"If some is good, more is better!" Unfortunately, this simple maxime does rarely apply when it comes to the physiological response to certain foods and/or supplements. For protein, however, it appears as if the relation holds - at least as long as protein does not become the only energy source in your diet.

Read more about ISSN and other studies at the SuppVersity

Vitargo, Red Bull, Creatine & More | ISSN'15 #1

Pump Supps & Synephrine & X | ISSN'15 #2

High Protein, Body Comp & X | ISSN'15 #3

Keto Diet Re- search Update | ISSN'15 #4

The Misquantified Self & More | ISSN'15 #5

BCAA, Cholos-trum, Probiotics & Co | ISSN'15 #6

• High protein, high GLP-1, ... highly beneficial? As a SuppVersity reader you are aware of the far-reaching metabolic effects of GLP-1 on appetite (suppression | Näslund. 1999), glucose and fat metabolism, as well as thermogenesis (Lejeune. 2006). Against that background, you will know that the small, but statistically significant increase in GLP-1 Franklin et al. (2015) observed in their latest study which compared the effects of a high protein and high mono-unsaturated fat meal on the well-known incretin hormone may have significant long-term effects even though the blood glucose levels of the study's twenty-four overweight or obese participants (male/female: 12/12; age: 38.7 ± 15.3 (mean ± standard deviation) years; BMI: 31.6 ± 4.0kg/m²), who consumed isocaloric meals containing either 35.2% energy from fat and 20.7% from monounsaturated fat (HMF meal) or 31.9% energy from protein (HP meal), did not trigger differences in post-prandial glucose levels at 30, 60, 120, and 180 min.
  
  

  Figure 1: Levels of active GLP-1 in response to high protein (HP) or high MUFA (HMF) meals (Franklin. 2015).

  To believe that "simply eating more protein" is going to solve all your weight problems, though, would be short-sighted - especially for the overweight obese for whom the study at hand as well as previous studies investigating the effects of GLP-1 on glucose metabolism suggest that they may benefit to a lesser extent from protein induced increases in GLP-1 than lean individuals, in whom the "satiety hormone" will trigger much more pronounced β-cell responses that in in patients with sign. insulin resistance and pre- or full-blown type 2 diabetes (Kjems. 2003).
  
  If that sounds like you, using the high(er) protein meals in conjunction with an energy restricted diet to lose weight and thus to improve your insulin sensitivity can obviously still be beneficial. Without a planned, reasonable caloric deficit, however, high(er) protein intakes alone are probably not going to "cut it" (all puns intended).

Even if weight loss is the goal, training fasted and thus hungry does not appear to provide significant benefits. Learn more about this longstanding myth and the reality in my write-up of Schoenfeld et al's seminal paper on fasted cardio and fat loss. A paper that finally had a long-standing and die-hard fat loss myth tumble.

Are you hungry before your workouts? In this case you may be interested in the results of a paper by Nystrom et al.' who suggest that athletes have to use "more proactive strategies [...] to optimize training adaptations". Why's that? Well, of the 481 (240 women, 241 men) NCAA Division I athletes representing eleven intercollegiate sports from three universities in three athletic conferences (i.e., Atlantic 10, Atlantic Coast Conference, Conference USA) who participated in the researchers investigation into the nutrient timing habits of Division I NCAA athletes, 79% reported feeling hungry prior to training, practice or competition - and that despite the fact that most of them had breakfast. It is thus well possible that the amount and types of foods athletes eat before their workouts do still receive (too) little by athletes and their athletic departments which often provide post-workout meals, but fail to do so pre-workout.

• Pimp my plant protein - digestive enzymes can do the trick! Despite the fact that pea and other protein powders have become widely (and cheaply) available over the past years, vegan and vegetarian athletes and gymrats are still having a harder time satisfying their protein requirements than their omnivore competition or gym-buddies. Against that background and in view of the fact that more and more athletes are "going vegan" or at least vegetarian, the latest study by Julie Minevich (2015) and colleagues from the University of Tampa and the formulators, manufacturers and vendors of digestive enzymes and respective supplements from Chemi-Source and Increnovo LLC, was in fact published quite timely. A study that was designed...

  "to investigate if co-ingestion of a plant protein specific digestive enzyme blend (Digest-All® VP, a proprietary enzyme blend consisting of protease 6.0, protease 4.5, peptidase, bromelain and alpha-galactosidase, Chemi-Source, Inc., Oceanside, CA) can reduce the significant differences in amino acid appearance in the blood between plant and animal proteins" (Minevich. 2015).

  To this ends, 11 resistance-trained male subjects (age: 21.4 ± 1.5 years, body weight: 82.5 ± 3.9kg, height: 177.3cm ± 6.1cm | average training status of 2.3 years ± 1.9 years) were randomly assigned to receive either 60 g of whey protein concentrate, or the same amount of protein in form of a 70:30 blend of pea and rice protein concentrates (Veg), either alone or alonside the enzyme blend Digest-All® VP in a double-blind, crossover study. All supplements were provided on an empty stomach after a 12 hour overnight fast. The three testing sessions, in which blood was drawn immediately prior to, and at 30 minutes, 1, 2, 3, and 4 hours following consumption of the supplements, were separated by a washout period of 7 days.
  

  Figure 2: Time to achieve peak amino acid levels and total amount of amino acids that made it to the blood stream with whey protein, the pea + rice mix and the pea + rice mix w/ digestive enzymes (Minevich. 2015).

  Ok, I have to admit that the differences are not exactly staggering and the standard deviations (see error bars) are large, but still. One potentially important determinant of skeletal muscle metabolism, the time it takes for the serum levels of essential amino acids - including leucine - to peak, i.e. T_max in Figure 2, was visibly improved by the addition of digestive enzymes to the otherwise comparatively slow digested rice + pea protein mix (if you look at the error bars, you will see that this was just a "trend", though).
  
  If you also take into account that the digestive enzyme blend brought the area under the EAA curve (see Figure 2) and the peak amino acid levels (not shown in Figure 2) of the vegetable protein blend up to the same level as it was observed with whey protein, it would seem as if the study would provide the missing evidence of the usefulness of proteases and co. for people who want to make the absolute most of their vegetable protein supplements - what is missing, obviously, is data that would allow us to quantify the downstream effects on muscle gains and other practically relevant study outcomes.
• High protein + training = WIN?! You will certainly remember the impressive results of Antonio et al.'s 2014 study on the effects of a 4.4g/kg protein diet on the body composition healthy resistance-trained men and women (learn more). Right after said study had been published the authors promised a follow up that would combine a similarly high protein intake with a controlled exercise intervention and... voila! The first results of this study were presented at this year's ISSN meeting.
  
  For the corresponding experiment, Ellerbroek et al. recruited forty-eight healthy resistance-trained men and women in their early twenties. who consumed either 2.3g/kg body weight per day (NP) or 3.4g/kg body weight per day (HP) of dietary protein during the treatment period. Moreover, all subjects participated in a split-routine, body part heavy resistance-training program. Training and diet (everyday) logs were kept by each subject.

Learn everything about the previous study.

Don't worry! I am going to write a full review of this study as soon as it will be published. In theory I would have had to skip it just like the other studies, but since I would have been mad at me if for doing that if I were you, I decided to give summarize the little information you can find in the abstract. Against that background I hope you will understand that I will refrain from making any definite conclusions until I've read the full-text. The abstract does after all lack a lot of potentially relevant information, such as the type of workouts, the way the subjects achieved the increase in protein intake (dietary or supplemental protein), the adherence, actual protein, carb & fat intakes, etc.

• As the scientists point out in the results section of the abstract, their two-time point (Pre, Post) by two-group (NP, HP) repeated-measures analysis of variance (ANOVA) showed (a) significant time by group (p ≤ 0.05) changes in body weight with weight gains and loss in the normal and high protein groups, respectively (1.3 ± 1.3 kg NP, -0.7 ± 4.0 HP), as well as reductions in total and relative body fat in both groups (-0.3 ± 2.2 kg NP, -1.7 ± 2.3 HP), and % BF (-0.7 ± 2.8 NP, -2.4 ± 2.9 HP) - both as you can see in Figure 3 with significant advantages for the HP group.
  

  Figure 3: Changes in body weight, fat and fat free mass in the normal and high protein groups during the diet + training intervention; mind the error bars = high inter-individual differences (Ellerbroek. 2015).

  In the absence of any form of ill health effects due to the high protein intake (both groups consumed significantly more than the recommended daily allowance of 0.8g/kg), Ellerbroek et al. also found a significant time effect for the increase in fat-free mass  (1.5 ± 1.8 NP, 1.5 ± 2.2 HP), 1-RM on the bench and squats and vertical jump and pull-up performance - albeit without significant diet-induced inter-group differences.

So what's not in this issue? Poster presentations I decided not to discuss "at length" in this issue are the allegedly interesting presentation by Galvan et al. on the "[e]ffects of 28 days of two creatine nitrate based dietary supplements on bench press power in recreationally active males." Just as it was the case for the previously referenced studies on BCAAs, I'd rather wait for the full-text to be published before I make up my mind on whether creatine nitrate is the first form of "advanced creatines" that's actually worth it's money (unlike the rest of the pack | Jäger. 2011).

Blocking Inflammation is Like Cho- king the Fire: Long Term Weight-, Visceral- and Android-Fat Gain in Human Study Emphasizes Essential Role of TNF-α in Metabolic Control!

The same must be said of a study by Detzel, et al. (2015) in which the researchers compared the effects of functional animal proteins on mTOR and endotoxins like , pro-inflammatory compounds, that arise as a consequence of intense training. There's no debating: The way serum the derived protein supplements (BioBeef, SerumPro, and SuperSerum) were capable of neutralizing endotoxin is is interesting, but to comment on the practical usefulness of blending of high-quality protein sources with functional serum protein supplements (SuperSerum and SerumPro) the abstract that does not provide numbers to assess the relevance of the reductions in IL-8 cytokine production by THP-1 monocytes is simply not sufficient | Comment!

• Detzel, Christopher J., et al. "Functional animal proteins activate mTOR and bind pro-inflammatory compounds." Journal of the International Society of Sports Nutrition 12.Suppl 1 (2015): P35.
• Ellerbroek, Anya, et al. "The effects of heavy resistance training and a high protein diet (3.4 g/kg/d) on body composition, exercise performance and indices of health in resistance-trained individuals-a follow-up investigation." Journal of the International Society of Sports Nutrition 12.Suppl 1 (2015): P37.
• Franklin, Brian, et al. "The effect of meal composition on postprandial glucagon-like peptide-1 response in overweight/obese participants." Journal of the International Society of Sports Nutrition 12.Suppl 1 (2015): P12.
• Galvan, E., et al. "Effects of 28 days of two creatine nitrate based dietary supplements on bench press power in recreationally active males." Journal of the International Society of Sports Nutrition 12.Suppl 1 (2015): P17.
• Jäger, Ralf, et al. "Analysis of the efficacy, safety, and regulatory status of novel forms of creatine." Amino Acids 40.5 (2011): 1369-1383.
• Lejeune, Manuela PGM, et al. "Ghrelin and glucagon-like peptide 1 concentrations, 24-h satiety, and energy and substrate metabolism during a high-protein diet and measured in a respiration chamber." The American journal of clinical nutrition 83.1 (2006): 89-94.
• Näslund, E., et al. "Energy intake and appetite are suppressed by glucagon-like peptide-1 (GLP-1) in obese men." International journal of obesity 23.3 (1999): 304-311.
• Nystrom, M. G., et al. "Nutrient timing habits of Division I NCAA athletes." Journal of the International Society of Sports Nutrition 12.Suppl 1 (2015): P33.
• Minevich, Julie, et al. "Digestive enzymes reduce quality differences between plant and animal proteins: a double-blind crossover study." Journal of the International Society of Sports Nutrition 12.Suppl 1 (2015): P26.

I don't know what exactly was in the ketogenic rodent chow that was used in the study at hand, but I doubt it were transfat laden sausages ;-)

Read more about ISSN and other studies at the SuppVersity

Vitargo, Red Bull, Creatine & More | ISSN'15 #1

Pump Supps & Synephrine & X | ISSN'15 #2

High Protein, Body Comp & X | ISSN'15 #3

Keto Diet Re- search Update | ISSN'15 #4

The Misquantified Self & More | ISSN'15 #5

BCAA, Cholos-trum, Probiotics & Co | ISSN'15 #6

• You can build muscle on a ketogenic diet - theoretically -- While previous studies on low carbohydrate diets have already demonstrated that eating tons of fat and almost no carbohydrates can trigger improvements in body composition, it is still not clear whether the consumption of virtually carbohydrate-free diets may impair the resistance training induced anabolic response in skeletal muscle. In a previous ISSN article, for example, Paoli et al. )2012) state that their observations in gymnasts on ketogenic diets confirms that

  "the mechanism underlying the increase of body fat utilization [on ketogenic diets] has some pathways in common with mechanisms contributing to the lack of muscle mass increase [which is why] during the ketogenic diet it is actually very difficult to increase muscle mass" (Paoli. 2012).

In their latest study, researchers from the University of Tampa tried to get to the bottom of this myth by looking at the degree of muscle protein synthesis (MPS) in rodents on carbohydrate-rich Western and low-carbohydrate "ketogenic" diets (see Figure 1 for the exact macronutrient ratios).


Figure 1: Macro composition of the non-isocaloric chow (KD - 5.2 kcal/g, W - 4.5kcal/g | Mobley. 2015).

In week seven and thus after six weeks on the respective diets, the right-leg plantarflexor muscles of the researchers'"subjects", male Sprague-Dawley, were acutely exercised under isoflurane anesthesia by the means of high-frequency electrical stimulations (4 sets of 8 repetitions with 2 min recovery between sets). 90, 180 and 270 minutes after this highly controlled exercise stimulus a group of 8 rodents, each, was sacrificed and the levels of a previously injected tracer (intraperitoneal puromycin) were used as a marker for skeletal muscle protein synthesis (MPS).


Figure 2: While the absolute figures have not yet been published, I can already tell you that - statistically speaking - the type of diet did not make a difference (Mobley. 2015)

As you can see in Figure 2, the scientists observed a "main time effect for MPS". In non-scientist English this means that the training resulted in statistically significantly increase in muscle protein synthesis in the trained vs. untrained legs at 90, 180 and 270 min. What is much more important, though, is that this effect was not significantly different for the ketogenic vs. Western diet group. In conjunction with the lack of difference in phosphorylated (p)-4E-BP1 (Thr37/46) and p-rps6 (Ser235/236), two important signalling proteins that are involved in the control of skeletal muscle protein synthesis, it is thus probably warranted to conclude that "these data demonstrate that rats fed a ketogenic diet present a similar anabolic response to resistance exercise compared to rats fed a Western diet" (Mobley. 2015). Whether that's a "fair", let alone practically relevant comparison (the Western diet was lower in protein and isn't exactly a good representation of the average diet true muscle heads will be consuming) is anyone's guess, though.

While some people make it appear as if we already knew that ketogenic diets are superior, you may remember that some recent studies show that balanced diets have more favorable effects on the body composition of certain athletes | learn more

Ketogenic diets and fat free mass - an issue that requires further research in general: Only recently Grant M. Tinsley and Darryn S. Willoughby from the Baylor University highlighted in a review that a "potential loss of fat-free mass (e.g. skeletal muscle)", is a "potential concern of these “ketogenic” diets" of which the "majority of studies" suggests that it was inevitable. Since the most of these studies involve "aggressive weight loss diets" and lack an exercise component, "further research is needed to determine whether resistance training can effectively slow or stop the loss of fat-free mass typically seen in individuals following a ketogenic diet" (Tinsley. 2015). The study at hand can thus be considered the first in a line of studies on the effects and "mechanisms underlying the effects of a ketogenic diet on fat-free mass" (ibid.).

