SuppVersity - Nutrition and Exercise Science for Everyone

Can phospholipid-bound N-3s as in krill ward off the fat gain on a bulk?

Your daily visits, comments, feedback, criticism and obviously commendations are not only what makes the hours of work I invest into this blog worthwhile, they are also a constant source of "inspiration" and, as the latest post by Roy Nelson on the SuppVersity Facebook Wall goes to show you, oftentimes point me towards the most interesting stuff. In that, it does not really matter that Roy's question was more or less unrelated to what I personally found absolutely newsworthy in the study he referenced, a study which deals with fish oil supplementation and its *yawn* anti-inflammatory effects.

You learn from me, I learn from you

Now, I guess some of you are similarly fed up with those rodent studies like I am, but bear with me folks, Roy did in fact shoot the bulls-eye with this one (not sure if you realized that Roy, but you did ;-) After all, there was a certain twist to this study. A twist you have actually read about on the suppversity roughly 7 month ago, in a post with the suggestive title "Phospholipid or Triglyceride? What's in Your Fish Oil Caps? Only Phospholipid Based DHA+EPA Reduces Fat Cell Growth & Elevated Insulin Levels Despite Obesogenic Diet" (read more). Both studies, the one at hand, which was published only a couple of days ago in Nutrition & Metabolism, as well as the "old" study by Rossmeisel et al. (read up on the results), dealt with the difference between the "real-rodent-world" differences between triglyceride and phospholipid based n3-PUFAs.

Why are you talking about "n-3 PUFAs" and not simply about fish oil? There are actually two reasons, I am trying to avoid the term "fish oil" in this context. Firstly, real fish has both, triglycerides which make up >90% of the fat in fatty fish like salmon & co. And secondly, the way fish oil supplements are produced usually removes the last phospholipid fractions leaving you with nothing but the triglycerides (another reason to stick to fish as an animal, instead of fish as a gelatine cap ;-)

Rossmeisel et al. have already been able to show that the phospholipid-bound n-3 PUFAs (DHA and EPA) posses physiological effects the cheap triglycerides don't have to offer: They decrease the size of the fat cells and thus provide a structural advantage, the common triglyceride-bound forms of DHA and EPA do not have to offer.

Why is a smaller adipocyte size significant?

Remember the post on choline as part of a weight loss stack (read more)? Guess what: Choline is also part of most phospholipids.

I have been dabbling with adipocyte sizes in previous posts and freely admit that this is a too complex matter to actually support the statement that "small adipocytes are best" (learn more in previous posts).

In a hypercaloric diet scenario, as the one in the study at hand, a decreased adipocyte size may yet well be considered the structural foundation of reduced baseline inflammation. after all, the size or you could as well say the filling level o the fat cells is directly associated with the amounts of pro-inflammatory cytokines they release (Skurk. 2007).

For those of you who are in fact dabbling with high levels of fat-induced inflammation (these are often the skinny fat guys and girls), this alone would therefore warrant the investment in Krill instead of fish oil, if you can't or don't want to get your dietary phospholipids from fresh fish. The new findings the study by Manar Awada and his (or her?) colleagues from the CarMeN Laboratory in Lyon, France, brings to the table are yet probably a more convincing argument for the majority of physical culturists:

Phospholipid-base N3-PUFAs reduce will cut body fat even on a HFD diet

Yep, that's right. If the results of the Awada study translate 1:1 from you rodents to physical culturists, you could infact up your caloric intake by 50% and still lose 14% body fat compared to following a "species-appropiate diet" (in the case of a rodent that's obviously a high carb diet, with a macronutrient ratio of 19.1% protein, 57.6 carbohydrates and12.8% fat in it).

Figure 1: Energy intake and body composition (left) and lipid, glucose, insulin and leptin levels (right); data expressed relative to values from the regular low-fat chow group (Awada. 2013)

Now the data in figure 1 and the notion that you could cut body fat on a bulk certainly sounds too good to be true and to be honest, I have my doubts that someone whose following all the nutritional advice you get on the SuppVersity on an almost daily basis will see identical "real-human-world" results (specifically if your diet already contents phospholipid bound N3-PUFAs, which it will if you follow my advice to have fish once or twice a week). But let's be honest, if the consumption of phospholipid bound DHA and EPA at a dosage of 0.08g/kg body weight did nothing but blunt the almost inevitable fat gain on an intense (+50% increase in energy intake) "bulk", that would be awesome - wouldn't it?

What are the underlying mechanisms, here?

Krill protein offers non-negligible health benefits, as well (learn more).

I know many of you mainly interested in the practical implications, but especially, when we are dealing with data from rodent studies, we have to understand how a supplement works, in order to tell something about the probability that it will work in humans as well.

Against that background, it's well-worth to take a final look at those cellular parameters that may provide some clues on what it is that makes the phospholipid forms of DHA and EPA so superior compared to their conventional triglyceride counterparts.

Aside from a highly more pronounced increase in intra-cellular vitamin E (2.8x higher than HFD alone and 1.5x higher than HFD + triglyceride-bound omega-3s), there were yet unfortunately no statistically significant inter-group differences. Even in conjunction with the (probably related) yet statistically non-significant difference in markers of lipid peroxidation (4HHE 104, 89, 128nM and 4HNE 13, 6, 9nM in high fat, high fat + PL and high fat + TG, respectively), this is simply not enough to gain insight into the underlying mechanisms which lead to these highly desirable anti-obesity effects. So that we will, for better or worse, have to contend ourselves with the scientists' own conclusion that "further research is required to better understand the mechanism of action of PL carrier".

Figure 2: The PL N-3 content (g/100g dry mass) of fish is very heat stable compared to the triglyceride fraction of which are partly (baking) or totally (frying) lost when you process the raw fillets (Mai. 1978). So even if your fish has a relatively low PL content, that will at least remain where it is supposed to be ;-)

Bottom line: Without knowing the underyling mechanism and in the absence of respective human data, I am honestly hesitant to suggest you go and buy tons of krill oil supplements. After all, the human equivalent dosage of the amount of phospholipid bound DHA+EPA that was used in the study at hand amounts to ~6g per day. So even if found a product that's 100% phospholipid, 0% triglyceride you would have to take ~30 1g caps of regular krill oil which usually have ~200mg of DHA and EPA in them.

So unless you happen to have a cheap source of the purified omega-3 phospholipids the scientists used in their study, it will probably be more prudent to wait for the third SuppVersity post on this matter and invest the buckloads of money this will save you into fresh fish fillets.

References:

Awada M, Meynier A, Soulage CO, Hadji L, Géloën A, Viau M, Ribourg L, Benoit B, Debard C, Guichardant M, Lagarde M, Genot C, Michalski MC. n-3 PUFA added to high-fat diets affect differently adiposity and inflammation when carried by phospholipids or triacylglycerols in mice. Nutr Metab (Lond). 2013 Feb 15;10(1):23.
Mai J, Shimp J, Weihrauch J, Kinsella JE. Lipids Of Fish Fillets: Changes Following Cooking By Different Methods. Journal Of Food Science. 1978; 43: 1669–1674.
Skurk T, Alberti-Huber C, Herder C, Hauner H. Relationship between adipocyte size and adipokine expression and secretion. J Clin Endocrinol Metab. 2007 Mar;92(3):1023-33.

Lots of good meats on Fury from the slaughterhouse ;-)

I am not sure if all of the US and other international students of the SuppVersity have already gotten wind of the huge "scandal" *rofl* about horse meat in convenient foods. In case you ain't no clue what I am talking about, here is the gist: About a week ago the first reports surfaced that some of the junk... ah, I mean instant meals that are sold by the largest supermarket chains in Europe and produced by such "reputable" companies as Nestlé and Co. are "adulterated" with horse meat (if you want to, you can read up on the whole story in the online version of the NY Times; read more).

Actually things started out with frozen Lasagna and now horse meat appears to be in everything the average convenient food lover packs into his shopping basket. Now, frozen lasagna (unless self-prepared) is nothing I would expect the average SuppVersity reader to consume on a regular basis, anyway. And the mislabeling of the products alone would certainly not qualify as being "SuppVersity newsworthy", either. The fact that it may be a smart move of yours to actually buy horse-meat lasagna (obviously not the one that was made with the meat of potentially sick animals) instead of regular one is however exactly the kind of stuff you read about here at the SuppVersity - and I would venture the guess only at the SuppVersity.

"Horse meat? You're kiddin' right?"

If we disregard the argument that horses are "amiable animals" that are "not supposed to be eaten" that's brought forward by many of the costumers as their main rationale why they would not buy horse-meat lasagna or a "Mac Fury" (would certainly be a major advantage over the other "Mac's" you are served at everyone's favorite fastfood chain ;-), there are actually no convincing arguments against the consumption of horse meat.

There is another study, unfortunately in Russian that reports 54% reduction in excess body weight in overweight individuals, whose diets contained obviously significant (yet in the abstract undisclosed) amounts of horse meat, of which the scientists write that it is "a product that possesses lipotropic and choleretic properties" and was the main reason for the "markedly" reduction in body weight, the participants experienced. Moreover, the latter went hand in hand with "a considerable improvement of liver function" (Kadyrova. 1984). Without access to the full-text, I am yet unable to say anything but "interesting" about this study... although, I guess I may add that it is not just interesting, but intriguing that these two were the only horse meat based dietary interventions I could come up with.

That being said, it's certainly no coincidence that the editors of the International Journal of Food Sciences and Nutition decided to finally include the 2012 paper by Chritian Del Bo et al. that has hitherto only been available as an ePub in the March 2013 issue of this monthly Journal. In the said study, the researchers from the Dipartimento di Scienze per gli Alimenti, la Nutrizione e l'Ambiente (that's what I call a well-sounding name ;-) at the University of Milano investigated the "long-term" (=90 days) effects of regular horse meat (2x 175g per week) consumption on the health of 26 of the 52 healthy volunteers who participated in their study and compared them to the 26 participants who were told to abstain from horse-meat for the full three months study period. The results were absolutely unequivocal: Horse meat, as red and culturally depreciated as it may be let to..

significant reductions in serum levels of total (-6.2%) and low-density lipoprotein cholesterol (LDL; -9.1%) and transferrin levels (- 4.6%), as well as
increases in total omega-3 content /+7.8%), omega-3s (+8%) and docosahexeanoic acid (DHA; +11%) in the red blood cells of the subjects (p < 0.005 for all)

As exciting as these observations may sound, the study design makes it difficult to say whether they were a result of replacing horse-meat for other meats or simply eating meat at all (I know you that common wisdom tells us that red meat kills, but you've heard me talk about the fallacy of this assumption on one of the last installments of the Science Round Up).

Aside from the common (and flawed) wisdom about the ill health-effects of meat eating aside, there is another important and obviously way more convincing argument for the former explanation (replacement effects), which pertains to the omega-6 to omega-3 ratio in horse-meat.

Table 1: Omega-6 (N6) to omega-3 (N3) ratio of selected foods (extended version of Bourre. 2005)

With an omega-6 to omega-3 ratio of 0.6 and thus 1 gram of omega-6 fatty acids per 1.7 grams of omega-3s, horse meat is almost on par with farmed salmon (see "Making the Right Fish Choices") and far superior to grass-fed beef, which contains 2 grams of omega-6 fatty acids for every single gram of omega-3s (n-6/n-3 ratio of 2.29; see previous SuppVersity post).

"Hold on! Where is the downside? Where the "on the other hands?"

With 100g of horse meat offering 21g of quality protein, 5g fat (approx. 1g saturated fat, 2g monounsaturated fat and 1g PUFAs) and obviously zero grams of carbohydrates, the ideal protein source, but wait: All this does in fact sound a little "too good too be true" and there are in fact a couple of "on the other hands" attached:

The Lance-Armstrong factor: As already mentioned before, there is currently a large concern about medicine residues in the horse meat that was added to the instant meals over here in Europe. Yet despite the fact that you can certainly argue that there is a certain chance you would be eating a former race-horse, which collapsed from an overdose of performance enhancing drugs, regular horse meat is as tightly controlled as all other meats and your chances to consume consume any sort of medication are thus not higher lower than with other meats, as long as you don't buy them on the gray market in Romania (where the horse meat in the scandal is supposed to come from) or China ;-)

I guess you may have heared about toxoplasma gondii being transfered from rodents to cat and accidentally to humans, but do you also know that infected men have higher testosterone levels? No? Well, in the end this is not a recommended way to up your testosterone production, anyway (lean more)

The nasty bugs factor: Another commonly heard argument against eating horse-meat is based on some horror stories about people dying from bacterial infections after consuming old, imported and improperly stored (the scaremongerish reports obviously don't mention that) raw horse-meat (Gill 2005). This is obviously another non-horse-specific problem and can be easily avoided by buying your meats from the right sources and heating them to temperatures >67°C. The heat will also take care of any Toxoplasma gondii contaminations and the larvae of Trichinella. Both parasites are often named in the same breath as "horse meat", despite the fact that they are not horse-specific and have almost exclusively been found in meats imported from overseas (Pozio. 2001; Pomares. 2011).

The polar-bear factor:Just as in the case of the polar bears this does not affect the meat of the horses, but their organs. Depending on the soil on which the horses were housed, their livers and kidneys may contained high amounts of heavy metals (cadmium, Gill. 2005; lead, Kosla. 1989) and are thus not recommended for human consumption unless prior testing was done.

So, basically this leaves us with only one "on the other hand": The "I don't want to eat Black Beatuy or Fury" Factor. But let's face it: Who of the bacon lovers would say he'd like a piece of Babe?

You have been eating dozens of "Babes" and now you refuse to eat the much healthier Black Beauty?

Bottom line: Unless your horse meat is imported from questionable sources, the only valid argument why you shouldn't eat horse meat, and maybe even prefer it over beef, let alone pork, are your own scruples culturally rooted scrouples about eating such a "noble" animal as a horse.

And by the way, when it's cooked its pretty hard to distinguish from beef, anyway. Only when you eat it raw (which is something I don't recommend) you may be able to recognize the slight tinge of sweetness that's a result of the 7x higher glycogen content of horse vs. beef meat.

References:

Bò CD, Simonetti P, Gardana C, Riso P, Lucchini G, Ciappellano S. Horse meat consumption affects iron status, lipid profile and fatty acid composition of red blood cells in healthy volunteers. Int J Food Sci Nutr. 2013 Mar;64(2):147-54.
Bourre, JM. Where To Find Omega-3 Fatty Acids And How Feeding Animals With Diet Enriched In Omega-3 Fatty Acids To Increase Nutritional Value Of Derived Products For Human : What Is Actually Useful. The Journal of Nutrition, Health & Aging. 2005; 9(4): 232-242.
Gill CO. Safety and storage stability of horse meat for human consumption. Meat Sci. 2005 Nov;71(3):506-13.
Kadyrova RKh, Salkhanov BA, Shakieva RA. [Effect of diet therapy using horse meat on liver function of patients with metabolic-alimentary obesity]. Vopr Pitan. 1984 May-Jun;(3):22-7.
Kośla T, Anke M, Grün M. The lead status of horses from central Europe depending on breed, sex, age and living area. Arch Tierernahr. 1989 Jul;39(7):667-74.
Pomares C, Ajzenberg D, Bornard L, Bernardin G, Hasseine L, Darde ML, Marty P. Toxoplasmosis and horse meat, France. Emerg Infect Dis. 2011 Jul;17(7):1327-8.
Pozio E, Tamburrini A, La Rosa G. Horse trichinellosis, an unresolved puzzle. Parasite. 2001 Jun;8(2 Suppl):S263-5.
Wise J. "Bute" in horse meat presents very low risk to health, says England's chief medical officer. BMJ. 2013 Feb 15;346:f1066.

While this installment of Adelfo's SuppVersity guest posts actually deals with the "optimal" exercises and form - I personally would say that physique-wise Adelfo is likewise on a good way towards achieving a form or rather overall physique even the most critical judges will have a hard time to ignore on the upcoming 2013 Wheelchair Nationals in March (learn more at wheelchair-bodydbuilding.com)!

Ok folks, the good news is, there is the promised update from your's truly Adelfo Cerame - what's even better: Adelfo is giving away some of his secrets discussing his favorite exercises for chest, back and arms, as well as the most common mistakes which forestall training progress.

The bad news is, there is no Science Round Up today and what's even worse is the sad reason for the unplanned break. Carl's mother passed away earlier this week and it goes without saying that the next round of "science news sniffing" will have to wait till next week.

If you can't wait so long, I suggest you go check out the latest SuppVersity facebook news. There are a couple of pretty interesting things there, but my absolute personal favorite is the latest study from Ristow's group at the University of Jena over here in Germany which has the potential to send the stupid "starve yourself to a longer life by reducing the metabolic rate and thus ROS generation"-hypothesis finally back into the dark abyss, from which it spread and infected scientists, the laypress and ultimately even a large parts of the public like the pest (read more). But enough of that, let's check out what Adelfo has to tell us about his favorites and your (?) mistakes.

Stick to the basics, not because you are a beginner, but because you are a pro!

This year under the tutelage of coach Alberto I have learned that especially experienced (or should I say even say seasoned ?) bodybuilder or weightlifter like myself should stick to staple exercises rather than doing each exercise he knows just to end up spreading himself thin in trying to do a new dance every time.

If you want to add to the staples, why don't you incorporate for increased strength & size gains (learn more).

A lot of lifters feel that they need to change their exercises every time when they feel they are no longer sore the next day or no longer feel the stimulation that they used to feel, when they first started (I was very guilty of this as well), in the past months, however I have learned that you’re not plateauing just because you’re “not feeling it” any more. You are actually improving on that exercise as you continue to perfect your craft. The reason you feel challenged most of the time, when you change your routine or perform a new exercise is 'cause you’re just learning a new dance- and this has little to do with "tricking your muscles".

Not that there’s anything wrong with changing routines or doing different exercise from time to time, I just learned that it’s more beneficial to pick a small staple of exercises that you can improve your craft in and have those variety of exercises to keep in your back pocket for those special occasions on which you may need them.

My favorite exercises and everyone's favorite mistakes

As mentioned before, I commit guilty of doing way too much exercise hopping in the past, as well. This year, however, I have really zoned in a couple of carefully selected staple moves, hit the individual body parts more frequently and tried to perfect my craft on each of of the exercises in the following list:

Video 1 (click to watch): Adelfo doing the wheelchair version of the Gironda Dips. Actually this is an older video, but if everything works out the way we planned it you will be able to watch him do more of the exercises in this list in the next installment of Adelfo's guest-posts.

Chest (A) - Weighted dips: This is one of my favorite chest exercises. I love weighted dips because it liberates me in a way from getting away from the norm of exercises when being in a chair, the same feeling of liberation I get when I do laps in the swimming pool for my cardio sessions. For me weighted dips (especially the Vince Gironda version, see video 1) really stimulates my chest like a decline movement would because you can control the depth and angle of how low you can go and really dig to get that stretch.

Chest (B) - Bench Press (flat angle): This is an exercise that I’ve had a love/ hate relationship with since high school. Just like every young man who picks up a weight, the bench usually tends to be the first exercise that we gravitate to. Ever since my spinal cord injury, the bench and I have been on rocky terms…

I guess due to the fact that I really didn’t feel comfortable or confident enough in my mobility to be able to get back on that saddle again so I avoided it like the plague most times and stuck to chest press exercises like the hammer strength and smith machine. Eventually as my confidence in my abilities (via mobility and balance) improved, so did my eagerness to get back under the barbell of a free weight bench and my love for the good old flat bench returned.

Figure 1: As this figure from the chest article in the SuppVersity EMG Series goes to show you, the barbell flat bench is still the "king" - well, at least as long as you don't compare it to it's brother, the BB bench press on a decline (learn more)

The flat press bench is one of the few core compound exercises that I can take pride in. Most people have squats, deadlifts and cleans, but obviously I cannot perform any of those exercises, so the only one I have left is the bench. I guess that's part of why I really take proud in each lbs I have been able to add to the bar over past years of training. Funnily it was only this year that I have finally been able to perfect my techniques. Without the leverage from my legs, I obviously have certain disadvantages compared to most of you and it took me years until I discovered that I could mimic engaging my glutes and arching my back so that I can use my whole body to push the weight rather than just arms and chest by tying a weight belt around my hips.

I have also embraced using a closer rather than my preferred wide grip that I have done all my life (that's actually something I read about in the EMG Series, here at the Suppversity, but never really implemented). The close grip has helped me tremendously in finally getting rid of my constant nagging shoulder pains and had me finally realized that I can indeed touch the bar with my chest and thus go over the full range of motion without any pain in my rotator cuff, whatsoever.

Chest (M) - "M" as in mistakes → Quarter presses!You know those guys, right? Those guys who load up the squat rack with tons of weight and then perform bench presses over what can hardly count as a quarter press (=going over just 25% of the range of motion)...yeah, I see you know them ;-) It's a mere waist of time and in the end you just have to look at the physiques of the "quarter presseres" to see that without going over the full-range of motion, focusing on the positives as well as the negatives and sticking to weight you can un-rack yourself your results will be "quartered", as well.

* * * * * * * * *

Adelfo says: "Hammer strength high rows, Hammer strength seated rows and unilateral vertical rows are the 3 main staple exercises I used to build my back this year."
Back (A) - Weighted Chin-ups: Even though I haven’t been able to do them in a while (due to unknown MRI results that my doctors are trying to figure out), this is by far my favorite back exercise to perform, it really allows me to stretch and isolate the lats and pull maximal weights. It also helps build a strong core. In fact, I personally believe that weighted chin ups are a way superior "abs" or rather core exercise than those stupid crunches everybody is doing for hours.

Back (B) - Hammer Strength High-Rows: This is what I call a very wheelchair friendly machine (well for me at least…): It’s easy to transfer unto and very versatile. I can go from regular high rows to single arm high rows without out having to make much adjustment. I feel that the frequency of being able to train my back with this machine alone has been able to help me bring up my back this year.

Back (C) - Hammer Strength Seated Rows: I like this exercise because it’s simple and efficient. It’s basically like a T-bar row for me but seated, and since it is chest supported, I can really go heavy without it catapulting myself of the machine.

Back (D) - Unilateral (vertical rows): This is actually one on the newest exercises that I learned from Coach Alberto and has really helped bring up my lower lats. It’s basically a unilateral vertical row with a spinal flexion movement/squeeze at the end to really engage the lower lat muscles. I have basically ditched the lat pulls for this exercise.

Back (M) - "M" as in mistakes → Chins gone wrong: People oftentimes don’t tense up their lower extremities and stabilize their pelvis and hips. It makes it a lot easier in my opinion to keep the core nice and tight and locking the hips and pelvis, to keep the lower extremities stale. Thus you won't be swinging back and forth, and you can actually focus on engaging your lats when doing a chin-up.

* * * * * * * * *

Adelfo says:"DB overhead presses, hammer strength overhead presses and DB lateral raises were the 3 staples exercise I used to build my shoulder and delts." And if you go by the looks there must be something to those moves, don't you think so?

Shoulders (A) - DB overhead press: I love DB overhead presses because the DB’s allow you to control the direction your shoulders go – I like to stay tight and keep my overhead movements compact and the DB’s allow me to do so. I also feel more connection with DB movements.

Shoulders (B) - Hammerstrength overhead press: I use this on my strength days. Due to my disability and mobility, I have limits on how heavy I can go on DB’s if I do not have my training partners with me, so the hammer strength overhead exercise allows me to go heavy without having to worry about safety issues or having spotters.

Shoulders (C) - DB lateral raises: Again, with lateral raises, I love using DB’s because of the range of motion it allows. I wont be able to lift as heavy as I would on a machine but I feel that I stimulate my delts more efficiently using DB’s.

* * * * * * * * *

The biceps brachii attaches directly to the shoulder joint and is probably the most overtrained body part of the male body ;-) Don't be a fool and do all the exercises you know. Rather pick those that work best for you - regardless of whether they are #1 or #5 in the EMG ranking - the activity is almost identical, anyway (read the details)

Arms (Biceps) - DB Biceps Curls: No preacher, forearm reverse, or EZ-bar curls, just DB’s this year. I either go with a regular or hammer grip. Again DB’s allows for better range of motion for movement

Arms (Triceps) - Triceps Extensions with rope: I’ve been sticking to the rope mostly this year. Either press downs or single-arm extensions.

Arms (M) - "M" as in mistakes → The DB, barbell, hammer, reverse, SZ-bar curl: Believe it or not but the most common mistake, when training arms is not doing one of the staples wrong, but rather not having a staple at all. That's particularly true for the biceps exercises where you see (funnily only) guys "hit their arms from every angle". Funnily those are the same people who will then come up to you and ask you which additional exercises you would do to build "those impressive biceps" *rofl*

Well that’s all I have for today but stay tuned next time as I will compare notes from this year to last years contest prep notes, from nutrition to training and how I mentally approached both preps… This was a topic suggestion by Primalkid,by the way ;-)

Don't be fooled. DHEA won't allow you to train forever day in and day out the study at hand does yet add to previous results which already suggested that it could have its merits whenever intensity and workloads are high (learn more)

I don't know if you have noticed, but as of late, there has been a definitive testosterone deficiency as far as the topics of the daily SuppVersity news are concerned. With today's article on the use of 50 mg of dehydroepiandrosterone aka DHEA "pre-workout" this will change dramatically (read all previous articles on DHEA). Why? Well, the protocol the researchers from the Taipei Physical Education College, the China Medical University, the Asia University and their overseas colleague from the University of Texas at Austin describe in their recently published paper will yield age-dependent increases in free testosterone ranging from +100%, for the twens, to +300% for the men in their prime of their lives (~49 years).

I see, guys, I got your full attention, now! And for the ladies, ...

