Could BIBA be the active ingredient in a pill that solves your weight problems once and for all? Or is that too good be true?

Some people say that caffeine is the last real "fat burner" left on the market

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Figure 1: 100mg/kg/day BAIBA may be an anti-weight gain supplement The data from obese rodents (rights) does yet suggest that it is not a weight loss supplement (Maisonneuve. 2004) | Anti-obesity, but not weight loss effects were also observed in obesity prone rodents in a 2008 study by Begrich et al. at the same dosage of BAIBA.

In obesity prone mice, BAIBA (100mg/kg) did not just ameliorate the body fat gain, it also reduced (c,d) the number of fibrotic leasons (a,b) of the liver that occured when the ob +/+ mice got fat (Begrich. 2008).

Is BAIBA even safe? In the absence of human studies that's difficult to say, but in rodents it had no ill effects on mtDNA replication (Mainonneuve. 2004) and displays a generally low toxicity. As Begrich et al. point out, their "further investigations are [still] requested to determine whether BAIBA could induce deleterious effects," even though, "it seems that this endogenous derivative could have a favourable safety profile that might be attractive for pharmacological usage" (Begrich. 2010). Deteriorations of the lipid or glucose metabolism, were not observed in any of the currently published studies and at a dosage of 100mg/kg BAIBA reduced the fibrotic leasons in the livers of obesity prone mice and improved the level of lactate dehydrogenase, a potential marker of liver problems (Begrich. 2008).

• While BAIBA may be useful to ameliorate the body fat gain in lean individuals and would thus in fact be an "attractive pharmacological strategy in order to prevent [...] obesity" (ibid.) in an obesogenic environment,
• it appears to be more than just 'a little too early' to assume that BAIBA supplements could also be used to "treat" (ibid.) obesity in individuals who are already carrying >50% more body fat on their frame than the average lean person.

It is however more than the fact that many of you are probably (still) lean that keeps BAIBA in the game: If you look at the data in Figure 2, it becomes obvious that BAIBA may do more than to prevent the body fat gain in people who have always been lean: its effect on leptin, in particular, could be of even greater use for people who have lost a significant amount of body fat and are now struggling with the nasty yoyo effect.

Figure 2: The increase in adipocyte (=fat cell) leptin and adiponectin production that was observed in the petri dish is particularly interesting for people who have already lost a significant amount of body fat (Begrich. 2010). If it translates into in vivo human studies, it may help those people to stay lean and reverse "metabolic damage".

As you can see in Figure 2, in vitro data shows that the direct exposure of fat cells (adipocytes) of mice, which are at a particularly high risk of becoming obese, will trigger a significant increase in leptin and adiponectin production. Why's that important? Well, of these...

• Metabolic Damage, Energy Intake & the Human "Energy Thermostat" - An Update Based on Recent Studies | read it!

  the increase in adiponectin that is produced by one's fat cells has been linked to important health markers, like increased insulin sensitivity and improved markers of lipid management.
• the increase in leptin production, however, may be of greater importance, because the diet- or rather fat-loss induced remodelling of the adipose tissue (many small empty fat cells) will reduce the production of the "you're fat enough" signal leptin and thus increase the risk of formerly obese individuals to regain every pound (or even more) of body fat they have painfully lost over months of hard dieting.

Bottom line: Whether an increase in leptin production is, as Figure 3 from Begrich's previously cited review suggests, the only (or at least the most important) mechanism of the beta-aminoisobutyric acid induced anti-obesity effect will yet have to be confirmed in future studies.

Figure 3: If Begrich et al. (2010) are right, the beneficial effects of BAIBA are mediated mostly, if not exclusively by leptin. Due to a lack of human data, BAIBA must - as of now - still be classified as "promising, but unproven" anti-obesity supplement.

Of even greater importance than investigations into what I would like to call the "leptin hypothesis of BAIBA's anti-obesity effects", though, is the simple confirmation of its effects in independent human studies. I mean, rodents are (often) a good model of human metabolism, but there are instances where slight metabolic differences between man and mouse can have a huge impact on several practically relevant research outcomes. It is thus well possible that unexpected human-specific "side effects" like an extreme increase in appetite and energy intake could reduce or blunt the purported anti-obesity prowess of BAIBA. Before the aforementioned human studies have not been conducted, peer-reviewed and published, I recommend to stay skeptical about BAIBA being the "next big thing in fat loss supplements." | Comment on Facebook!