• Even if it wasn't for the questionable control diet, there would still be one thing the data from Mobley's study cannot tell us and that's whether the putative reduction in IGF-1 that has been observed on low carbohydrate diets (Caton. 2012) may have long(er)-term detrimental effects on muscle gains. There is, as you as a SuppVersity reader will know, good evidence that IGF-1, despite its irrelevance for short term increases in muscle protein synthesis, may play an important role in the long-term adaptational response to exercise (I suggest you go back to this SuppVersity Classic Article if that's news to you). It's thus not just the fact that we are dealing with a rodent study here that makes me want to say that future long(er) term studies in humans are necessary before the myth that ketogenic diets may impair (long-term) gains can be put to rest once and for all.
• Is weight gain hardly possible on the ketogenic diet? Actually this is another common ketogenic diet myth: When you are consuming a ketogenic diet you cannot get fat. Sounds stupid, right? Well, if you look at a recent study that comes - just as the previously cited study - from the University of Tampa (Holland. 2015), would certainly appear as if there may be something to this claim.
  
  In their 6-week rodent study, Angelina M. Holland and colleagues compared the effects of ketogenic (KD), Western (WD), and standard chow (StdChow) control diets on fat deposition and serum health-related biomarkers (exact macronutrient ratios are given in Figure 3).
  

  Figure 3: Macronutrient composition of the diets in Holland's study (Holland. 2015).

  Over the course of the study, the scientists'"subjects", male Sprague-Dawley rats (~9-10 weeks of age) were provided isocaloric amounts of either a KD (5.2 kcal/g, 20.2% protein, 10.3% carbohydrate, 69.5% fat; n = 50), WD (4.5 kcal/g, 15.2% protein, 42.7% carbohydrate, 42.0% fat; n = 66), or StdChow (3.1 kcal/g, 24.0% protein, 58.0% carbohydrate, 18.0% fat n = 10). At the end of the study the exact daily food intake and body weights were recorded and the animals were sacrificed in order to analyze the weight of four different fat depots.
  
  As it was to be expected, the rats on the ketogenic diet consumed slightly less energy (3,540 ± 74 kcal) than those on the western diet (3,638 ± 83 kcal) over the course of the six week study. It is thus not surprising that there was a significant inter-group difference in terms in terms of the total amount of weight rodents in the KD and WD group gained: 397g vs. 494g to be precise.
  

  Figure 4: Due to a significantly reduced feed efficacy (weight gain per energy intake) the rats on the ketogenic diet gained sign. less weight than both, the rats on the Western diet and standard chow (Holland. 2015).

  What may come as a surprise, though, is the generally reduced feed efficiency (=amount of body weight gained per kcal the rodents consumed) of the ketogenic diet. With a feed efficacy of only 0.018g/kcal, the ketogenic diet was significantly less fattening than the Western diet (0.042 ± 0.007g/kcal) and the standard chow (0.045 ± 0.012g/kcal).
  
  That's a quite a remarkable result, but if the lack of weight gain applied only to the total amount of body weight, it would be difficult to decide whether that's a good or a bad thing. When the scientists took a look at the weight of the fat depots, however, it became clear that the lion's share of the weight difference was mediated by a lack of fat, not just weight gain.

  "KD and StdChow had significantly less absolute and relative omental (absolute omental: 0.8 ± 0.3g and 1.2 ± 0.4g vs 1.6 ± 0.6g, respectively, p < 0.05; relative omental: 2.1 ± 0.7 and 2.4 ± 0.7 vs 3.2 ± 1.2g/kg, respectively, p < 0.05) compared to WD rats. KD and StdChow also had significantly less perirenal adipose tissue compared to WD (absolute perirenal: 4.2 ± 1.3 and 5.4 ± 1.4 vs 7.8 ± 1.8g, respectively, p < 0.05; relative perirenal: 10.6 ± 2.8 and 11.4 ± 2.4 vs 15.6 ± 3.0g/kg, respectively, p < 0.05). KD had significantly less absolute inguinal subcutaneous (SQ) and scapular brown fat than WD (absolute SQ: 4.3 ± 1.5 vs 6.6 ± 2.4g/kg; absolute brown fat: 0.6 ± 0.2 vs 0.8 ± 0.3g) but similar relative SQ and brown fat weights" (Holland. 2015).

  In view of the concomitantly reduced serum triglyceride levels (WD - 319.7 ± 109.8mg/dL versus StdChow 163.0 ± 67.0mg/dL and KD 69.9 ± 21.2mg/dL; p < 0.05), serum cholesterol and glucose levels glucose, the claim that ketogenic diets may help mammals to maintain stable body weights while improving, not messing with their glucose and lipid metabolism does therefore appear to be clearly supported by the study at hand. All that still has to be done before we can remove the "?" from the subheading that precedes the previous paragraphs would be a human study with a similar / identical design to exclude that any differences in glucose and, more importantly, fat metabolism in human beings increase the feed efficacy of the ketogenic diet to an extent that nullifies the benefits.

Are you looking for an unconventional nootropic? Look no further. Morning cardio on empty could be just what you've been looking for. Learn more in "Breaking the Fast, Cardio & Your Brain: Cardio on Empty is Fatiguing. Fasting Without Exercise, However, Can Have Nootropic Effects"

Which studies didn't make it into this installment of the ISSN '15 Research Review? This time, three studies didn't make the cut. There's Jason Cholewa's study on the "effects of a sports nutrition education intervention on nutritional status, sport nutrition knowledge, body composition, and performance in NCAA Division I baseball players," which may make it into a special on the importance of sport nutrition knowledge, when the full text is published, Solomon et al.'s study on the "efficacy study of alpha BRAIN®" as a nootropic where I would like to see the absolute improvements and the respective standard deviations in cognitive performance before discussing the study in the SuppVersity news, as well as Jones' and Davidson's investigations into the "proportionality of skeletal muscle before and after intervention" the significance of which would go unappreciated if I simply summarized the little information from the abstract | Comment on Facebook!

Exercise induced joint and muscle pain - Can a few grams MSM help?

Read more about ISSN and other studies at the SuppVersity

Vitargo, Red Bull, Creatine & More | ISSN'15 #1

Pump Supps & Synephrine & X | ISSN'15 #2

High Protein, Body Comp & X | ISSN'15 #3

Keto Diet Re- search Update | ISSN'15 #4

The Misquantified Self & More | ISSN'15 #5

BCAA, Cholos-trum, Probiotics & Co | ISSN'15 #6

• The benefits of inositol-stabilized arginine silicate as a workout ingredient - Over the past years the way people thought and think about arginine has changed significantly. While it was originally considered a super-supplement that would increase pump, gains and vascularity, most recent studies on its effects on relevant markers of exercise performance and training adaptation yield similarly disappointing results as Gary Cooks honor thesis from 2015 in which he observed that neither arginine supplementation 20 minutes prior to exercise, nor arginine supplementation two hours post exercise had an effect on the increase in strength performance or hypertrophy following a 4-week resistance training regime (Cook. 2015).
  
  

  Only few studies show ergogenic effects of plain arginine. This one, however reports a sign. increase in to exhaustion in a group of elite wrestlers.

  With more and more consumers becoming aware of the lack of effect of regular arginine, supplement producers are forced to develop "alternatives" - alternatives that promise to finally do what regular l-arginine supplements promised to do: Boost your nitric oxide levels, exercise performance and overall gym experience. With inositol-stabilized arginine silicate (ASI; Nitrosigine®) there's a true newcomer that is set about revolutionizing the pre-workout supplement scene ... that's at least if we believe in what the patent holders tell us about the "new standard for pumped results" (manufacturer's homepage).
  
  In fact, ASI has been previously shown to enhance blood levels of arginine up to six hours post-dose and increase nitric oxide levels, acutely (Kahlman. 2014). In the long(er) term, Whether that would produce practically relevant increases in perceived intra-workout energy, muscle pump, and stamina, as well as post-workout muscle recovery was now the subject of a new study by Rood-Ojalvo et al. (2015).

• The randomized double-blind placebo-controlled cross-over study study was conducted with 16 male subjects with limited exercise routines prior to participating in the study. The subjects took 1,5g/day of ASI or a placebo supplement daily for 4 days before they completed an intense leg extension exercise protocol to induce muscle soreness. Subjects then returned to the lab after 24, 48, and 72 hours for additional study measurements. After 72 hours, subjects repeated the leg extension exercise protocol to assess whether the provision of ASI (or placebo) had measurable effects on the recovery protocol.
  

  Figure 1: In spite of significant changes in blood flow velocity and leg circumference (which is interpreted as increased blood flow / hyperemia by the authors) the study at hand cannot prove practically relevant ergogenic effects of ASI simply because corresponding outcome variables were not assessed (Rood-Ojalvo. 2015).

  The scientists' analysis of the data they got produced two important results: Firstly, the 19-33 year-old subjects felt significantly more energetic and less fatigued (at least based on inertia sub-scores) on the 72 hour retest compared to placebo (p = 0.039). Secondly, the provision of the supplement lead to significant increases in leg circumference. Unfortunately, this increase in leg circumference is not a sudden muscle gain. Rather than that, the increased leg circumference appears to be a result of increased hyperemia (=increase of blood flow).
• In conjunction with the significant decrease in CK levels - a purported, albeit unspecific marker of muscle damage - in the ASI group at 24 (p = 0.040), 48 (p = 0.017) and 72 (p = 0.034) hours, the overall results of the study at hand do thus suggest that short-term supplementation with inositol-stabilized arginine silicate could have ergogenic effects. In the absence of meaningful outcome measures such as the number of reps (=volume) or the maximal weight lifted during the exercise tests, it would yet be premature to say that ASI is a proven ergogenic. 
• MSM for muscle and joint pain in marathoners and other athletes -- As Withee et al. point out in the introduction of the abstract to their poster presentation "[p]articipants in organized running commonly experience muscle and joint pain while training for and competing in distance events" for them a supplement that is able to reduce the pain associated with osteoarthritis could be a true game changer; and methylsulfonylmethane (MSM), a sulfur-based nutritional supplement, could be that supplement.
  
  Several previous studies have shown that MSM has anti-osteoarthritic and anti-inflammatory properties. Whether it would also help managing exercise-induced muscle and joint pain, effectively, was now the research question of a recent study from the National College of Natural Medicine in Portland (Withee. 2015). The design of the study is simple:

  "Twenty-two healthy females (n = 17) and males (n = 5) (33.7 ± 6.9 yrs.) were recruited from the 2014 Portland Half-Marathon registrant pool. Participants were randomized to take either MSM (OptiMSM®) (n = 11), or a placebo (n = 11) at 3g/day for 21 days prior to the race and two days after (23 total). Pain was recorded using a 100 mm Visual Analogue Scale (VAS) for both muscle pain (MP) and joint pain (JP) on a single questionnaire. Participants completed the questionnaire at five time points. Baseline levels (T0) were recorded approximately one month prior to the race. Post-race pain levels were recorded at 15 minutes (T1), 90 minutes (T2), 1 Day (T3), and 2 days (T4) after race finish. Data were analyzed using linear mixed models controlled for baseline, with time point as a repeated factor. Simple contrasts compared post-race time points to baseline, and Student's t-tests assessed between-group time point comparisons" (Withee. 2015)

  Unfortunately, this cannot be said for the study results, which showed nothing but a trend of lower pain levels in the MSM group - with non-significant time-by-treatment effects in either of the groups.
  

  Figure 2: Muscle and joint pain  15 minutes (T1), 90 minutes (T2), 1 Day (T3) after half-marathon race with methylsulfonylmethane (MSM | 3g/day) or placebo supplementation (Withee. 2015)

  In view of the fact that the provision of the 3g of MSM did result "in nearly significantly lower MP at T1 (MSM = 27.3mm vs. placebo = 49.8mm, p = 0.063), and lower MP at T2 (27.1mm vs. 40.0mm; p = 0.300), and T3 (30.0mm vs. 41.9mm; p = 0.306)" (my emphasis in Withee. 2015), as well as similar changes in joint pain (see Figure 2), it does still appear warranted to conclude that MSM supplements (3g/day) may be worth trying for anyone suffering from persistent joint and/or muscle pain after workouts.
• MSM as an inflammatory cytokine modulator -- While the previously discussed study by Withee et al. (2015) clearly indicates that MSM supplementation helps managing the level of exercise-induced inflammation, Withee et al. did not investigate the mechanism that was responsible for their observations. A recent study from the University of Memphis, however, did just that: In said study, Godwin et al. determined the effect of MSM on lipopolysaccharide (LPS) - induced inflammatory mediators after a single bout of acute eccentric exercise.
  
  To do so, they had five recreationally active, healthy men consume either 3g/day of MSM or a placebo supplement for 28 days. At the end of the supplementation program, a single bout of acute exercise (10 sets of 10 repetitions of eccentric knee extensions) was performed and blood samples were collected (immediately = 0 h, as well as 24 h, 48 h and 72 h post exercise) and analyzed.
  
  

  Do you remember that MSM can also act as a GH booster & bone builder | more

  The most significant results of the analysis are hardly surprising: The supplementation of MSM blunted the increase in the systemic levels of inflammatory cytokines (IL-6 and IL-1β) immediately after exercise.
  
  What is surprising, though, is the fact that the inflammatory response to LPS exposure in an ex-vivo study with blood that had been drawn at various time-points during the study shows a "dramatic increase in inflammatory cytokine secretion (IL-6, IL-1β and TNF-α) only after exercise for samples that was exposed to MSM" (Godwin. 2015).
  
  So what does that mean - practically speaking? Well, the authors are certainly right, when they point out that ...

  "[t]his response is specific to the stimulation with LPS as secretion of LPS-non responsive proteins is not increased, as evident by the stable levels of IL-17a [... and thus suggestive of the fact that] MSM is able to reduce the initial cytokine surge that is induced by acute exercise, while allowing for an efficient response to infectious stimuli after a single bout of acute exercise" (Godwin. 2015).

  On the other hand, this assumption stands in contrast to the 2-3 fold increase in IL-10 production after LPS stimulation for the subjects in the MSM group whose pre-exercise levels of the IL-10 levels before exercise. Previous research did after all suggest that greater IL-10 production my be the motor of the exercise induced "depression of immunity commonly reported in athletes engaged in high training loads" (Handzlik. 2013). Whether the chronic use of MSM supplements entails an increased risk of infection may thus warrant further investigations.

3x 1.3g/day cordiceps synensis can significantly increase time to exhaustion and have (individually different) beneficial effects on the ventilatory threshold (Hirsch. 2015).

Two more to go... two more studies that is: While the total number of ISSN '15 studies I haven't discussed or at least mentioned in this series yet is larger than two, there are only two studies I'd like to single out before the end of this installment of this Suppversity series. The Cordyceps synensis study by Hirsh et al. who were able to show that 4g of the mushroom can improve oxygen kinetics, and peak power non-significantly, as well as time to exhaustion significantly in recreationally active subjects who completed  a maximal graded exercise test, 6 min sub-maximal cycle test, and 3 min all-out cycle test, each separated by at least 24 hrs when the supplement is consumed chronically, i.e. in thee servings of 1.3 g equally spread across the day for three weeks (Hirsch. 2015).