... who may now believe that this article wasn't for them, I have a 2008 study from Steroids, one of the journals dealing with endocrine issues, which shows that DHEA is an important player in subcutaneous fat reduction in women (Hernandez-Morante. 2008), as well as a study in hypoadrenal women (any one suffering from the athlete's triad probably qualifies for self-induced hypoadrenalism, learn more) from Diabetes the journal of the American diabetes association showing profound improvements in insulin sensitivity after 12-weeks on 50mg/day DHEA. So don't click this article away, thoughtlessly, ladies!

5x 1 min is obviously not the only sensible HIIT protocol. Read the SuppVersity Series on Making HIIT a HITand find out which HIIT-style would be right for you (learn more)

50mg that was, as mentioned in the introduction also the dosage Liu et al. gave their sedentary young (aged 21.4±0.3 years, N=8) and middle-aged (aged 49.3±2.4 years, N=8) male participants 12 h before the exercise challenge under supervision of staff personnel. This exercise challenge was a standardized High Intensity Interval Training (HIIT) comprising 5x2min of cycling at 100% VO2max with 1 min rest between each cycling interval. The exercise was perfomed at 9:00AM and in a fasted state. The latter is probably significant, as the hormonal response of the adrenal gland - albeit only that of cortisol (cf. Labsy. 2013) - depends on the time of the day with a 2-3x higher response in the morning compared to the afternoon (cf. Thuma. 1995; Oskis. 2012).

This protocol was meant to shed some light unto the hitherto unknown effects of DHEA supplementation on testosterone levels during the recovery period after a bout of vigorous exercise. Interestingly, enough, you as a Suppersity addict (or soon to be addict ;-) will be aware that DHEA's beneficial effects on recovery in general have actually been proven - even in a scenario of temporary overreachig (=strategic overtaining for a short time period to elicit a maximal training stimulus; see figure 1 and read all the details in my May 2012 article).

Figure 1: Changes in DHEA-S serum levels and exercise induced elevations of creatine kinase =marker of muscle damage) in 16 healthy untrained college aged men receiving 100mg/day DHEA or placebo during a 5-day "mixed-type exercise" regimen (this graph was originally discussed on May 27, 2012 and is based on Liao. 2013)

While the dosage in the study at hand was 2x lower than in the Liao study and administered only once, it could still give us some insights into whether or not the decrease in creatine kinase (and thus muscle damage) Liao et al. observed in 2012 (the study was officially published only 1 month ago) was accompanied by an increase in total and/or free testosterone. Aside from the DHEA-S levels and the amount of luteinizing hormone (LH), the latter were the two main study outcomes in the Liu study (see figures 2 & 3):

Figure 2: Dehydroepiandrosterone (DHEA-S) and total testosterone levels (TT) during the interention; the asterisk (*) over the TT bars signifies significantly different from placebo in the same age group (Liu. 2013)

If you take a closer look at the data in figure 2 you will realize that there were increases in total testosterone in both groups. Contrary to the very unsurprising increase in DHEA sulfate, the latter were yet only significant in the middle-aged study participants (mean age 49 years).

"Nice, but where's the data on cortisol and what about free test & LH?"

What is not shown in figure 1 are the cortisol levels of the study participants, which were not significantly different at baseline. After the exercise intervention, the levels did yet increase significantly - irrespective of whether or not the participants were young or middle aged or received the placebo or the actual DHEA pills. Intriguingly, the drop that occured after 24h in both age groups was much more pronounced in the middle-aged guys.

Figure 3: Free testosterone and luteinizing hormone levels during the intervention (Liu. 2013)

Contrary to the total testosterone levels, the amount of free testosterone increased significantly in both, the young and old study participants (see figure 3), it actually goes without saying that

"[...] the free testosterone to cortisol [FT/C] ratio increased significantly during the training recovery for both the middle-aged and young control groups." (Liu. 2013)

Now all that is good news, but what's even better news is that, at least in the short run, these profound elevations in free testosterone did not lead to lower levels of the "testosterone production trigger" luteinizig hormone (LH), which is released by your hypothalamus and tells your testes to produce more sex hormones. Now why is that important? Well, the answer is simple, a reduction in LH is not just a sign of the dreaded HTPA shut-down, it is the shutdown - or I should say the mechanistic cause of being "shut down" (=not producing any or too little sex hormones on your own).

Ok, higher T levels, lower testosterone to cortisol ratio, but what about estrogen?

A note on performance and estrogenic side-effects: An 8-week exercise intervention by Brown et al. which used 50mg DHEA /day combined with 3x total body workouts per week did not produce significant changes in any of the study parameters. Neither beneficial ones, such as greater strength increases or hypertrophy, nor negative ones such as increases in estrogen or deteriorations of the lipid profile (Brown. 1999). In 2010, on the other hand, Ostojic et al. reported that 4 weeks of 100mg DHEA, despite having no effects on the body composition of the 19-21 year-old soccer players who participated in the study, led to statistically significant increases in total testosterone (+37%), DHEA-S (+197%) and estradiol (+21% compared to the subjects in the placebo group; Ostojic. 2010). The overall significance of these results is yet questionable, since both studies were pretty underpowered (N=10 and N=20 for Brown and Ostojic, respectively). It is still noteworthy that the DHEA induced "estrogen dominance", which is one of the most frequenly heardt arguments against DHEA supplementation was not observed in either of the two studies.

If the above is the question that's just praying on your mind, then this is probably not the first article on DHEA administration you've read and what's more, the other ones were probably not published on the SuppVersity. While it is true that a handful of previous studies have in fact shown an increase of estrogen in response to the administration of DHEA, the important ratio of testosterone to estrogen was maintained even in the majority of those studies, where this effect was observed (for more details read the text in the red box on the right).

Regardless of how "real" the danger of elevated estrogen levels may be, there is actually another way more important question to be answered, which pertains to the sustainability of the results. In view of the fact that the DHEA was only administered once, it is way more likely that the unquestionably beneficial effects the scientists observed could be of very transient / short-lived nature. The minimal changes in luteinizing hormone for example could well become significant (and negative) in the long run. After all a +100% increase in free testosterone is nothing your body is going to ignore for weeks. It's more likely that it will slowly bounce back to the former steady state by either reducing the production of testosterone or that of DHEA.

So even if it's unlikely that the small dosage of 50 mg would eventually shut you down, you may well lose the benefits after one months of continuous supplementation.

That being said, you could also argue that the exogenous DHEA has, just as TRT or performance enhancing drugs, the advantage of not being subject to diet-, training- and obviously age-induced reductions in their endogenous production. If any of the latter reminds of a situation / period of your life you are in, your chances of seeing benefits would at least be higher - whether they would be high enough to actually manifest in beneficial training outcomes remains questionable, though.

It is unfortunate that science gave up on DHEA, when it became clear that it's not the fountain of youth. I mean, greater fat-inhibition effects than testosterone are nice, no (learn more about those)?

Bottom line: The new information the Liu study has to provide does actually go hand in hand with what the data from the Liao study already suggested. The purported "fountain of youth" hormone has potent ergogenic effects in training scenarios, which focus on vigorous physical activity.

Unfortunately, the evidence from these short-term interventions does not tell us anything about the beneficial and detrimental effect the low and high dose protocols from the Liuand the Liao studies will have. Personally I would assume that the benefits will wane off, but in the absence of corresponding studies, this is mere guesswork. After all, 99% of the previous research on DHEA has been done in sedentary old men and women. Few trials investigated the effects on young or middle aged subjects and less than a handful did that in an exercise scenario with any resemblances to yours or mine.

So there is probably need for at least another SuppVersity article (obviously based on a novel study), before you will hear me recommend the use of DHEA as an ergogenic supplement. Now, if you want to make sure, you don't miss that, I suggest you start following the SuppVersity on Facebook, Twitter or simply with your favorite RSS reader (click here to get to the channel ;-)

References:

Brown GA, Vukovich MD, Sharp RL, Reifenrath TA, Parsons KA, King DS. Effect of oral DHEA on serum testosterone and adaptations to resistance training in young men. J Appl Physiol. 1999 Dec;87(6):2274-83.
Hernández-Morante JJ, Pérez-de-Heredia F, Luján JA, Zamora S, Garaulet M. Role of DHEA-S on body fat distribution: gender- and depot-specific stimulation of adipose tissue lipolysis. Steroids. 2008 Feb;73(2):209-15.
Labsy Z, Prieur F, Le Panse B, Do MC, Gagey O, Lasne F, Collomp K. The diurnal patterns of cortisol and dehydroepiandrosterone in relation to intense aerobic exercise in recreationally trained soccer players. Stress. 2013 Mar;16(2):261-5.
Liao YH, Liao KF, Kao CL, Chen CY, Huang CY, Chang WH, Ivy JL, Bernard JR, Lee SD, Kuo CH. Effect of dehydroepiandrosterone administration on recovery from mix-type exercise training-induced muscle damage. Eur J Appl Physiol. 2013 Jan;113(1):99-107.
Liu TC, Lin CH, Huang CY, Ivy JL, Kuo CH. Effect of acute DHEA administration on free testosterone in middle-aged and young men following high-intensity interval training. Eur J Appl Physiol. 2013 Feb 17.
Oskis A, Clow A, Thorn L, Loveday C, Hucklebridge F. Differences between diurnal patterns of salivary cortisol and dehydroepiandrosterone in healthy female adolescents. Stress. 2012 Jan;15(1):110-4.
Ostojic SM, Calleja J, Jourkesh M. Effects of short-term dehydroepiandrosterone supplementation on body composition in young athletes. Chin J Physiol. 2010 Feb 28;53(1):19-25.
Thuma JR, Gilders R, Verdun M, Loucks AB. Circadian rhythm of cortisol confounds cortisol responses to exercise: implications for future research. J Appl Physiol. 1995 May;78(5):1657-64.

Won't take long until China is the world economy #1 and not much longer until they are the fattest economy, as well ;-)

Let's see which one do I pick? Oh, ok... The SuppVersity Figure of the Week is 0.19. This is the correlation coefficient that describes the statistical relation - which is as every SuppVersity student knows no evidence of causal relationships (!) - between the per capita gross domestic product (GDP) and the prevalence of obesity as it was calculated by Mario Siervo and colleagues from the Newcastle University and the UCL Institute of Child Health in London as part of their analysis of country-specific prevalence estimates of overweight, obesity and hypertension and their relation to nutrient and food intakes and (and this is new!) the economy (Siervo. 2013).

The scientists used the WHO Global Infobase database, year- and country-specific Food Balance Sheets (FBS) and information on urbanization rates, per capita GDP and physical inactivity and did so much statistical shenanigan that of all the baseline correlations (incl. milk consumption and egg consumption, as predictors of obesity and high blood pressure) only the already mentioned per capita GPD, as well as physical inactivity (PA) and cereal consumption (CE) remained as highly significant predictors of being overweight (GPD), being obese (PA) and not being obese (CC). Statistical significant, but very low correlations were also observed for obesity and the relative energy intake from sugar (regression coefficient B = 0.03).

Makes me wonder what the addition of the average population-based magnesium intake would have had to contribute to the results... why? Well, the diabesity-protective role of magnesium is the first topic of today's installment of On Short Notice.

The importance of adequate magnesium intake can hardly be overestimated

The latest issue of the Journal of Nurtition (US) features yet another article showing how important adequate magnesium intakes are for an optimal glucose metabolism. Since a messed up glucose management it one of the root causes of most of the features of the metabolic syndrome, the results Adela Hruby and a ton of colleagues present in their latest paper are of great importance not just for individual, but also for public health. The latter is particularly true in view of the fact that the researchers who started out with the hypothesis that single nucleotide polymorphisms (SNPs ~= minimal genetic differences between person A and B) would explain / influence the potential differences of the association between magnesium intake and fasting glucose and insulin on an individual level.

It's not going to work for everyone but there is scientific evidence that 500mg/day magnesium can help with headaches (learn more)

To verify / disprove this hypothesis the researcher analyzed data from fifteen studies from the CHARGE (Cohorts for Heart and Aging Research in Genomic Epidemiology) Consortium . The studies provided data from up to 52,684 participants of European descent without known diabetes. In a fixed-effects meta-analyses, they quantified

cross-sectional associations of dietary magnesium intake with fasting glucose (mmol/L) and insulin (ln-pmol/L) and
interactions between magnesium intake and SNPs related to fasting glucose (16 SNPs), insulin (2 SNPs), or magnesium (8 SNPs) on fasting glucose and insulin.

After adjustment for age, sex, energy intake, BMI, and behavioral risk factors, the found that each 50-mg/d increment in magnesium intake was inversely associated with fasting glucose (β = −0.009 mmol/L, P< 0.0001) and insulin (−0.020 ln-pmol/L, P< 0.0001). Plus - and this is the actual news - these improvements (within a "normal" intake of magesium wa below the 2xRDA dose of 720mg) was not generally related to the individual genetic make-up of the healthy stud participants.

However, rs2274924 in magnesium transporter-encoding TRPM6 showed a nominal association (uncorrected P = 0.03) with glucose, and rs11558471 in SLC30A8 and rs3740393 near CNNM2 showed a nominal interaction (uncorrected, both P = 0.02) with magnesium on glucose.

Now what's interesting, here, is that previous studies investigating the effects of familial TRPM6 polymorphisms showed that a mutation / loss of the former SNP, i.e. TRPM6, will disrupt the regular magnesium flux in the kidney and epithelial tissue an is accompanied by hypo- (=low) not hyper-(=high) glycemia (Schlingmann. 2003; Chubanov. 2005).

Are there other reasons you may be set to be obese (learn more)?

These observations, as well as results from a case-controlled study by Romero et al. who did not find gene variations in TRPM6 and its cousin TRPM7 to "be useful predictors for T2DM risk assessment" (Romero. 2010). Clearly point towards the negligent effects genes have on the magnesium <> diabetes connection. In other words: Keeping an adequate magnesium intake is one of the easiest ways to reduce your risk of developing type II diabetes regardless of your genetic make-up.

What's the best magnesium supp? Cap, tablet or powder? Oxide, citrate, lactate, ...?

Speaking of solutions, magnesium and glucose management - Did you know that no-calorie sweeteners disrupt early response to glucose ingestion, reduce GLP-1 expression and could thus promote overeating (learn more)

Although the urinary excretion of magnesium after the ingestion of equal amounts of magnesium oxide in the form of everescent tablets vs. regular powder-filled caps is not a direct quantitative indicator of tissue accumulation (t's still better than the serum mg / creatinine ratio; cf. Bøhmer. 1990), the +100% increase in this parameter Siener et al observed in 2011 with the former preparation is still good evidence for the superiority of the highly soluble tablet preparation (Siener. 2011).

In a similar study, Marcelín-Jiméne et al. found that the pharmacokinetics of a single 500mg oral dose of Mg-valproate 500-mg ingested eiher as a solution, suspension, or in form of enteric-coated tablets were identical (Marcelín-Jiméne. 2009). So, if we discard the initial surge in magnesium with the solution an suspension that was absent with the enteric-coated tabs (they took ~2.5h to fully kick in) it is probably not necessary that you crush your tabs to make a "crushed tab magnesium suspension" out of them ;-)

I do yet suspect that you will probably be more interested in the results of one one of the most comprehensive evaluations of the consequences of chronic supplementation with different types of magnesium supplements, namely the inorganic magnesium salts MgCl2, MgSO4, MgCO3 and magnesium-acetate and their organic cousins in which the magnesium is bound to pidolate, citrate, gluconate, lactate or aspartate from a 2005 rodent study by Coudray et al.:

Figure 1: Plasma an bone (primary axis) as well as red blood cell (RBC; 2ndary axis(!)) content after 14 days of supplementation with identical amounts of magnesium in different organic and inorganic forms (Coudray. 2005)

Now regardless of which of these magnesium supplements you pick, one thing probably holds for all of them, if your levels are already saturated you will only increase the workload on your kidneys (Altura. 1994). Or put simply, if you pick one of the expensive versions such as mg-lactate the result is expensive urine (matches well with the tons of B-vitamins you hopefully peeing out and not retaining from your 12x overdosed "high potency B-supplement") - So, if you eat tons of magnesium rich foods already, save the money for more of those goods foods.

Review underlines the importance of adequate energy intake in reproductive function

Figure 1: Reproductive hormone changes in exercising cynomolgus monkeys undergoing energy restriction (Williams. 2001)

Everyone who has read all parts ot the SuppVersity Athlete's Triad Series has hopefully absorbed the message that "under-eating" is the main reason for the endocrine disturbances in both men and women. The latter and the non-significance of cortisol outside of its function as a glucocorticoid (=hormone that does everything to keep your blood glucose from dropping) is also what Fuqua and Rogol emphasize in their latest review of the literature (Fuqua. 2013):

The data in figure 1, which shows parameters of the endocrine . function of female monkeys who were placed on a fixed caloric intake and then trained to run on a treadmill for increasing lengths of time, shows that after only 2 blocks, the reproductive function was totally lost (again, usually male mammals remain fertile, but often loss of libido, sexual dysfunction, as well as depression and the obvious weight loss and exercise performance plateaus are non-sex-specific).

As Fuqua et al. point out, the onset of amenorrhea was accompanied by decreases in gonadotropins, estradiol, and progesterone. In that, the endocrine hormones are yet nothing but "slaves" to the changes in ghrelin, leptin and PYY, of which particularly the former, i.e. ghrelin suppresses pulsatile LH secretion in adult men and women. If you are interested in learning more, check out the Athlete's Triad Series, if you haven't done that already.

Glutamine & maltodextrin keep anaerobic power up to the last sprint

It wasn't part of the post of PWO glucose repletion, but theoretically glutamine could help here as well.

In an article that was published ahead of the next print issue of the Asian Journal of Sports Medicine Roohi and Khorshidi, two researchers from the Tehran University of Medical Sciences report that the ingestion of both 50 mg of maltodextrin and/ or 0.25g/kg body weight glutamine has significant ergogenic effects on repeated sprint performance.

What's interesting about this study is that the participants were all "well-trained physical education students who were participating in a training regimen (three or more days a week for at least an hour)" and not the next best sedentary volunteers the scientists were able to find (most importantly, they were not smoking water pipe - you got to love those cultural differences ;-)

As you can see in figure 2 the provision of the supplements two hours before the first of three RAST test, which consisted of 6x35m discontinuous all-out sprints, with 10 seconds rest between the individuals sprints (all six sprints are one bout), did yield ergogenic effects from the very first exercise bout on.

Figure 2: Minimal and maximal power on subsequent 6x35min sprints (1h in between bouts) with or without matlodextrin and/or glutamine supplementation 2h before the workout (Raahdi. 2013)

Statistical significant were yet only the difference between the placebo supplement (water) and the combined treatment during the third of the RAST tests. What's particularly interesting is the additive nature of the effects about which the Iranian researchers speculate that it could be "due to greater storage of carbohydrate in sites other than skeletal muscle, the most likely candidate being the liver" (Roohi. 2013), as well as glutamine's own role as a substrate for gluconeogenesis in the liver.

"Real world" evidence: Early exposure to mercury precipitates diabetes in man

From rodent studies, we already know that early mercury exposure increases the susceptibility to develop diabetes later in life. With the soon-to-be-published results from a prospective cohort of 3,875 American young adults who were 20-32 years old and free of diabetes in 1987, when the first data-set was acquired, the number of subjects who had abnormally high toenail mercury levels was extraordinarily high in the 288 incident cases of diabetes that occurred in the years up to the 18 years of follow-up.

Did you know that there is no correlation between amalgam fillings and Hg levels in the toe nails? At least according to a 2007 study by Björkman et al. who analyzed brain, blood, muscle and toenails of 30 deceased individuals the statistically non-significant correlation between the surface area of amalgam fillings and toenail mercury is even negative (meaning more fillings = lower Hg levels in the nails; Björkman. 2007). This is yet no reason to be relieved. In fact, it's rather the exact opposite: While the Hg levels in the toenails may have been low, the levels of the hardly less toxic inorganic mercury in the brain, as well as the total mercury concentrations in the pituitary and thyroid were significantly correlated with the surface area of amalgam fillings.

After adjustment for age, sex, ethnicity, study center, education, smoking status, alcohol consumption, physical activity, family history of diabetes, intakes of long-chain n-3 fatty acids, as well as serum magnesium, and toenail selenium levels the toenail mercury levels were still positively associated with the incidence of diabetes. With a probability of only 2% that we are dealing with a statistical outlier and an increased diabetes risk of 65% this provides another reason to give all mercury containing stuff an extra wide berth (He. 2013).

Against that background it appears to be all the more important to keep an adequate dietary intake of nutrients such as selenium and zinc, which have only recently been shown to useful adjuvants to a standard treatment of thiol chelator (DTT) regimen in a rodent model of acute mercury exposure (Deepmala. 2013) . The latter is obviously the extreme version of the slow, but constant onslaught of mercury most of us are exposed to, but our bodies' very own detoxification mechanism rely on the presence of adequate amounts of zinc (for the necessary metallothioneins; cf. Durnam. 1997) and selenium (for glutathion repletion; read more about selenium).

Since these "Short News" got a little longish, I have just updated the facebook news with a couple of shorter items, influcing among others...

Man or woman, trying to build muscle or get ripped, always prefer whole proteins (and whole foods in general) over isolated nutrients. That this is particularly true for amino acids has been addressed in way more than the two most recent posts on the repartitioning effects of isoleucine and respective peptides in whey (learn more) and the related post "Don't Judge a Protein By Its Amino Acids" (read it) here at the SuppVersity

EAA induced protein synthesis - Additional energy from carbohydrates or alanine does not increase protein synthesis beyond what 10g of essential amino acids alone will do (read more)

Human data on ergogenic effects of fish oil "inconclusive" - Scientists also point towards problems with increased immunosuppression and prolonged bleeding times (read more)
Probiotics for bone health -An exclusively male thing? At least in rodents their beneficial effect on bone density appears to be sex-specific (read more)
Alternate day fasting and exercise make a perfect match - 2x higher weight loss exclusively from body fat and greater improvements in cholesterol particle distribution in the combination group (read more)

There are as usual more sort news for you to spend the hours to whatever you have planned for Saturday night, so I suggest you briefly surf over to www.facebook.com/SuppVersity check out the rest and comment and discuss the latest news.

References:

Altura BT, Wilimzig C, Trnovec T, Nyulassy S, Altura BM. Comparative effects of a Mg-enriched diet and different orally administered magnesium oxide preparations on ionized Mg, Mg metabolism and electrolytes in serum of human volunteers. J Am Coll Nutr. 1994 Oct;13(5):447-54.
Björkman L, Lundekvam BF, Laegreid T, Bertelsen BI, Morild I, Lilleng P, Lind B, Palm B, Vahter M. Mercury in human brain, blood, muscle and toenails in relation to exposure: an autopsy study. Environ Health. 2007 Oct 11;6:30.
Bøhmer T, Røseth A, Holm H, Weberg-Teigen S, Wahl L. Bioavailability of oral magnesium supplementation in female students evaluated from elimination of magnesium in 24-hour urine. Magnes Trace Elem. 1990;9(5):272-8.
Coudray C, Rambeau M, Feillet-Coudray C, Gueux E, Tressol JC, Mazur A, Rayssiguier Y. Study of magnesium bioavailability from ten organic and inorganic Mg salts in Mg-depleted rats using a stable isotope approach. Magnes Res. 2005 Dec;18(4):215-23.
Chubanov V, Gudermann T, Schlingmann KP. Essential role for TRPM6 in epithelial magnesium transport and body magnesium homeostasis. Pflugers Arch. 2005 Oct;451(1):228-34.
Deepmala J, Deepak M, Srivastav S, Sangeeta S, Kumar SA, Kumar SS. Protective effect of combined therapy with dithiothreitol, zinc and selenium protects acute mercury induced oxidative injury in rats. J Trace Elem Med Biol. 2013 Feb 18.
Durnam DM, Palmiter RD. Analysis of the detoxification of heavy metal ions by mouse metallothionein. Experientia Suppl. 1987;52:457-63.
Fuqua JS, Rogol AD. Neuroendocrine alterations in the exercising human: Implications for energy homeostasis. Metabolism. 2013 Feb 14.
He K, Xun P, Liu K, Morris S, Reis J, Guallar E. Mercury Exposure in Young Adulthood and Incidence of Diabetes Later in Life: The CARDIA trace element study. Diabetes Care. 2013 Feb 19.
Marcelín-Jiménez G, Angeles-Moreno AP, Contreras-Zavala L, Morales-Martínez M, Rivera-Espinosa L. A single-dose, three-period, six-sequence crossover study comparing the bioavailability of solution, suspension, and enteric-coated tablets of magnesium valproate in healthy Mexican volunteers under fasting conditions. Clin Ther. 2009 Sep;31(9):2002-11.
Romero JR, Castonguay AJ, Barton NS, Germer S, Martin M, Zee RY. Gene variation of the transient receptor potential cation channel, subfamily M, members 6 (TRPM6) and 7 (TRPM7), and type 2 diabetes mellitus: a case-control study. Transl Res. 2010 Oct;156(4):235-41.
Schlingmann KP, Waldegger S, Konrad M, Chubanov V, Gudermann T. TRPM6 and TRPM7--Gatekeepers of human magnesium metabolism. Biochim Biophys Acta. 2007 Aug;1772(8):813-21. Epub 2007 Apr 3. Review.
Siener R, Jahnen A, Hesse A. Bioavailability of magnesium from different pharmaceutical formulations. Urol Res. 2011 Apr;39(2):123-7.
Siervo M, Montagnese C, Mathers JC, Soroka KR, Stephan BC, Wells JC. Sugar consumption and global prevalence of obesity and hypertension: an ecological analysis. Public Health Nutr. 2013 Feb 18:1-10.
Williams NI, Caston-Balderrama AL, Helmreich DL, et al.Longitudinal changes in reproductive hormones and men-strual cyclicity in cynomolgus monkeys during strenuous exercise training: abrupt transition to exercise-induced amenorrhea. Endocrinology 2001; 142(6):2381–9

The left part of the image shows what scientifically proven hypoxic training looks like. You wear a mask with an exogenous supply of low oxygen air. The right part of the image shows you what the fitness industry will try to sell you as "hypoxic training". That being said, did you know that at least the left version could also help you shed 11%% of your body fat in three weeks (learn more)?