• Begriche, Karima, et al. "β‐Aminoisobutyric Acid Prevents Diet‐induced Obesity in Mice With Partial Leptin Deficiency." Obesity 16.9 (2008): 2053-2067.
• Begriche, Karima, Julie Massart, and Bernard Fromenty. "Effects of β‐aminoisobutyric acid on leptin production and lipid homeostasis: mechanisms and possible relevance for the prevention of obesity." Fundamental & clinical pharmacology 24.3 (2010): 269-282.
• Maisonneuve, Caroline, et al. "Mitochondrial and metabolic effects of nucleoside reverse transcriptase inhibitors (NRTIs) in mice receiving one of five single-and three dual-NRTI treatments." Antimicrobial agents and chemotherapy 47.11 (2003): 3384-3392.
• Maisonneuve, Caroline, et al. "Effects of zidovudine, stavudine and beta-aminoisobutyric acid on lipid homeostasis in mice: possible role in human fat wasting." Antiviral therapy 9.5 (2004): 801-810.

Is it worth to replete vitamin D, but not to train super-slow, right?

If you periodize appropriately you may actually be able to benefit from super-slow training.

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• (Super-)slow training and its inferior effects on early-phase satellite cell and myonuclear domain adaptation (Herman-Montemayor. 2015) -- The purpose of one of the latest studies from the Rocky Vista University was to identify adaptations in satellite cell (SC) content and myonuclear domain (MND) after 6-week slow-speed vs. “normal-speed” resistance training programs.
  
  To this ends, thirty-four untrained women were divided into slow speed (SS), traditional strength (TS), traditional muscular endurance (TE), and nontraining control (C) groups. The ladies performed a leg work consisting of three sets of each of the following exercises twice per week in the first and thrice per week in the fifth week: Leg press, squat, and knee extensions. To investigate how the way these workouts were performed would affect the adaptive response, the scientists randomly assigned their subjects to four different groups:
  • The Super-Slow (SS) group performed 6– 10 repetition maximum (6–10RM) for each set with 10-second concentric (con) and 4-second eccentric (ecc) contractions for each repetition.
  • The Traditional Strength (TS) group and the Traditional Muscular Endurance (TE) group who performed 6–10RM and 20–30RM, respectively, at “normal” speed (1–2 seconds per con and ecc contractions).
  • The sedentary control group (C) which did not work out at all.
  To allow for a similar number of reps in the TS and SS group, the intensity (=weight used) in the SS group was reduced to the same 40–60% of the 1RM that was also used in the TE group. The TS group, on the other hand trained at 80–85% 1RM.

• I know that this is not ideal, but there's no way you do 6-10 reps with a time-under-tension (TUT) of 10-0-4 with the same weight you'd do 6-10 reps at a normal TUT of 1-0-1 or 2-0-2, accordingly, the results the scientists' analysis of the pretraining and posttraining muscle biopsies the authors analyzed for fiber cross-sectional area, fiber type, SC content, myonuclear number, and MND still have practical relevance.
  

  Figure 1: Percentage change (%) in mean fiber cross-sectional area, myonuclear domain size (domain), and number of myonuclei per fiber cross-section (myonuclear number) from pretraining to posttraining for each group (TS, SS, TE, and C). *Significant increase after training, p , 0.001. §Significant increase after training, p # 0.05. #Significantly greater increase after training compared with all other groups (SS, TE, C), p , 0.01. TS = traditional strength (Herman-Montemayor. 2015).

  And what does the scientists' analysis tell us? Well, along with the data in Figure 1, the exclusive increase in satellite cell content of type I, IIA, fibers (IIX and IIAX increased in both SS and TS, but not TE or control) that was observed in the traditional strength (TS) training group appears to confirm the superiority of this way of training when it comes to lying the foundations of further myonuclear domain growth (learn more in the "Muscle Hypertrophy 101").
  