Also worth mentioning, but in the absence of hard evidence of causality hardly worth discussing in much detail is Marc Bubbs' observation that basketball players who are training at high-intensity "seem more likely to have insufficient levels of vitamin 25(OH)D" (Bubbs. 2015) - if a follow up shows that normalizing these levels with supplementation will have performance enhancing effects, though, this would be really news-worthy | Comment on Facebook!

In view of the inaccuracy of the standard equations that are used to calculate our energy requirements we are approaching the age of the "misquantified self".

Read more about ISSN and other studies at the SuppVersity

Vitargo, Red Bull, Creatine & More | ISSN'15 #1

Pump Supps & Synephrine & X | ISSN'15 #2

High Protein, Body Comp & X | ISSN'15 #3

Keto Diet Re- search Update | ISSN'15 #4

The Misquantified Self & More | ISSN'15 #5

BCAA, Cholos-trum, Probiotics & Co | ISSN'15 #6

• Eating according to your genes may help you retain lean mass -- You will have noticed that the number of companies that do gene testing in order to tell you "exactly" what and how to eat is exploding lately. Unfortunately, the same cannot be said of research that would confirm that any of the test results people often pay several hundred dollars for are worth the paper they are printed on.
  
  Against that background, a recent study from the Texas A&M University comes quite handy for the shareholder value of said companies. The corresponding poster presentation at the ISSN Conference 2015 expanded on the results of a 2015 study by Coletta et al. (2015a), in which the researchers observed "that correctly matching diet type to some obesity-related genes promoted greater fat loss during the first 3 months of a diet and exercise intervention" (Coletta. 2015b). In the study at hand the researchers did now examine "whether these changes were observed following a 6-month diet and exercise training program" (ibid.).
  
  Over the course of the 6-months study, fifty sedentary, obese women (41.6 ± 12 yrs, 35.4 ± 8 kg/m²) who had been genotyped before the intervention, were either truly matched (T) to their diet group based on genotype (n = 28) or falsely matched (F) based on genotype (n = 22).
  

  Figure 1: Macronutrient composition of the diets (Coletta. 2015b).

  Irrespective of the group they were assigned to, all subjects consumed the same amount of energy (1,500 kcal/d), but with either a high or low ratio of carbohydrate:fat:protein percentages (see Figure 1). But the women didn't just eat less, they also had to perform a supervised circuit-style resistance-exercise program four days/week and followed a standardized walking program that consisted of 10,000 steps/day on three days/week. 

High carbohydrate diets for metabolic syndrome? A question of your genes - Study suggests that diets high in carbohydrate may not be appropriate for rs328 G carriers with the metabolic syndrome. In said study, two districts in Shanghai, China were randomly selected to be the intervention and control group, and patients (n=235) with metabolic syndrome within these two districts were selected based on a multistage sampling method.

"Three Days on Pasta, Muffin & Bread Diet (84% CHO) = 1kg Add. Lean Mass and a Sign. Trend for Decreased Fat Mass" - Probably the subjects in the study discussed in this SV Classic Article simply had the right genes ;-)

Fasting glucose was reduced in rs328 CC homozygotes (p=0.028) but not G carriers (p=0.686) within the intervention group.

Also an ancillary study with greater statistical power by combining the baseline measurements across both the intervention and control groups was conducted to test the cross-sectional statistical interactions between carbohydrate/fat and lipoprotein lipase genotypes for homeostasis model assessment of insulin resistance/insulin/fasting glucose. Increased carbohydrate intakes were positively associated with homeostasis model assessment of insulin resistance and insulin in rs328 G carriers but not CC homozygotes (p for interaction was 0.025).

"These results indicate that diet high in carbohydrate may not be suitable for metabolic syndrome rs328 G carriers, calling for the development of personalized dietary intervention for metabolic syndrome subjects," (Zhang. 2015) scientists say.

• Unsurprisingly, the combination of both, diet and exercise triggered significant reductions in weight and body fat in both diet groups (high and low carb). Nevertheless, both, the carbohydrate content of the diet and the genotype < > diet match, had significant effects on the study outcomes, as well. More specifically, ...
  • the participants following a more carbohydrate restricted diet experienced significantly greater weight loss and slightly greater body composition changes (the low-carb-fat-loss-advantage), and
  • matching diet based on gene-type exhibited better retention of fat free mass, albeit with no significant differences between groups in changes in weight or fat mass (the genotype-lean-mass-advantage).
  Now that sounds pretty much like genotyping your diet was always the way to go, right? Well, in view of the fact that the falsely assigned subjects experienced a slightly greater reduction in body fat percentage, the interpretation of the study results does actually depend on one's individual goals and is thus less obvious than it may appear to be when you read the abstract.
• How much should you eat, ladies? Study shows: No equation can answer this question exactly -- You may believe that your apps and fitness trackers were able to tell you "exactly" how much energy you need, but  eventually their recommendations are also based on equations like those Kisiolek et al. tested in their latest study.
  
  

  Do We Systematically Underestimate the Energetic Costs of Push-Ups, Pull Ups, Squats & Co? Study Says Anaerobic Exercises Burn 2x More Energy Than Previously Thought | learn more

  For the experiment on which I base the above statement, the scientists recruited twenty-five recreationally active, college-aged women (20.72 ± 0.97 yrs; 163.04 ± 5.67 cm; 67.08 ± 10.40 kg; 29.04 ± 5.80% BF) who underwent a single day of testing, consisting of determination of REE by indirect calorimetry (TrueOne® 2400 Metabolic Measurement system, ParvoMedics, Sandy, UT) followed by body composition assessment.
  
  To avoid interferences by exercise or dietary factors, all subjects were instructed to refrain from strenuous exercise 48 hrs prior to testing in addition to fasting >8 hrs prior.
  
  During the actual testing, the participants laid motionless without falling asleep for 15-20 minutes during REE determination. Data were recorded during a period of time in which criterion variables (e.g., VO2 L/min) changed less than 5% every 5 minutes. In addition, the subjects' body composition was assessed using air displacement plethysmography (BODPOD, Cosmed, USA) via the Siri equatio and fed into the three equations the scientists tested, i.e. the (1) Nelson Equation the (2) Mifflin-St. Jeor Equation and the (3) Harris-Benedict Equation (with a moderate activity factor).
  

  Figure 2: Energy expenditure (kcal/24h) according to indirect calorimetry (measured) and the three tested equations (calculated); %-ages indicate differences to measured values (Kisiolek. 2015).

  For all three tested equations the results were significantly different than indirect calorimetry (p < 0.001; see Table 1). More specifically, ...
  • the Nelson and Mifflin-St. Jeor equations underestimated REE when compared to indirect calorimetry by 345.5 ± 51.5 and 220.6 ± 47.3 kcals, respectively,
  • while the Harris Benedict overestimated REE by 272.4 ± 49.3 kcals.
  Against that background it could be considered a "success" that all three equations were moderately correlated with the subjects' objectively measured resting energy expenditure (REE) as determined by indirect calorimetry.
  
  Well, "success" or not, the implications of Kisiolek's study should be clear: "Practitioners should exercise caution when providing dietary recommendations based upon predicted REE values as certain equations may over or underestimate energy requirements by several hundred kilocalories" (Kisiolek. 2015); and I would like to add: If you want to make sure you're nailing it, log your dietary intake during a weight stable week - that's the only way to know for sure how much energy you need.

So what didn't make the "cut"? Worth mentioning, but not discussing in detail are the observations Mullins et al. made when they investigated the effects of Iron Cuts®, a thermogenic supplement from MusclePharm, that appeared to improve the subjects strength, but had no significant effects on the health or body composition of 20 recreationally trained men who participated in Mullins' prospective, double-blind, placebo controlled randomized trial (Mullins. 2015).

Statistical significance was only observed for the small increase in fatty acid oxidation in response to Shred-Matrix® from -3h to pre-workout not for the post increase (Seijo. 2015). Neither of them means that the supplement will actively promote fat loss, though.

The increase in fatty acid oxidation Seijo et al. observed when they studies the acute effects of Shred-Matrix® on fat oxidation is certainly more impressive than the results of Mullins study, but eventually it is of even less practical relevance. As a SuppVersity reader you should now that the currently available research refutes the existence of a reliable mechanistic link between the acute increases in fatty acid oxidation the scientists observed before and after the workout and long-term fat loss (the post-workout increase in fatty acid oxidation was not even significantly higher than the increase in the placebo group, by the way).

In view of the lack of effect on mood state and perception of hunger it is thus very questionable, whether the supplement can actually do what the scientists say their results would "suggest" and augment "the weight-loss benefits at rest and during exercise" (Seijo. 2015) | Comment!

Are you trying to build a body like this? Maybe one of the supplements discussed in this article can help.

Read more about ISSN and other studies at the SuppVersity

Vitargo, Red Bull, Creatine & More | ISSN'15 #1

Pump Supps & Synephrine & X | ISSN'15 #2

High Protein, Body Comp & X | ISSN'15 #3

Keto Diet Re- search Update | ISSN'15 #4

The Misquantified Self & More | ISSN'15 #5

BCAA, Cholos-trum, Probiotics & Co | ISSN'15 #6

• Ten weeks of branched chain amino acid supplementation improves select performance and immunological variables in trained cyclists -- Unlike previous studies which used either relatively low amounts of BCAAs or investigated only the acute effects of BCAA supplementation on performance and immune markers in athletes, the latest study from the Auburn University used a total of 12g BCAAs per day (6g/d L-Leucine, 2g/d L-Isoleucine and 4g/d L-Valine) or a maltodextrin placebo that was consumed by the N=18 trained cyclists (32 ± 2 yr, 77.8 ± 2.6 kg, and 7.4 ± 1.2 yr training) who participated in the study for 10-weeks.
  
  Before and after the 10-week study, the following was assessed: a) 4-h fasting blood draws; b) dual X-ray absorptiometry body composition; c) Wingate peak power tests; and d) 4km time-trials.
  

  Figure 1: While there were no improvements in body composition, the scientists observed sign. increases in selected performance markers in response to 10-weeks on high dose BCAA (Kephart. 2015).

  The analysis of the data shows no group*time interactions existed for total lean mass (p = 0.27) or dual-leg lean mass (p = 0.96). A significant interaction existed for body mass-normalized relative peak power (19% increase in the BCAA group pre- to post-study, p = 0.01), and relative mean power (4% increase in the BCAA group pre- to post-study, p = 0.01), however.
  
  Non-significant, but still noteworthy were the improvements in 4km time-trial performance which shows a borderline significant interaction (p = 0.08) - with the BCAA group improving their TT performance by a non-significant +11% from pre- to post-study. To which extent this improvement was mediated by the increase in serum BCAA: L-Tryptophan ratio would have to be investigated separately, though (l-tryptophan is still suspected to mediate the exercise induced increase in central fatigue | Fernstrom. 2006).
  
  Of similarly unclear practical significance are the interactions the scientists observed for neutrophil numbers (p = 0.04), which increased only in the placebo (+18%), yet not in the BCAA group. In view of the association of increased neutrophil levels and the exercise-induced suppression of immunity, it is yet logical to follow the scientists' conclustion that "BCAAs may benefit immune function during a prolonged cycling season" (Kephart. 2015).
• Caffeine and coffee don't differ in their effects on exercise performance -- As Trexler et al. point out, coffee (COF) and caffeine (CAF) "have not yet been directly compared in the context of strength and sprint performance" (Trexler. 2015). To fill this gap in the available research Trexler et al. conducted a randomized, double-blind study that was to compare the effects of acute COF and CAF intake on strength and sprint performance.
  
  In the study, fifty-four resistance-trained male participants (mean ± SD; age = 20.1 ± 2.1 yrs; height = 177.3 ± 5.6cm; weight = 78.8 ± 8.8 kg; habitual caffeine intake = 32.9 ± 59.6mg/day) completed a baseline test that consisted of both one-rep max (1RM) and repetitions to fatigue (RTF) for leg press (LP) and bench press (BP).

  "Following strength testing, a friction-loaded cycle ergometer was loaded with a resistance of 95g/kg of bodyweight and participants completed a repeated sprint protocol consisting of five, ten-second sprints separated by one minute of passive rest. Peak power (PP) and total work (TW) were recorded for each sprint, along with average PP and TW values for the entire protocol (all five sprints). At least 48 hours later, participants returned for post-testing and ingested a beverage containing either CAF (300mg), a caffeine-matched dose of instant COF (8.9g, yielding 303mg of caffeine), or a flavored placebo (PLA) 30 minutes prior to exercise. Prior to each visit, participants were instructed to maintain similar dietary habits, abstain from strenuous exercise for at least 24 hours, and avoid caffeine intake for at least 48 hours. Change scores were compared using one-way ANOVAs, and 95% confidence intervals (mean ± 1.96 × SEM) were constructed for each dependent variable" (Trexler. 2015).

  The analysis of the data the experiment generated yielded significant performance increases on the on the leg press where the 1RM was improved more by COF compared to CAF (Δ = 32.2 ± 18.6 vs 15.3 ± 16.9lb, p = 0.04), but not to PLA (p = 0.99).
  

  Figure 2: At least in comparison to the placebo treatment, the improvements in exercise performance are not debatable. Whether caffeine or coffee is the better ergogenic is albeit still not 100% clear (Trexler. 2015)

  No significant interactions were not observed for bench press (BP) 1RM, BP RTF, or leg press (LP) RTF (p > 0.05). The total work during the spring, however was increased for CAF [81.4, 623.9J], but not COF [-121.0, 376.2J] or PLA [-239.9, 180.1J]. In addition, both caffeine and coffee blunted the significant reductions in peak power and total work during the latter sets of the spring training. In spite of the lack of general improvements of strength outcomes, the improvements that were observed during the repeated sprint test support the notion that both caffeine and coffee have practically relevant ergogenic effects.
• Bio-Gro™, a commercial food-based bio-active peptide product, may augment your gains and enhance your recovery -- I guess the question that's preying on your mind at the moment is "Bio-Gro? Wtf..." Well, I wish I could answer this question precisely, but all I can tell you is that it's a peptide-based powder (serving size 1.5g) of which the manufacturer, Isatori, says that it is extracted from bovine colostrums and contains ...

  "an exact concentration of bioactive:  Proline-Rich Peptides (PRP's), Growth Factors (IgF, TGF beta-2, EGF, PDGF), Immunoglobulins (IgG, IgA), Lactoferrin and Fibroblast-GF." (manufacturer website)

  Against that background it is not really surprising that Patrick Jacobs' study on the safety of the product did not find unwanted side effects in twenty recreationally resistance trained men who consumed the supplement that is available both in powder- and capsule-form.
  
  What is surprising, though, is that the provision of the supplement over 8-weeks also yielded significant enhancements in the rate of body mass and lean body mass gains with supplementation of a bio-active peptide in conjunction with eight weeks of resistance training. To be precise, Jacobs' analyses of the data revealed that ...

  "Bio-Gro™ produced significantly greater (p < 0.05) changes in total body mass as assessed with BodPod (+6.3 pounds) than the placebo condition (+2.8 pounds). [In addition, l]ean body mass changes were also significantly greater with Bio-Gro™ (+5.8 pounds) compared with placebo (+3.7 pounds) (p < 0.05)" (Jacobs. 2015).

  Similar benefits were observed for the subjects sleeve sized of which mid-arm flexed measurements (+0.74 inches) indicate that they increased more than 2x more in the treatmet vs. placebo condition (+0.31 inches) (p < 0.05).
  

  Figure 3: Pre- / post changes in body composition and mid-arm flexed circumference (Jacobs. 2015).