Based on the feedback I got on the mini-summary of the latest review on "Kaatsu" aka blood flow restricted training I posted as part of last Monday's Exercise Science Round Up, I gather that many of you will be interested to hear about the results of a pertinent experiment that has been conducted only recently at the Lincoln University in Christchurch; New Zealand (Manimmanakorn. 2013).

To elicit, whether a combination of resistance training and vascular occlusion would modify the patterns of muscle activation, the development of muscle strength and hypertrophy, and whether these effects could be replicated by training under hypoxic conditions, the scientists who were involved in this research recruited 30 female netballers (age 20.2 ± 3.3 years, height 168.4 ± 5.8 cm; body mass 65.2 ± 6.5 kg, mean ± SD).

Ladies, hold your breath ;-)

The women were in their pre-competition training phase, and matched on their netball ability (had equal training volume, and were trained by the same physical conditioner). They were randomly assigned to either hypoxic training (HT), vascular occlusion (=Kaatsu; KT) and control training (CT) and had them perform bilateral knee extensions and ﬂexions from 0 to 90° on a regular leg extension machine.The detailed experimental protocol for the three groups looked like this:

If you don't intend to suffocate yourself or at least your leg muscles, but still have (for whatever reason) to use lighter weights, you may be interested in another recent study, which was able to show that ballistics lunges activate muscles to the same extent as 34% lighter standardlifts and that this effect can be improved by using elastic band & dumbbells (learn more)
"During each set of knee extensions and ﬂexions, participants in the HT group received normobaric hypoxic gas from a face mask via a hypoxicator system . The fraction of inspired oxygen (FIO2) was automatically adjusted by the hypoxicator using a biofeedback control system to maintain saturation of peripheral oxygen (SpO2) at *80 % (normal SpO2, approximately 99 %). The KT group performed training with restricted leg vascular blood ﬂow in both lower limbs. During training, the pressure exerted by the Kaatsu cuffs (which were approximately 5 cm in width) at the root of the thigh,was gradually increased by 10 mmHg each day, starting from 160 mmHg at Day 1 going up to 230 mmHg at Day 8. The pressure then remained unchanged throughout the remaining of the training (Abe 2006). Heart rate and SpO2 were monitored by a pulse oximeter at the end of each exercise set. The CT group performed knee extension and ﬂexion exercises with the Kaatsu cuffs on but not inﬂated (<5 mmHg) and breathed normal ambient room air." (my markups in Manimmanakorn. 2013)

In the course of the 5-week training period the participants completed three training sessions per week. Each training session consisted of three sets of knee extensions followed by three sets of knee ﬂexions to failure (unable to complete the exercise successfully). The total number of sets was thus six, with 30s rest between sets and 2-min rest between exercises and a TUT (time under tension) of 1 0 1, which means that the women performed the exercise with a 1s concentric, 0 seconds rest at the top and a 1s eccentric contraction.

"Building strength with 20% of the 1-RM? You are kiddin' me, right?"

The resistance used was light - very light in fact: 20 % of the 1-RM. And as if that was not already light enough, the HT and CT groups of which the scientists expected that they would be able to perform more reps were advised to match the repetitions performed by the KT group "to ensure equal training load between groups" (during the tests the subjects were obviously required to perform as many reps as they could). Against that background, it's actually not surprising that there were no increases in any of the measured parameters in the control group:

Figure 1: Relative changes (in %) in the peak maximum voluntary contraction in 3 s, area under the 30 s MVC curve,the number of repetitions able to be performed at 20 % 1-RM (left) and changes in surface electromyogram (EMG) amplitude (root mean square RMS %) during the Reps20 test before (pre) and after (post) 5 weeks training (Manimmanakorn. 2013)

As you can see in figure 1 the hypoxia training turned out to be the most effective if training methods - at least, if we go by the absolute increases in maximal voluntary contraction. The difference to the Kaatsu condition, however was trivial for all three parameters: The MVC3, the MVC30 and the total number of reps at 20% of the 1-RM.

The gym of the future a torture chamber or just an "old-school" gym in the basement?

Whether the gyms of the future will hand out cuffs at the door or "simply" have a low oxygen environment... wait a second: Now I know why all the strong guys train in these non-air-conditioned old-school gyms. It's to create a hypoxic environment, one of which the researchers say that it furthers "substantial increases in strength and endurance", which were "undoubtedly" brought about in part due to increased skeletal muscle hypertrophy.

Takarada et al. found that low inten- sity occlusion training can induce greater increases biceps CSA than regular high intensity training even in trained subjects (Takarada. 2000)
"However, indications of speciﬁc neuromuscular adaptation were also detected in the form of an increased EMG signal during the MVCs, particularly in the vascular occlusion group, indicating that increased motor unit activation probably also played a role in enhanced force production in these participants. Additionally, during a dynamic fatiguing exercise (Reps20) improvement in performance by the hypoxic and vascular occlusion groups post-training was in part due to improved efﬁciency of the force production machinery of the muscle." (Manimmanakorn. 2013)

Unfortunately, the actual increases in muscle cross sectional area (CSA) were not measured in the study at hand, but based on the findings of previous studies, which did report (in some cases) pretty impressive increases in CSA (see image next to the citation for one impressive example), I guess the scientists assumption that the ladies in the hypoxia and Kaatsu groups will also have gained more muscle than their peers is more than plausible.

Looking for readily available intensity techniques? "Unleash the Neanderthal Within" with Adelfo Cerame's "Fav Five Intensity Techniques" (learn more)

Bottom line: Now, let's get back to the "gym of the future" - I am not yet convince that we are soon going to see the air being sucked out of the gyms, but I am more and more convinced that blood flow restriction, Kaatsu, vascular occlusion or whatever else you may be using to reduce the oxygen supply to the muscle and thus increase the amount of eu-stress (=beneficial stress, learn more), will probably become the "intensity technique" of the future - if not on a "whole gym level", then maybe in form of one or two of those neat cages (see image at the bottom of the article).

Whatever the future may hold, I still feel that it is very unlikely that Katsuu and hypoxic training with light weights are ever going to replace "regular" strength training completely.

After all, working out should be more to you than just a means to develop sleeve bursting biceps. Honestly, if you seriously can say for yourself that you would not miss lifting heavy weights and would willingly content yourself with the knowledge that you should be able to do that, it's no wonder that you are clutching to any straw to finally make those gains you have been chasing for years.

Kaatsu training on methodological dope: Where is the level playing ground?"

You should also keep in mind that neither the study at hand, nor the previously mentioned and unquestionable impressive study by Takarada offered a level playing ground for the contestants, i.e. classic hypertrophy vs. Kaatsu or training in hypoxic conditions.

Is this how the gym of the future looks like? I guess, the results of the study at hand are still not enough to predict the future, but when I was looking for a nice video to go with this article, I found an ABC report that underlines that Victor Conte (yep, the "Balco guy") believes in the success of hypoxic training (watch video)

The "high intensity" condition in the Takarada condition prescribed training loads from 50-80% and would be considered "moderate" by the majority of muscle heads. Manimmanakorn study, on the other hand, the fact that the "HT and CT groups were then instructed to match the repetitions performed by the KT group to ensure equal training load between groups" (Manimmanakorn. 2013) is a major downside to its real world significance and makes me wonder what the ladies in the HT group could have achieved, when they would not have had to stop "before their time"...

... ah, and I don't have to mention that not having a high intensity group in the Manimmanakorn study reminds me of those sponsored pre-workout supplement studies, here the placebo is either plain water or simple sugar - when you want to prove something is superior to common practice you better test it against common practice or your data is of highly questionable practical value.

References:

Abe T, Kearns CF, Sato Y (2006) Muscle size and strength are increased following walk training with restricted venous blood ﬂow from the leg muscle, Kaatsu-walk training. J Appl Physiol 100:1460–1466
Manimmanakorn A, Manimmanakorn N, Taylor R, Draper N, Billaut F, Shearman JP, Hamlin MJ. Effects of resistance training combined with vascular occlusion or hypoxia on neuromuscular function in athletes. Eur J Appl Physiol. 2013 Feb 15.
Takarada Y, Takazawa H, Sato Y, Takebayashi S, Tanaka Y, Ishii N. Effects of resistance exercise combined with moderate vascular occlusion on muscular function in humans. J Appl Physiol. 2000 Jun;88(6):2097-106.

A bigger biceps and less body fat to cover your precious gains? At least for CLA this has in fact been observed in a human study (see figure 1).

About two weeks ago, I stumbled across an interesting paper that had just been published in the peer-reviewed journal Nutrients, filed it and got so much to do that I would almost have forgotten about it. When I was just thinking about which topic to address next, I did yet remember the auspicious conclusion to the abstract, which says "we can hypothesize that fat supplements may improve the anabolic effect of exercise." (Macaluso. 2013). "May" and "hypothesis", those are terms I like and since fish oil and CLA were implicated in the previous lines, I suppose you are going to like it as well. So what would be more obvious than to apply the "SuppVersity Sniff Test" (I am beginning to like this term, Carl often uses on the Science Round-Up) to this ostensibly well-researched review of the literature?

"May improve the anabolic effect of exercise"

Usually things that "may" do just that, namely "improve the anabolic effect of exercise" end up in a pricey and useless testosterone booster.

Check out the overview of the Intermittent Thoughts on Building Muscle and learn how testosterone, growth hormone, IGF-1, mTOR and the rest of the pack orchestrate skeletal muscle hypertrophy and why boosting your testosterone levels from mid will not translate into visible muscle gains (read more)

Personally, I don't know of any test booster though, which boasts that fish oil or CLA were it's main ingredients and without taking away too much of the results of this sniff test, I can already tell you that there is a good reason for why this is the case: It's even less likely to produce significant effects than the next best herb that "grows but in one place" in the Amazonian rain forest, where the CEO of company X harvests it at the hazard of his own life... ah, you know that spiel, so I don't have to repeat it here.

If you take a look at the tables the researchers provide as part of their review and have basic mathematical and reading skills, it's not difficult to count the number of which would remotely support the notion that fish or CLA supplementation have any effects at all: It's 5 out of 9 for fish oil and 4 out of 7 for CLA. Certainly reason enough to "hypothesize" a bit.

Fish oil is good for your heart, but not for your physique

In the next step we need a little more than to identify those studies with the "no effect" label from the tables and take a the ones we were left with after our initial glance at the data. If we do just that the number of studies we have to look at decreases from 9 to 4 studies, as none of the fish oil studies survives the "Sniff Test", after all, neither

They probably ain't anabolic either, but could help you to stay lean on a bulk: DHA-phospholipid, as you would find them in krill vs. common fish oil supplements (learn more).
improved cardiovascular function in the absence of increased endurance performance or recovery in football players (Buckley. 2009)

a minimal reduction in O2 cost in the absence of effects on the endurance performance in cyclists (Peoples. 2008),

improvements in VO2max in previously sedentary men a non-placebo-controlled study (Brilla. 1990)

a reduced acute phase inflammatory response in a non-randomized non-placebo controlled intervention with average Joes (Ernst. 1991)

would qualify as convincing evidence for any "anabolic effects" - in fact, even if we were talking about ergognenic effects in general, only the study by Guezennec would survive 2nd phase of the Sniff Test.

Now, what's interesting about the Guezennec study, though, is that the "beneficial" effects (a profound decrease red blood cell deformability; RCD) were hypoxia specific and could easily turn against you. After all, one of the reasons athlete "train high and compete low" (meaning they train at high altitudes with less oxygen in the air and thus hypoxic conditions to outperform the competition at sea level) is that this will increase the production of red blood cells. Now guess why that happens!? Correct! It's a result of the hemolytic effect of hypoxic training... now, what will happens if you copy the 6g /day EPA-max supplementation regimen of the 19-38 years old guys in the Guezennec study? Right, this effect will be absent. I wouldn't go so far and call this "ergolytic", but you could certainly make a point that huge amounts of EPA are - at least in this scenario - anti-ergogenic.

So what about CLA, then? Isn't that simply a fat burner

So, if even the widely hailed fish oil has little data to support its usefulness as an ergogenic supplement for athletes and aspiring physical culturists, what about CLA, then? I mean, we all know that the benefits researchers observed in human trials were miles apart from what they had expected to happen based on previous experiments in rodents (click on the image to the right to be redirected to a study, where the CLA treated ice dropped 77% body fat and did nevertheless display statistically significant increases in endurance capacity).

Adequate dosing still remains an issue

These discrepancy in terms of the body fat reducing effects of conjugated linoleic acid supplementation, as Dilzer and Park pointed out only recently, at least in parts a result of insufficient doses:

In July 2012 I wrote about what I believe is the unquestionably most impressive study on the fat burning and endurance enhancing effects of conjugated linolic acid. 77% body fat reduction - that's bordering lipodystrophy. The dosage used in this study would be roughly equivalent to 30g/day for human being and supports the notion that profound effects are only observed with amounts of CLA that have yet not been administered to humans in controlled trials (learn more)!
"Studies with mice used diets containing 0.5 w/w%* CLA, which is equivalent to about 56 g CLA/day/70 kg (Malpuech-Bruger. 2004). Most human studies used CLA doses ranging between 0.7 g and 6.8 g per day, which is lower than doses used in mice." (Dilzer. 2012)

*Addendum: Anonymous pointed out correctly, that the figures in the above quotation (which is dirertly from the FT) are inconsistent. 0.5% would be only 5.6g. I guess that's a typo in the Dilzer study, because the Malpuech-Bruger study they reference says "a daily intake of 0.70 g/kg body mass was effective in mice". (Malpuech-Bruger. 2004) - sloppily as they are, they don't say that this is already in human equivalents, though. That becomes clear in the next sentence only, which says "A value of 0.70 g/kg body mass in humans would correspond to a daily intake of 56 g of CLA." (ibid.) The July 2012 study I reference under the image to the right used a HED of ~30g (learn more), so even if the exact figures are questionable, the argument obviously still holds.

Since the same goes for studies investigating the "anabolic" effects the abstract to Macaluso et al.'s review explicitly mentions, chances are that increases in endurance performance, as they were observed in the previously mentioned rodent study (read the full story, here), were likewise species or at least dosage specific.

Is CLA "anabolic" or at least ergogenic?

If we take a look at the 7 studies the researchers included in their review (I guess you will be hard-pressed to find more than those seven, as CLA is not exactly the typical supplement researchers use as an ergogenic), we can easily exclude three of them. In these studies that were conducted on healthy young women, trained male bodybuilders and physically active men and women, supplementation with 3g, 6g and 3.9g/day of CLA did exactly nothing.

This leaves us with a set four studies to take a closer look at - three of them report improvements in body composition, two of them also observed increases in endurance performance and a single one even found "slight increases in testosterone":

Improvements in body composition were observed by Thom (2001), Colakoglu (2006) and Pinkonski (2006); all studies were placebo controlled and the participants were physically active or at least healthy men (only in the Thom study) and women who consumed 1.8, 3.6 and 5g of CLA per day.

While the former two studies by Tho and Colakoglu used exhaustive and medium intensity endurance programs, the study by Pinkonski et al. used a stardardized full-body workout with 12 exercises ranging from leg presses, bench and shoulder presses, to lat pull downs, biceps curls, and some core exercises. Each exercise was performed three times per week consisting of 3–4 sets of 4–10 repetitions at approximately 75–90% of one-repetition maximum (1RM).
Figure 1: Relative changes in body composition biceps and quadriceps size and strength parameters after 7 weeks of serious strength training with or without 5g of CLA per day (Pinkoski. 2006)
This protocol and the high number of study participants (76 men and women) and their training status - the majority had more than 2 years of weight training experience under their belts - make the results of the Pinkoski study so interesting for us. The results, on the other hand (cf. figure 1), are not exactly earth shattering, especially in view of the fact that only the fat loss and the increase in biceps size reached statistical significance and that despite a pretty high number of participants. Whether or not CLA really is "anabolic" and not "just" a mediocre fat burner has thus still to be determined.

Figure 2: Increases in cortisol (top) and testosterone (bottom) and respective increases in lean body mass in response to a 12-week hypertrophy oriented resistance training program (West. 2012)

Increases in testosterone, as Macaluso et al. observed them in 10 "physically active" male subjects (age, 27.4) in a previous study in response to 6g CLA per day, on the other hand, would probably qualify as "anabolic" if the latter had not been measure right the workouts, as part of a short 3-week study with no corresponding effects on body composition (Macaluso. 2012).

The latter should actually not come as a surprise to any seasoned SuppVersity student. After all you've learned that (1) endocrine induced changes in body composition take their time in the Intermittent Thoughts on Building Muscle, that (2) the role of testosterone levels in the normal range in the whole process is fundamentally overrated and (3) that the seminal paper by West & Phillips, on which the data in figure 2 is based, clearly refutes the notion that post-workout increases in testosterone have any impact on skeletal muscle hypertrophy.

If we also take into account that numerous rodent studies do in fact support the notion that CLA posses "ergogenic", yet not necessarily "anabolic" qualities. Macaluso et al. are certainly correct, when they conclude their paper with the scientific equivalent to "And they lived happily ever after" stating that "additional research".

Milk from pastured cows has a relatively high amounts of both, CLA and DHA + EPA. The absolute amounts are however so low that you would probably have to drink more than the notorious gallon of milk per day to see any effect - and let's be honest, even if CLA + DHA make a good fat burner, the gallon of milk certainly makes a better weight gainer ;-)

Bottom line: I guess, you'd like to hear a supplement recommendation now, right? Well, as far as ergogenic and/or anabolic effects are concerned, CLA is unquestionably the more promising fatty acid off the "two" (actually we are talking about four fatty acids, here: DHA + EPA = fish oil and cis-9,trans-11 and trans-10,cis-12 CLA). CLA's anti-PPAR-gamma effect, which is probably responsible for the reductions in insulin sensitivity and detoriations of the lipid metabolism that have been observed in numerous studies (only trans-10,cis-12 CLA), is probably not so much of a problem for lean, physically active people and the upside of the PPAR-gamma blockade is a reduced rate of fat storage....

Ah, you see I am diverting to the fat loss effects again. And if we are honest, the results of this review do actually only confirm that what you've read here at the SuppVersity roughly 3 months ago the combination of CLA + DHA could turn out to be a safe and effective fat burner (learn more), if we would finally see adequately doses, long(er) term supplementation trials in humans.

As ar as the "anabolic" nature of either of them, i.e. EPA + DHA or cis-9,trans-11 and trans-10,cis-12 CLA. The jury may still be out there, but the verdict is - at least in the case of regular fish oil almost certainly "not guilty", .. ah I mean, "not anabolic".

References:

Brilla, L.R.; Landerholm, T.E. Effect of fish oil supplementation and exercise on serum lipids and aerobic fitness. J. Sports Med. Phys. Fitness 1990, 30, 173–180.
Buckley, J.D.; Burgess, S.; Murphy, K.J.; Howe, P.R. DHA-rich fish oil lowers heart rate during
submaximal exercise in elite Australian Rules footballers. J. Sci. Med. Sport 2009, 12, 503–507.
Colakoglu, S.; Colakoglu, M.; Taneli, F.; Cetinoz, F.; Turkmen, M. Cumulative effects of conjugated linoleic acid and exercise on endurance development, body composition, serum leptin and insulin levels. J. Sports Med. Phys. Fitness 2006, 46, 570–577.
Dilzer A, Park Y. Implication of conjugated linoleic acid (CLA) in human health. Crit Rev Food Sci Nutr. 2012;52(6):488-513.
Ernst, E.; Saradeth, T.; Achhammer, G. n-3 fatty acids and acute-phase proteins. Eur. J. Clin.
Invest. 1991, 21, 77–82.
Guezennec, C.Y.; Nadaud, J.F.; Satabin, P.; Leger, F.; Lafargue, P. Influence of polyunsaturated fatty acid diet on the hemorrheological response to physical exercise in hypoxia. Int. J. Sports Med. 1989, 10, 286–291.
Lenn, J.; Uhl, T.; Mattacola, C.; Boissonneault, G.; Yates, J.; Ibrahim, W.; Bruckner, G. The effects of fish oil and isoflavones on delayed onset muscle soreness. Med. Sci. Sports Exerc. 2002, 34, 1605–1613.
Macaluso, F.M.; Catanese, P.; Ardizzone N.M.; Marino Gammazza, A.; Bonsignore, G.; Lo Giudice, G.; Stampone, T.; Barone, R.; Farina, F.; Di Felice, V. Effect of conjugated linoleic acid on testosterone levels in vitro and in vivo. J. Strength Cond. Res. 2012, 26, 1667–1674.
Macaluso F, Barone T, Catanese P, Carini F, Rizzuto L, Farina F, Di Felice V. Do Fat Supplements Increase Physical Performance? Nutrients 2013; 5:509-524.
Malpuech-Brugère C, Verboeket-van de Venne WP, Mensink RP, Arnal MA, Morio B, Brandolini M, Saebo A, Lassel TS, Chardigny JM, Sébédio JL, Beaufrère B. Effects of two conjugated linoleic Acid isomers on body fat mass in overweight humans. Obes Res. 2004 Apr;12(4):591-8.
Oostenbrug, G.S.; Mensink, R.P.; Hardeman, M.R.; De Vries, T.; Brouns, F.; Hornstra, G. Exercise performance, red blood cell deformability, and lipid peroxidation: Effects of fish oil and vitamin E. J. Appl. Physiol. 1997, 83, 746–752.
Peoples, G.E.; McLennan, P.L.; Howe, P.R.; Groeller, H. Fish oil reduces heart rate and oxygen consumption during exercise. J. Cardiovasc. Pharmacol. 2008, 52, 540–547..
Peoples, G.E.; McLennan, P.L.; Howe, P.R.; Groeller, H. Fish oil reduces heart rate and oxygen consumption during exercise. J. Cardiovasc. Pharmacol. 2008, 52, 540–547.
Pinkoski, C.; Chilibeck, P.D.; Candow, D.G.; Esliger, D.; Ewaschuk, J.B.; Facci, M.; Farthing, J.P.; Zello, G.A. The effects of conjugated linoleic acid supplementation during resistance training. Med. Sci. Sports Exerc. 2006, 38, 339–348.
Thom, E.; Wadstein, J.; Gudmundsen, O. Conjugated linoleic acid reduces body fat in healthy exercising humans. J. Int. Med. Res. 2001, 29, 392–396.
Toft, A.D.; Thorn, M.; Ostrowski, K.; Asp, S.; Moller, K.; Iversen, S.; Hermann, C.; Sondergaard, S.R.; Pedersen, B.K. N-3 polyunsaturated fatty acids do not affect cytokine response to strenuous exercise. J. Appl. Physiol. 2000, 89, 2401–2406.
West DW, Phillips SM. Associations of exercise-induced hormone profiles and gains in strength and hypertrophy in a large cohort after weight training. Eur J Appl Physiol. 2012 Jul;112(7):2693-702.

Concentration curls are among those exercises, where eccentrics can easily be incorporate. Plus. As the EMG Series shows, this increases the biceps activity by almost 50% compared to the regular barbell curl (learn more). But will it also make you grow faster?

Just let me get this straight right away: I am well aware that it is still debated if and if so to which extend skeletal muscle damage affects or even determines the training induced gains in strength and/or lean body mass and it is not my intention to rekindle this never-ending debate. At least in my humble opinion, it does yet appear that a certain degree of "damage" is necessary for "optimal" gains. Anything that passes this threshold is however, as Schoenfeld points out in what I believe is the most recent review of the literature, not going to "further augment muscle remodeling and may in fact interfere with the process" (Schoenfeld. 2012).

The potential of negative interference is obviously particularly pronounced, when the the potentially muscle damaging physical activity is performed during the recovery phase. But how long it going to take until the repair and restructuring processes are completed?

In other words: How long would be optimal rest interval for someone who trains really intense with a focus on eccentric overload?

At first sight it seems as if the results of a recent study from the State University of Campinas should help us to bring light into the darkness, but as we are soon going to see, things are (once again) more complicated than common sense would tell us.

The main intension of the researchers was to (I quote) "observe the time course of muscle damage and inflammatory responses to resistance-training with EO [eccentric overload]" (Neme Ide. 2013). To this ends, they recruited 3 women and 5 men in their early twenties who had at least one year of previous strength training experience and had them perform a standardized workout program with the following parameters:

No idea how to schedule your workouts? Learn how to do that and much or in the Step By Step Guide to Your Own Workout Routine!

total duration: 13 sessions (total) distributed evenly across 7 weeks; 2x full body workouts trained every Tuesday & Thursday

set & rep scheme: 4 sets of 8 reps at 80% of the 1-RM max for eccentrics; since that's more than you can "lift", i.e. move concentrically, the researchers who supervised the sessions had to help the participants on the eccentric part of the movement

exercises: classic full body workout consisting of bench presses, 45-degree leg presses and bent-over rows

The blood samples were taken 96h after training session 2, 7, 9, 11 and 13, respectively and the creatine kinase, CRP and various hematological parameters were measured to evaluate the impact the eccentric workouts had on ...

muscle damage - indicated by the amount of creatine kinase (CK) that leaked from the musculature into the blood,

overall inflammation - indicated by the change in C-reactive protein (CRP) levels,

hemtaological paramaters - including red blood cell count (RBC), hemoglobin concentration (Hb), hematocrit (Ht), mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC), erythrocyte distribution width (RDW), white blood cell (WBC) count, lymphocyte (LYNF) count, neutrophil (NEUTR) count, and platelet count (PLT).

The reasoning behind the constant monitoring of CK, CRP and blood parameters was that the scientists expected that there would be an attenuation of the damaging effects of the workouts as the participants bodies got accustomed to the bi-weekly torture.

Don't let your Dr send you to the ER without letting him know that you trained the day before you got your latest bloodwork done.

If you take a look at the creatine kinase (CK) data I plotted in figure 1 (left) there are two things you should take a mental note of. Firstly, the increase in creatine kinase is "exorbitant" and could - assuming your doctor either doesn't know you are strength training or has no clue about the effects a heavy workout can have on the amount of the enzyme that "recycles" creatine into pohosphocreatine (PCr) that's floating around in your blood stream - be enough to have your physician send you to the ER - misdiagnosis: rhabdomyolysis (please bear in mind that Kraemer et al. (2004) suggest a reference interval for physically active subject of 1,309U/L; that's almost 4x more than the regular lab range that usually says everything past 400U/L would be pathological)

Figure 1: Creatine kinase (CK) levels (left) and C-reactive protein (CRP) levels (right) at different timepoints of the 7-week exercise intervention (Neme Ide. 2013)

And secondly, this increase in creatine kinase is hard to predict and varies from subject to subject (the numbers in the upper line of the label of the horizontal axis are the subject numbers):

"CK and CRP presented significant changes at specific time points, but not for all subjects. Four subjects presented significant changes in CK activity at P2 (+1719%, +1250%, +1281%, and +312% resp.), and other two at P13 (+391% and +139%, resp.). For CRP six subjects presented significant changes at P2 (+1100%, +243%, +3800%, +2500%, +1400%, and +2400%, resp.), one at P4 (+567%), other at P9 (+3200%), three at P11 (+300%, +3400%, and +3900%, resp.), and other at P13 (+1500)." (Neme Ide. 2013)

Interestingly, there was no significant correlation between the changes in creatine kinase (CK) and C-reactive protein (CRP) as you would expect if muscle damage and systemic inflammation went hand in hand.

Accommodation? yes! Unequivocal results? No.

Despite the fact that the expected pronounced initial CK response was present only in four out of the eight individuals, the scientists are confirmed that the data they gathered does support their initial hypothesis that there would be an attenuation of muscle damage in the course of the 7-week study period and ascribe the latter to the repeated bout effect a term, scientists use to refer to the protective effects a single bout of eccentric exercise has on the muscle damage during subsequent bouts (Mc Hugh. 2003).

"The potential adaptations that explain the phenomena have been categorized as neural, mechanical, and cellular. Regarding the cellular adaptations there is evidence of longitudinal addition of sarcomeres and adaptations in the inflammatory response following an initial bout of eccentric exercise, limiting also the proliferation of damage." (Neme Ide. 2013)

While a similar trend was observed for the CRP levels, the initial increase of the latter was by far less pronounced than for the CK values, so that the levels remained within the physiological norm for active people (the average CK values, on the other hand, were 2x elevated over the already high reference interval for physically active individuals).

Changes in hematological parameters were the exception

In case your workout program looks anywhere like Adelfo's Overkill Program from April 2012, you better make sure to come up with a new one after no more than max. 3-4 weeks!

If we acknowledge the reasoning Plaisance and Grandjean present in their 2006 review of the literature and take the comparatively low exercise related increases in C-reactive protein levels (CRP) as an indicator of damage in non-skeletal muscle tissue, it is also not surprising that this unquestionably intense and obviously muscle damaging exercise regimen did not have more pronounced effects on the blood panel of the study participants.

Only two subjects presented significant changes in neutrophils with an unpredictable up and down for subject 7 and a significant 60% increase after the final session in subject 6. In view of the fact that subject 7 was also the only one with detoriations in almost all other blood parameters, it's yet pretty unlikely that this was a result of the workout protocol and not the result of some sort of infection or whatever.

Ok, so what exactly have we learned now? This is actually a pretty good question. I guess one thing we have learned is that physically active individuals can actually shock their doctors with "exorbitantly" high (yet still normal) creatine kinase levels. This does not mean that you can simply ignore constantly elevated / abnormal CK values, but it's important to realize that the 400U/L range your lab report lists is probably not sufficient for your personal CK values if you get blood drawn in the vicinity of a hard workout (on a related note: especially when you are low-carbing and eating high amounts of protein the increase in CK usually goes hand in hand with increases in the "turn protein to energy" enzymes AST and ALT, which are in this case not necessarily indicative of "liver damage").

There is evidence that the expression of the local factions of IGF-1, MGF & Co., depends on the exercise induced wear and tear (learn more), it would be stupid to assume that there was no turning point at which the beneficial damage turns against you.

What we unfortunately didn't learn (and I feel that the scientists really missed out on this opportunity) is what the underlying reasons of the differential CK response to the workout may have been. Would it really have been too difficult to ask the "non-responders" what kind of exercise protocol (including set + rep schemes, frequency, weights and exercises) they had been following before they enrolled in the study? I don't think so. In fact, I would rather argue that it would have been obligatory. For me, for example, the eccentrics would have been the only novel stimulus in this workout. I have however been training with a female friend of mine a couple of days ago who would certainly qualify as having been training for at least a year and following a training program consisting of 3–5 sets of 6–12 repetitions with 1-2-minute rest interval between sets, performed 4-5 times per week (these were the inclusion criteria for the study at hand), for whom all of the exercises would have constituted a whole new stimulus in and out of itself (she usually works out on those fancy machines).

Now this may be a pity, but int the end, the differential CK response could have been totally irrelevant anyway. The pertinent evidence from human studies may be more than scarce, but if we go by the few studies we have, it appears that even a 5x higher CK response to eccentric exercises as it was observed in the non-preconditioned group in a 2011 human study by Flann et al. does not result in significantly different increases in either muscle size, or strength (cf. figure 2).

Figure 2: Strength and hypertrophy (left) and creatine kinase (CK, right) response in pre-trained and naive individuals in the course of an 8-week eccentric training protocol (Flann. 2011)

The fact that Neme Ide et al. did not measure the strength and/or hypertrophy response, still baffles me. I do however believe that (most) scientists are not just clever, but also very rational beings and therefore I would suspect that there is soon going to be a follow-up paper with the respective data. Why's that? Well, in a scientific community, where the number of publications is unfortunately more important than their quality, tricks like these may eventually give you the edge over the competition on your next job application ;-/

References:

Flann KL, LaStayo PC, McClain DA, Hazel M, Lindstedt SL. Muscle damage and muscle remodeling: no pain, no gain? J Exp Biol. 2011 Feb 15;214(Pt 4):674-9.
Kraemer WJ, French DN, Paxton NJ, Häkkinen K, Volek JS, Sebastianelli WJ, Putukian M, Newton RU, Rubin MR, Gómez AL, Vescovi JD, Ratamess NA, Fleck SJ, Lynch JM, Knuttgen HG. Changes in exercise performance and hormonal concentrations over a big ten soccer season in starters and nonstarters. J Strength Cond Res. 2004 Feb;18(1):121-8.
McHugh MP. Recent advances in the understanding of the repeated bout effect: the protective effect against muscle damage from a single bout of eccentric exercise. Scand J Med Sci Sports. 2003 Apr;13(2):88-97. R
Neme Ide B, Alessandro Soares Nunes L, Brenzikofer R, Macedo DV. Time course of muscle damage and inflammatory responses to resistance training with eccentric overload in trained individuals. Mediators Inflamm. 2013;2013:204942.
Schoenfeld BJ. Does exercise-induced muscle damage play a role in skeletal muscle hypertrophy? J Strength Cond Res. 2012 May;26(5):1441-53.

This is how the "buffered" alternate day fast works: You eat 1/4 of the White Choc Banana Cream Pie on your fasting day and a whole pie on the next one - well, not really, but the ratios would be right ;-)

I guess at least the SuppVersity facebook friends are probably going to remember the study today's article is dealing with: "Alternate day fasting and endurance exercise combine to reduce body weight and favorably alter plasma lipids in obese humans." To me that sounded like Intermittent Fasting Done Wrong Does Still Produce Great Results, When You Combine It With an Aerobic Exercise Regimen", when I first read the abstract. After taking a brief look at the full-text (thx John!), however, my perspective on the study changed from "even a dog has its day" to "that oes look interesting, let's see whether this kind of buffered alternate day fasting" is able to take bear up with a classic intermittent fast.

A brief warning with respect to the data in figure 1: I know that a couple of you are too lazy to actually read the article and do headline + figure hopping. If you intend to to that, please keep in mind that the data in figure 1 is from another recent study, I used to illustrate the negative effects of "real" alternate day fasting.

Not all alternate day fasting is created equal

For the course of this 12-week, randomized, controlled, parallel-arm feeding trial the participants, 61 women and only 3 men aged 25 to 65 years, overweight / obese (BMI 30-39.9kg/m²) and weight stable for at least 3 months were randomized to one of the four study arms (unfortunately the data does not allow for any conclusions, whether the men and women reacted differently to the intervention or "real" alternate day fasting the data from the rodent study I discuss in the interlude surrounding figure 1 shows that this is the case, though):

control group (C): sedentary, no diet

exercise group (E): 25, 30, 35, 40min at intensities of 60, 65, 70, 56% of the calculated HRmax (intensity and duration were increased in week 4, 7 and 10)

alternate day fasting group (ADF): after 4-week controlled feeding period the study concluded with an 8-week self-selected feeding period.

As long as study subjects just have to eat what scientists serve them, every diet works. When they are however told to eat a high protein diet, for example, even the reported nutrient intake diverges massively from what the scientists had in mind, when they devised the protocol - you don't believe me? Well, then read for yourself, "What Really Happens, When Science Meets the Real World"
"During the controlled feeding period (week 1-4) participants consumed 25% of their baseline energy needs on the "fast day” (24 h) and consumed food ad libitum on each "feed day” (24 h). [...] The diet consisted of a 3-day rotating menu plan, and all fast day meals were prepared in the metabolic kitchen of the Human Nutrition Research Unit (HNRU). Fast day meals were consumed between 12.00 pm and 2.00 pm to ensure that each subject was undergoing the same duration of fasting.[...] During the self-selected feeding period (week 8-12) subjects continued with the ADF regimen but no the fast day food was provided to them. Instead, each subject met with a dietician at the beginning of each week to learn how to maintain the ADF regimen on his or her own at home." (Bhuatin. 2013)

During the counseling sessions the participants were also instructed to make (I quote) "healthy foodchoices on the ad libitum feed days by choosing low fat meat and dairy options and
increasing fruit and vegetable intake." (Bhutani. 2013)

combination group (ADF + E): combination of alternate day fasting and exercise protocol

Table 1: Nutrient composition of the fast day diet provided to the combination and ADF groups (Bhutani. 2013)

So, as you've learned from the above overview this was no "alternate day fast", as I had expected it to be, when I read the term "Alternate Day Fasting (ADF)" in the abstract of the study. With 450kcal/day and a nutrient composition providing 50% of the energy in form of carbohydrates, and 25% (each) from fat and protein the "fasting days" were characterized by a low caloric intake (see table 1), but should not have triggered a similar starvation response as the classic alternate day fasting regimen in a recently published rodent study by Kamur et al. from which the data in figure 1 is derived.

Let's briefly take a look why "real" alternate day fasting may not be a good idea

As you can see the effect of the alternate day fasting regimen in the Kumar study, in the course of which the rodents simply did not receive any food for a whole day, had profound negative effects on the hypothalamo-gypophysial-gonadal axis - especially in the female rodents.

Figure 1: Effects of every-other day fasting vs.ad libitum feeding on ovarian weight, estradiol, lutenizing hormone, leptin, and testosterone in female and male rodents (Kumar. 2013)

Now the first thing that will jump your eye is certainly the profound increase in serum estrogen in the IF group. Looks strange and certainly not anywhere near what you would have expected right? If you think that this cannot be that bad, you are probably a man, is that right? I see... so what really is bad about the estrogen explosion is actually that it is "living proof" of the total disruption of the cyclic interplay between estrogen and progesterone that's at the heart of female (in-)fertility (on a side note: the male rodents simply got skinny fat on that regimen).

Now why didn't these adverse events occur in the study at hand?

Actually I am only assuming that there were not similar negative effects in the study at hand. After all, we don't have the respective hormonal and even in the rodents it took it's time (2 cycles) until the females were totally infertile. Changes like these would thus probably have gone unrecognized. I do however suspect that the major factors contributing to the overall hormonal decline in the rodent study were the extendended time-span without food and the overall caloric deficit, which is usually ~30-40% of the habitual intake in rodents on alternate day fasting regimen, as they do not compensate for the fasting day on the subsequent day.

Figure 2: Changes in body composition in the combined, ADF, exercise and control groups (Bhutani. 2013)

With the extended fast being absent and a ~75% reduction in calorie intake on the fasting days, only (humans are unfortunately much better in "compensating" for a lack of food on a fasting day, anyway ;-) and the huge amount of adipose tissue the rodents in the Kumar study obviously did not have as an "emergency reserve", it is therefore unlikely that the beneficial changes in body composition Bhutani and his colleagues observed in their 64 subjects (see figure 2) were accompanied by hormonal deteriorations (although 61 of them were, as previously mentioned, female).

Figure 3: Changes in lipid profile (left) and glucose metabolism in the combined, ADF, exercise and control groups (Bhutani. 2013)

It is nevertheless interesting to see that there were no significant improvements in fasting glucose, insulin or HOMA-IR (the measure of long-term blood glucose levels; not shown in figure 3) in any of the groups. Moreover, the improvements in total LDL and HDL cholesterol were only significant in the combined group and that the total amount of the inflammatory marker CRP remained essentially the same in all four arms of the 12-week intervention study.

Image 2: Ramadan fasting can serve as a relatively well studied "model" of intermittent fasting. With the additional restriction of water intake and the common practice of rising early to have breakfast there are yet non-negligible differences. You can find more information about the strengths and limitations of this model in Part 2 and Part 3 of the IF series.

A brief reminder for everyone who missed the Intermittent Thoughts on Intermittent fasting series back in the day: If there is one thing we can take away from studies investigating the effects Ramadan fasting (a Muslim fasting ritual, where you eat only when the sun goes down) it is that eating the same amount of food at different times of the day alone is not going to make you lose weight. If you do intermittent fasting in order to lose weight you still have to achieve a caloric deficit. Plus, when you are doing it during a bulk, I personally suspect that you are more likely to gain body fat, simply because your body cannot make "good use" (=muscle glycogen and skeletal muscle protein) from all the food you will be cramming down in a small fasting window. So, if you insist on IF on a bulk, do at least increase your feeding window to 8h to be able to spread your energy intake more evenly.

Based on a comparison of the data from all three groups, we can yet also conclude that it is the alternate day fasting (or probably rather the caloric deficit) that exerts the beneficial effects on what the scientists subsume under the umbrella term "CHD risk indicators":

"the combinationof ADF plus exercise decreased LDL cholesterol (12% from baseline) while increasing HDL cholesterol (18% from baseline); a change that was not noted for any other intervention. The combination group also experienced an increase in LDL particle size, and a reduction in the proportion of small LDL and HDL particles." (Bhutani. 2013)

Only later in the discussion of their results do they mention that those "CHD risk indicators" improved to the same extend in the ADF only group - with even more significant changes in the particle profile.

Learn why breakfast is probably not the "most", but rather the least "important meal of the day" (read more).

Bottom line: The weight and fat loss are certainly intriguing. The regimen appears to be reasonably easy to follow and the fact that the improvements in glucose metabolism were marginal could well be related to the fact that the subjects were - despite being seriously overweight (!) - not diabetic.

Keeping all that in mind I am still not convinced that a regular intermittent fasting routine (16-18h fasting window on every day; learn more about intermittent fasting here at the SuppVersity) and a combined aerobic + strength training regimen would not have yielded even superior results. The average physical culturist probably will be better of with this by now almost "classic" diet routine.

References:

Bhutani S, Klempel MC, Kroeger CM, Trepanowski JF, Varady KA. Alternate day fasting and endurance exercise combine to reduce body weight and favorably alter plasma lipids in obese humans. Obesity (Silver Spring). 2013 Feb 14.
Kumar S, Kaur G. Intermittent Fasting Dietary Restriction Regimen Negatively Influences Reproduction in Young Rats: A Study of Hypothalamo-Hypophysial-Gonadal Axis. PLoS ONE. 2013; 8(1): e52416.

Crossfit doesn't fit well with everyone. In fact you have to be pretty fit already if you intend to benefit - specifically if you don't have someone who tailors the workouts to your specific needs. If you don't or are still miles apart from being fit, don't be bamboozled by the results of people who have been training for years.

This certainly sounds a little sadistic, but I hope you've been missing the Science Round-Up last Thursday. If that's the case, you will be happy to hear that Carl and I are back on track, and ready to talk about topics ranging from magnesium supplementation over the potentially fatal combination of NSAIDs and exercise and what's that got to do with gut health / integrity, how light therapy won't make you lighter, but help you cut body fat, how intense workouts compromise your sleep, and how intense sweeteners make you fat - at least if you add them on top of a Western diet. If we will have time, we will also take a look at how much protein it actually takes to preserve lean mass on a diet and how protein supplementation is not necessary and in a recently published study not even conducive to building muscle. And while these were only 50% of the news I've on my list of potential topics, I won't give away more... just tune in live at 1PM EST on the Super Human Radio Network.

For the time that remains and for those of you who are just arriving here after having listened to the live-stream, I still have a special goodie... have you ever pondered over the following question:

How much can you achieve within 10 weeks of training?

Even if you have already decided on a certain type of training, for example HIIT, you will have to adjust your routine to "Make HIIT a HIT" read Part I and Part II of the eponymous series and learn how to turn a HIIT workout into your HIIT workout to avoid overtraining and maximize its efficacy (learn more)

There is obviously no definite answer to this question. I mean, it goes without saying that we would first have to define, whether we are talking about muscle growth, overall conditioning, fat loss, etc. - what people often overlook, however it also depends on where you are coming from. Sometimes I feel like I am the only one who dares telling someone who's been "running" - in most cases this is rather sitting and driving - around at 2x his/her normal weight for years, is past his early 20s and has a life beyond working out and dieting is very unlikely to ever achieve a cover model physique. On the other hand, we've got the average trainee, who's been training for years has a high degree of leanness and is just about to see his sixpack shine through, who will necessarily make much smaller improvements within a given time-frame than his obese colleague who's just about to start working out for the first time of his/her life.

The previous paragraph should have made it quite clear, compared to the (overweight) beginner, an advanced trainee must invest much more thought into his/her diet and exercise regimen. That real intermittent fasting would probably be a better alternative for him/her than the "buffered every other day fat" has already been mentioned in yesterday's SuppVersity Article, but what about the exercise regimen?

Working out for fat loss and conditioning - Crossfit rules!

Fast paced high intensity workouts are gathering more and more momentum even outside of Crossfit gyms. Some of them may look somewhat "Jane Fonda", but as a previous review of the workout DVDs Insanity vs. TurboFire revealed, even hopping around in front of your TV set is more productive than the fat burning zone on the treadmill in next to your sofa (learn more)

Let's say he or she is working out primarily to increase his/her conditioning and drop a (if by any means possible) a significant amount of body fat? What would be the best way to train, then?

According to the results of a soon-to-be-published study from the Ohio State University Health & Exercise Science in Columbus, Ohio (Smith. 2013), there is no question that this would be a Crossfit-esque workout - or, as the scientists refer to it, a crossfit-basedhighintensitypowertraining (HIPT) program, they describe as follows:

"[...] a crossfit-based HIPT program using basic gymnastic skills (hand- stands, ring, and bar exercises) and traditional multiple-joint, functional, resistance exercises (squat, press, deadlift, Olympic lifts) performed as quickly as possible at a high intensity (low repetition, high percentage of 1-RM)." (Smith. 2013; my italics)

The 10-week program was varied so that some exercises were performed for a best time, and others were performed in the “as many rounds as possible” style (AMRAP; for a little more versatility check out Adelfo's EDT-CrossOver training) within anything from 10 to 20 minutes.

While there were no prescribe recovery times during the strength/skill portion of the exercise session, the WOD portion of the session did not allow for any real "rest" between the sets, as all the exercises were to be performed as quickly as possible.

Wow, who survived that? - Good question, indeed!

Only the fittest survive: Please do me a favor - If you are the aformentioned overweight person who's still carrying around another guy/gal's weight as body fat, don't even think of crossfitting, if you don't want to end up like 9 of the 11 dropouts (the study started with 54 participants), who retired willingly due to overuse or injuries, ok?

I guess you won't be surprised to hear that the 23 men and 20 women who survived and of whom the scientists state that they were "spanning all levels of aerobicfitness and bodycomposition" were actually the typical already reaonably fit Crossfit clientele of whom Smith et al. somwhat awkwardly point out that they "had already been following a 'Paleolithic' type diet prior to and following completion of the training protocol." In other words the "levels of aerobic fitness" the participants spanned ranged from the untrained yet 100% healthy male with a VO2max of ~35 ml/kg/min to the hardcore crossfitter with a starting VOMax of >50ml/kg/min - the aforementioned heavily overweight and thus by now average (see "Obese is Going About to Become the New Normal") Westerner was yet not part of the study population.

Still, the presence of subject spanning the divide between "just healthy" and ripped and well-conditioned is in fact what attracts me as the author of a webpage that's dedicated to anyone ranging from those who just want to be / get / remain healthy and look not all-too shabby in front of the mirror to those who are looking to max out on their own physical performance and appearance. Long story short: The data you see in figure 1 is relevant for all of you. Even if you are still a couple of inches away from matching at least the initially criteria, you will sooner or later arrive at a point, where you'll find a representative counterpart of yours among the subjects of the study at hand.

Figure 1: Body fat percentage (left) and VO2Max (right) before and after the intervention (Smith. 2013)

I guess the data in figure 1 do actually speak for themselves: There is actually pretty much you can achieve within just 10-weeks of serious training: A significant (P<0.05) improvement of VO2max of 2.64% if you are a man and 11.78% if you are a women and (probably much sexier in the eyes of most of you) a 4% respectively 3% decreaes in body fat!

"To our knowledge no research on the aerobic benefits of HIPT has been conducted. HIPT focuses on high intensity resistance training usingmultiple joint exercises, with little to no focus on traditional aerobic activities. In spite of this, our results show that this type of training also provides aerobic and body composition benefits. Theincreased aerobic capacity of the subjects in our HIPT study were similar to those found in past research (Tremblay. 1994; Burgomaster. 2005). Based on the results presented here, individuals of all fitness levels and either gender can realize body composition and aerobic benefits from HIPT. Given that our subjects were following a Paleolithic diet, we cannot relate all of the observed weight loss to HIPT training. However, HIPT and Paleolithic diet in combination could be used to promote positive changes in body composition."

Now, all the scientists write is unquestionably true (also the part on the "paleo diet", as long as it is not very low carb paleo, cf. "Carbohydrate Shortage in Paleoland") and still, for me there are two things Smith et al. don't mention in the paragraph cited about and these are (A) the sex differences in terms of the VO2Max gains (maybe a result of the fact that women are not the ones who would otherwise do HIIT-esque workouts (=aerobic training at high intensities), so that the new stimulus will yield a greater results and (B) the fact that Crossfit is a workout regimen, from which even those benefit who are already fit and lean (keep in mind that the 16% in the lean group are for men and women, so that is lean!).

Bottom line: Crossfit appears to be the high intensity workout regimen which can help experienced trainees to make the transition from lean to ripped!

Want to do some more aerobics but also stick your classic weight lifting routine and just add cardio in? Now you are asking yourself, when this would make sense? Before, after or in between? Is that's you, go back in the SuppVersity archives and learn more.

As exciting as this may seem, a brief glance at the data in figure 1 will yet also tell you that those who are not up to the intensity and athletic demands of crossfitting don't just risk getting injured (please read the red box further up in the article, as well), they are also wasting their time with a workout that's not designed for their fitness level an will thus yield suboptimal results. This may not necessarily be the case in absolute terms - after all -4% body fat reduction certainly is not bad, but that's -4% from a pretty chubby baseline of 33% and actually could be achieved with basically any well-planned nutrition + exercise regimen. The latter obviously cannot be said of the -50% relative reduction in body fat percentage in the lean subjects on the other side of the "body fat divide". These men and women are most likely people who have been working out for all their lives in one way or another.

The "gifted ones" are in fact rather the ones who are often literally accused of being "genetically gifted" by accusers who simply don't take into consideration that it is above all the epigenetic priming of years of high school, college and other sports that renders them ostensibly resistant to the "obesity virus".

If you are still infected with the obsisty virus and have just found your way to physical culture you hardly qualify as one of those individuals by whom the original Crossfit workouts were created and are therefore certainly not among those people for whom these metabolically and technically demanding workouts were and still are designed.

If you do "qualify", however (and that is nothing you have to be born wirth, I myself once believed that I just did not have the genes to see my abs), cross fitting could fit in particularly well in your "beach-ready" plan, of which I'd hope you are already thinking about... I mean, spring is less than 3 weeks away (click here to learn more about setting up a workout routine)!

Addendum: Since I got several people asking for the lean mass changes, I thought I'd mention that there was a +1kg increase in lean mass in men and women. Unfortunately the scientists don't provide differential information for lean and heavier subjects, but if your body fat percentage decreases you do at least have to lose much more fat than lean mass and since there was no dieting involved, I bet the lean guys and girls did not lose any muscle..