  In view of the lack of differences in other circumferential change scores, and the lack of statistical significance of the lean mass when the latter were assessed by skinfold measurements, I would still like to see an independent confirmation of the results (also a comparison to whey protein / the use of Bio-Gro™ alongside whey protein) before I invest 52.5 cents per serving. This is particularly true in view of the fact that the supplement appears to have boosted the subjects' fat gains, too (see Figure 3 where the difference between total mass and lean mass increases is probably fat, not organ or bone weight ;-).
• Caloric restriction is easy on "intermittent fasting", but fat loss does not ensue -- Bad news for intermittent fasting enthusiasts comes from the Baylor University, where Grant M Tinsley investigated the effects of intermittent fasting combined with resistance training on body composition, muscular performance, and dietary intake.
  
  For the course of the 8-week study, 18 adult men were randomly assigned to do either resistance training alone (RT) or resistance training plus IF, in the form of termed time-restricted feeding (RT+TRF). Both groups followed a 3-days-per-week resistance training program for 8 weeks.

  "The TRF program was implemented on non-workout days (i.e. 4 days per week) and consisted of consuming all calories within any 4-hour period between 4 PM and midnight. Both groups were allowed unrestricted food intake during feeding periods. Research visits were conducted at baseline, 4 weeks, and 8 weeks after beginning the study and consisted of body composition assessment via dual-energy x-ray absorptiometry (DXA), 1-repetition maximum (1-RM) strength testing and muscular endurance testing on bench press and leg press exercises, and subjective measures of program difficulty. Diet records, workout logs, and compliance forms were used to track and encourage program adherence, as well as examine dietary differences. One-way and factorial ANOVAs were conducted using R (version 3.1.1)" (my emphasis in Tinsley. 2015).

  For intermittent fasting enthusiasts, the results were - as previously said - disappointing: No group*time interactions were found for any measures of body composition (lean mass, fat mass, and body fat percentage), muscular performance, or dietary intake.
  
  Interestingly, the intermittent fasting group did still display a slightly higher leg press 1-RM as well as an increased bench press endurance compared to the resistance training only (RT) group. That this occurred in the presence of a significantly reduced energy and fat intake in the RT+TRF group on the fasting days, but in the absence of significant differences on the non-fasting days is surprising. It does after all suggest that the subjects in the intermittent fasting (RT+TRF) group must have consumed significantly less energy. Now, it's up to you to decide what you find more surprising:

  • Intermittent fasting can make you fat | learn why!

    The fact that the subjects in the intermittent fasting group consumed significantly less energy without losing body weight or fat?
  • Or the fact that the subjects in the intermittent fasting group saw greater performance increases despite consuming significantly less energy and dietary fat?
  Whatever your personal answer to this question may be, the most significant results of the study is probably that there were "[n]oticeable differences in individual responses to the programs" (Tinsley. 2015) - an observation that should remind you of the conclusions to previous articles on Intermittent Fasting, here at the SuppVersity: Eventually, you will have to try it to find out if IF works for you.
• Probiotic muscle protectors -- Muscle protecting probiotics? I have to admit: That sounds awkward. Nobody would doubt that GanedenBC30 a probiotic supplement that contains Bacillus coagulans GBI-30, 6086, supports healthy digestive and immune function. I am even willing to believe that supplement-induced changes in the make-up of its users gut microbiome can increase the absorption of protein, but I would not have expected that it can actively promote muscle recovery through gut microbial modulation.
  
  Just that is yet what a recent study from the University of Tampa suggests. In said study, 30 healthy recreationally-trained males (mean+/-SD; age: 21.5 ± 2.8 years; height: 177.4 ± 8.0 cm; weight: 89.7 ± 28.2 kg) were randomly assigned to consume either 20 g of casein (Control = CON) or 20 g of casein plus probiotic (500M CFU GanedenBC30, = BC30) twice daily in a crossover, diet-controlled design for a two-week time period.

  "Subjects performed a damaging exercise bout consisting of 10 sets × 10 repetitions unilateral leg press at 70% 1 RM with 1 minute rest, one legged - leg extension (5 sets × 12 reps), and rear foot elevated split squat 5 sets × 12 reps with one minute rest at baseline and after two weeks of supplementation. Athletic performance consisting of peak power (Wingate 10 sec Peak Power Assessment at 7.5% BW at 175RPM threshold loaded drop), vertical jump power (Tendo unit, single-leg jump), and 1-RM single-leg press; and muscle damage was analyzed by muscle swelling (ultrasonography) and blood draws (creatine kinase (CK), blood urea nitrogen (BUN)) were taken at baseline (pre-supplementation) and 48 hours after damaging exercise bout. Perceptual measures (perceived recovery, soreness) were taken before, 24, 48 and 72 hours after exercise" (Jäger. 2015).

  The analysis of the data the tests generated shows that the damaging exercise bout significantly increased muscle soreness (p < 0.001), reduced perceived recovery (p < 0.001) in both groups. Compared to the control group, however, the subjects in the casein + BC30 group show a significantly increased rate of recovery at 24 and 72 hours, and decreased soreness at 72 hours post exercise.
  

  Figure 4: Changes in CK and Wingate peak power in the control and treatment group (Jäger. 2015).

  The perceptual measures were confirmed by increases in CK (CON: +266.8%, p = 0.0002; BC30: +137.7%, p = 0.01), with BC30 showing a trend towards reduced indices of muscle damage (p = 0.08). It is thus only logical that the significant reduction in athletic performance in the control group (Wingate Peak Power; CON: (-39.8 watts, - 5.3%, p = 0.03)), was ameliorated, yes even blocked, in the BC30 group (+10.1 watts, +1.7%).
  
  Whether similar effects can be seen with non-patented strains of probiotic bacteria warrants further investigation. What I can tell you already, though, is that even regular yogurt has immuno-supportive effects (Lollo. 2013). Previous studies also indicate that more commonly used lactobacillus strains have similar anti-oxidant effects in athletes (Martarelli. 2011). Whether their effects are more or less pronounced than those of the Bacillus coagulans strain in BC30 will now have to be elucidated in future studies.

Nootropics for the bottom line: In view of the inconclusive results of Parker et al.'s study on the effects of alpha-glycerylphosphorylcholine, caffeine or placebo on markers of mood, cognitive function, power, speed, and agility, I have "banned" it into the bottom line, where I'd like to cite the scientists's conclusion that "future research should focus on dosage of [alpha GPC for certain physical and mental performance tasks], timing of consumption before testing measurement, bioavailability, longer term supplementation, and subject selection, in order to reduce individual variability" (Parker. 2015) and add that you may want to memorize that the provision of 200mg of caffeine did not improve the 10 male and 10 female participants' performance on subsequent (30 min) tests for reaction time, hand-eye coordination, power, speed, and agility.

You have to adjust volume, intensity and frequency of your workouts according to your goals | learn how!

At first sight, the lack of efficacy of caffeine appears to stand in contrast to the results Trexler et al. present in their study. Eventually, however, it could well be nothing but the test that makes all the difference. After all, acute performance benefits were observed by Trexler et al. only in the total work during a sprint test - the total work, however, wasn't even assessed by Parker et al. So, if there's one important take-away it's that supplements must always be chosen according to one's personal goals...

Now, this which brings me back to the increased sleeve sizes in the Jacobs study. You will be happy about these inches only if you don't care about the purported fat gain Jacobs doesn't address in the abstracts to his 8-week study on cholostrum peptide supplementation | Comment on Facebook!

Not just for women who are always afraid of an increase in water retention, loading protocols may not exactly be the best way of taking creatine monohydrate.

You can learn more about creatine at the SuppVersity

Creatine Doubles 'Ur GainZ!

Creatine, DHT & Broscience

Creatine Pre or After Workouts?

ALA + Creatine = Max Uptake?

Creatine Blunts Fat Loss?

Build 'Ur Own Buffered Creatine

"randomly placed 25 subjects into 1 of 3 groups: (1) creatine supplementation of 3 g·d21; (2) creatine supplemen tation of 20 g·d21 for 7 days, followed by creatine supplementation of 5 g·d21 for the remainder of the study; or (3) a placebo group" (Wilder. 2001).

"For the first week (loading phase), ingestion occurred 4 times per day. High-dose creatine (5 cre atine tablets), low-dose creatine (3 creatine tablets and 2 placebo tablets), or placebo (5 placebo tablets) was taken when the subjects awoke, before and after the workout session, and in the evening before bed. For the subsequent 9 weeks, the high or low dose of creatine or the placebo dose was ingested once per day after workouts and at the same time on off days" (Wilder. 2001).

• Strength program: The primary exercises in the strength program were the front squat, back squat, hang clean, power clean, overhead press, bench press, single-arm dumbbell press, 1-arm rows, straight-leg dead lift, power shrugs, upright rows, chin-ups, dips, medicine ball plyometrics, and bumper-plate push-ups. 
• Periodization scheme: The periodization protocol was a 5-week base hypertrophy phase (4 to 6 sets at 50% to 80% 1-RM), followed by a 2-week power phase (3 to 5 sets at 80% to 88%). After this 7- week period, a 2-week strength phase (1 to 3 sets at 90% to 95%) was implemented, followed by a 1-week peak strength phase (1 to 3 sets at 95% to 100%). 

Figure 1: Changes in strength and lean mass gains over the course of the 10-week study (Wilder. 2001).

• Creatine loading + high dose supplementation did not produce significantly different effects on strength, urinary creatinine, or percentage of body fat than training, alone.
• There were no significant inter-group differences for loading + high dose vs. low dose supplementation over the course of the 10-week study.
• Significant side effects weren't observed in any of the three study groups.

Figure 2: Pre- / post changes in body fat (%) - Note: The differences didn't reach statistical significance due to inter-individual differences (Wilder. 2001)

"Creatine & Caffeine Don't Mix" - Another myth you to forget? Read my recent article on the matter and make up your mind! More.

Bottom line: I am not saying that the study at hand can prove the superiority of low vs. high dose (+loading) supplementation for creatine monohydrate. All that I am saying is that the still commonly used loading scheme for creatine, as well as the often practiced "more helps more" approach to creatine supplementation lack scientific backup - unless, obviously, it is used specifically to maximize the phosphocreatine stores in your muscles in the shortest amount of time (in this case loading may be the way to go).

Eventually, it would obviously be nice if we had more studies that investigate the differential effects of loading and/or high vs. low dosing. In view of the number of creatine studies, it is pretty surprising that Wilder's study practically the only one dealing with this issue, right? Comment!

• Kim, Hyo Jeong, et al. "Studies on the safety of creatine supplementation." Amino Acids 40.5 (2011): 1409-1418.
• Wilder, Nathan, et al. "The effects of low-dose creatine supplementation versus creatine loading in collegiate football players." Journal of athletic training 36.2 (2001): 124.

Just look at the guys surrounding you, girls. How on earth will you get bulky if they are training like maniacs and still look like size-zero bans?

Learn more about dieting and not ruining your metabolism @ www.suppversity.com

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Figure 1: There's little doubt that the overall improvements in body composition (figures are effect sizes for loss of fat, increase in lean mass) are the most pronounced in response to diet + resistance training (but non-existent w/ resistance training, only - not shown). What is surprising is the low efficacy of combined training programs, though (Clark. 2015).

Figure 2: The effect sizes of the interventions' effects on insulin, leptin, cholesterol & co yields similar results: The combination of resistance training and diet has (on average) the most favorable effects (Clark. 2015).

"resistance training (RT) was more effective than endurance training (ET) or combination of RT and ET, particularly when progressive training volume of 2-to-3 sets for 6-to-10 reps at an intensity of ≥75% 1RM, utilizing whole body and free-weight exercises, at altering body compositional measures (ES of 0.47, 0.30, and 0.40 for loss of BM, FM, and retention of FFM respectively)" (Clark. 2015)

Figure 3: The good results some studies on combined training show suggest that the lack of benefits in the meta-analysis may be a statistical phenomenon, or a result of certain aspects of the individual study design (e.g. low volume or intensity) in some of the studies (data from Donnely. 1991).

Bottom line: If you still need material to convince your significant other that hitting the weights is not only more time-efficient and less daunting than hours on the treadmill, but also more effective when it comes to improving his/her body composition and/or health, I'd suggest you print this article and pin it on your fridge.

Losing Weight Doesn't Have to Ruin Your Metabolism | more

Eventually, though, the article has another, even more important message than "resistance beats cardio training". Which one? Well, there is "no relationship between any treatments effectiveness for inducing acute changes in energetic balance with the effectiveness for induced responses to body composition or biomarkers of health from said treatment program" (Clark. 2015). A revelation that reinforces the idea that our individual body composition is not a function of energy intakes vs. expenditure. The effects of metabolic stress, which is obviously greater for resistance and HIIT training (compared to steady state, the HIIT studies in the meta-analysis yielded better results, too), on the other hand is still underappreciated by both practitioners and scientists of who James E. Clark is one of the first to conclude that the "focus of treatment should be on producing a large metabolic stress (as induced by RT or high levels of ET [don't overdo it on "cardio", though | learn why]) rather than an energetic imbalance for adults who are overfat" (Clark. 2015) | Comment on Facebook!

• Clark, James E. "Diet, exercise or diet with exercise: comparing the effectiveness of treatment options for weight-loss and changes in fitness for adults (18–65 years old) who are overfat, or obese; systematic review and meta-analysis." Journal of Diabetes & Metabolic Disorders 14.1 (2015): 31.
• Cuff, Darcye J., et al. "Effective exercise modality to reduce insulin resistance in women with type 2 diabetes." Diabetes care 26.11 (2003): 2977-2982.
• Donnelly, Joseph E., et al. "Effects of a very-low-calorie diet and physical-training regimens on body composition and resting metabolic rate in obese females." The American journal of clinical nutrition 54.1 (1991): 56-61.

Yes, I do suggest that it may be beneficial to drink these two and another two cups of coffee w/ lots of sugar after your workout - if you are an athlete, at least.

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Caffeine Resis- tance - Does It Even Exist?

Figure 1: Total glycogen [proglycogen (PG) macroglycogen (MG)] glycogen concentrations during 5 h of recovery in the placebo trial (A) and caffeine trial (B | Battram. 2004).

"In conclusion, Caf ingestion does not impede the resynthesis of PG or MG after an extensive depletion of muscle glycogen and with the provision of exogenous dietary carbohydrate" (Battram. 2004).

Even though Beelen's study does not support the the superior effect of caffeine on muscle gylcogen, it does at least show that the effect (if it occurs) would probably be identical for fast- and slow-twitch muscles and thus similarly beneficial for strength and endurance athletes (Beelen. 2011).

So, there is no doubt that this works? Well, as usual, there is doubt. Another 2011 study by Beelen et al. did not find the same increases in glycogen resynthesis. It is well possible, though that this was due to either the fact that they pumped their subjects up with even higher amounts of carbs, though (1mg/kg/h in Pedderson vs. 1.2mg/kg/h in Beelen) and lower amounts of caffeine (15% less). In view of the fact that the exercise protocol used in the study only halved the glyocogen levels of the subjects, while it was reduced by >75% in the Pedderson study, the lack of effect may also be a result of the lack of full glycogen depletion in Beelen's study (unfortunately, the authors don't provide their values only in arbitrary units - that's why I can't tell you with certainty to which degree this may have influenced the results).

• CHO [4 g/kg body mass (BM)] alone or
• CHO [4 g/kg body mass (BM)] with Caff (8 mg/kg BM)

Figure 2: High dose caffeine (8mg/kg) increases glycogen resynthesis after exhausting workouts without having ill effects on the resynthesis of ATP and PCr (Pedderson. 2008).