References:

Burgomaster KA, Hughes SC, Heigenhauser GJ, Bradwell SN, Gibala MJ. Six sessions of sprint interval training increases muscle oxidative potential and cycle endurance capacity in humans. J Appl Physiol. 2005 Jun;98(6):1985-90.
Smith MM, Sommer AJ, Starkoff BE, Devor ST. Crossfit-based high intensity power training improves maximal aerobic fitness and body composition. J Strength Cond Res. 2013 Feb 22.
Tremblay A, Simoneau JA, Bouchard C. Impact of exercise intensity on body fatness and skeletal muscle metabolism. Metabolism. 1994 Jul;43(7):814-8.

99% of the guys & gals on this photo are not going to see anywhere similar improvements in body composition from marathon running as the highly trained 7x7 runners in the Karstoft study.

It's Friday and that means its time for the wrap-up of yesterday's installment of the Science Round-Up on SHR. Well, let's see then what this weeks Round-Up of the Round-Up has to offer. Somehow I felt like picking up something we did actually cover in the live-show yesterday (download the podcast here). I guess I want to give everyone the chance to look at the data himself in order to decide whether "rare sugar syrup" (RSS) is going to be the savior of the Western world and the unfortunate rest who's currently "westernized" by the big Ms, the big As and the rest of the corporate alphabet soup with a vested interest in the prosperity of mankind, or - to be precise - that the part of mankind who owns their shares ;-)

Rare Sugar Syrup has 90% of the sweetness of regular sugar + "cleaner taste" than HFCS

(IIda. 2013) -- Assuming that you've by now all listened to the podcast, I will stick to some additional explanations, citations and graphs in this follow up.

While D-psicose is not the only fructose epimer in rare sugar syrup, it is probable the one with the most potent beneficial effects on blood glucose management (learn more). One potential caveats of RSS is that its d-psycose content is only 5% with te rest being other hexoses including D-allose, D-sorbose, and D-mannose,

As the scientists point out, the main intention of their study was to assess whether their rare sugar syrups would suppress

"body weight gain and abdominal fat accumulation in rats fed on diets composed of different carbohydrate sources: starch, starch + HFCS (50:50), and starch + RSS (50:50) were examined. (Iida. 2013)"

Accordingly, they maintained their rodents on otherwise identical diets containing (on a per weight not per kcal basis!) 57% carbs, 18% protein, 4% fat, cellulose, added methionine and a couple of vitamin and trace elements with either plain corn starch, corn starch and HFCS or cornstarch and rare sugar syrup (see figure 1, left).

Now, as mentioned in the show, there is no debating that this feeding regimen worked and with "90% of the sweetness of sucrose, and a more rich and clean taste than HFCS" replacing HFCS with RSS could even improve the taste of respective products, but let's be honest: How likely is it that we are going to see products without HFCS and 50% of rare sugar syrup actually making up the lion's share of the processed junk in the super market anytime soon?

Figure 1: Carbohyrate content of the diets and weight of different visceral fat pads after the 8-week dietary intervention in otherwise healthy rodents on a cornstarch only, cornstarch + HFCS or cornstarch + RSS diet (Iida. 2013)

Isn't it more likely that you will see labels like "now with rare sugars" on the front of the packaging and the hardly legible figure "contains 3% carbohydrates from rare sugars" hidden on its back? I would think so and the fact that neither this study nor the general existence of this HFCS substitution did as of now hit the media certainly doesn't refute contradict this hypothesis.

7 marathons (!) in 7 days - A marathon a day keeps the fat stores at bay?

(Karstoft. 2013) -- I probably don't have to preface this part of the seconds with a "don't do this at home" (or anywhere else ;-), but I think it's nevertheless newsworthy that accordingly trained people can actually run 7 marathons in 7 days without the dreaded negative effects the average bro is expecting when he is just walking for 40min on a treadmill.

Figure 2: Body composition before and after the race (left) and changes in markers of muscle damage as well as hormonal changes and differences in markers of blood glucose management (right) in 8 experienced recreational runners participating in a multiple-marathonrunning event in which 7 marathons were completed on consecutive days (Karstoft. 2013)

Doesn't look so bad, ha? The reason I still stick to the initially voiced recommendation not to copy this protocol if you intend to lose body fat is pretty simple. The main reason "nothing" happened here is that the subjects were conditioned to run marathons.

That's the same "repeated bout effect, we have seen only a couple of days ago in the "No Pain No Gain" post (click here to go back) and the ~2kg of "muscle mass" are (despite being measured with DEXA) probably rather a result of glycogen hyper-compensation from tons of energy gels and pasta (the subjects did not follow a prescribed diet, but simply ate, drank and supplemented what had helped them on previous marathons), than structural increases in muscle tissue.

No high intensity training before a good night's sleep

Unless you have read the SuppVersity Circadian Rhythm Series, you have no right to complain about being overweight or undermuscled (read it ;-)

(Wong. 2013) -- After listening to the show, you know what you got to do once you got out of the bed, namely to switch on your bright light therapy lamp, but what do you have to do before you go to bed? I did actually discuss most of the things you should do (curtains, ear-plugs, turn the temperature down, etc.) in the Circadian Rhythm Series, but with the recent publication of a study by Wong et al. there is another thing you should - or in this case should not do and that's working out at a high intensity.

According to the results the researchers present in their soon-to-be-published paper in the Journal of Sports Science, a cycling exercise at intensities of 65% and 75% VO2Max lead to significant increases in light sleep and reductions in the recuperative REM sleep from 22.5% to 19& and 18.7% of the total sleep time.

Light exercise, in this study done at 45% and 55% of the VO2max, on the other hand did not have these side effects it did however not improve sleep, which is by the way an urban myth of which Driver and Taylor wrote in a Y2k paper in the Sleep Medicine Review that it "has yet to be established empirically" (Driver & Tailor. 2000).

That's it for today, unless you want to head over to the SuppVersity Facebook Wall and check out some of the news that are already available over there, e.g.

Newsweek title from the year 2000 - "Fat for Life?"; did his mother love her soy protein more than her son's health? (learn more)
"High" dose supplementation with vitamin C and/or E increases cataract risk - 1,000mg of vitamin C increase the risk +36% and 100mg of vitamin E by 57% (read more)
Aerobic fitness could have greater impact on academic achievement than obesity -- Although obesity is a concern for children, this study shows that aerobic fitness can have a greater effect on academic performance than weigh (read more)
Aqua Mel, Portuguese "folk medicine" works for the alleviation of simple symptoms of upper respiratory tract -- Effect probably mitigated by the phenols in the honey this product is made of (read more).
Serum albumin carries cholesterol out of the cells -- Hitherto scientists thought that this was a prerogative of HDL (read more)

If you don't like these or the other ones I did not mention just wait for further news to be posted. Alternatively switch of the computer and your mobile devices and head off into a well deserved weekend!

Don't worry, there is going to be a whole heap of short news tomorrow, you won't get bored... ah, you don't get bored on the weekend, anyway - do you?

References:

Driver H.S., Taylor SR. Exercise and sleep. Sleep Medicine Reviews. 2000; 4(4):387–402
Iida T, Yamada T, Hayashi N, Okuma K, Izumori K, Ishii R, Matsuo T. Reduction of abdominal fat accumulation in rats by 8-week ingestion of a newly developed sweetener made from high fructose corn syrup. Food Chem. 2013 Jun 1;138(2-3):781-5.
Karstoft K, James Solomon TP, Laye MJ, Pedersen BK. Daily Marathon Running for a Week - the Biochemical and Body Compositional Effects of Participation. J Strength Cond Res. 2013 Feb 25.
Wong SN, Halaki M, Chow CM. The effects of moderate to vigorous aerobic exercise on the sleep need of sedentary young adults. J Sports Sci. 2013 Feb;31(4):381-6.

You still have a couple of milli- or centimeter too much on your waistline? Let's hope this spring will provide ample time to work out in the sun, after all that's the energizing way to work out, something even virtual reality indoor exercise cannot compete with (Plante. 2006)

The SuppVersity figure of the week is "90". That was the average total amount of sunshine hours we got here in North-Rhine-Westphalia within the winter months (DWD. 2013; and there were places with only 40h!). A pretty depressing figure, in the literal sense. If you listened to the last installment of the Science Round Up (click here to download the podcast), you may remember that I was actually somewhat surprised to hear that this was the darkest Winter ever since the sunshine hours have been recorded - after all, I got my 45min of "artificial sunshine" in, every morning. So, just in case you are still wondering how it's possible to write a blogpost everyday, the data from a 2012 series of studies in Dutch schools would support that it's all about the right lighting (Sleeges. 2012).

Apropos news, here is your weekly serving of short news on all sorts of things... you are missing the exercise related news? Well, I saved those for a round-up and one or two individual posts in the course of the next week ;-)

Fiber renders mammalian guts colon proof (Nagy-Szakal. 2013) -- As a recent rodent study from the Baylor University suggest, it can hardly be too early to keep an eye on fiber intake. The mice in the pertinent study that had been randomly assigned to a low-cellulose (indigestible fiber that's present in fruits, veggies, whole grains etc.) diet had little to no protection against experimentally induced cholitis.

Semisynthetic non-fermentable viscous fiber Hydroxpropyl-Methylcellulose is imported pound-wise from China and ends up as E464 from in all sorts of food - obviously at too low dosages to do the anti-obesity trick, though (learn more).

Murine pediatric cellulose supplementation, on other hand, induces transient trophic and anticolitic effects, which is - and that's important (!) - dependent on a continuous supply of adequate amounts of dietary fiber. The same goes for the benefifical changes in the diversity of the gut microbiome which did largely decline after only 10 days.

The protective effect on the epithelial cell lining and the increase in surface area in response to cellulose supplementation should also facilitate the uptake of those vitally important nutrients, people with Crohn's etc. are lacking - a result that may well be significant for those of you who are trying to make the most of the nutrients and not just the energy in their diets.

Edit: As George Henderson rightly said, the study at hand does not talk about cancer protection, I simply inferred that from previous human studies such as Mendez (2007), Terry (2001) or Roth (2001), without mentioning that, my mistake, sorry for that. I still changed the headline to reflect the contents of the study and want to point out that George also makes a valid point stating that (a) fiber often replaces other less healthy nutrients in the diet and (b) that (my addition) "once the baby has been thrown out with the bathtub" and you already have Crohn's and co different rules may apply.

The diabesity syndrome - Is it the soda, or the bottle it's packaged in? (Indumathi. 2013) I am well aware that the doses of BPA we are supposed to get from our "diets" is way below those that are uses in rodent studies like the one by Indumathi et al., but don't you think that it is still remarkable that the same plastic poison aka BPA that leaches so readily into the acidic brown soup 50% of the US citizens guzzle on a daily basis, induces exactly the same nasty reductions in insulin receptor and GLUT-4 transporter expression, as well as glucose oxidation and the phosphorylation of Akt which are currently still ascribed exclusively to the soda itself (see figure 1).

Figure 2: Effects of 20 or 200mg/kg body weight of BPA on insulin receptor and Akt phosphorylation, GLUT-4 expression in skeletal muscle and systemic insulin and testosterone levels (Indumathi. 2013)

Now what's worst is that these pathological changes are not likely to be observed, because it happens "silently"; i.e. in the absence of elevated blood glucose levels.

Did you know that the amount of BPA that leaches from plastics increases by x40, when you dishwash and reuse them (Brede. 2003)? And worst of all, these figures were observed in baby bottles and thus objects those of us get in contact for whom the otherwise probably harmless exposure could actually be dangerous (DiVall. 2013). Exposure to higher temperatures of liquids in plastic containers in the summer (>40°C) is another factor which contributes to an increased leakage of BPA from the container into the liquid (Makris.2013)

With the latter being the only blood parameters that are evaluated on a regular basis within at least a reasonably large cross section of the population it's no wonder that many of us don't see how the diabetic beast and the BPA castrator are sneaking up on them before it's already too late. Obviously no reason for the FDA or any other governmental body to even bother. Aside from the U.S. Environmental Protection Agency which has published a reference dose of 0.05 mg/kg/day for BPA in 1993 (IRIS. 1993) an official acceptable daily reference intake for BPA is still lacking. Even if the current research does not suggest that our daily exposure is high enough to actually do any harm, I would expect the reference levels to reflect that - what about you?

In 1998 the Consumer Union wrote a letter to the FDA compaining about "endocrine disrupting chemicals" in cheese and dairy in plastics wrappings. I wonder if they knew about the masked phtalates in hygiene products, as well.

More news for the"Plasti-Nations" (various): A couple of days ago Wu et el. published a paper on the TSH and estrogen suppressive effects of phtalates in Taiwanese children. With >40% lower TSH levels and estrogen levels the changes, in the 4-5 year olds with the highest (500ppm) phtalate exposure from food stuff is alarming. The only good news is that it these changes appear to be reversible, when further exposure is avoided (Wu.2013).

Apropos good news, in December 2012, Fierens et al. investigated the effects of cooking at home on the phtalate content of foods and found that, except for veggies, the phtalate content of almost all foods decline after cooking (Fierens. 2012). I guess, I don't have to mention that this is not going to happen in a crock pot unless you pour away the brew.

What you should also keep in mind is that your diet is by far not the only way you are exposed to phtalates, as a group of scientists working at a University right around my corner elucidated (Koch. 2013). The "pro-breast cancer" monoethyl carboxylpentyl phthalates (MEPs) for example usually come from personal hygiene products (it's the stuff thats called "fragrance"). The dosage, by the way, was high enough for the scientists to be able to actually measure rises in MEP concentrations after people (esp. men, by the way) took a shower. Ah, and not to forget a non-negligible amount of the low molecular weight phtalates is simply with ubiquitous sources including dust and indoor air. Up to now convincing evidence for the role of this constant assault in any of the ailments our society is suffering from is not conclusive.

Don't like oats? Buckwheat has similar benefits (Stringer. 2013) -- In a recently published paper in the scientific journal Metabolism, a group of researchers from the University of Manitoba in Winnipeg, Canada, reports that the consumption of buckwheat cracker either instead of rice crackers or simply on their own could help both diabetics and non-diabetics maintain a healthy weight.

4x more iron, 3x more calcium, >9 times more magnesium, ~6x more potassium and about twice as much zinc, copper and manganese that's what buckwheat flour has to offer compared to wheat (de Francischi. 1994). If you like those figures, what about havin' one of the pancakes you see above (recipe)

Yet, despite an increased satiety effect and improvements (increases / decreases) in the corresponding hormones glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic peptide (GIP) and pancreatic polypeptide (PPY) the glucose response to the buckwheat crackers was not significantly different from the one the scientists observed after the consumption of rice crackers.

What's intriguing, though is that it appears as if these effects were not exclusively fiber-specific. After all, the rice crackers had almost as much fiber as the buckwheat. Moreover, a 2003 study Kawa et al. confirmed that even fiber-free buckwheat extracts exert potent anti-diabetic effects, the researchers ascribed to the presence of d-chiro-inositol in the extracts (Kawa. 2003).

Anabolic vibes - Vibrate your way to higher testosterone levels (Couto.2013) -- If you still believe vibrators were for women only you got to check out the latest issue of the International Journal of Sports Medicine, in which a group of Brazilian scientists reports that the use of one of those fancy vibration devices (20-Hz and 12-mm) during the lat pulldown induced greater increases in testosterone and lactate concentrations. Dunno if that will also work if you just swipe your girlfriends vibrator and honestly, I don't even want to know that ;-)

Does the testosterone and overall hormonal response to workouts even count, or are we still chasing a hormonal ghost? (Schoenfeld. 2013) -- In his latest review of the literature, Brad Schoenfeld who has been busy writing reviews on everything muscle heads are interested in within the last couple of weeks, picks the role of the endocrine response to exercise apart. In that, Schoenfeld points out that it is important to look close before you can tell whether or not a certain "hormone" will effect or even drive skeletal muscle hypertrophy.

Check out this previous analysis of post-workout anabolism here at the SuppVersity (read more)
There is for example ample evidence for the involvement of the muscle specific IGF-1 isoform IGF-1Ec, or its locally expressed splice-variant MGF and the presence of high and low responders (cf. West. 2012). Studies using its parent growth hormone, which used injections of the artificially produced recombinant growth hormone are of questionable value, since they lack the natural diversity of "growth hormones" (different GH peptides). Schoenfeld also points out that the evidence that testosterone is anabolic "is inconvertible" (Schoenfeld. 2013) and that the debate would thus have to center around its influence in the vicinity of a workout, where - and this is interesting - we actually know that the effects should occur only after the initial repression of androgen receptors is reversed.

In accordance with what I have pointed out in the Intermittent Thoughts on Building Muscle Series Schoenfeld comes to the conclusion that it would be inappropriate to totally discard the importance of the endocrine response to workouts (IGF-1 & Co, in particular), just because it does not promote the (imho totally overrated) short term protein synthetic response to exercise:
"Based on limited cellular signaling data, it is conceivable that the primary effect of post-exercise hormonal elevations is to increase satellite cell activity as opposed to mediating acute increases in muscle protein synthesis. If so, this could favor greater long-term increases in muscle hypertrophy without significantly impacting short-term gains." (Schoenfeld. 2013)
Obviously (and rightly so) Schoenfeld concludes this paragraph of the discussion of this excellent review with the sentence "This hypothesis requires further study." -- And you bet, I will keep an eye on the topic in order to let you know whether the 8% of which West and Phillips say that it's the upper limit of the contribution the transient increases in endocrine hormones have on skeletal muscle hypertrophy (West. 2012) is an over- or underestimation.

Excess magnesium is good for your testosterone levels, bad for your prostate and could potentially become fatal for your heart (Chandra. 2013) -- According to the latest results from a rodent study, it appears as if an excess intake of magnesium, ingested not as supplement but in form of magnesium sulfate in the chow, can boost testosterone levels by almost 30% (figure 1):
Figure 1: Testosterone levels prostate weight, luteinizing hormone and serum magnesium levels (all data expressed relative to baseline) after 15 or 29 days on diets with different magnesium content.
The increase in testosterone does yet not come without downsides in the form of slight, but significant increases in prostate size as well as a profound increase in magnesium levels, which would - if they were observed in human beings already mark the early stages of hypermagnesemia. So, as important an adequate amount of magnesium in your diet may be, it should be obvious that 1.5% of the diet or ~350mg/kg magnesium sulfate and thus 35mg elemental magnesium per kilogramm body weight (the HED of the dosage that was administered to the rodents; ) is simply too much - honestly, I am surprised that the rodents did not get chronic diarrhea, anyway ;-)

Since a wise man facebooked me earlier today to keep the SuppVersity posts short on this weekend, spending some time idling around, in order to avoid ending up totally burned out (I wonder if that really was an all altruistic advice of him ;-), I will now do just that - cut it short; yet not without pointing you towards the SuppVersity Facebook Wall, which does - as every day - hold 6-10 new short news for you to read up on.

+++ Have a nice weekend, everyone! +++

References:

Brede C, Fjeldal P, Skjevrak I, Herikstad H. Increased migration levels of bisphenol A from polycarbonate baby bottles after dishwashing, boiling and brushing. Food Addit Contam. 2003 Jul;20(7):684-9.
Chandra AK, Sengupta P, Goswami H, Sarkar M. Effects of dietary magnesium on testicular histology, steroidogenesis, spermatogenesis and oxidative stress markers in adult rats. Indian J Exp Biol. 2013 Jan;51(1):37-47.
Couto BP, Silva HR, Filho AG, da Silveira Neves SR, Ramos MG, Szmuchrowski LA, Barbosa MP. Acute Effects of Resistance Training with Local Vibration. Int J Sports Med. 2013 Feb 26.
de Francischi ML, Salgado JM, Leitão RF. Chemical, nutritional and technological characteristics of buckwheat and non-prolamine buckwheat flours in comparison of wheat flour. Plant Foods Hum Nutr. 1994 Dec;46(4):323-9.
DiVall SA. The influence of endocrine disruptors on growth and development of children. Curr Opin Endocrinol Diabetes Obes. 2013 Feb;20(1):50-5.
DWD. Press Release from February 27, 2013. < http://www.dwd.de/presse >
Fierens T, Vanermen G, Van Holderbeke M, De Henauw S, Sioen I. Effect of cooking at home on the levels of eight phthalates in foods. Food Chem Toxicol. 2012 Dec;50(12):4428-35.
Indumathi D, Jayashree S, Selvaraj J, Sathish S, Mayilvanan C, Akilavalli N, Balasubramanian K. Effect of bisphenol-A on insulin signal transduction and glucose oxidation in skeletal muscle of adult male albino rat. Hum Exp Toxicol. 2013 Feb 19.
Integrated Risk Information System (IRIS). Reference Dose (RfD): Description and use in health risk assessments. 1993 < http://www.epa.gov/ncea/iris/subst/0356.htm >
Kawa JM, Taylor CG, Przybylski R. Buckwheat concentrate reduces serum glucose in streptozotocin-diabetic rats. J Agric Food Chem. 2003 Dec 3;51(25):7287-91.
Koch HM, Lorber M, Christensen KL, Pälmke C, Koslitz S, Brüning T. Identifying sources of phthalate exposure with human biomonitoring: Results of a 48h fasting study with urine collection and personal activity patterns. Int J Hyg Environ Health. 2013 Jan 17.
Makris Kc, Andra S, Jia A, Herrick L, Christophi C, Snyder Sa, Hauser R. The Association Between Water Consumption From Polycarbonate Containers And Bisphenol-A Intake During Harsh Environmental Conditions in Summer. Environ Sci Technol. 2013 Feb 28.
Mendez, A M, Pera G, Agudo A, Bueno-de-Mesquita HB, Palli D, Boeing H, Carneiro F, Berrino F, Sacerdote C, Tumino R, Panico S, Berglund G, Manjer J, Johansson I, Stenling R, Martinez C, Dorronsoro M, Barricarte A, Tormo MJ, Quiros JR, Allen N, Key TJ, Bingham S, Linseisen J, Kaaks R, Overvad K, Jensen M, Olsen A, Tjønneland A, Peeters PH, Numans ME, Ocké MC, Clavel-Chapelon F, Boutron-Ruault MC, Trichopoulou A, Lund E, Slimani N, Jenab M, Ferrari P, Riboli E, González CA. Cereal fiber intake may reduce risk of gastric adenocarcinomas: the EPIC-EURGAST study. Int J Cancer. 2007 Oct 1;121(7):1618-23.
Nagy-Szakal D, Hollister EB, Luna RA, Szigeti R, Tatevian N, Smith CW, Versalovic J, Kellermayer R. Cellulose supplementation early in life ameliorates colitis in adult mice. PLoS One. 2013;8(2):e56685.
Plante TG, Cage C, Clements S, Stover A. Psychological benefits of exercise paired with virtual reality: Outdoor exercise energizes whereas indoor virtual exercise relaxes. International Journal of Stress Management, Vol 13(1), Feb 2006, 108-117
Roth J, Mobarhan S. Preventive role of dietary fiber in gastric cardia cancers. Nutr Rev. 2001 Nov;59(11):372-4.
Schoenfeld B. Post-exercise hypertrophic adaptations: A re-examination of the hormone hypothesis and its applicability to resistance training program design. J Strength Cond Res. 2013 Feb 25.
Sleeges PJC, Moolenaar MN, Galetzka M, Pruyn A, Sarroukh BE, van der Zande B. Lighting affects students’ concentration positively: findings from three Dutch studies. Lighting Research and Technology.June 22, 2012.
Stringer DM, Taylor CG, Appah P, Blewett H, Zahradka P. Consumption of buckwheat modulates the post-prandial response of selected gastrointestinal satiety hormones in individuals with type 2 diabetes mellitus. Metabolism. Available online 26 February 2013.
Terry P, Lagergren J, Ye W, Wolk A, Nyrén O. Inverse association between intake of cereal fiber and risk of gastric cardia cancer. Gastroenterology. 2001 Feb;120(2):387-91
West DW, Phillips SM. Associations of exercise-induced hormone profiles and gains in strength and hypertrophy in a large cohort after weight training. Eur J Appl Physiol. 2012 Jul;112(7):2693-702.
Wu MT, Wu CF, Chen BH, Chen EK, Chen YL, Shiea J, Lee WT, Chao MC, Wu JR. Intake of phthalate-tainted foods alters thyroid functions in taiwanese children. PLoS One. 2013;8(1):e55005.

Dexter Jackson was not the 26-year old natural bodybuilder in the study at hand, but he is the Winner of the Arnold '13 (Photo bb.com)

Who would have thought that!? Dexter Jackson won the Arnold Classic 2013. "The Blade" as Jackson is also called has been competing ever since 1999 and will thus probably be able to tell you one thing or another about the hardships bodybuilders have to go through during the pre-contest phase. It is these hardships today's SuppVersity post will be dealing with - the hardships of those who do (almost) everything to "peak" (=achieve the best conditioning possible) at day 0 and in this particular case without resorting to all the readily and less readily available "helpers" from the arsenal of the "big guys".

People like the 26 year-old caucasian, natural, professional bodybuilder, whose latest contest prep has been monitored by Lindy M. Rossow and her colleagues from the Department of Health and Exercise Science at the University of Oklahoma and her colleagues from the Creighton University and the University of Central Florida (note: the whole study period comprised 12 months, 6 months prep and 6 months follow-up and the data on diet and training volume were derived from the subjects meticulous food and workout logs).

Diet, meal planning and nutrient timing

With 5 meals per day and occasional week-by-week reductions in fat and carbohydrate intake (5-10g), whenever he felt he stagnated, neither the meal pattern nor the total energy intake (~2,500kcal/day) of the subject changed dramatically over the course of the pre-contest period.

With a ratio of 36/36/28 % the macronutrient ratio of the pro-bobyduilder who started out with a body-fat percentage of 14.8% (4-C model based on DXA and BOD POD data vs. 8.9% when measured by chest, abs and thigh skinfolds), was very balanced and actually pretty close to what I suggested in my interview with Sean for CasePerformance for both average Joes and Janes and aspiring gymrats alike (read the whole interview here).

Figure 1: Overview of the key aspects of the nutritional regimen in the pre-contest (Prep), immediately pre-contest (last wee before the show) and the subsequent recovery period (based on data from Rossow. 2013)

With two moderate carb-refeeds per week during which he increased his carbohydrate intake to 48% (see figure 1), the subject, who had won his pro-card two years before he agreed to participate in this study, stuck to the above macronutrient ratios until "just prior" to competition, when he dropped the carbohydrate intake to <30% and increased the protein intake to 46% keeping fats almost stable at 25%. When we do the math in order to calculate the corresponding nutrient intakes in grams we get ~207g of protein (, 130g of carbohydrates and 112g in the last phase of the contest prep.

There is evidence that a high carb bulk works best the classic way, i.e. with almost zero fat (read more)

"I don't want to gain fat too quickly afterwards": While the subjects declared goal for the post-competition phase was "not to regain body fat too quickly", his irregular and unquestionable ravenous eating habits tell us that he must have forgotten about that ;-)

No wonder his body fat levels shot up to 15.5% (higher than precontest) within 5 months, then stabilized and despite constant overeating began to drop again. What is an interesting side-note that over the whole study period, but especially in the off season, the often hailed skin-fold measurements hilariously underestimating the body fat content (the values were up to 8% off).

The only supplements the subject took were 5g/day of creatine and whey protein, which was already part of the regular diet and thus included in the macro-breakdown in figure 1 and the ~200g/day of protein I calculated based on the not exactly exhausting information about the exact macronutrient and energy content of the diet.

Strength and cardio - working out every day is key

A key contributer to the sustained weight- and, as we are going to see in figure 3 further below, fat loss at a relatively high energy intake (2,500kcal at a starting weight of ~100kg is obviously below maintenance, but no starvation diet) is probably the versatile workout routine with daily workouts, except on days before the exercise tests at the lab were conducted.

"During competitive preparation, per week on average, the subject performed four days of resistance training (5 hourst total per week), two days of high intensity interval training (HIIT, 40 minutes total per week), and one day of low-intensity, steady-state, aerobic exercise (30 minutes per week). This resistance training split allowed for the athlete to train each major muscle group twice per week."

This training regimen, as well as the often underestimated 30-60s isometric contractions during the 15-30 min posing practices the subject performed only once in the initial 1-6 weeks and 2-4 times per week during weeks 20-26, will have done one last thing to propel the fat loss in face of a constantly declining resting metabolic rate. The latter, as well as the hormonal changes, the dropping blood pressure and the - for a non-athlete - dangerously low heart rate all point towards one thing: Metabolic shutdown (see figure 2):

Figure 2: If you want to know about the hormonal / metabolic consequences of cutting down to sub-natural body fat levels (4.5% for the guy in the study) this is the graph to look at (data expressed relative to pre-prep values; based on Rossow. 2013).

As I have already hinted at in one of the infoboxes in figure 2 the resting metabolic rate the scientists measured only thrice during the 12-months observation phase, i.e. twice before and once after the contest dropped by >1,000kcal from week -25 to week -1 (=one week before the contest) and did not fully recover within the 12 weeks up to the subject's last REE assessment with a metabolic cart.

A note to the desperate haters out there: No, I did not check the guy's urine for additional "supplements", so I cannot know for sure whether he was indeed natural. What I do however know is that you were just about to post something along the lines of "you cannot achieve this level of conditioning without drugs" - obviously, without daring to do so under your own name. Do me and yourself a favor and spend the time and energy in the gym instead - thank you!

Starvation mode without starvation = continuous fat loss?

In view of these metabolic changes the drastic reduction in body fat (%) from 14.8% to 4.5% appears surprising. Likewise, common sense would tell you that the cortisol increase (more than +100%) would (a) burn away your muscles in no time and (b) stop your fat loss in tracks. The data in figure 3 does yet speak a very different language.

Figure 3: Body mass, fat free mass and body fat % over the 12-months study period (Rossow. 2013)

What the increase in cortisol did, was saving our dieter's brain from starving while getting him shredded by facilitating the catecholamine induced lipolysis (=squeezing the fat out of the cells) and bugging the liver to produce more glucose (Exton. 1972; Lamberts. 1975). That the substrate for the increased hepatic gluconeogenesis was not exclusively fat, but also protein should be obvious. As obvious as the fact the contribution of muscle protein was still negligible compared to the energy that came from the adipose tissue. Otherwise you could hardly explain that the subject lost not even 3kg of lean mass, while he dropped 14kg of body weight and kept the hydration level constant (62.6% at the beginning and 62.12% on contest day).

Chronically fatigued? Taking a meditative time-out with qigong twice weekly will improve mental + physical symptoms by ~50% & increase telomere-length by 75%! (learn more)

Bottom line: If you look at the time it took the subject of the study to get down to the <5% body fat range and at how his body reacted (cf. The Athlete's Triad), I probably don't have to mention that the notion that any of these guys, drugged or not, is running around like you see him on stage or in the magazines all year is hilarious.

This does also mean that any training program that aims at running around at real (and not caliper measured) single-digit body fat levels year round is destined to fail and will go hand in hand with hypogonadism, low thyroid levels, 6-7x elevated fatigue levels, confusion, anger, hostility and overall 7x higher levels of mood disturbances. I bet your significant other will like neither the former nor the latter symptoms and let's be honest, even if you are single, would this be worth it?

"So are natural bodybuilders stupid idiots?"

Certainly not! The exact opposite is the case, people like the subject in the study at hand have a goal and the plan, the determination and the guts to achieve it. They want to show up on stage in the best form possible, never knowing whether this will be enough to take the trophy home. They are sportsmen like so many other athletes; and while it may be debatable how healthy these ups and downs in body weight eventually are, I would venture the guess that natural bodybuilding is not unhealthier than American football.

So, if there is anything "idiotic" about bodybuilding, it would probably be its unintended downstream effects on some of the gymrats who believe they can have the upsides, i.e. the hyper-muscular contest-ready sub 5% body fat look, without the downside, i.e. the time spend at a normal body fat level of ~12-15%.

Moreover, if you look at the way the guy in the study broke through the 5% body fat wall, there is just one thing that sticks out: persistence! Patience and a stubborn persistence. No low-to-no-carb diets, no no-fat interventions, no protein only days, not even intermittent fasting or thermogenics and certainly no natural test boosters. If you feel that you have the persistence and want to step on stage, go for it, but be aware that it's not going to be an easy ride.

References:

Exton JH, Friedmann N, Wong EH, Brineaux JP, Corbin JD, Park CR. Interaction of glucocorticoids with glucagon and epinephrine in the control of gluconeogenesis and glycogenolysis in liver and of lipolysis in adipose tissue. J Biol Chem. 1972 Jun 10;247(11):3579-88.
Lamberts SW, Timmermans HA, Kramer-Blankestijn M, Birkenhäger JC. The mechanism of the potentiating effect of glucocorticoids on catecholamine-induced lipolysis. Metabolism. 1975 Jun;24(6):681-89.
Rossow LM, Fukuda DH, Fahs CA, Loenneke JP, Stout JR. Natural Bodybuilding Competition Preparation and Recovery: A 12-Month Case Study. Int J Sports Physiol Perform. 2013 Feb 14.

Is he (or she?) going to be muscular when he grows up, or is this kind of exercise just making him strong?

I guess we all know that the most muscular guys are not necessarily also the strongest men in the gym - but why is that the case? And moreover, how does this fit in with the notion that you'd have to use heavy weights to induce skeletal muscle hypertrophy? Yeah, I know. Many scientists believe that's nothing but "broscience" (cf. Burd. 2012) and if you look at the muscle fiber composition of a bodybuilder in this previously published article, you will see that it is by no means type II and thus "strength-specific". And let's be hones does not the advent of blood flow restricted training signify that we are about to witness a "paradigm change"? With the classic approach (heavy weight and 8-10 reps) being on the upper end of a "optimal growth continuum"?

Notwithstanding this contemporary trend towards "making light weights heavier" (let's be honest, BFR for example does exactly that), a group of researchers from the Health and Human Performance Laboratory at the Hofstra University and the Gridiron Training Facility in Hempstead, New York, did actually dare to "waste" their time on research on the opposite extreme of the heavy vs. light lifting divide.

Don't forget: The paradigm determines the research design

Before we delve further in to the methodological issues, let me briefly get one thing straight. Ghigiarelli and his colleagues firmly believe in the significance of the immediate and early endocrine response to a workout. They specifically cite the work from Stuart Phillips lab, I have been referring to numerous times times, but (and this is science, guys!) politely disagree with the conclusion that the relationship between elevated endogenous testosterone levels and hypertrophy function was non-existent or at least irrelevant, stating that...

Suggested read "Anabolic Workouts Revisited"
"[...] a much larger body of evidence supports the integral role that the acute hormonal response to RE [resistance exercise] has on muscle hypertrophy (Schoenfeld. 2010; Vingren. 2010) and its role in strength training adaptation (Hansen, 2001;Kvorning. 2006). Those in support of an endogenous testosterone response stand by the belief that RE causes an initial downregulation on AR content in the target tissue (i.e., skeletal muscle) followed by a subsequent upregulation during the recovery period, thus increasing free testosterone uptake facilitating protein synthesis." (Ghigiarelli. 2013)

It is therefore not a design flaw, when the scientists take the acute testosterone response to the workout as a measure of it anabolic potential and speculate that a strongmen-esque workout, which engages much more muscle fibers than even a compound based bodybuilding workout does, would elicit a stronger hormonal response than a "classic" hypertrophy training (additional read => the Saturdaily installment of On Short Notice) .

Real trainees, real workouts, real (?) results?

To probe their hypothesis the scientists recurited trained athletes from various athlete backgrounds. The mean age of the

tan recreational strength trainees (>4 training sessions per week, >2 years of training),
one wrestler and one football player,
two competitive bodybuilders,
one competitive powerlifter and one competitive o-lifter

was 24 years, whose mean 3-RMs , i.e. the weight the participants can maximally perform for 3 reps, were 161kg for the squat and 126kg for the bench press.

Main result: Not superior, but "similar"testosterone responses

I guess, when you read the word "similar" (which is a real quotation from the full text) in the above subheading and take a loot at the actual data in figure 1 some of you may not without good reason complain that Ghigiarelli et al. use the word "similar" pretty generously.

Figure 1: Salivary testosterone response to immediately after (post) and 30 min after work-matched classic hypertrophy, strongmen and mixed routines (Ghigiarelli. 2013)

If you look at the raw data on the left, it does after all look as if the classic hypertrophy workout with its squats, the leg presses, bench presses and seated rows was way more "anabolic" than

its strongmen counterpart that consisted of tire flips, chain drags, farmers walks, keg carries and stone lifts,

the mixed protocol which was build around tire flips, squats, chain drags, bench presses and stone lifts

when all exercises were performed for 3 sets x 10 reps with 75% of the weight the subjects could lift... and what should I say? You are right!

"Hold on! I don't see any 'similar' response!?"

What the average data in figure 1 (left) does yet not convey, are the large inter-individual differences. If you take those into account and use some statistical shenanigan to compensate for differences in the workout duration and the individual exercise intensity (whatever that may be, see Steele's recent paper on the absence of a clearcut definition of "intensity"), the superiority does turn into "a nonsignificant trend of greater testosterone release after the H protocol" (Ghigiarelli. 2013) - a trend, the researchers ascribe to the "abnormal response" they observed in response to the hypertrophy training (abnormal as compared to other studies, where the reponse hypertrophy training is usually in the 70% range, as well), which in turn would be attributable to 6 high responders with extreme spikes testosterone spikes of 165-493%.

Does true mastery of the exercise determine skeletal muscle anabolism?

Usually outliers like that are a problem, but sometimes there are cases where the exception from the rule has the greatest explanatory value and in this case, the latter may well be the case. How come? Well, the two hypothesis Ghigiarelli et al. come up with to explain the differences is simply too attractive to discard it as being irrelevant. Firstly, the scientists believe that it would be plausible that the anxiety level due to the unfamiliarity of strongman lifts may have reduced the testosterone spike.

You have no goals or don't track your results? Huge mistake (learn why)!
"This possibility is supported by previous literature examining the hormonal responses to different RE protocols in seasoned trainers (Beaven. 2008). Beaven et al. suggested that the novelty and stress of the situation are likely to be perceived based on experience. Thus, the stressors of the ST and XST sessions and the lack of familiarity of the exercises can suppress the actual physical nature of the stimulus. This psychological nature of the hormonal response in our subject pool may have caused a different response to protocols with which they were unfamiliar with or disliked." (Ghigiarelli. 2013)

Now, if you go one step further and expand on this idea by involving my mantra that training is not about moving weights from point A to point B and rephrase all that using a term Nicolas Burd et al. mentioned in their recent review in Applied Phyisology and Nutrition, in which they advance the idea that it does not really matter on which extreme of the low vs. heavy weight continuum you train, as long as your protocol elicits "high intensity contractions" (Burd. 2012), you could also argue that the subjects may have moved the weight for 3 sets of 10 when they did the farmer's walk etc., but did not to so using "high intensity contractions".

The intensity of the contraction determines the gains

Knowing the "101 of Pre Workout Protein Supplementation" can make a difference. Over all the supplement shenanigan many trainees do yet tend to overlook the basics and simply assume that as long as they move weight from A to B the use of the right powders and popping the right pills at the right times would have the largest impact on their results - big mistake!

In other words, the calculated "intensity" and the real muscular tension, i.e. the intensity of the contraction, were not identical and certainly sub-optimal for those of the trainees who have never flipped tires or carried kegs before. The bodybuilders and certainly also most of the recreational athletes may well have been so focused on the novel exercise that they could not pay any attention to the one thing that's at the bottom of skeletal muscle growth the "high intensity contraction".

Now, it is probably undebatable that the actual work that is done by the muscle and not the physical work, you would calculate by multiplying the weight (respectively the force you would apply to it in an ideal scenario) and the length of the way along which you dragged, carried or flipped it, is the physiologically relevant number here. In this context it would also be irrelevant, if the endocrine response to a workout does actually correlate with the net gains in muscle size or strength, as long as the "intensity of the contraction" did. In the end, it is thus not the weight or the exercise that determines the actual growth stimulus, but rather your ability to use a given weight in a given exercise to induce those damn high intensity contractions.

Bottom line: For 90% of the trainees out there, the first step to improve their gains would thus to improve their game. To take the true meaning of "training", of which the venerable Oxford English Dictionary says that it is "the sustained instruction and practice (given or received) in an art, profession, occupation, or procedure, with a view to proficiency in it." (OED Online. 2012). For the majority of trainees I see at the gym, it would thus be much wiser to follow Adelfo Cerame's recent advice and focus on a handful of exercises, instead of hopping from one exercise to the next, whenever a study says: Subjects, X,Y and Z gained 0.5% more mass doing farmer's walks vs. squats.

For others, it may yet be time to move on or to expand their arsenal of exercises with what Ghigiarelli et al. feel are "unique and exciting" exercises which provide "effective alternative to traditional resistance training, but require a lot of training to even master them "manipulate the specific combinations of rest intervals, loading, and volume toward [your] desired training goals" (Ghigiarelli. 2013).

References

Beaven CM, Gill ND, Cook CJ. Salivary testosterone and cortisol responses in professional rugby players after four resistance exercise protocols. J Strength Cond Res. 2008 Mar;22(2):426-32.
Burd NA, Mitchell CJ, Churchward-Venne TA, Phillips SM. Bigger weights may not beget bigger muscles: evidence from acute muscle protein synthetic responses after resistance exercise. Appl Physiol Nutr Metab. 2012 Jun;37(3):551-4. doi: 10.1139/h2012-022. Epub 2012 Apr 26.
Ghigiarelli JJ, Sell KM, Raddock JM, Taveras K. Effects of strongman training on salivary testosterone levels in a sample of trained men. J Strength Cond Res. 2013 Mar;27(3):738-47.
Hansen S, Kvorning T, Kjaer M, Sjøgaard G. The effect of short-term strength training on human skeletal muscle: the importance of physiologically elevated hormone levels. Scand J Med Sci Sports. 2001 Dec;11(6):347-54.
OED Online. "training, n.". December 2012. Oxford University Press. < http://www.oed.com/view/Entry/204425 > accessed March 04, 2013.
Kvorning T, Andersen M, Brixen K, Madsen K. Suppression of endogenous testosterone production attenuates the response to strength training: a randomized, placebo-controlled, and blinded intervention study. Am J Physiol Endocrinol Metab. 2006 Dec;291(6):E1325-32.
Schoenfeld BJ The mechanisms of muscle hypertrophy and their application to resistance training.J Strength Cond Res. 2010; 24: 2857–2872.
Steele J. Intensity; in-ten-si-ty; noun. 1. Often used ambiguously within resistance training. 2. Is it time to drop the term altogether? Br J Sports Med. 2013 Feb 12.
Vingren JL, Kraemer WJ, Ratamess NA, Anderson JM, Volek JS, Maresh CM. Testosterone physiology in resistance exercise and training: the up-stream regulatory elements. Sports Med. 2010 Dec 1;40(12):1037-53.

Protein, sugar or plain water - what if it would not even matter what was in his bottle, as long as he is still young, works out hard and gets his 1.2g+ protein per kg body weight from whole foods?

If this is not the first time you're here at the SuppVersity you are unquestionably aware that the effect size of the tried and proven peri-workout supplementation is totally overrated. Notwithstanding, a protein supplement and especially a fast digesting whey protein is one of the SuppVersity Suggested Staple Supplements; one of those supplements of which even I claim that 99% of the trainees can benefit. So what do we do with the results of a recently published paper by Ashley A. Walter and her colleagues from the University of Kansas Medical Center, the University of Kansas, the California State University-San Bernardino, the University of North-Carolina-Chapel Hill and the University of Central Florida?

Have we been doing it wrong, all the time?

Do we simply ignore their data, which indicates that 8 weeks of resistance training (three times per week, chest + legs) does increase muscle performance and size similarly among all groups "regardless of supplementation" (Walter. 2013). Why no? I mean let's wrap this up and simply say, the study must be flawed. No wonder, actually, after all the idea to investigate the differential effects of different forms of protein (regular vs. "bioenhanced" = pegylated* whey), different workout volumes 3 vs. 5 sets and a placebo vs. a "no supplement at all" control group looks like one of the classic mistakes science greenhorns ake. A mistake I know only all to well fro the real world university (not the SuppVersity), where overeager students of mine who try to write the "Jack of All Traits" Bachelor or Master thesis in 99% of the cases produces a garbled mess with little or no scientific value.

What is pegylation? Pegylation refers to the process of binding a molecule, like a small peptide or amino acid to polyethylene glycol in order to increase its bioavailability. It's common practice with pharmaceuticals and has already shown some promise in previous studies with pegylated creatine (e.g. Camic. 2010). Especially in the case of PEG creatine, it is however questionable, whether the higher bioavailability, which does nothing, but reduce the dosage requirements (Herda. 2008), would be worth the additional costs. My personal answer to that question clearly is "no" and the fact that these expensive products actually never had a breakthrough on the market would confirm that the marginal utility is zero (or negative ;-)

On the other hand, there is no debating that the study at hand, with its 106 healthy active male volunteers (mean age 21 years, body fat 10-25%; ~60% with aerobic training, ~40 percent with resistance training experience or both, as well as 60% performing other recreational sports regularly) and thus ~20 subjects per group is not underpowered, as you would expect and should thus in fact be able to spot differences between the 5 arms of the 8-week randomized, placebo controlled clinical trial:

bio-enhanced whey* protein with low volume training (BWP LV , n=22)
bio-enhanced whey protein with moderate volume training (BWP MV, n=20)

standard whey protein with moderate volume training (SWPMV, n=22),

placebo with moderate volume training (PLA, n=21),
control (=no suppleent) with moderate volume training (CON, n=21).

The supplement itself was chocolate-flavored and ingested on both workout days and off days: one before, one after the workout or a single shake at a self-chosen timepoint on the off day. The main difference between the "bio-enhanced" and the regular whey was the addition of 5g of polyethylene glycosylated (PEG) leucine to the baseline amount of 20g of whey. The placebo contained pure maltodextrin and the control group did not receive any drink whatsoever... actually this is something I have not seen before - a neat way to answer the question: How much of the efficacy of a tried and proven staple supplement lke Whey is actually in your head, only?

Enough of the presquabble let's take a look at the results

Looking at the plots in figure 1 certainly does not look like there would not be any differences to begin with, but once you realize the "differences" are almost exclusively negligible and well within the standard deviations of the respective parameters.

Figure 1: Changes in body composition (left), strength and strength endurance (right; Walter. 2013)

There are just two things that stick out, #1 is the statistically non-significant but still obvious fat loss advantage of not supplementing at all (marked by an arrow) and the other one is the lean and total mass disadvantage of the ...

Note: Both programs involved training chest and legs thrice a week, which should obviously be enough of a growth stimulus. If you doubt that or believe that it may even be too much, take a look at the success of the guys in the control groups.
low volume training program , which involved an onramp up to 3 sets of 6 reps with 80% 1-RM on the bench and the leg press,compared to the

high volume program, in the course of which the subjects performed 5 sets of 6 reps with 80% 1-RM on the bench and the leg press

This observation does in fact fit pretty well with rationale the scientists use to explain the non existence of any measurable differences between the 5 arms. "[A]midst the anabolic stimulus of resistance training." (Camic. 2013), the additional growth stimulus any amount of protein could add to the already high basal level of workout induced MPS in young men would simply be negligible (cf. Volpi. 2001; Yarasheski. 2002).

"This may partially explain why this study showed no significant effects of protein supplementation beyond the resistance training during the 8- week study period, regardless of treatment group.[...] Our primary outcome variable was muscular strength changes. While the present study indicated strength changes in all groups, the importance of a lack of additional change in the groups with protein supplementation." (Walter. 2013)

What is yet interesting is tthat not just the protein supplementation but also the ~40-45% higher volume in the "-MV"-groups (medium volume training) vs. the "-LV"-group (low volume training) did bring about significant changes in 55-59% of the resistance training volume elucidated significant differences in strength or size gain.

Suggested read "Greater & Steadier Strength Gains w/ 8 Sets of Squats." (Article I) and "Higher Volume Increases Strength Gains in Legs, Satellite Cell Recruitment and Fiber Size in Legs & Traps." (Article II)

Unfortunately, it cannot be said if the protein supplementation did in this case create an equal playing field or not, although the researchers' statement that

"[...] these findings suggest that when a moderate- or high-volume of resistance training is not possible, consuming protein and amino acids in conjunction with a low-volume resistance training program may be sufficient for achieving equivalent results" (Walter. 2013).

appears to suggest just that: The fallicious believe that you can "out-supplement" suboptimal training routines. This does not necessarily mean that you got to to 5 sets of every of the X exercises you do, but if you stick to only one, you better make sure to have at least five sets esp. for legs and other large muscle groups (check out the suggested reads on the right for more information: Article I, Article II)

Apropos level playing field

A brief glance at the data in figure 1 shows that (a) the protocol did work out as it is supposed to be and only the guys in the protein supplement groups did actually exhibit a significant increase in protein intake, and (b) that the overall protein intake on a per kg of body weight base was - quelle suprise (!) - exactly where the many ofthe latest reviews say it has to be, in order to support optimal protein synthesis in young men: in the +1.2g range (e.g. Coleman. 2012).

Figure 2: Protein intake before (pre, no supp) and during the study period in the different arms of the study (left) and respective protein intakes relative do body weight in the different groups (right)

Without significant differences in any other of the established nutritional parameters - first and foremost the overall energy intake, the only argument left would be that consuming even more protein on a daily basis may make the difference.

The lack of MPS data is a definitive, but by no means rare downside of the study

Figure 3: Fractional protein synthesis (FSR) in the Moore study (young participants leg curls + leg extension medium intensity, red), in which a ceiling effect occurred and the Yang study (old participants rel. light workout, blue), where the latter was absent (originally published on February 11, 2012)

If we did yet follow this rational we would have to discard 90% of the muscular protein synthesis (MPS) data from previous studies we have become so fond of. After all, 90% of the pertinent and heavily cited data is based on trials using only 20-30g of whey after a workout. And if taking the protein before and after the workout would be a problem this would only compromise the body recompositioning effect, superior strength and size gains should yet still be visible. And taking more? Well, the 40g of whey (20g pre and 20g post) used in this do actually already approach the "ceiling level" after which the marginal utility of additional protein approaches zero - at least in young trainees and after a reasonably intense workout (read up on my previous comparison and elaborations on the data from young and old individuals from studies by Moore et al. and Yang et al.; cf. figure 3).

In the end, comparisons like the former involving MPS / FSR studies like the ones by Moor et el. with the study at hand would yet require the presence of respective data for the early mid- and end-phase of the Walter study. Since this data is not present and in view of the fact that we do actually have to be as skeptic about the prognostic value of MPS data measured in the immediate vicinity of a workout as we are about the heavily scrutinized "anabolic" response to a workout (cf. yesterday's post and the suggested reads), the overall significance of the study at hand remains questionable.

As questionable, by the way, as the researchers discussion of the "practical implications". After stating for the fifth time that supplementation clearly did nothing to augment the exercise induced increase in size and strength, the researchers suddenly don't dare to speak out the only logical consequence, i.e. "there is no use in protein supplementation" and walk the eggshells instead when they state:

Acutually you could also argue that using stevia as a sweetener may benefit older trainees and people on low volume routines. I've written about its potential effect on satellite cell recruitment over a year ago, already (learn more)
"Furthermore, athletes could benefit from a low-volume regimen in conjunction with protein supplementation while recovering from injury and completing their prescribed rehabilitation program. This may potentially speed up the recovery process and decrease the event of post-injury complications. As active adults age, they are encouraged to maintain or increase activity. However, less is known about how older adults may respond to whey protein and leucine supplementation in conjunction with chronic resistance exercise. A lower-volume of resistance exercise plus supplementation can potentially benefit untrained or detrained individuals, similar to moderate-volume without protein supplementation.