Figure 3: Exercise capacity during the Loughborough Intermittent Shuttle Test for the carbohydrate (CHO), CHO plus caffeine (CHO+CAFF), and water (WAT) trials. Lines represent individual subject responses (Taylor. 2011).

• Battram, Danielle S., et al. "Caffeine ingestion does not impede the resynthesis of proglycogen and macroglycogen after prolonged exercise and carbohydrate supplementation in humans." Journal of Applied Physiology 96.3 (2004): 943-950.
• Beelen, Milou, et al. "Impact of caffeine and protein on postexercise muscle glycogen synthesis." Med Sci Sports Exerc 44.4 (2012): 692-700.
• Pedersen, David J., et al. "High rates of muscle glycogen resynthesis after exhaustive exercise when carbohydrate is coingested with caffeine." Journal of Applied Physiology 105.1 (2008): 7-13.
• Taylor, Conor, et al. "The effect of adding caffeine to postexercise carbohydrate feeding on subsequent high-intensity interval-running capacity compared with carbohydrate alone." International Journal of Sport Nutrition andExercise Metabolism 21.5 (2011): 410.
• Thong, Farah SL, and Terry E. Graham. "Caffeine-induced impairment of glucose tolerance is abolished by β-adrenergic receptor blockade in humans." Journal of applied physiology 92.6 (2002): 2347-2352.
• Van Nieuwenhoven, M. A., R-JM Brummer, and F. Brouns. "Gastrointestinal function during exercise: comparison of water, sports drink, and sports drink with caffeine." Journal of applied physiology 89.3 (2000): 1079-1085.

With overtraining you have to undertrain to reverse the damage you've done. Doing so in intermittent hypoxia, returns important markers of OT to normal in less than 4 weeks in T&F athletes.

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"15 athletes with OTS volunteered to participate and undertook a conditioning programme consisting of repeated exposures to hypoxia (O2 at 10%) and hyperoxia (O2 at 30%) (6–8 cycles, total time 45 min–1 h), three times a week, delivered 1 5–2 h after a low-intensity exercise session (2 bouts of 30 min, running at 50% of VO2max with 10 min rest between bouts) over 4 weeks" (Susta. 2015). 

Figure 1: Pre vs. post results of the PWC170 (Boreham. 1990) performance test in overtrained and normal athletes (Susta. 2015) indicate that even with hypoxic training the time it takes to recover is a throwback for athletes.

Figure 2: The most significant marker that indicates the normalization of the training status in the overtrained group is the LH/HF Index, the only variable that is plotted against the secondary axis (Susta. 2015).

If you've tried to use overraching to increase your performance, the hypoxia-hyperoxia protocol used in the study could come very handy to help you recover | learn more.

Bottom line: While the scientists are right to conclude that their "pilot study showed that intermittent hypoxia–hyperoxia training and low-intensity exercise can facilitate functional recovery among athletes with OTS in a relatively short time" (Susta. 2015). They forget to mention that they didn't test their protocol vs. a regular light intensity exercise protocol.

A follow up study in which this is being done and the effects on performance and the normalization of the sympatho-parasympathetic index are compared between the regular and hypoxia training group is thus necessary before one could recommend training in hypoxia for athletes and/or gymrats suffering from the very existent overtraining syndrome | Comment on Facebook!

• Boreham, C. A., V. J. Paliczka, and A. K. Nichols. "A comparison of the PWC170 and 20-MST tests of aerobic fitness in adolescent schoolchildren." The Journal of sports medicine and physical fitness 30.1 (1990): 19-23.
• Susta, Davide, Elena Dudnik, and Oleg S. Glazachev. "A programme based on repeated hypoxia–hyperoxia exposure and light exercise enhances performance in athletes with overtraining syndrome: a pilot study." Clinical Physiology and Functional Imaging (2015).

Old or young, who is going to benefit and who is going to benefit most from vitamin D supplementation during a 12-week resistance training regimen. That was the question the study at hand sought to answer and this was a question it didn't find an unambiguous answer to.

There are many ways to get your vitamin D learn more the SuppVersity

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Vitamin D Helps Store Fat

"We hypothesized that intake of vitamin-D plus calcium would improve the outcome of three months of resistance training in healthy untrained individuals resulting in greater muscle strength and hypertrophy compared to a training control-group supplemented with calcium alone (placebo). Moreover, we hypothesized that resistance exercise would increase the mRNA expression of VDR and CYP27B1. The study included a group of young and a group of elderly individuals to elucidate a possible blunted hypertrophic response in the aging muscle" (Agergaard. 2015).

• placebo supplementation with 800mg of calcium per day, or
• vitamin D + calcium at a dosage of 48µg (1920 IU) vitamin-D 3 + 800 mg calcium/day

Figure 1: Flowchart showing a young and b elderly subjects from first contact to end of study (Agergaard. 2015)

• During the first 6 training sessions, participants completed 3 sets of 12–15 repetitions at 65–70 % of 1RM. 
• During session 7–12, participants performed 3 sets of 10–12 repetitions at 70–75 % of 1RM, increasing to 4 sets at 70–75 % of 1RM during session 13–18. 
• From session 19 and onwards, participants performed 5 sets with training load progressing from 8–10 repetitions at 75–80 % of 1RM in session 19–27 to 6–8 repetitions at 80–85 % of 1RM in session 28–36 [38]. 

The complex ways in which vitamin D supplements interact with both the levels of the active form of vitamin D 1,25(OH)2D and the binding proteins vitamin D binding protein and serum album has yet not been considered in any of the "vitamin D and gains" studies - epic fail ? (data from Glendenning. 2015)

Vitamin D Binding Protein, Bioavailable Vitamin D & Receptor Polymorphisms - Although it has been known for decades that only 0.1% of the vitamin D in our body and only ~10% of the metabolites in our blood are free, the effects of being bound to its specific binding protein (VDBP) or albumin are still largely unknown. One of the reasons is that studies still rely on unreliable measurements of total vitamin D that are then run through algorithms to elucidate if there's a difference between the effects of free and bound vitamin D (Chun. 2014). This is not only problematic because it assumes that we'd all have the same / similar amounts of vitamin D binding protein, but also because it ignores already established genetic polymorphisms (e.g. inter-racial / whites are more likely to have a low binding affinity than blacks) in how VDBP works and how it affects our health and is affected by supplementing with vitamin D (sign. increases are seen w/ vit D2 or D3 | see Fig.).

A similar negligence can be observed with regard to the role of the vitamin D receptors on its various target organs. While we know that their expression increases with resistance training (no added increase was observed with vitamin D supplementation in the study at hand in contrast to a recent study by Makanae et al. (2015) in rodents), we still have almost no clue how they interact with free and bound vitamin D; and only recently researchers like Jia et al. (2015) have begun to investigate how certain vitamin D receptor polymorphisms (gene types) like the rs739837 gene are associated with increased risk of T2DM. In conjunction with the role of genetic polymorphisms of the binding proteins, the whole system is at the moment thus way too too complex for us to make predictions on a population or even sub-population levels (like the elderly, men and women at an increased risk of cancer, or patients with autoimmune diseases, or athletes). 

Figure 2: Serum vitamin D levels at all time-points during the study (I added the markups for the zones to the original figure from Agergaard to make it easier for you to interpret the data).

Figure 3: Cross sectional area (CSA), Isometric strength and strength/CSA of Quadriceps muscle. Change in a CSA, b isometric strength and c strength/CSA of quadriceps muscle for young and elderly vitamin-D and placebo groups, respectively. Data shown as mean percentage change from week 0 ± SEM. * different from week 0 (p < 0.05)

• No group effects - The first thing you should realize is that there were no significant inter-group differences and thus no group effects in response to the provision of vitamin D3 vs. placebo. This does imply that neither the increased size gains (A) in the vitamin D group in the young nor the decreased gains in the vitamin D group in the old subjects was statistically significant. The same can be said, albeit in the opposite directions for the strength increases (B) and the relative strength increases (C) in the young subjects.
• Significant time effects - Since subjects in both groups still gained significant amounts of muscle and strength, the one thing the study does confirm is the efficacy of resistance training as strength and mass builder in young and old.
• Significant group effect on relative strength in the elderly - Due to the reversal of the observations compared to the young group (lower size gains + higher strength gains in the older, higher size + lower strength gains in the younger subjects), the relative strength of the older subjects has improved by vitamin D supplementation (p = 0.008, not correctly indicated in Figure 3) - a result that stands in line with previous research like Moreira-Pfrimer et al. (2009) where the provision of 150,000 IU once a month during the first 2 months, followed by 90,000 IU once a month for another 4 months enhanced both, the 25(OH)D levels and the lower limb muscle strength of the > or =60 year old subjects, even in the absence of any regular physical exercise practice.

Figure 4: The optimal ranges, Bischoff-Ferrari et al. estimated are based on the above observational data from a 8-foot-walk and sit-to-stand test done in the elderly. That's super reliable and just like you, right? No? Well, that's why I believe those "optimal values" have no relevance for the young and low relevance for the old subjects (Bischoff-Ferrari. 2006)

Figure 5: Correlation between Quadriceps ΔCSA, ΔIsometric strength, Δstrength/CSA and 25(OH)D (Agergaard. 2015)

So vitamin D supplementation is finally disproven? It is not just the specific study population (unhealthy individuals or athletes may benefit more, men and women may differ (Ko. 2015) etc.) that precludes making overgeneralized conclusions such as "vitamin D supplementation doesn't do anything for your gains". There is more! Firstly, there is the increase in what the scientists call "muscle quality", i.e. the ratio of strength/size increases in the elderly. Now, the data in Figure 5 indicates that this is clearly not a function of the serum 25OHD levels. If that's not the case, however, it could only be mediated by vitamin D3 directly or metabolites that haven't been tested in the study at hand (most prominently active vitamin D, i.e. 1,25-dihydroxycholecalciferol aka calcitriol). If that's the case, age may explain that the older subjects did not see the same changes in fiber type morphology (greater increase in type IIa) and myostatin expression the young ones did.

Figure 6: Significant treatment specific changes in fiber type (%), i.e. increases in fast-twitch type IIa fibers and decreases of the protein synthesis inhibitor myostatin were observed only in younger subjects (Agergaard. 2015).

I highlighted these changes with arrows in Figure 6 and would like to point out that they are the most interesting reason to still supplement w/ vitamin D. Eventually, both effects could affect your gains in the long-term: (I) lower myostatin = higher protein synthesis; (II) more type IIa fibers = higher growth potential. In only 12-weeks, however, newbies don't reach a level where myostatin and / or the fiber composition of their muscle is holding them back, significantly. For athlete and after longer training periods, however, the scientifically proven (albeit in vitro | Garcia. 2013, 2014)  ability of active vitamin D aka calcitriol (and / or vitamin D3 directly - not proven in human muscle) to increase the myogenic differentiation (would explain myofiber changes) and suppress myostatin in human myoblasts could turn out to be game changers.

To find out whether these purported long-term effects exist and / or if similar effects can be seen in non-sedentary adults, like athletes who would benefit the most of reduced myostatin levels and further changes in the muscle architecture, we do yet need more studies. Randomized controlled studies, maybe with different dosing schemes (the ~2,000 IU are not exactly much, if we consider potential direct effects) and no more observational bogus on vitamin D | Comment on Facebook!

• Agergaard, Jakob, et al. "Does vitamin-D intake during resistance training improve the skeletal muscle hypertrophic and strength response in young and elderly men?–a randomized controlled trial." Nutrition & metabolism 12.1 (2015): 32.
• Bischoff-Ferrari, Heike A., et al. "Estimation of optimal serum concentrations of 25-hydroxyvitamin D for multiple health outcomes." The American journal of clinical nutrition 84.1 (2006): 18-28.
• Chun, Rene F., et al. "Vitamin D and DBP: the free hormone hypothesis revisited." The Journal of steroid biochemistry and molecular biology 144 (2014): 132-137.
• Garcia, Leah A., et al. "1, 25 (OH) 2 vitamin D 3 enhances myogenic differentiation by modulating the expression of key angiogenic growth factors and angiogenic inhibitors in C 2 C 12 skeletal muscle cells." The Journal of steroid biochemistry and molecular biology 133 (2013): 1-11.
• Garcia, Leah A., et al. "1, 25 (OH) 2vitamin D3 stimulates myogenic differentiation by inhibiting cell proliferation and modulating the expression of promyogenic growth factors and myostatin in C2C12 skeletal muscle cells." Endocrinology 152.8 (2011): 2976-2986.
• Glendenning, Paul, et al. "Calculated free and bioavailable vitamin D metabolite concentrations in vitamin D-deficient hip fracture patients after supplementation with cholecalciferol and ergocalciferol." Bone 56.2 (2013): 271-275.
• Guralnik, Jack M., et al. "Lower-extremity function in persons over the age of 70 years as a predictor of subsequent disability." New England Journal of Medicine 332.9 (1995): 556-562.
• Jia et al. "Vitamin D Receptor Genetic Polymorphism Is Significantly Associated with Risk of Type 2 Diabetes Mellitus in Chinese Han Population." Arch Med Res. (2015): Ahead of print. 
• Ko, Min Jung, et al. "Relation of serum 25-hydroxyvitamin D status with skeletal muscle mass by sex and age group among Korean adults." British Journal of Nutrition (2015): 1-7.
• Koplin, Jennifer J., et al. "Polymorphisms affecting vitamin D–binding protein modify the relationship between serum vitamin D (25 [OH] D 3) and food allergy." Journal of Allergy and Clinical Immunology (2015).
• Makanae, Yuhei, et al. "Acute bout of resistance exercise increases vitamin D receptor protein expression in rat skeletal muscle." Experimental physiology 100.10 (2015): 1168-1176.
• Moreira-Pfrimer, Linda DF, et al. "Treatment of vitamin D deficiency increases lower limb muscle strength in institutionalized older people independently of regular physical activity: a randomized double-blind controlled trial." Annals of Nutrition and Metabolism 54.4 (2009): 291-300.

Don't expect weight loss wonders from high(er) protein and dairy intakes, but especially when the energy intake is not controlled both can have benefits the study at hand could not detect.

Learn more about women's weight loss & co a the SuppVersity

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• the JumpStart phase (weeks 0–2), being intended to kickstart the subjects' weight loss on a ~35% energy deficit, phase (2), 
• the Weightloss phase(weeks 3–12; total of 12 weeks), during which the subjects were supposed to adhere to a 1,500-1,700kcal diet which came close to a 25-30% energy deficit compared to their baseline energy intakes, and
• the Weightloss Maintenance phase, (weeks 13–24; total of 12 weeks), over the course of which the subjects had to stick to a dietitian designed "energy-balanced" diet which had still ~20% less energy than the subjects baseline diet (see Figure 4, right)

Figure 1: Macronutrient compositions of the prescribed diets in the intervention and comparison group (Shlisky. 2015).

Figure 2: Total intake (g) of carbohydrates, proteins and fats during the 12 week weight loss and maintenance phases (Shlisky. 2015)

"[w]eekly educational sessions were held for both INT and COM groups throughout the 6- month study and included lessons on basic nutrition knowledge, exchange patterns of eating, portion size and control, purchasing and preparing food and modifying recipes as well as motivational lessons on outcome expectations, selfregulation and monitoring, problem- solving, lifestyle modification, emotion eating and motivation for walking" (Shlisky. 2015) 

Thorpe et al. were able to show that high(er) protein intakes from dairy will decrease calcium loss and preserve bone mass (WB = whole body; LS = lumbar spine) while dieting. Don't fall for the "protein is bad for your bones" lie!