It is also possible that older adults and elderly patients may have a higher aptitude to respond to the anabolic effects of protein supplementation and resistance exercise. Additionally, it is possible that PEG may be more beneficial for the absorption of the amino acids in those with difficulties digesting nutrients, rather than healthy young men that already have a high basal MPS rate." (Walter. 2013; my emphases of the conditionals and speculations)

I don't know about you, but in my mind the best term to describe aftertaste that remains after reading this "conclusion" is "Much Ado About Nothing" ;-)

Bottom line: Since the above "practical implications" are probably of little use to you, let me give you mine. Forget about everything but the fact that protein synthesis may not be the best indicator of long(er) term real world strength and size gains and stick to the tried and proven. Mix 20-30g of whey (plus 10-20g casein, optional) after your workout add 1-2 bananas / or some instant oats (amount depends on whether you are trying to build muscle or cut body fat), head home, have a full meal within the next hour or so (don't freak out if it takes 61 or even 90min until you get something to eat) and - last but not least - make sure that each of your whole food meals has at least 20-30g of EAA rich whole protein in it. That's it! Easy, right?

Hydrolysates have clear advantage over EAAs (learn more). Plus, w/ the isoleucine-dipeptides they may even outperform regular whey. The study to prove that in a realistic scenario has yet to be conducted, though.

What? Oh yeah, you want to know if you should buy PEG whey? Well, I guess the results of this study speak for themselves, don't they? So even if the claims I've found in a patent by someone who goes by the telling surname "Guru" and reports a 5x higher amino acid accumulation from micronized PEG enriched whey compared to its conventional counterpart were not just the result of non-peer-reviewed "experiments" (Ramanathan. 2010), which have been conducted for only one purpose, i.e. making the patented product shine, you probably don't have to worry that you could be missing out on this one.

If you insist on trying something different, I would rather suggest you take a look at the readily available and as of now no longer that expensive protein hydrolysates. No, not for their fast absorption, but rather for their unique small peptide structure (suggested reads: Isoleucine-dipeptides and GLUT-4, hydrolysate vs. EAA)

References:

Aragon AA, Schoenfeld BJ. Nutrient timing revisited: is there a post-exercise anabolic window? J Int Soc Sports Nutr. 2013 Jan 29;10(1):5.
Camic CL, Hendrix CR, Housh TJ, Zuniga JM, Mielke M, Johnson GO, Schmidt RJ, Housh DJ. The effects of polyethylene glycosylated creatine supplementation on muscular strength and power. J Strength Cond Res. 2010 Dec;24(12):3343-51.
Coleman, E. Protein Requirements for Athletes. Clinical Nutrition INSIGHT: September 2012; 38(9):1–3.
Herda TJ, Beck TW, Ryan ED, Smith AE, Walter AA, Hartman MJ, Stout JR, Cramer JT. Effects of creatine monohydrate and polyethylene glycosylated creatine supplementation on muscular strength, endurance, and power output. J Strength Cond Res. 2009 May;23(3):818-26.
Moore DR, Robinson MJ, Fry JL, Tang JE, Glover EI, Wilkinson SB, Prior T, Tarnopolsky MA, Phillips SM. Ingested protein dose response of muscle and albumin protein synthesis after resistance exercise in young men. Am J Clin Nutr. 2009 Jan;89(1):161-8.
Ramanathan, Guru. Dietary Ingredient With Enhanced Bioavailability. United States Patent Application. Pub. No. US2010/0209558A1. August, 2010.
Volpi E, Sheffield-Moore M, Rasmussen BB, Wolfe RR. Basal muscle amino acid kinetics and protein synthesis in healthy young and older men. 2001; JAMA 286:1206-1212.
Walter AA, Herda TJ, Costa PB, Ryan ED, Stout JR, Cramer JT. Muscle Performance, Size, And Safety Responses After Eight Weeks Of Resistance Training And Protein Supplementation: A Randomized, Double-Blinded, Placebo-Controlled Clinical Trial. J Strength Cond Res. 2013 Feb 25.
Yang Y, Breen L, Burd NA, Hector AJ, Churchward-Venne TA, Josse AR, Tarnopolsky MA, Phillips SM. Resistance exercise enhances myofibrillar protein synthesis with graded intakes of whey protein in older men. Br J Nutr. 2012 Nov 28;108(10):1780-8.
Yarasheski KE, Welle S, Nair KS. Muscle protein synthesis in younger and older
586 men. JAMA. 2002; 287:317-318.

I know it's difficult to resist guys, but first things first: Study confirms, you better train the large muscle groups of the upper body first, before you go progress to what many of you probably love the most... no, not what you think now, I am talking about training arms ;-)

I know that you probably think that I had forgotten about the exercise science quickie I announced in Saturday's installment of On Short Notice. Today's SuppVersity article is written proof that this is not the case. With topics that range from the redundancy of Kaatsu aka blood flow restriction and intense workouts and the beneficial effects of training the large muscle groups first in your workout to the usefulness of the internal and external application of cold water and other stuff before and after workouts to elicit performance gains and speed up recovery and the unique benefits only heavy resistance training has to offer to elderly bones, I'd hope that everybody will find at least one item he / she is interested in.

And in the fortunate case that you know all the "right" to the true or false", already, you may want to pick up a couple of recent SuppVersity Facebook news to satisfy your cravings.

Adding blood flow restriction on top of already intense workout is probably useless

(Holis. 2013) -- No further improvement if intensity is already high!? Yep, that's at least what a recently published study by scientists from the Universityof Exeter would suggest. The researchers subjected 9 physically-active male participants to three weeks of intensive single-leg knee-extensor exercise training. Each training session consisted of 25 min of interval training. During those sessions the subjects had one leg cuffed (F(I)O(2) 14.5 ± 0.1%; IHT leg - don't worry if you don't get what this means; that just means that you would need someone to apply the cuffs for you, anyway ;-) while the other served as a control (INT).

Suggested read: A brief summary of a summary o the current state of the art as far as blood flow restricted (BFR) / Kaatsu training is concerned (read it).

When they evaluated the results, Holis et al. found that neither the most straight forward parameter, namely the time-to-exhaustion during incremental exercise nor the changes in muscle metabolite concentrations during the workout were significantly different between the groups.

Now this does not necessarily mean that there may not be minimal or other benefits you could derive in the long run (I am thinking about mitochondrial biogenesis) by making an already intense routine even more intense via BFR. However, if there was such an effect, it is probably going to be minuscule and certainly not something anyone, but an Olympic athlete would benefit from.

Large muscle groups first! Common BB-wisdom confirmed once again

(Simã. 2013) -- You've certainly heard about the "growth promoting effects" of squats, deadlifts etc., right? Of course you have! And as a diligent student of the SuppVersity you will also be aware that this growth promoting effect is supposed to be the result of the workout induced endocrine response.

Want another Exercise Science Quickie? What about news on light training with high TUTs, the HIIT vs. Liss Formula for more T, DHT & cortisol and the effects your left leg has on your right one (learn about all).
.
"The results indicate that the GH concentration increased after both sessions, but the increase was significantly greater (p < 0.05) after the sequence in which larger muscle-group exercises were performed prior to the smaller muscle-group exercises. No differences were observed between sessions for TT [total testosterone], FT [free testosterone], SHBG [sex hormone binding globulin], C [cortisol], or the T/C [testosterone / cortisol] ratio at baseline or immediately after resistance exercise. These results indicate that performing larger muscle-group exercises first in an upper-body resistance-exercise session leads to a significantly greater GH response." (Simã. 2013)

Don't worry I am not going to discuss for the 1003rd time, whether the absence of any hormonal difference outside of the increased growth hormone response is good or bad for your gain. I just want your to memorize that the GH response corresponds with the workout volume, which was significantly higher, when the 20 male subjects trained the large muscle groups of the upper body before the smaller ones. So even if it was only a question of workout economy, the longstanding rule of thumb to train large muscle groups first would obviously still have its place in today's in parts sometimes ueber-scientificated workout planning.

Competitive sports is not a good means to protect your bone mineral density

(McCory. 2013) -- According to the latest study from the University of Pittsburgh Clinical and Translational Research Center old the mere participation in regular (intense), bot not strength specific physical activity alone does not offer any protective effect against age induced bone loss.

"Our results imply that participation in highly competitive senior athletics does not have a protective effect on BMD, perhaps because of a lower bodyweight or other confounding factors." (McCory. 2013)

Among the parameters which did apparently figure were (you guessed it) bodyweight, and calcium and vitamin D intake. The higher those three parameters were the better the bone mineral density. Plus: The knee extension peak torque explained another 3.4% of the variance, but only in the hips.

Taking calcium supplement has been associated w/ prostate cancer and CVD in some, but not all studies (Baron. 2005; Spence 2013) With up to 14x elevated lead levels in some OTC calcium supplements the differences may well depend on whether you pick the wrong one (learn more).

That being said I personally believe we'd have seen very different study outcomes if the researchers had not made the common mistake of confusing "sports" with endurance exercise and would thus not have narrow-mindedly focused on those participants of the "Senior Olympics", who competed in running events longer than 400 m (n = 44; 28 males, 16 females), cycling events longer than 5K (n = 17; 11 males and 6 females), and any swimming event (n = 43; 25 males and 18 females). After all, a very recent study from the Catholic University of San Antonio did just confirm that high resistance circuit training (HRC) and heavy strength training can improve the bone mineral density in an elderly population (Romero. 2013). And what's more, the high resistance had the added benefit of inducing significant improvements in body composition in the thirty-seven healthy men and women (61.6±5.3years) who participated in the randomized trial.

Is cooling a useful tool for performance recovery?

(Poppendieck. 2013) -- According to the latest review by scientists from the University of Saarbrücken, Germany, "the average effects of cooling on recovery of trained athletes were rather small (2.4%, g=0.28)" (Poppendieck. 2013) With a peak in performance increase roughly 4-days after the initially exercise bout and the greatest benefit being observed with endurance athletes, it does also look as if there were particular subgroups of athletes who'd benefit most: Those expose their bodies to several high intensity stimuli within a relatively short timespan, namely.

What about pre-cooling, then? With average performance increases of +8.6%, +6.0% and +4.2% endurance athletes performing open-end tests, graded exercise tests and time trials are the ones who benefit most. Similar effect was observed for intermittent sprints (+3.3%, g = 0.43), whereas performance changes were smaller during short-term, high-intensity sprints (−0.5%, g = 0.03). Across all sports included in the most recent review of the literature (Wegman. 2012), cooling the musculature before a training session will have a larger effect on performance in hot (+6.6%, g=0.62) than in moderate temperatures (+1.4%, g = 0.004).

The most promising cooling methods were cold drinks (+15.0%, g= 1.68), cooling packs (+5.6%, g = 0.70) and a cooled room (+10.7%, g = 0.49), whereas a cooling vest (+4.8%, g = 0.31) and water application (+1.2%, g = 0.21) showed only small effects. Regardless of the method, the best trained subjects (highest VO2Max) saw the greatest benefits.

For those who want to try it and don't have access to a cryotherapy chamber (effect +3.8%), I'd recommend to go "hard core" and do - irrespective of which muscle group you may have been training - a full-body water immersion. The latter has been shown to be 70% more effective than water immersion of individual body parts. The use of icepacks, on the other hand, will rather compromise than promote recovery (-1.4%).

Two bad, one good news: The first bad news is that this was it for today - at least if you don't count the facebook news that are already available, e.g.

Black cohosh for breast cancer prevention? The jury is still out there (learn more)
Adiponektin does not work in women? With a low type II fiber count and correspondingly lower receptor density it is at least not as effective as in men (learn more)
Whole grains taste like sh*t? That's at least what the participants of a recent epidemiological study thing and probably also the reason they won't eat them (learn more)

as well as as those I am still going to post within what probably would count as "today" at least for some of you.

These pics are more than 2 weeks old and I can tell you that Adelfo's "anatomy chart" physique has kept improving ;-)

The 2nd bad news is that there won't be a SuppVersity Science Round-Up tomorrow. I had hoped that my voice would recover, but since it failed me several times in the cause of the day, I heavily doubt that you would understand anything I would be grunting into the phone, anyway.

But don't worry, there is also good news. Tomorrow is one of those "every other week" Thursday's where Adelfo Cerame is "in the house" and will (at least that was the pan last week) fill you in on the differences between the current and previous content preps... and I can assure you that's going to be a post even those who are not planning to compete will probably find very useful (I hope you read this Adelfo, 'cause I am just rising the bar, here ;-)

References:

Baron JA, Beach M, Wallace K, Grau MV, Sandler RS, Mandel JS, Heber D, Greenberg ER. Risk of prostate cancer in a randomized clinical trial of calcium supplementation. Cancer Epidemiol Biomarkers Prev. 2005 Mar;14(3):586-9.
Holliss BA, Fulford J, Vanhatalo A, Pedlar CR, Jones AM. Influence of intermittent hypoxic training on muscle energetics and exercise tolerance. J Appl Physiol. 2013 Jan 10.
McCrory JL, Salacinski AJ, Hunt Sellhorst SE, Greenspan SL. Competitive Athletic Participation, Thigh Muscle Strength, And Bone Density In Elite Senior Athletes And Controls. J Strength Cond Res. 2013 Feb 25.
Poppendieck W, Faude O, Wegmann M, Meyer T. Cooling and Performance Recovery of Trained Athletes - a Meta-Analytical Review. Int J Sports Physiol Perform. 2013 Feb 02.
Romero-Arenas S, Blazevich AJ, Martínez-Pascual M, Pérez-Gómez J, Luque AJ, López-Román FJ, Alcaraz PE. Effects of high-resistance circuit training in an elderly population. Exp Gerontol. 2013 Mar;48(3):334-40.
Simão R, Leite RD, Speretta GF, Maior AS, de Salles BF, de Souza Junior TP, Vingren JL, Willardson JM. Influence of upper-body exercise order on hormonal responses in trained men. Appl Physiol Nutr Metab. 2013 Feb;38(2):177-81.
Spence LA, Weaver CM. Calcium intake, vascular calcification, and vascular disease. Nutr Rev. 2013 Jan;71(1):15-22.
Wegmann M, Faude O, Poppendieck W, Hecksteden A, Fröhlich M, Meyer T. Pre-cooling and sports performance: a meta-analytical review. Sports Med. 2012 Jul 1;42(7):545-64.

2013 ain't 2012: Different diet, different training, different macros, different physique... different placing!?

I am not sure if all of you read yesterday's SuppVersity Exercise Science Quickie, but those who did have probably already told their boss that they don't need an extended lunch-break today to listen to the "Thursdaily" 1PM EST installment of the SuppVersity Science Round Up on Super Human Radio. My voice did recover somewhat within the last 24h, but after a hefty dose of NAC I am now sniffin' and snortin' 24/7 - probably not exactly what you want to hear, I guess.

What you want (at least I'd suspect so) to read, however, is Adelfo's last blogpost before he is making his third and imho by far best-conditioned and thus promising attempt on winning his pro-card at the NPC Wheelchair Nationals on March 16, 2013... ah, I guess, I'd better let him tell the story... enjoy!

Roughly 11 days out & looking back

I am approximately 11 days out from CJ’s NPC Sunshine Classic & Wheelchair Nationals in Palm Beach, Florida, where I will try to make another attempt at trying to win the overall and possibly earn my IFBB pro card for the wheelchair division. So far I feel great! My food intake is high, my energy is up and I’m very confident that I have made all the right moves, adjustments and improvements this year to put myself in the best possible position to take it all down this year ;-) I joined a great team in 3DMJ, and am being mentored by a great coach in Alberto Nunez, who is a seasoned and experienced bodybuilder.

So, let's recap a couple of key features of this to previous ones....

As I reflect on this years contest prep/ bodybuilding season, I thought it would be interesting to compare notes from last years season to this year.

Nutritional Regimen - Which "diet" have I been following?

2012 = IF (Leangains)

2013 = IF (Leangains) + IIFYM (flexible dieting)

From a physiological perspective, 125g of carbs per day shouldn't be a problem for any non-diabetic - even if he/she does not work out (learn more)

In 2012 I followed an intermittent fasting meal protocol using a 16h to 8h fasting vs. feeding window. This year I used the same IF meal protocol (since I found success with it last year and it’s a protocol that works with my daily life schedules) but combined it with a flexible style of dieting that is also known as the acronym IIFYM "If It Fits Your Macros".

As I mentioned in previous posts, I don't abuse the IIFYM paradigm to stuff myself with all sorts of junkfood, my diet is still mostly clean, but the leeway it gives you is refreshing and takes away a lot of stress related to picking, preparing, packaging etc. foods (see next point, i.e. Food Choices, as well).

Food Choices - What type of foods have I been eating?

2012 = Stuck to your so called “clean foods”

2013 = I am not depriving myself of any type of foods; I’m eating what I want but use a 80/20 to 90/10 ratio of whole “nutrient dense” foods to processed foods, or what you would call “junk” food but I don’t like the word junk so I call it “fun” foods ;-)

Last year; even though I started to veer away from the whole “eating chicken breast and broccoli and brown rice” mentality and began to broaden my horizons in eating more variety of whole foods, I still basically stuck to your so called "clean foods" and I was just in the beginning phases of getting over my phobia of carbohydrates since I consider myself coming from a high fat/ low carb camp for almost 2 years on a dietary regimen that was more or less identical to the "anabolic solution diet".

So yes, even though I was eating a greater variety of lean meats, fruits, veggies, fats and whole food carb starches like tubers, I still deprived myself of foods like bread, oatmeal, grains, cereal because I still believed that they were evil, when it came to a body composition standpoint or even just when it came to general health.

Believe it or not, but the quote on the left, is actually from Adefo's very first post, here at the SuppVersity.

However, as you all know if you’ve ever read my very first Blog here on Suppversity and I’ll quote from it:

"My diet and training methods have evolved and will continue to keep evolving, because of my willingness to keep an open mind and apply and experiment with new strategies, methods and philosophies to my diet and training" - me

(Yes! I just quoted myself! Hahaha!) And that’s exactly what I did, I kept an open mind and gave IIFYM a shot just like I gave “IF” a chance last year, and guess what?

It all worked out for the greater good because the combination of an IF meal protocol combined with a flexible method of dieting has really taken me a step closer to that goal of finding a perfect diet that I can convert into a lifestyle and do long-term. Like I mentioned before… A diet should be able to synergistically co-exist with your daily life and social schedules, and is something that you can convert into a lifestyle and do long-term - that's fundamentally different from a "dietary intervention", under which you can easily subsume all the fad, single-sided and unflexible dietary regimen that work in the short run, but have you plateau before you even see your abs.

Training - Which type, how much and how intense was my training regimen?

2012 = Low volume/ high intensity – cardio was non-existent

2013 = hypertrophy/ strength split using an RPE scale – cardio was all throughout prep

Last year the majority of my training was very low volume/ heavy weight. My training consisted of 5x5 and EDT’s and reverse pyramids. The highest rep range I ever flirted with was 6-8. This year, I’m doing a split between hypertrophy and strength training using an RPE scale, and I would say the majority of my workouts would fall into the high volume category by common standards.

Does rest matter? Study finds 7-9% greater increase in muscle size w/ decreasing rest periods (learn more).

The main difference this year was the frequency of hitting the muscles and using just a handful of exercises as my staple and improving on them.

Last year I barely did any cardio except for probably the last 4 weeks of my prep to try to expend a little bit more energy but that was it. This year I incorporated a cardio regimen all throughout my prep... but to be honest: it was very easy – I started the first 2 to 3 weeks with none, then Alberto eventually prescribed 2x cardio session per week for 9 laps each session around a track. I completed those at a self-chosen until a couple o weeks ago, when he reduced the volume by 50%

As you may imagine this type of cardio regimen really wasn't a big issue... nothing compared o my previous HIIT sessions, for sure. I still feel that the additional laps on the track allowed me to keep my food high via carbohydrates -- and if I've learned one thing from this prep, then it is that the higher you can keep your carbs up while dieting the more beneficial it is for your physique.

Calories/ Macros - How much did I eat at the beginning of the prep?

Caloric zigzagging? (Re-)Read Adelfo's guest post "How I Break My Fast, Plan & Time My Macros and Use Caloric Zigzagging & Re-Feeds on a LeanGains Inspired IF Regimen" and learn more!

2012 = eeehhhh…??? around 1700/ 2000 kcal. (non-training/ training); 55-7g5 fat/ 150-200g carbs/ 150-200g protein (non-training-training) – skiploading style re-feed (basically eat as much high GI carbs as you can while keeping fat intake as low as possible.

2013 = 1960 kcal w/ a re-feed day 1x/ week; 40g fat/ 200g carbs/ 200g protein – 300g carb re-feed

Last year I experimented with caloric zigzagging, so my calories were higher on training days with a higher carb/ low fat intake and my calories were lower on non-training days with a higher fat/ low carb intake. And I didn’t start incorporating refeeds till later towards my prep or until I got lean enough to feel comfortable doing refeeds. This year I stayed consistent with my numbers and just had one re-feed day – so I had low days and one high day

Calories/ Macros - How much did I eat towards the end?

Adelfo has already written about the beneficial effects of a higher carb intake on your physique in a previous post onThursday, January 31, 2013: "Intermittent Carbohydrate Modulation as a Stepping Stone Towards an Anatomy Chart Physique"(read up on the article)

2012 = 1300/ 1600 kcal (non-training/ training days)
50-60g fat/ 50-100g carbs/ 150-190 protein (non-training-training day) – skiploading style re-feed

2013 = 2305 kcal w/ a re-feed day 1x/week
50g fat/ 240g carbs/ 200g protein – 325g carb re-feed

Last year I floated around sub 100g of carbohydrates for about the last 11 weeks of my prep and this year I started to gradually increase my food intakes 5-6 weeks out. I used weekly 25g increments (I’ll explain the process of how I started to bring my food later before I wrap up my blog)

With regards to my re-feeds; it was a bit more controlled this year compared to last years Sunday carb feasts I use to have. My fats this year were also on the lower end but still 20% of my total calories and I feel that this was another of the decisive factors that contributed to the clear improvements in my physique - with the low(ish) fat intake, I simply had way more room for carbs in my diet.

Comparison of Adelfo's pre-contest physique 2012 vs. 2013 (photos (c) Adelfo Cerame. 2012-13)

Well that’s all I got for today! I hope you enjoyed the notes PrimalKid ;-) but before I sign off, as I said I would; here’s a brief overview of how I started to gradually bring my food up to where it’s at now.

At about 6-5 weeks out is when coach Alberto started to gradually bring food back up via carbs but prior to that I was on about a 2 ½ week intensive dig of 100g/ day, then we increased 25g (125g) for about a week and a half, then increased another 25 the next (150g), then increased by 50g (200), then increased by just 25g last week (225g) and now increased by 15g this week (240g)… Oh and fat got increased by 10 somewhere during that week. lol.

But yeah… Coach Alberto felt that my body was lean enough for carbohydrates to start having a positive stimulating effect on my physique, and that my body was more capable of partitioning carbohydrates much more efficiently now that I am leaner.

I know this photo from motivationblog.org borders sexism, but you must understand ladies: Men are simple and lazy folks and you know about the importance of squats, anyways, right?

No, you're not mistaken exercise and fat loss science (at least statistically your favorites) in a single blogpost. And as if that was not already enough, two of my favorites are also part of the game: For one thing the subjects in the latest study from the National Institute of Fitness and Sports in Kanoya, Kagoshima, Japan deals with ways to tackle childhood obesity and for another thing, the results are quite impressive, despite the ingenious simplicity of the approach the scientists used to improve the body composition, increase the fitness level and build muscle strength and size in their adolescent study particpiants:

Do 100-rep body weight squats everyday after school!

For the ninety 13.7 ± 0.6 boys who participated in the study this meant that they were squatting to parallel for roughly 3 minutes 4-6 times per week, without extra weight.

Now you are probably thinking about some of the pampered and fattened Chinese children and how a body weight squat for them equals your 5-RM max, right? As unfortunate as it may be that this could in fact be the case, we are talking about Japan, here - not China - and our young subjects were by no means sedentary couch potatoes. On the contrary, they were 100% average Japanese school boys from a pilot school in Kagoshima (Japan). There were kids who played table tennis (n = 12) and volleyball (n = 11), participated in track and field (n = 5), and Japanese archery (n = 8) in the active arm of the study and baseball (n = 24) and soccer (n = 22) players, as well as boys who were swimming(n = 5) and practicing kendo (n = 3), regularly. In fact,

"[t]he number of times participating in a week and duration involved in their athletic activities in a day were 5.0 ± 2.0 days/week and 2.4 ± 0.9 h/day respectively." (Takai. 2013)

And what's more, all of the active students did take part in competitions at a regional level. The effects you see in figure 1 were thus not of the "Biggest Loser" variety.

Figure 1: Changes in body composition (left) muscle size and strength (right) in adolescent boys after 8 weeks of doing 100 body weight squats 4-5x per week (Takai. 2013)

Ok, the total amount of body fat, the boys lost was not earth shattering, but contrary to the aforementioned "biggest losers" there was not much be lost in the first place; plus, and this is really important, whenever we are talking about body recompositioning in adolescents. The effect was highly squat-specific and not a result of a group specific growth spurt (body height increased 6-7% in both groups in the course of the 8 weeks.

Let's not forget: There is more to physical culture & health than fat loss!

I know that fat loss probably is the "sexiest" benefit the (almost daily) squat episodes had, but let's not forget about the rest, i.e.

increases in lean body mass,
increases in muscle thickness and strength of the knee extensors, and
improved vertical jump height.

Which are certainly enough to validate the scientists conclusion that this simple and above all highly practical "exercise regimen" is a ...