What does previous research tell us? If you look at previous research by Bowen (2004 & 2005), Josse (2011), Thorpe (2008) and Zemel (2004), there is significant evidence that high(er) protein intakes will augment fat loss and lean mass retention while increased dairy intakes may benefit bone mass and metabolic markers in men, women, young and old. In particular, when they are consumed alongside true exercise regimen, high(er) protein intakes have been proven have additive effects on body comp. during weight loss (8.8kg vs. 5.5kg fat loss in 16wks | Layman. 2005).

Against that background I would be very hesitant to take use the study at hand to argue that you can shed body fat just as effectively on the bogus "recommended diet" (=15-20% protein, 60% carbohydrates and 20-25% fat).

Figure 3: Relative changes in markers of body composition after the weight loss and weight maintenance phase; all values expressed as percent difference to the respective pre-values in both groups (Shilsky. 2015).

Figure 4: Reduction in energy expenditure (% of baseline) and total step count (activity level) of the subjects in the weight loss and weight maintenance phases of the study (Shlisky. 2015)

"[h]ealthy premenopausal women with excess adiposity effectively lost BW and fat mass and improved some metabolic risk factors following an ERD with approximately 20% protein and 3 svg/d of nonfat dairy intake." (Shlisky. 2015)

The actual macronutrient ratio during the weight loss and maintenance phase (figure shows averages) was by no means what it was supposed to be. The women ate ~8% less protein than they were supposed to do.

So, there's no benefit to high(er) protein and dairy intakes? No, there isn't - at least in a study with such a questionable design. Did you recognize the culprit? Yes, you're right: What on earth do you expect to happen if you design a "weight maintenance phase" during which the subjects still have to consume an energy reduced diet... I mean, it is well possible that the dietitians equations said that the diet was "energy-balanced". If you compare their intake to the ad-libitum diets of the subjects (=their baseline diet), the women still consumed 18% (HP) and 27% (NP) less energy during the weight maintenance phase - this time with a significant inter-group difference in favor of the high(er) protein high(er) dairy (yogurt) group who consumed more energy during both the weight loss and maintenance phase with identical results.

I am not sure what you think, but I personally would refute any statement about the standard diet recommendation being as efficient as a high(er) protein + high(er) dairy variety based on the study at hand. The increased satiety effect, a potential increase in thermogenesis, etc. - all the purported benefits of high(er) protein intakes couldn't show due to (a) non-adherence (instead of 30%, the subjects in the intervention group consumed only 23% and 20% protein during the weight loss and maintenance phase, respectively, and were thus not far off of the 20% and 18% in the COM group) and (b) the stupid idea not to let the women eat an ad-libitum with a fixed macronutrient ratio during the weight maintenance phase. This is after all a more realistic scenario and one in which real benefits of high(er) protein can show | Comment on Facebook!

• Bowen, Jane, Manny Noakes, and Peter M. Clifton. "A high dairy protein, high-calcium diet minimizes bone turnover in overweight adults during weight loss." The Journal of nutrition 134.3 (2004): 568-573.
• Bowen, J., M. Noakes, and P. M. Clifton. "Effect of calcium and dairy foods in high protein, energy-restricted diets on weight loss and metabolic parameters in overweight adults." International journal of obesity 29.8 (2005): 957-965.
• In particularly in conjunction with exercise, high(er) protein intakes have been proven have additive beneficial effects on body composition during weight loss (Layman. 2005)
• Josse, Andrea R., et al. "Increased consumption of dairy foods and protein during diet-and exercise-induced weight loss promotes fat mass loss and lean mass gain in overweight and obese premenopausal women." The Journal of nutrition 141.9 (2011): 1626-1634.
• Shlisky, Julie D., et al. "An energy‐reduced dietary pattern, including moderate protein and increased nonfat dairy intake combined with walking promotes beneficial body composition and metabolic changes in women with excess adiposity: a randomized comparative trial." Food Science & Nutrition (2015).
• Thorpe, Matthew P., et al. "A diet high in protein, dairy, and calcium attenuates bone loss over twelve months of weight loss and maintenance relative to a conventional high-carbohydrate diet in adults." The Journal of nutrition 138.6 (2008): 1096-1100.
• Zemel, Michael B., et al. "Calcium and dairy acceleration of weight and fat loss during energy restriction in obese adults." Obesity research 12.4 (2004): 582-590.

Probiotics act on in the digestive tract, but their effects are still systemic.

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Learn everything about overfeeding! How do the effects of high vs. low fat, high vs. low protein and high vs. extra-high energy intake differ, what's the effect on thyroid and other important hormones and more

"All testing took place at the Human Integrative Physiology Laboratory between the hours of 5:00 and 11:00 am. Participants fasted for 12 h, did not consume caffeine or alcohol, performed no vigorous physical activity for the prior 48 h, and were free from acute illness for the prior 2 weeks.

[...]Following a 2-week eucaloric control diet, participants underwent dual X-ray absorptiometry to determine body composition, an intravenous glucose tolerance test to determine insulin sensitivity, and a skeletal muscle biopsy for measurement of in vitro substrate oxidation" (Osterberg. 2015). 

Figure 1: Composition (in g/day) and energy consumption (kcal/day) of the lead in and high fat diet (Osterberg. 2015).

Figure 2: Changes in body composition in response to 4-week high fat overfeeding with or without probiotic supplementation (VSL#3, a 900 billion multi-strain probiotic) in 20 normal-weight young men (Osterberg. 2015).

Bottom line: In spite of the statistically significant weight and fat gain differences, the interpretation of the study at hand is not 100% straight forward. This may be due to the fact that within only 4 weeks other changes (esp. health relevant parameters) did not occur in either group.

While this study shows no immediate health benefits, there's evidence that gluten sensitive individuals may benefit from supplementing /w certain strains.

Furthermore, it must be said that the reduced lean mass gains in the probiotic strain and the subsequent lack of changes in body fat percentages, suggest that the amelioration of the subjects' weight gain is mediated by a mere reduction in energy-availability (this assumes that the intakes in both groups were identical to begin with). If this is the case, the supplement still has its merits: According to the questionable approximation that says that it takes 7,000kcal extra to gain 1kg of body fat, the probiotic supplementation would have compensated for 1.3 kg x 7000 kcal/kg = 9100kcal over 4 weeks and 325 kcal/ day (note this is not a scientifically accurate calculation).

Still, much more research is going to be necessary - not only to elucidate the exact mechanism, but also to find out if the effect might depend on the type of diet: A high fat diet, for example, has been shown to have significant, potentially detrimental effects on the human gut microbiome, which may be meditated by the bile acid resistance of several strains of bacteria, i.e. more fat = exuberant bile production = death to many good bacteria (David. 2014) |  Comment on Facebook!

• David, Lawrence A., et al. "Diet rapidly and reproducibly alters the human gut microbiome." Nature 505.7484 (2014): 559-563.
• Osterberg, et al. "Probiotic Supplementation Attenuates Increases in Body Mass and Fat Mass During High-Fat Diet in Healthy Young Adults." Obesity (2015): Ahead of print.

Single-legged leg presses that make both legs stronger are only one of many topics, today.

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• Long rest periods prolong testosterone response to bench press exercise -- From various previous SuppVersity articles you know that resistance training triggers an acute increase in testosterone. That this increase may depend on the rest between sets, though, is news. News from a recent article in the Journal of Strength and Conditioning Research.
  
  The purpose of the study was to examine the influence of rest period duration (1 vs. 3-minute between sets) on acute hormone responses to a high intensity and equal volume bench press workout (5x3 sets at 85% of the 1RM, to be specific).
  

  Figure 1: Mean (left) and individual (right) free testosterone levels before and after performing bench presses with 1 min or 3 min rest (Scudese. 2015).

  To this ends, Scudese et al. (2015) recruited ten resistance trained men (25.2 +/- 5.6 years; 78.2 +/- 5.7 kg; 176.7 +/- 5.4 cm; bench press relative strength: 1.3 +/- 0.1 kg/kg of body mass) and had them perform two bench press workouts separated by one week. Each workout consisted of 5 sets of 3 repetitions performed at 85% of 1-repetition maximum, with either 1 or 3-minute rest between sets. The rates of perceived exertion and serum levels of growth hormone (GH), cortisol, free and total testosterone were sampled at three different timepoints right (PRE), right after (T0) before, 15 (T15) and 30 (T30) minutes after. The results were as follows:
  • For total testosterone, both rest lengths enhanced all post-exercise verifications (T0, T15 and T30) compared to PRE, with 1-minute showing decreases on T15 and T30 compared to T0.
  • For free testosterone, both 1 and 3-minute rest protocols triggered augmentations on distinct post-exercise moments (T0 and T15 for 1-minute; T15 and T30 for 3-minute) compared to PRE.
  • Since the the cortisol values did not change throughout any post-exercise verification for either rests, the total testosterone/cortisol ratio was significantly elevated for both rests in all post-exercise moments compared to PRE.
    The growth hormone values did not change for both rest lengths.
  Now, that's exciting, right? The free testosterone levels kept increasing... well, not exactly. If you look at the data in Figure 1 right, you will notice interpersonal differences that suggest that the elevation would not have lasted for much more than those 15 extra-minutes .
  
  What's of significantly greater importance for the interpretation of the study results is yet a study by West et al. (2012) who observed that the testosterone response (both free and total) to resistance training is not associated with either strength or size gains. So what? It is very likely that the results of the study at hand are of zero practical relevance for your gains (strength- and sizewise, as West's study indicates).
• Blood flow restriction before strength training? It works - just as well as placebo! -- You will probably remember my recent article about the benefits of using blood flow restricting cuffs before a sprint workout, right (click here if not)? With the publication of the results of Moacir et al.'s (2015) latest study, we do now know that similar benefits will be seen with subsequent resistance training, too.

  The study at hand should make you question the results of the previously discussed study which did not have a placebo group | learn more

  "Thirteen men participated in a randomized crossover design that involved 3 separate sessions (ischemic preconditioning, placebo and control). A 12-RM load for the leg extension exercise was assessed through test and retest sessions prior to the first experimental session. The IPC session consisted of 4 cycles of 5 minutes occlusion at 220 mmHg of pressure alternated with 5 minutes of reperfusion at 0 mmHg for a total of 40 minutes. The PLACEBO session consisted of 4 cycles of 5 minutes of cuff administration at 20 mmHg of pressure alternated with 5 minutes of pseudo-reperfusion at 0 mmHg for a total of 40 minutes. 

  The occlusion and reperfusion phases were conducted alternately between the thighs, with subjects remaining seated. No ischemic pressure was applied during the control (CON) session and subjects sat passively for 40 minutes. Eight minutes following IPC, PLACEBO or CON, subjects performed three repetition maximum sets of the leg extension (2min rest between sets) with the pre-determined 12-RM load. Four minutes following the third set for each condition, blood lactate was assessed" (Moacir. 2015)

  When the researchers analyzed the results, they found that for the first set, the number of repetitions significantly increased for both the IPC (13.08 +/- 2.11; p = 0.0036) and PLACEBO (13.15 +/- 0.88; p = 0.0016) conditions, but not the CON (11.88 +/- 1.07; p > 0.99) condition.
  

  Figure 2: Significant increases in the number of reps (left) were observed for both the placebo and IPC group. The fatique index (right) did not differ between treatments, but the large inter-individual variety in the IPC group clearly suggests that BFR as a means of preconditioning ain't for everyone (Moacir. 2015).

  Similarly, the IPC and PLACEBO conditions resulted in significantly greater repetitions versus the CON condition on the 1st set (p=0.015; p=0.007) and 2nd set (p=0.011; p=0.019), but not the 3rd set (p=0.68; p>0.99). No significant difference (p=0.465) was found in the fatigue index and lactate concentration between conditions.
  
  As the researchers point out, their results "indicate that IPC and PLACEBO ischemic preconditioning may have small beneficial effects on repetition performance over a CON condition" (Moacir. 2015). It is thus not completely logical that they suggest "that ischemic pre-conditioning might be practiced gradually to assess tolerance and potential enhancements to exercise performance" (ibid.). What? Oh, you think your clients would notice that their blood flow is not actually impaired and the placebo effect would be lost? Right, now I understand why you should keep using it. Unfortunately that does not exclude that it is still a placebo effect which seems not unlikely in view of the larg(er) inter-individual differences in the IPC vs. any other group. Further studies are necessary... obviously!
• Train your right leg, and your left leg will become stronger, too - on leg presses, at least -- What sounds like a joke (or magic) is actually science. Science that is going to be presented in an article in a future edition of the Journal of Strength and Conditioning Research; and more precisely from a study that assessed the cross education of strength and changes in the underlying mechanisms (muscle size, activation, and hormonal response) following a 4-week unilateral resistance training (URT) program.
  
  In said study by Beyer et al. (2015), a group of nine untrained men completed a 4-week URT program on the dominant leg (DOM), while cross education was measured in the non-dominant leg (NON); and were compared to a control group (n=8, CON).

  "Unilateral isometric force (PKF), leg press (LP) and leg extension (LE) strength, muscle size (via ultrasonography) and activation (via electromyography) of the rectus femoris and vastus lateralis, and the hormonal response (testosterone, growth hormone, insulin, and insulin-like growth factor-1) were tested pre- and post-training" (Beyer. 2015).

  In all strength and size related measures, the trained group improved significantly better than CON. Significant group x time effects for PKF, LP, LE, and muscle size were observed only in the dominant leg (DOM), the non-dominant (NON = untrained leg), on the other hand, the scientist observed not just a trend, but rather an actual and statistically significant increase in leg press strength.
  

  Figure 3: Relative leg press and leg extension strength relative to body weight; the values above the post-bars indicate the relative difference between post and pre-test (2015).

  Whether that's related to the acute hormonal response to URT, the scientists observed, is more than questionable, after all the strength increase in the non-dominant leg didn't just occur in the absence of "detectable changes in muscle size, activation (EMG), or the acute hormonal response" it did also occur only during leg presses - if it was the result of any of the aforementioned factors one would expect to see at least something like a trend for leg extensions, as well.
  
  Against that background it should also be clear that you must not neglect one leg or arm when you train in the definitely false hope it would grow and the almost certainly false hope it would get stronger as you train your "favorite" limb. 

There's more: In view of the fact that the bottom lines to the individuals studies discussed in SuppVersity Research Overviews are always provided at the end of the respective item, I have room for mentioning two other interesting results at least briefly.

Figure 4: Energetic demands of 5x3 vs. 5x1 set upper body workout in men and women. Needless to say that the inter-group difference between 3 vs. 1 sets and the inter-group difference between men and women (not shown) were significant (Mookerjay. 2015).

Firstly, Hatfield et al.'s study of the "Effects of circadian rhythm on power, force, and hormonal response in young men" that indicates that "high force and power exercises utilizing  bench press-throws or jump squats may be performed any time of day without detrimental decreases in acute performance" (Hatfield. 2015). And secondly, Mookerjay et al.'s "[c]omparison of energy expenditure during single vs. multiple-set resistance exercise" (Mookerjay. 2015) that yielded a very obvious result which was that the multi-set protocols yield greater metabolic and cardiovascular demands than single set protocols when the number of exercises performed are the same (see Figure 4). In the study 5 upper-body exercises of either 1 or 3 sets per exercise performed in random order the gross and net energy expenditure was determined for the workout + 5 minutes of recovery. You can see the exact data in Figure 4, in case you're interested | Comment on Facebook!

While this picture shows loaded cardio in its most beautiful form, the study investigated loaded cardio on the treadmill and compared it (for questionable reasons) to non-loaded cardio on a stationary bike and guess what: Both burn the same amount of muscle - NET: Zero!