"feasible and effective method for improving body composition, the strength capability of the knee extensors and jump performance in adolescent boys." (Takai. 2013)

I guess few of you will consider themselves "adolescent boys" any longer. Thinking of my 90-year old grandpa who did his squats and push ups every morning and made the German Sports Batchwith ease even in the summer before he passed away, I am however pretty sure that you will be hard pressed to find a man or women of any age who would not benefit from something as practical and time-efficient as doing 100 squats every morning before they hop under the shower.

Watching TV & eating junk is only part of the equation; what's missing here is the lack of sleep kids don't get, when they watch TV canned with coke and energy drinks all night (learn more).

A primer on frequent activity!? If you look at the number of studies associating the time you spend in a sedentary state with health outcomes ranging from cardiovascular disease over diabetes up to stroke and Alzheimer's that have been published only within the last months, it becomes more and more evident that the four workouts you may be squeezing into your tight "sit on your but and work" schedule ain't enough to keep you healthy, as long as you spend most of the rest of your time sitting (worst of all in front of a screen; cf. Wijndaele. 2007; Mark. 2008; George. 2013).

Now this wouldn't be science if there was not someone with counter-evidence such as Chaput et al. or Kwon et al. (2013), who found that moderate-to-vigorous (MVPA; ≥488 counts per 15 s) activity could very well protect adolescents from getting obese - whether the same applies to old(er) individuals is yet another story. That this probably ain't the case is supported by a study that's less than a week old and was published in the electronic version of the renowned journal Diabetologia ahead of print. According to Henson et al. who used "objectively measured" activity levels, breaks from sedentary time and total physical activity and MVPA of subjects with increased type II diabetes risk "were significantly inversely associated with measures of adiposity, but not with any other cardiometabolic variables after adjustment for sedentary time and BMI" (Henson. 2013; see Celis-Morales (2012) if you don't believe that using accelerometers instead of questionnaires makes a difference)).

My best bet is that we will never get a definite answer on this chicken or egg question, but an "in office" or "launch break" mini-workout is certainly not going to harm you - the same goes for taking the stairs instead of the elevator, for using the bike instead of the car or for walking to the small supermarket around the corner if you just forgot to buy some tomatoes or whatever.

The only thing that startles me is the absence of increases in sprint performance. It's difficult to say, but if you take a closer look at the baseline sports the participants were engaged in, my best bet is that the 24 baseball and soccer players in the control group, or rather their sports-specific training regimen are responsible for the difference. On the other hand, if we expand on this thought of confounding factors that may skew the study results, we would also have to expect that these boys should have major "fat burning advantage" over their table tennis, volleyball and esp. Japanese Archery counterparts in the active group. That being said, on a level playing field, the effect size may, in fact have been even more pronounced if the scientists had simply randomized the participants to the squat ad control groups.

If you also have something to hold to and do underhand chins, you can do a whole and in fact very effective full-body even when you are traveling. I mean, you still remember that the underhand pull-up is a formidable biceps exercise, as well (learn more)?

Bottom line: Much in line with the astonishing fat loss results Smith et al. observed in already fit crossfit athletes (cf. "Crossfit Your Way Down from 16% to 8% Body Fat"), the study at hand provides further evidence in favor of "light" full body workouts or plyometrics (cf. "Building the Jack-of-All-Traits Legs Workout With Squats, Jump Squats and Body Weight Plyometrics"), not necessarily as a replacement, but rather as an adjunct / way to diversify your habitual routine.

Tweaks / adjuncts like these may well be able to rekindle and maintain constant progress - especially in terms of physical conditioning and explosive performance. Not to mention that adding 50 push ups and pull-ups to the equation would make a perfect "travelers workout", which can be performed wherever you can bring and install a doorway pull-up bar. And if you can't do 50 in a row, just use a rest pause technique: Do as many as you can, rest, take 10-12 deep breaths and continue counting from where you stopped in your previous "set" until you hit the targeted rep range.

References:

Celis-Morales CA, Perez-Bravo F, Ibañez L, Salas C, Bailey ME, Gill JM. Objective vs. self-reported physical activity and sedentary time: effects of measurement method on relationships with risk biomarkers. PLoS One. 2012;7(5):e36345.
Chaput JP, Lambert M, Mathieu ME, Tremblay MS, O' Loughlin J, Tremblay A. Physical activity vs. sedentary time: independent associations with adiposity in children. Pediatr Obes. 2012 Jun;7(3):251-8.
George ES, Rosenkranz RR, Kolt GS. Chronic disease and sitting time in middle-aged Australian males: findings from the 45 and Up Study. Int J Behav Nutr Phys Act. 2013 Feb 8;10:20.
Henson J, Yates T, Biddle SJ, Edwardson CL, Khunti K, Wilmot EG, Gray LJ, Gorely T, Nimmo MA, Davies MJ. Associations of objectively measured sedentary behaviour and physical activity with markers of cardiometabolic health. Diabetologia. 2013 Mar 1.
Kwon S, Burns TL, Levy SM, Janz KF. Which Contributes More to Childhood Adiposity-High Levels of Sedentarism or Low Levels of Moderate-through-Vigorous Physical Activity? The Iowa Bone Development Study. J Pediatr. 2013 Jan 7.
Mark AE, Janssen I. Relationship between screen time and metabolic syndrome in adolescents. J Public Health (Oxf). 2008 Jun;30(2):153-60.
Smith MM, Sommer AJ, Starkoff BE, Devor ST. Crossfit-based high intensity power training improves maximal aerobic fitness and body composition. J Strength Cond Res. 2013 Feb 22.
Takai Y, Fukunaga Y, Fujita E, Mori H, Yoshimoto T, Yamamoto M, Kanehisa H. Effects of Body Mass-Based Squat Training in Adolescent Boys. Journal of Sports Science and Medicine. 2013; 12:60-65.
Wijndaele K, Duvigneaud N, Matton L, Duquet W, Delecluse C, Thomis M, Beunen G, Lefevre J, Philippaerts RM. Sedentary behaviour, physical activity and a continuous metabolic syndrome risk score in adults. Eur J Clin Nutr. 2009 Mar;63(3):421-9. Epub 2007 Oct 31.

Believe it or not a soon-to-be published study that was sponsored by a the German LBS and presented to the public two days ago found that 1 out of 20 German kids below the age of 14 thinks about having liposuction done (figures based on LBS Kinderbarometer. 2013).

5% that's the SuppVersity Figure of the Week and it's the percentage of German kids below the age of 14 years who are thinking about getting liposuction done. I am not sure, whether I should feel sorry or enraged... not about the kids obviously who probably feel miserably in their own skin, but for the parents, the food industry and the government with their "expert" advisers whispering into their left ear and the junk food industry lobbyists who are holding a megaphone to the politicians right ear and a razor-blade to their throat. I guess, I'll settle for both, feeling sorry for the kids and being mad at the adults.

But enough of this let's get to some recent science news. Let's see... oh yeah, why don't we just start out with something 15% of the German kids (this is the number of already obese kids) are probably going to need sooner or later: diabetes medication.

Metformin not unique, green tea just as effective?!

(Sundaram. 2013) -- I know this sounds almost like a marketing scam from some snake oil... ah, green tea vendor, but according to a soon-to-be-published paper in Phytomedicine does have almost identical effects on the glucose metabolism of diabetic (streptozotocin + high at diet = std. model of type II diabetes), as metformin does.

Figure 1: Glucose and insulin levels in healthy and streptozotocin induced diabetic rodents receiving different doses of green tea (75, 150, 300mg/kg) or metformin (500mg/kg; Sundaram. 2013)

In fact, a short glimpse on the data in figure 1 should suffice to tell you that green tea is on a mg/mg basis even more potent than metformin. I would still caution any true diabetics out there not to drop their medication for the endproduct you get if you buy1 kg of fresh green tea leaves from the plant C. sinensis from the Nilgiris, India, dry them in the shade for two weeks, pulverize them and finally create a 1:10 ethanol extract, store that in the fridge for one week and then finally filter and evaporate it at a temperature of <50°C.

Did you know that the macronutrient composition (esp. the protein content) can have major impacts on your neurotransmitters and mood? No, then revisit this older SuppVersity article and learn more.

Not diabetic, then you may be interested in this: A non-negligible side note of the study at hand is that the GTE that was so good for the sick rats, did nothing, I repeat, absolutely nothing for the glucose metablism of the healthy rats on the high carb, low fat chow. Still, a recent study from Japan suggests that your psychological well-being (not tested in the rodents ;-) alone would justify the consumption of one, two or even three cups of green tea or coffee per day (Pham. 2013). After all, Pham et al. observed in their most recent study which is going to be published in one of the future installments of the peer-reviewed journal Public Health Nutrition that both, green tea and coffee consumption are inversely related with the odds ratio of depression in the Japanese working population. In this case, the scientists are yet pretty sure that it's none of the fancier components, but simply the caffeine content that is responsible for the >40% reduced risk of depression in tea/coffee aficionados.

You may be asking yourself why I mention the lengthy procedure of preparing that extract, right? Well, different source, different preparation methods, different effects. This and the fact that a human diabetic is not a streptozotocin treated rodent of a high fat diet put a huge question-mark behind and premature conclusions like "green tea is a better anti-diabetic than metformin".

After all those years, 1-Andro still works.

(Granados. 2013) -- It is certainly debatable in how far this qualifies as "news", after all, 1-androsterone is the "mother of all prohormones", but I still guess that one or another of the average muscle heads out there will still be intrigued to hear that researchers from the Human Performance Research Laboratory of the Department of Sports and Exercise Sciences at the West Texas A&M did actually dare to test the effects of 330mg/day 1-AD, which were administered for 4 week with 16 session of a structured RT program, on the physique and health of 16 males (23±1yrs; 13.1±1.5%BF; 5.3±1.0yrs RT experience; the 1-AD used in the study was probably that of a larger US producer that's still available online and has a slightly different nomenclature, i.e. 3-hydroxy-5alpha-androst-1-en-17-one).

Figure 2: Relative changes in muscle mass (total change above the bars) and kidney, "liver" and lipoprotein metabolism after four weeks on a 1-AD clone (Granados. 2013)

The results I plotted for you in figure 2 actually speak for themselves: Increases in lean mass and strength on the positive and deteriorations of the kidney (creatine), liver (S-GOT) and lipid metabolism (HLD, LDL, total cholesterol) are exactly what you can expect from a mild prohormone like this.

EPA triggers protein synthesis and inhibits breakdown... in the petri dish

CLA and fish oil, are they "anabolic" in human trials (learn more)?

(Kamolrat. 2013) -- You will probably remember the SuppVersity article on the potential "anabolic" effects of fish oil and CLA from February, 25, 2013, where not a single of the human studies showed beneficial effects of fish oil supplementation on training induced muscle gains, right?Well, a soon-to-be-published paper from the Biochemical and Biophysical Research Communications does at least confirm that Maculoso et al. were not totally off the track, when they suspected that fish oil could be "anabolic". Contrary to their hormonal understanding, the results of the study at hand do yet suggest that high serum concentrations of EPA may increase the expression of local control factors of protein synthesis in a way that does not necessarily render them anabolic, but would suggest that they may help people with muscle wasting disorders.

If you take a look at the data in figure 3, which holds all the statistically significant effects the scientist observed, the most important advantage of EPA vs. DHA in murine C2C12 myotubes after L-leucine stimulation unquestionably is the EPA-specific decrease in protein breakdown.

Figure 3: Protein breakdown, marker of protein synthesis and apoptosis in EPA or DHA treated C2C12 myotubes in the petri dish (Kamolrat. 2013)

What the scientists don't tell you though is that the effect size may be negligible, that the enhanced anti-protein breakdown (note:protein breakdown does not equal cell death) effects are only present when the cells are incubated with leucine and - most importantly - that FOX3a, which was likewise significantly elevated, "is necessary and sufficient for the induction of autophagy in skeletal muscle in vivo" (Mammucari. 2007), is upregulated in catabolic states of testosterone deficiency (White. 2013), and is suppressed by HSP70 (heat shock protein expressed in response to eustress such as exercise; cf. Senf. 2008). No wonder no human trial was ever able to demonstrate the anabolic effects of fish oil.

Phthalates in your food chain - addendum to last week's short news

Once again, I am not trying to make you panic about the individual serving of whatever is on the following list. The current state of research clearly suggests that the individual contribution of endocrine disrupting plastics from each of these items is way below what can harm an adult (and sexually mature) individual. When I went through the latest data Arnold Schecter et al. present in their latest paper in Environmental Health Perspectives, there were - for my liking - still too many patterns emerging to simply ignore this paper (I cannot simply copy & paste all the data, but the you can download the supplemental data here):

Figure 4: The metabolites of all measured phtalates in a 2012 study from the Columbia University were significantly elevated in 56 infertile vs. 56 fertile couples (Tranfo. 2012). I know, correlation is not causation, but I would venture the guess that none of the 1/6 couples who are infertile (McArthur. 2007) will care about the difference...

Pork, the supposedly unhealthiest meat source has the highest estimated mean phthalate concentration of any food group.

The "good apple" juice of which Dennison et al. report that daily intakes equal or greater than 12 fl oz/day are associated with shortstature and with obesity in two and five-year old children in New York (Dennison. 2013), is topped in terms of its phthalate content only by diet lemon tea - another of those "healthy" beverage.
The "healthy" vegetable oils are the absolute #1 dietary source of BBzP, of which a group of researchers from the Columbia University has only recently been able to show that children who were exposed to BBzP prenatally had a >50% higher risk of developing eczema within the first 2 years of their lives (Just. 2013).

I guess, I could cite a couple of other "happy coincidences", but I don't want to bore you away, before we get to something that should really make us reconsider the convenience of our "Plasti-Nation(s)", specifically the convenience of getting "scientifically formulated baby foods" for your children.

Figure 5: Dietary exposure (in µg/kg body weight; calculated on average intake of the various food items) from beverages, milk, other dairy, fish, fruits/vegetables, grain, beef, pork, poultry, vegetable oils and condiments (Schecter. 2013)

I wonder which science says that the foods babies eat should contain 4.3x more phthalates (on a per kg body weight basis), than the junk adults are eating.

Several studies have reported an increased risk of allergic disease among children with higher childhood phthalate exposure, as well as increased airway inflammation.
Some human studies suggest that in-utero phthalate exposure could lead to abnormal genital and behavioral development.
Based on our current understanding, diet and dust are the predominant sources of DEHP and BBzP, while cosmetics are the major source of DEP.

Ok, this is of course a result of the fact that babies weight less than adults do, but it is also a consequence of the fact that the baby foods are freaking "plasticized" - regardless of whether you buy them in glass or plastic containers. A fruit homogenate sold in glass bottles for example contained 235ng/g DEHP (about as much as paper-packaged butter, by the way) and was topped only by plastic food such as ham (1158ng/g). Again, way below the amount of DEHP that's deemed to be toxic, but is it really coincidence that a group of scientists from the University of Washington and the Havard Medical School only recently published an opinion paper (Braun. 2013), in which they formulate the take home messages I quote in the red box to the right... just food for thought, of course!

I guess you know what's next!? Correct: "That's it for today! Check out the facebook news, such as

Wolverine doesn't care about the phthalates in milk, but what about homogenization? (read more) could be the only face of the "Got Milk" campaign who does not have to care about potential negative health effects of homogenized milk.

Thyroglobulin levels could be a measure of adequate iodine intake -- Both, too high and too low iodine intakes will result in increased thyroglobolin levels (read more)

Dairy & blood pressure - revisited & acquitted -- "[....]the preponderance of evidence indicates dairy foods are beneficially associated with blood pressure" (read more)

Supplement users are a special kind of people -- Specifically health conscious, for example, and this will necessarily distort all epidemiological guesswork like "taking supplement X is associated with Y" (read more)

Retinoic acid & testosterone: While vitamin A does not figure in the LH induced increase in testosterone production it's presence in the testes appears to be necessary to keep the basal testosterone production up (read more)

if you still can't get enough of the latest on exercise, nutrition and supplementation science and have a nice Saturday evening (+ night)!"

References:

Braun JM, Sathyanarayana S, Hauser R. Phthalate exposure and children's health. Curr Opin Pediatr. 2013 Feb 16.
Dennison BA, Rockwell HL, Baker SL. Excess fruit juice consumption by preschool-aged children is associated with short stature and obesity. Pediatrics. 1997 Jan;99(1):15-22.
Granados J, Gillum T, Hodges C, Kuennen M. 3-hydroxy-5alpha-androst-1-en-17-one Enhances Muscular Gains but Impairs the Cardio-metabolic Health of Resistance Trained Males. International Journal of Exercise Science. TACM 2013.
Just AC, Whyatt RM, Perzanowski MS, Calafat AM, Perera FP, Goldstein IF, Chen Q, Rundle AG, Miller RL. Prenatal exposure to butylbenzyl phthalate and early eczema in an urban cohort. Environ Health Perspect. 2012 Oct;120(10):1475-80. doi: 10.1289/ehp.1104544. Epub 2012 Jun 13.
Kamolrat T, Gray SR. The effect of eicosapentaenoic and docosahexaenoic acid on protein synthesis and breakdown in murine C2C12 myotubes. Biochem Biophys Res Commun. 2013 Feb 21.
Mammucari C, Milan G, Romanello V, Masiero E, Rudolf R, Del Piccolo P, Burden SJ, Di Lisi R, Sandri C, Zhao J, Goldberg AL, Schiaffino S, Sandri M. FoxO3 controls autophagy in skeletal muscle in vivo. Cell Metab. 2007 Dec;6(6):458-71.
McArthur SL. Infertility Fact Sheet. ABC Health & Well-Being. 2007 <http://www.abc.net.au/health/library/stories/2007/05/30/1919840.htm> retrieved March, 09, 2013.
Schecter A, Lorber M, Guo Y, Wu Q, Yun SH, Kannan K, Hommel M, Imran N, Hynan LS, Cheng D, Colacino JA, Birnbaum LS. Phthalate Concentrations and Dietary Exposure from Food Purchased in New York State. Environ Health Perspect. 2013 Mar 6.
Senf SM, Dodd SL, McClung JM, Judge AR. Hsp70 overexpression inhibits NF-kappaB and Foxo3a transcriptional activities and prevents skeletal muscle atrophy. FASEB J. 2008 Nov;22(11):3836-45.
Sundaram R, Naresh R, Shanthi P, Sachdanandam P. Modulatory effect of green tea extract on hepatic key enzymes of glucose metabolism in streptozotocin and high fat diet induced diabetic rats. Phytomedicine. 2013 Feb 27.
Tranfo G, Caporossi L, Paci E, Aragona C, Romanzi D, De Carolis C, De Rosa M, Capanna S, Papaleo B, Pera A. Urinary phthalate monoesters concentration in couples with infertility problems. Toxicol Lett. 2012 Aug 13;213(1):15-20.
White JP, Gao S, Puppa MJ, Sato S, Welle SL, Carson JA. Testosterone regulation of Akt/mTORC1/FoxO3a signaling in skeletal muscle. Mol Cell Endocrinol. 2013 Jan 30;365(2):174-86.

Is HIT obesity incompatible? One thing appears to be sure - the purported post-workout increase in energy expenditure is reversed in the obese.

You may remember the positive results of the 100 squats a day challenge from the SuppVersity news on Friday, right? If you do, you will probably also remember the red box in which I mentioned the ongoing debate that's revolving around the issue, whether or not regular bouts of vigorous physical activity can protect you from the detrimental effects of sitting around 8h+ per day (see "100 Squats A Day Challenge"). While it may not really help us to answer the question whether "sporadic" activity is enough, a recently published study in the journal of the International Association for the Study of Pediatric Obesity certainly provides an interesting and novel angle on the debate.

What happens after you've burned those extra calories?

In a series of three experiments, a group of French researchers tried to elucidate why most of the studies that investigate the effect of physical activity on the change / loss of body fat report sub-optimal results. Within the last two decades, researchers such as Goran et al. (1992), Morio et al. (1998) or Donelly, et al. (2003), have repeatedly suggested that the primary reason for insufficiency of physical activity alone to modulate body weight was not restricted to the compensatory intake of food, but would - at least partly - be mitigated by a compensatory decrease in total daily energy expenditure (DEE).

As usual the existing evidence in ambigous, but a 1999 study by Kriemler et al. provided evidence that the high intensity exercise early in the morning will result in a decreased energy expenditure during the res of the day and the following day (Kriemler. 1990). Since Kriemler and his colleagues relied exclusively on the heart rate of their subjects to assess the energetic expenditure, Thivel et al. re-investigate the purported metabolic slow down in response to high intensity exercise in a series of three experiments.

The fitter you are the greater the benefits of working out at high intensities (learn more)
Study 1 involved only obese adolescents and used a combination of heart rate and accelerometer data to evaluate the energy expenditure

Study 2 was conducted with lean (17% body fat) and obese (44% body fat) adolescents and evaluated the energy expenditure by the means of a SenseWear Armband

Study 2 involved only obese adolescents and used the most sophisticated measuring technique, a open-circuit whole-body calorimeter in a metabolic chamber

In study 1 and 2 the subjects had to perform a cycling exercise consisting of 3 x 10 min at 70%VO2max (EX), while study 3 compared a 3 x 11 min at 75% VO2max high intensity (very long) interval protocol to a 3 x 20 min at 40% VO2max low intensity extremely long interval protocol (click here to learn how to design a real high intensity interval workout).

Does HIIT slow down the obese metabolism or does it simply increase laziness?

While the general trend, the scientists observed was pretty meaningless (more on that in the "bottom line"), the differences we see between the studies and between lean and obese subjects are quite telling and do in fact relate back to the initially mentioned question of "working out like crazy" and "sitting around lazy" the rest of the day.

Figure 1: "Energy expenditure" in the exercise and control trials of the three studies (Thivel. 2013)

In order to appropriately interpret the data we have to remind ourselves of what the scientists actually measured in the different studies. Study 1 used accelerometer and heart rate data and did thus access a mixture of metabolic and physical activity. Study 2 used just the SenseWear Armband with a build-in accelerometer, which - despite being more sophisticated than a simple pedometer, still measures only physical activity. Lastly, in study 3, the metabolic chamber actually measures the "true" energy expenditure irrespective of whether that's due to an increase / decrease in metabolic rate or in response to exercise / sitting around.

Let's start with the third study, since it's the most sophisticated one. What do we see in the middle of figure 1? Right, we see that conducting a 30min HIIT workout reduces the energy expenditure during the afternoon (-9.2%), but the total daily energy expenditure in a well-controlled scenario and measured with sophisticated equipment is still 8.9% higher than in the non-exercise scenario.
So what about study two then? There is no debating that the afternoon energy expenditure in the obese groups dropped, but wait... what do we actually measure here? Right. That's not necessarily the amount of energy the obese youths actually expended. It's just a measure of their physical activity. It is thus not sure, if the obese youths did, as the scientists imply, not still end up with a higher daily energy expenditure. After all, the heart rate remains elevated after a workout in unfit vs. fit individuals. Plus, even with the "physical activity only" measure the exercise trial yielded a marginal, but statistically non-significant higher total energy expenditure for the day. In the lean subjects the exercise advantage amounted to 233kcal and was thus clearly significant - irrespective of the (imho) inadequate measuring method.
The results of study one actually speak for themselves: The energy expenditure, which does, as we have noted before, include both, physical activity (accelerometer data) and metabolic rate (heart rate data), simply does not decline after the morning workout.

I guess, I actually don't have to "summarize" the above even more, but since I understand all of you who have been complaining about missing "summaries" in many of the older SuppVersity posts I still will provide you with the obligatory bottom line.

Now that you know it's not bad for you, read up on all previous HIIT articles at the SuppVersity.

Bottom line: "High intensity" exercise is not useless and it does not (in the presence of adequate nutrient intakes) shut down your metabolism. It may be true that especially people who are not used to working out and will thus be correspondingly fatigued after a by no means "high" intensity "HIIT" workout at 70% of their VO2max (actually this is more of one of those stupid "fat burning workouts") tend to decrease their activity levels during the rest of the day, but the beauty of high intensity workout is that they increase your conditioning and as you are getting fitter, this behavioral but not metabolic compensatory effect is going to decline.

And best of all, as long as you don't succumb to the "I worked out, so I can have my cream pie today" idiocy, you are going to lose weight even while this adaptation process is still taking place. Why? Well, the two studies that don't rely on physical activity (study 1 & 3) only to determine the energy expenditure are telling me that you spend ~9% more energy if you work out for half an our at a not too intense pace in the morning. Whether this will help you to escape the detrimental health effects of sitting around the rest of the day is yet questionable, because health in not determined by the difference between caloric intake and expenditure... but whom am I telling that? You know that anyway, right?

References:

Donnelly JE, Kirk EP, Jacobsen DJ, Hill JO, Sullivan DK, Johnson SL. Effects of 16 mo of verified, supervised aerobic exercise on macronutrient intake in overweight men and women: the Midwest Exercise Trial. Am J Clin Nutr 2003; 78: 950–956.
Goran MI, Poehlman ET. Endurance training does not enhance total energy expenditure in healthy elderly persons. Am J Physiol 1992; 263: E950–E957.
Kriemler S, Hebestreit H, Mikami S, Bar-Or T, Ayub BV, Bar-Or O. Impact of a single exercise bout on energy expenditure and spontaneous physical activity of obese boys. Pediatr Res 1999; 46: 40–44
Morio B, Montaurier C, Pickering G, et al. Effects of 14 weeks of progressive endurance training on energy expenditure in elderly people. Br J Nutr 1998; 80: 511– 519.
Thivel D, Aucouturier J, Metz L, Morio B, Duché P. Is there spontaneous energy expenditure compensation in response to intensive exercise in obese youth? Pediatr Obes. 2013 Feb 28.