HIIT is the ideal complement to classic "cardio" training!

Never Train To Burn Calories!

Tabata = 14.2kcal /min ≠ Fat Loss

30s Intervals + 2:1 Work/Rec.

Making HIIT a Hit Part I/II

Making HIIT a Hit Part II/II

HIIT Ain't For Everyone

• Two groups performed CE and the other two performed LC. 
• One of each of the exercise groups received EAA drinks to consume during exercise, and the other groups received control (CON) drinks. 

"[...] intent was not to determine temporal changes in MPS within an exercise mode (with or without EAA), but to examine MPS responses between LC and CE during exercise and recovery independently" (Pasiakos. 2015).

"Volunteers completed 3 d diet and activity records at baseline, and similar to our previous work (Pasiakos. 2011), these records were used to individually prescribe 7 d lead-in diets to maintain body weight and to limit the potential confounding effect of diet on outcome measures. Compliance was confirmed by 24 h dietary recalls conducted every two days during the lead-in phase (Food Processor SQL1, version 10, ESHA Research, Salem, OR) (Table 1). Volunteers were also instructed to maintain activity levels reported at baseline for the first five days of the lead-in phase. All resistive and endurance-type activity was prohibited 48 h before data collection to minimize any potential residual effects of previous exercise on protein turnover" (Pasiakos. 2015).

Illustration 1: Graphical overview of the study design (Pasiakos. 2015) | EAA = 10g of EAAs, CON = non-nutritious control drink; LC = load carrying cardio on a treadmill, CE = control endurance exercise on a stationary bike.

"[m]atching the intensity and energy cost was done to isolate the effects of the possible differences in mechanical force and contractile properties of LC and CE from the relative intensity and energy cost of the exercise bout [and a] familiarization trial was conducted to ensure the accuracy of the exercise prescription and the ability of the volunteer to complete the prescribed exercise bout" (Pasiakos. 2015).

Figure 1: Overview of protein fluxes (synthesis vs. breakdown and oxidation) and subsequent net protein balance in the four treatment groups, i.e. loaded and control cardio with and with out EAA (Pasiakos. 2015)

Figure 1: Protein synthesis. Mixed-muscle (A), myofibrillar (B), and sarcoplasmic (C) muscle protein synthesis (MPS) during exercise and mixed-muscle (D), myofibrillar (E), and sarcoplasmic (F) MPS in recovery from a 90 min, metabolically matched load carriage (LC) or conventional endurance (CE) exercise bout, with and without (control, CON) essential amino acid (EAA) supplementation. Data are mean ± SD, n = 10 per group. †Mode main effect; LC different than CE, P < 0.05. *Drink main effect; EAA different than CON, P < 0.05 (Pasiakos. 2015).

1. The EAA-mediated decrease in muscle breakdown was complemented by both enhanced mixed-muscle and sarcoplasmic MPS during exercise.
2. During the recovery phase, the mixed muscle and sarcoplasmic protein synthesis in response to loaded cardio training were higher than they were in the control group.

Yes! You can use whey or even regular milk protein, as well and benefit. Better don't eat a steak during your workout though. Learn more in this SV Classic "23g of Dairy Protein + 5g of Leucine Turn Cardio Sessions Into Muscle Building Workouts"

So, loaded endurance exercise is not much, but a little better? Well, in this study it appears to be as if the former was the correct conclusion to be drawn. Generalizations, however, must be made with utmost care. Especially in view of the unfair comparison of walking on a treadmill with cycling on a bike, of which you could argue that it is naturally less anabolic than walking - irrespective of whether you're carrying an extra-load or not. Thus, the researchers have weakened the generalizability of their results by making the (imho unnecessary) decision to rely on a tried and proven method, i.e. cycling, only to (as I suspect) make it easier to standardize the workload in numbers. This, however, is bogus: I mean, you all have probably worked out for say 500kcal on an exercise bike and for 500kcal on a treadmill. Now tell me: What did you feel was more exhausting and had a subjectively significantly larger impact on your metabolism? You answer probably is 'treadmill'.

Eventually, the most practically relevant information you can draw from the study at hand are thus: (A) You can do both 90 minutes of loaded cardio on the treadmill and 90 minutes of classic cardio on an exercise bike without any muscle loss (at least from the exercised muscles) even if you consume only water (see net balance = 0 in Figure 2). (B) If you bring 10g of EAA and consume them over the course of your workout you may even hop off the treadmill or bike with a few micrograms extra muscle on your legs. And (C) if you chose the treadmill and loaded cardio this will trigger a better post-workout anabolic response than the bike. How meaningful all that is - in terms of gains, I mean - will yet have to be seen in future long(er)-term studies | Comment!

• Pasiakos, Stefan M., et al. "Leucine-enriched essential amino acid supplementation during moderate steady state exercise enhances postexercise muscle protein synthesis." The American journal of clinical nutrition 94.3 (2011): 809-818.
• Pasiakos SM, McClung HL, Margolis LM, Murphy NE, Lin GG, Hydren JR, et al. "Human Muscle Protein Synthetic Responses during Weight-Bearing and Non-Weight-Bearing Exercise: A Comparative Study of Exercise Modes and Recovery Nutrition." PLoS ONE 10.10 (2015): Online only.

The way we eat and live is not just obesogenic it is also acidogenic... or is the former just a consequence of the latter?

You can learn more about bicarbonate and pH-buffers at the SuppVersity

The Hazards of Acidosis

Build Bigger Legs W/ Bicarbonate

HIIT it Hard W/ NaCHO3

Creatine + BA = Perfect Match

Bicarb Buffers Creatine

Alkalosis Boosts Muscle Activity

Figure 1: Correcting a diet-induced low grade metabolic acidosis with K-bicarbonate reduces the nitrogen loss of 750mg - 1000mg per day (per 60kg BW) in post- menopausal women in a prev. study (Frassetto. 1997)

• In Study A, two 10-day high NaCl diet (32 g/d) periods were conducted, one supplemented with 90 mmol KHCO3/day.
   
• In Study B, participants received a high and a low NaCl diet (31 vs. 3 g/day), each for 14 days. During low NaCl, the diet was moderately acidified by replacement of a bicarbonate-rich mineral water (consumed during high NaCl) with a non-alkalizing drinking water. 

Even Low Grade Acidosis Will Increase Your Diabetes Risk | learn more!

Beware! It does not take much to mess you up! A quantitative analysis of the data from the study at hand shows that even increases of dietary acid loads in the magnitude of only 30 mEq/d, which drive the renal net acid excretion into a range that is commonly seen in people on the standard Western diet (60–70 mEq/d), suffice to affect glucocorticoid activity in ways that may ruin your bone, heart and muscle health. In that, the main offenders are grains, not meats. Grains contribute an estimated 38% to the net acid load of the avg. Westerner (Sebastian. 2002).

Figure 2: aily adrenal cortisol secretion as indexed by the sum of excretion rates of the 3 major urinary glucocorticoid (GC) metabolites tetrahydrocortisol, 5a-tetrahydrocortisol, and tetrahydrocortisone (THF + aTHF + THE) as well as excretions of potentially bioactive-free GCs (UFF + UFE | Buehlmeier. 2015)

Bottom line: As the authors point out, their study is the first to provide convincing evidence that the ill effects of chronic low-grade metabolic acidosis are mediated via enhanced glucocorticoid activity and secretion. In that, the pro-acidic effects of NaCl, as well as the lack of alkalizing foods and nutrients in the Western diet are the main motors of dietary induced glucocorticoid elevations.

Inactivity amplifies the ill effect of glucocorticoids on muscle loss by up to 213% (Ferrando. 1999).

These elevations are - in spite of being still in the physiological range - significant enough to compromise bone quality (Bedford. 2010; Shi. 2015), cardiometabolic health & diabetes (Prodam. 2013; Qi, 2007), and protein turnover (Frassetto. 1997 | see Figure 1; Buehlmeier. 2012), and appear to be particularly unfavorable under conditions of physical inactivity (Ferrando. 1999 | see Figure on the right). Reason enough for the authors to conclude that "[a]ccordingly, higher dietary acid loads may, in the long run, constitute an independent GC-driven musculoskeletal and cardiometabolic risk factor related with western dietary habits" (Buehlmeier. 2015) | Comment!

• Bedford, Jennifer L., and Susan I. Barr. "The relationship between 24-h urinary cortisol and bone in healthy young women." International journal of behavioral medicine 17.3 (2010): 207-215.
• Buehlmeier, Judith, et al. "Alkaline salts to counteract bone resorption and protein wasting induced by high salt intake: results of a randomized controlled trial." The Journal of Clinical Endocrinology & Metabolism 97.12 (2012): 4789-4797.
• Ferrando, Arny A., et al. "Inactivity Amplifies the Catabolic Response of Skeletal Muscle to Cortisol 1." The Journal Of Clinical Endocrinology & Metabolism 84.10 (1999): 3515-3521.
• Frassetto, L., R. Curtis Morris Jr, and A. Sebastian. "Potassium bicarbonate reduces urinary nitrogen excretion in postmenopausal women." The Journal of Clinical Endocrinology & Metabolism 82.1 (1997): 254-259.
• Qi, Dake, and Brian Rodrigues. "Glucocorticoids produce whole body insulin resistance with changes in cardiac metabolism." American Journal of Physiology-Endocrinology and Metabolism 292.3 (2007): E654-E667.
• Prodam, Flavia, et al. "High-end normal adrenocorticotropic hormone and cortisol levels are associated with specific cardiovascular risk factors in pediatric obesity: a cross-sectional study." BMC medicine 11.1 (2013): 44.
• Sebastian, Anthony, et al. "Estimation of the net acid load of the diet of ancestral preagricultural Homo sapiens and their hominid ancestors." The American journal of clinical nutrition 76.6 (2002): 1308-1316.
• Shi, Lijie, et al. "Higher glucocorticoid secretion in the physiological range is associated with lower bone strength at the proximal radius in healthy children: importance of protein intake adjustment." Journal of Bone and Mineral Research 30.2 (2015): 240-248.

Can you pump them up w/ silicon and to negate their atherosclerotic effects!?

Read more short news on various topics here at the SuppVersity

Exercise Research Uptake Nov '14 1/2

Exercise Research Uptake Nov '14 2/2

Nutrition and (Anti-)Aging News Special

Exercise Supplementation Quickie

Exercise Research Uptake Jan 12, 2015

Read the Latest Ex. Science Update

• Breakfasts Higher in Protein Increase Postprandial Energy Expenditure, Increase Fat Oxidation, and Reduce Hunger in Overweight Children from 8 to 12 Years of Age - In the eponymous study, Baum et al. determined whether consumption of a protein-based breakfast (PRO) increases postprandial energy metabolism and substrate oxidation, reduces hunger, and reduces food intake at lunch compared with a carbohydrate-based breakfast (CHO) in normal weight (NW) vs. overweight/obese (OW) children. Both, the normal and over-weight children participated in the same randomized, crossover protocol that arranged for all participants to be served a
  • high PRO [344 kcal, 21% protein (18 g), 52% carbohydrate, and 27% fat] or 
  • high CHO [327 kcal, 4% protein (3 g), 67% carbohydrate, and 29% fat]
  breakfast, after which the energy expenditure (EE), substrate oxidation, appetite, and blood glucose were measured over a 4 h period. To access whether the high protein intake would also affect the participants appetite, the subjects had free access to a lunch buffet and food intake was recorded.
  

  Figure 1: Energy expenditure, fat and carbohydrate oxidation in the 4h post breakfast (Blum. 2015).

  The results were unambiguous: After breakfast, OW children in the PRO group had higher (P < 0.0001) EEs and fat oxidation over the 4 h period than did the NW children in the CHO and PRO groups. Of these, the increase in energy expenditure was transient and didn't last for the full 4h period. The increase in fat oxidation in response to the high protein intake, on the other hand, lasted for the full 4 h period (+16%; P < 0.05) and went hand in hand with a surprisingly pronounced 32% increase in carbohydrate oxidation in the PRO vs. CHO (P < 0.01) trial.
  

  Table 1: Despite decreased hunger and increased fullness, the protein breakfast did not reduce the total energy intake or modify the macronutrient ratio of the foods the kids selected at the lunch buffet (Baum. 2015).

  Now, all this sounds great, but even though the subjects experienced decreased feelings of hunger (−14%; P < 0.01) and increased fullness (+32%; P < 0.05) after the PRO than the CHO breakfast, the lack of effect on the intake at the subsequent ad-libitum lunch is disappointing to say the least. This and the lack of long-term data make it very difficult to predict if a similar increase in protein during breakfast only would actually help the subjects lose weight.  
• Silicon ... not breasts, but enhanced meat may protect older individuals against atherosclerosis - That's at least what a recent rodent study by Garcimartin et al. (2015) suggests.

  "Research has shown that silicon can play an important role in protecting against degenerative diseases. Restructuring pork by partially disassembling meat would permit the incorporation of active components with potential functional effects. However, there has been no research to date on the impact that silicon, as a functional ingredient in restructured pork (RP), has on lipoprotein composition, metabolism, and oxidation" (Garcimartin. 2015).

  In order to find out whether the addition of silicon would actually have a meaningful effect, the scientists added 1.3g/kg silicon to sausages that were then fed to one group of old rodents while the rest received regular, non-enriched sausages as part of regular and pro-atherogenic cholesterol-enriched diets.
  
  The results were quite astonishing, as is partially normalized the changes induced by the high cholesterol diet. Compared with the rodents who received the regular sausages, those on the silicon sausages had lower VLDL compound concentrations (P < 0.001; e.g., 75% less VLDL cholesterol) and a significantly reduced VLDL oxidation (65% less conjugated dienes and 85% less TBARS) that went hand in hand with an increase in LDL-receptor expression (200% more).
  

  Figure 1: The silicon in the sausages increased the LDL receptor density to (almost) normal, the amount of cholesterol protecting AE in the blood and liver, as well as its ratio to the amount of cholesterol. The result is obvious: With as little oxidized VLDL in the blood as the control, we can safely assume that the rodents that consumed the silicon enriched sausages have a sign. lower atherosclerosis risk (Garcimartin. 2015).

  In spite of the fact that there are differences in the susceptibility of mouse and man to the pro-atherogenic diets of the results do - just as the authors point out - still suggest that silicon added to restructure pork can strongly counterbalanced the negative effect of high-cholesterol-ingestion and, as I would like to add, the negative effects of endogenous cholestrol (by increasing its uptake by LDL receptors and decreasing its susceptibility to oxidation) thus "functioning as an active hypocholesterolemic, hypolipemic, and antioxidant dietary ingredient" (Garcimartin. 2015).
• Healthy eating requires a controlled (not restricting) energy intake to increase one's chance of "aging healthily" by almost 50% - If you question if eating "healthy" and not eating everything in sight is even worth it, you will like the results of a recent study from the Sorbonne in Paris (Essmann. 2015).
  
  In her latest study Karen E Essmann and her colleagues analyzed the diets of a subgroup of 2769 participants of the SU.VI.MAX (SUpplémentation en Vitamines et Minéraux AntioXydants) trial. They identified subjects consuming "healthy" and those on the "standard Western diet", adjusted the data for a large number of potential confounders and the influence of high(er) and low(er) energy intakes.
  

  Table 2: Overview of the criteria the scientists applied to identify "healthy eating" - CES-D, Center for Epidemiologic Studies–Depression Scale; DKTMT, Delis-Kaplan version of the Trail Making Test; IADL, instrumental activities of daily living; MMSE, Mini-Mental State Examination; RI-48, 48-item cued recall test; SF-36, Medical Outcome Study Short Form 36; SPPB, Short Physical Performance Battery.

  In that, the scientists found that the association between "healthy eating" and "healthy aging" was mediated by low(er) energy intakes. Only in subjects with median or lower energy intakes, the association between "healthy eating" and "healthy aging" reached statistical significance, so that the non-gluttonous "healthy eaters" were 49% more likely to age healthily.
  
  Since we are already talking "healthy eating", let's briefly mention that scientists from the University of Eastern Finland just confirmed the obvious (Haapala. 2015): A poorer diet quality is associated with worse cognition in children. What is a bit surprising, though, is that the relationship was stronger in boys than in girls.

In contrast to Blum's study, a previous study with high fat breakfasts showed sign. reduced 24h food intakes | more

Bottom Line: So what did we learn today? I guess if you want to find a general bottom line it is as simple as "when it comes to nutrition, things are never as straight forward as it is often portrayed in the mainstream media". High protein breakfasts, for example will help you to control your energy intake (by increasing satiety and fullness) and increase your energy expenditure, but they (certainly) won't make you lose weight in a scenario where you simply eat whatever is in sight. The same goes for the link between "eating healthy" and "aging healthy" which is significant (+49%) only in those who don't overeat on their healthy diets (note: a median intake is enough, you don't have to fast!).

And if that was not complex enough, take a look at the silicon sausage study. With the right additives even something as junk-foody as sausages can have almost "medical" effects. Whether silicon supplements have the same effects in men and women, though, would require future (long-term) studies | Comment on Facebook!

• Assmann, et al. "A Healthy Dietary Pattern at Midlife, Combined with a Regulated Energy Intake, Is Related to Increased Odds for Healthy Aging." J. Nutr. first published on 5 August 2015 doi:10.3945/jn.115.210740
• Baum, et al. "Breakfasts Higher in Protein Increase Postprandial Energy Expenditure, Increase Fat Oxidation, and Reduce Hunger in Overweight Children from 8 to 12 Years of Age." J. Nutr. first published on 12 August 2015 doi:10.3945/jn.115.214551
• Garcimartín, et al. "Silicon-Enriched Restructured Pork Affects the Lipoprotein Profile, VLDL Oxidation, and LDL Receptor Gene Expression in Aged Rats Fed an Atherogenic Diet." J. Nutr. first published on 5 August 2015 doi:10.3945/jn.115.213934
• Haapala, et al. "Associations of diet quality with cognition in children – the Physical Activity and Nutrition in Children Study." British Journal of Nutrition (2015): FirstView Article.

With the publication of Learsi's latest paper the list of things metformin can do for you has just gotten been expanded with another item: Doping!

Like antioxidants metformin could blunt the hormetic response & long-term(!) adaptation

Is Vitamin E Good for the Sedentary Slob, Only?

Even Ice-Baths Impair the Adapt. Process

Vit C+E Impair Muscle Gains in Older Men

C+E Useless or Detrimental for Healthy People

Vitamin C and Glucose Management?

Antiox. & Health Benefits Don't Correlate

Figure 1: Overview of the study design. The active / placebo treatment, i.e. 500mg of metformin or an identically looking placebo were administered 60 min before the supramaximal tests. The whole procedure was repeated twice, with at least 72h between the first and the second testing session (Learsi. 2015).

Figure 2: Changes in time to exhaustion and EPOC, both stat. significantly w/ metformin (Learsi. 2015).

Alpha Lipoic Acid, GABA, Taurine, Green Tea, Gooseberry & Fenugreek. Plus: Metformin the No.1 Drug? Supplements to Improve and Restore Insulin Sensitivity - Read the First Installment of This Series | read more

Bottom line: This is the first human study to confirm that the AMPK-booster and frequently prescribed diabetes drug can trigger statistically and practically relevant increases in endurance performance during a supra-maximal VO2 max test. If we assume that a similar performance increase occurs in trained athletes, the Learsi study makes taking a bunch of grandma's metformin pills before the next race quite attractive. For the WADA, however, it means that they will have to watch and test for yet another commonly prescribed and readily available medication. And last but not least, for the "wonder-drug" metformin, it is yet another area of application: athletic performance enhancement or as we usually call it "doping" | Comment on Facebook!

• Gudat, U., G. Convent, and L. Heinemann. "Metformin and exercise: no additive effect on blood lactate levels in healthy volunteers." Diabetic medicine 14.2 (1997): 138-142.
• Johnson, S. T., et al. "Acute effect of metformin on exercise capacity in active males." Diabetes, Obesity and Metabolism 10.9 (2008): 747-754.
• Learsi, et al. "Metformin improves performance in high-intensity exercise, but not anaerobic capacity." in healthy male subjects." Clin Exp Pharmacol Physiol. 2015 Aug 7. doi: 10.1111/1440-1681.12474. [Epub ahead of print]

This could have been the HP breakfast. Egg-based pancakes + ham.

Learn more about fasting and eating / skipping breakfast at the SuppVersity

Breakfast and Circadian Rhythm

Does Meal Timing Matter?

Breakfast & Glucose Metab.

Break the Fast, Cardio & the Brain

Does the Break- Fast-Myth Break?

Breakfast? (Un?) Biased Review

Table 1: Subject characteristics at baseline (Leidy. 2015). As you can see the subjects were randomly assigned to the three groups at a ratio of 1:2:2 to breakfast skipping, normal protein (NP) and high protein (HP) breakfast.

Figure 1: Macronutrient composition (g) of the test meals used in the study (Leidy. 2015)

In Schlundt's 12-week study in which the subjects had to follow the same energy reduced diet pattern one time with, one time without breakfast the marginal differences in weight loss and fat loss (the former favors breakfast, the latter skipping it) were just as statistically non-significant as the other inter-group differences the US scientists observed (Schlundt. 1992).

In the long run, calories count. So if you are counting calories it doesn't matter if you have breakfast or don't. There are bazillions of "breakfast eating vs. skipping"-studies, but this is only study #3 to test the long-term effects. Yes, sometimes science is pathetic and stupid - and trying to elucidate the health effects of eating vs. skipping breakfast in studies on three testing days is both: pathetic and stupid.

One of the two non-pathetic studies comes from Schlundt et al. who examined the effects of consuming breakfast vs. breakfast skipping during a 12-week energy restriction weight loss diet in 52 adult women with obesity without finding significant differences.

More recently, Dhurandhar et al. completed a 16-week study in 309 adults with obesity and included a general recommendation to either "eat breakfast" or "skip breakfast". As it was to be expected when energy intake is controlled for, again, no differences in weight loss were observed in those who began eating breakfast compared to those who continued to skip breakfast.

Figure 2: Comparison of the changes in fat mass, the daily food intake, hunger and fullness ratings in the subjects from the CON (=kept skipping breakfast), NP (normal protein) and HP (high protein) breakfast groups (Leidy. 2015).

• "Breakfast!? An (Un-)Biased (?) Review of the Breakfast Myth" | read it!

  made the subjects magically lose (HP) or at least not gain (NP) superfluous body fat.
• significantly reduced the daily energy intake in the high protein condition and buffered the significant increase in energy intake in the no breakfast condition if the breakfast had a normal protein content,
• reduced the total time during which the subjects were hungry not just in the morning, but 24/7, and
• increased the subjects' fullness, especially in the morning.

The study at hand is an excellent example that shows that the previously observed effects of habitation can be overcome if you adhere to your new breakfast protocol meticulously.

So what? If you have a teenage son or daughter, serve him / her a high protein breakfast containing 40% protein, 40% carbohydrates, and 20% fat, like an egg-based pancakes and ham; egg-based waffles with pork-sausage; egg and pork scramble; and an egg and pork burrito (all these were options the subjects in the study at hand were provided with on a weekly basis. It's going to help them manage their weight, food cravings, and hunger pangs and it's not going to take you an hour to prepare (rather 15 min - max). The scientists assertion that "it is unclear as to whether the daily consumption of a high-protein breakfast, containing 35 g of protein, is feasible in a free-living environment" (Leidy. 2015) is just more pathetic evidence that people care so little about their health that they'd rather die from eating ready-made cereals than to invest the 10-15 minutes to prepare delicious and healthy protein pancakes into their health.

If you are now contemplating to switch back to having breakfast, yourself, let me remind you that it is not possible to extrapolate study results that were generated with a specific group of subjects, in this case overweight, but still healthy adolescents to whomever you want. If you are on an energy controlled diet and skipping breakfast as a means to do intermittent fasting and reduce your overall energy intake, you won't reduce your 24h energy intake (after all, you're eating X kcal everyday, anyway).  It is thus unlikely that you'd lose more weight than you'd do without breakfast and if you are like many people you will probably even feel hungrier now that you're able to eat only 3 small vs. 1-2 large(r) meals | Comment on Facebook!

• Dhurandhar, Emily J., et al. "The effectiveness of breakfast recommendations on weight loss: a randomized controlled trial." The American journal of clinical nutrition 100.2 (2014): 507-513.
• Leidy, Heather J., et al. "A high‐protein breakfast prevents body fat gain, through reductions in daily intake and hunger, in “Breakfast skipping” adolescents." Obesity (2015).
• Schlundt, David G., et al. "The role of breakfast in the treatment of obesity: a randomized clinical trial." The American journal of clinical nutrition 55.3 (1992): 645-651.
• Thomas, Elizabeth A., et al. "Usual breakfast eating habits affect response to breakfast skipping in overweight women." Obesity 23.4 (2015): 750-759.

I can almost guarantee that the results of this study are not sex-specific. Ladies, pick up the weights fater you hit the treadmill, stairmaster, elliptical or other torture instrument you like to use!

You can learn more about the optimal exercise order at the SuppVersity

Before, After or In-Between?

bef
Exercise Order & Leptin

Cardio First for Anabolism?

Large Muscle Groups First?

Combine Cardio & Strength, Right

Exercise Order Reloaded

"running with 70—75% of maximal heart rate (HRmax) for 10 minutes which gradually increased to 80% HRmax for 21.5 minutes [plus] resistance training consisted of 3 sets of 8 repetitions at 80% of 1 repetition maximum (1RM) in 5 resistance exercises (leg extensions, lying leg curl, triceps pushdown, bench press and lateral pull down)" (Sheikholeslami-Vatani. 2015). 

Figure 1: Relative changes in hormone levels (left) and absolute and relative changes in body fat fat free mass and body fat % (right) after 8 weeks of doing nothing (C) or doing cardio (CER) or weights (CRE) first (Sheikholeslami-Vatani. 2015).

• Similar gains w/ weights vs. cardio first in trained men | more.

  normalization of leptin levels (health)
• slight increases in testosterone (health)
• increases in cortisol (which are benign | learn why)
• significant reductions in body fat (health + physique)
• increases in fat free mass (health and physique)

Weights or Cardio? What's the Best Visceral Fat Burner + How Often, Long and Intense Do You Have to Train | Learn more!

So, weights first is the way to go? Well, I assume I should write that doing both on separate days and thus doing having 5-6 workout days per week may have even more pronounced effects on the body composition of obese young men. In the end, though, I have no evidence to prove that doing the same amount of cardio on a separate day would actually have yielded greater improvements in body composition. Against that background and in view of the fact that three workouts per week is everything that fits into the busy schedules of the average trainee, we are left with the confirmation that (a) doing (intense) cardio and weights in one session feasible and effective when the goal are health and physique improvements and that (b) if you or your clients combine both, you better start with the weights, not the cardio part | Comment!

• Sheikholeslami-Vatani, D., et al. "The effect of concurrent training order on hormonal responses and body composition in obese men." Science & Sports (2015).
• West, Daniel WD, and Stuart M. Phillips. "Associations of exercise-induced hormone profiles and gains in strength and hypertrophy in a large cohort after weight training." European journal of applied physiology 112.7 (2012): 2693-2702.

Dude, it won't suffice to just bring your chains to the gym to show them off, you will also have to attach them to the barbell before squatting and benching to see results... and bro, the science on the benefits of elastic bands is much more solid - even though they are not as "cool"!

Want to become stronger, bigger, faster and leaner? Periodize appropriately!

30% More on the Big Three: Squat, DL, BP!

Block Periodization Done Right

Linear vs. Undulating Periodizationt

12% Body Fat in 12 Weeks W/ Periodizatoin

Detraining + Periodization - How to?

Tapering 101 - Learn How It's Done!

Figure 1: Relative strength increase in bench press (BP), back squat (BSQ), leg press (LP) and squat (SQ) in response to regular and variable resistance training; if not indicated otherwise, the variable resistance training was done with bands, only the study by Ghigarelli, et al. compared bands to chains (Soria-Gila. 2015).

Figure 2: Absolute increase in 1-RM strength (all values in kg) in the respective exercises (see Figure 1 for abbreviations) in the seven 7-week plus studies that were part of the meta-analysis (Soria-Gila. 2015).

• An extra 5% increase in 1RM and thus 2x greater strength gains on the bench.
• An extra 11% increase in 1RM and thus 2.6x greater strength gains for squats.

Are you looking for more ways to maximize your strength gains? Find out if training to failure or modifying your rest times can help in thisSuppVersity article.

Variable resistance training for explosive gains? In relative terms, the effects are huge. Two-fold larger increases in 1-RM strength in trained subjects speak for themselves. The absolute strength gains, on the other hand, are - and that's typical for people who have been training for several years - relatively small. Accordingly, you should not expect to start gaining strength like a rookie again, when you incorporate bands (which are better researched than chains) in your training regimen. What you can expect, though, is that your progress will accelerate significantly. For the next 2-3 months this would mean that you may be able to add 4 kg to your bench instead of just 2 kg. That's not exactly earth-shatteringly much, but it's still a 100% increase in 1-RM strength and in my humble opinion worth the effort... no? | Comment on Facebook!

• Anderson, Corey E., Gary A. Sforzo, and John A. Sigg. "The effects of combining elastic and free weight resistance on strength and power in athletes." The Journal of Strength & Conditioning Research 22.2 (2008): 567-574.
• Bellar, David M., et al. "The effects of combined elastic-and free-weight tension vs. free-weight tension on one-repetition maximum strength in the bench press." The Journal of Strength & Conditioning Research 25.2 (2011): 459-463.
• Cronin, John, Peter Mcnair, and Robert Marshall. "The effects of bungy weight training on muscle function and functional performance." Journal of sports sciences 21.1 (2003): 59-71.
• Ghigiarelli, Jamie J., et al. "The effects of a 7-week heavy elastic band and weight chain program on upper-body strength and upper-body power in a sample of division 1-AA football players." The Journal of Strength & Conditioning Research 23.3 (2009): 756-764.
• McCurdy, Kevin, et al. "Comparison of chain-and plate-loaded bench press training on strength, joint pain, and muscle soreness in Division II baseball players." The Journal of Strength & Conditioning Research 23.1 (2009): 187-195.
• Rhea, Matthew R., Joseph G. Kenn, and Bryan M. Dermody. "Alterations in speed of squat movement and the use of accommodated resistance among college athletes training for power." The Journal of Strength & Conditioning Research 23.9 (2009): 2645-2650.
• Shoepe, Todd, et al. "The effects of 24 weeks of resistance training with simultaneous elastic and free weight loading on muscular performance of novice lifters." Journal of human kinetics 29 (2011): 93-106.
• Soria-gila, Miguel A., et al. "Effects of variable resistance training on maximal strength: a meta-analysis." Journal Of Strength And Conditioning Research/National Strength & Conditioning Association (2015): Accepted article.