  The fact that myonuclear domain increases of type I, IIAX, and IIX fibers occurred exclusively in the TS, yet not in the SS group, where only the domains of the type IIA fibers increased, does still appear to confirm the common prejudice that - for the average trainee - training at higher times under tension (TUTs) does not offer benefits that suggest faster or more robust size gains. Compared to strength-endurance training, however, super-slow training is still the better option. On a "per load basis" it is thus more effective to do fewer reps slower vs. more reps at a normal speed if your goal is to "grow" muscle.
• Vitamin D affects muscle recovery directly (Owen. 2015) -- We already know that vitamin D figures in one way or another in (a) the adaptive response to exercise and (b) the recovery process after strenuous workouts. Unfortunately our "knowledge" is based mostly on correlations and associations and can thus hardly be considered reliable evidence. That's something researchers from the Liverpool John Moores University, the Charité in Berlin, the Norwich Medical School and other European labs weren't happy with, either. Accordingly, they designed a randomised, placebo-controlled trial that involved twenty males with low serum 25[OH]D (45 ± 25 nmol.L-1) who performed 20×10 damaging eccentric contractions of the knee extensors with peak torque measured over the following 7 days of recovery prior to and following 6-weeks of supplemental Vitamin D3 (4,000 IU.day-1) or placebo (50 mg cellulose).
  
  To complement the results of this human trial, the authors conducted a parallel experimentation using isolated human skeletal muscle derived myoblast cells from biopsies of 14 males with insufficient serum 25[OH]D (37 ± 11 nmol.L-1) that were subjected to mechanical wound injury. Thus, the scientists tried to emulate the process of muscle repair, regeneration and hypertrophy in the presence and absence of 10 nmol or 100 nmol 1α,25[OH]2D3 in the petri dish.
  

  Figure 2: In view of the fact that the scientists used active vitamin D3 (calcitriol) in the in-vitro study, the improved recovery in the human trial is all the more the more relevant results of the study. It does yet pose the question whether similar or any effects had been observed in subjects with sufficient vitamin D levels in whom the provision of extra vitamin D3 may have increased 25OHD, but not the systemic calcitriol levels of which the scientists' in-vitro dta shows that it is responsible for the effects (Owens. 2015).

  What the results of both studies have in common is that they support the previously claimed role of vitamin D in muscle repair and regeneration. How's that? Well, the supplemental Vitamin D3 the D-ficient human subjects received didn't just increase the serum 25[OH]D levels. It also lead to measurable improvements of the recovery of peak torque at 48 hours and 7 days post-exercise. In conjunction with the observation that 10 nmol 1α,25[OH]2D3 aka calcitriol (=active vitamin D3, not the supplement you consume) improved muscle cell migration dynamics and resulted in improved myotube fusion/differentiation at the biochemical, morphological and molecular level in the cell study, where it also increased the myotube hypertrophy at 7 and 10 days post-damage, these preliminary data do just as the scientists say "characterise a role for Vitamin D in human skeletal muscle regeneration and suggest that maintaining serum 25[OH]D may be beneficial for enhancing reparative processes and potentially for facilitating subsequent hypertrophy" (Owens. 2015).

"Explosive Reps May Pay Off - At Least on the Bench: Fast Reps = Higher Muscle Activity, Higher Volume... Gains?" Find the answer to this question from a previous SuppVersity article here.

So what? Yes and no! Those are the answers to the questions you are probably about to ask. Yes, it does make sense to keep an eye on your vitamin D (25OHD in serum) levels, to do blood tests regularly and to supplement according to your personal needs. Yes, it does also make sense to get 1,000 IU of vitamin D3 per day even if you don't know you're deficient. And yes, all that may actually help you to recover faster.

What neither vitamin D3 nor super-slow training will do, though, is to turn you into a ripped super-muscular freak. In fact, the answer to the rarely asked question whether it makes sense to switch from a regular hypertrophy training regimen with a TUT of 1-0-1 or 2-0-2 to a super-slow regiment, is "no". Or more precisely: No, it is not generally recommendable to do super-slow training instead of regular resistance training if your goal is max. muscle hypertrophy.

A question the study by Herman-Montemayor cannot answer, however, is whether doing super-slow training only least temporarily (as part of a perdiodization scheme, for example) would help pro-athletes to make further or faster progress. Even without a study, though, it can be said that someone who has been training with a TUT of 1-0-1 and weights corresponding to his/her 6-10RM (=80-85% of 1RM) for years and for whom the super-slow training would constitute a novel training stimulus is probably more likely to benefit from intermediate super-slow training than the subjects in the study at hand for whom this was the first 6-week gym experience | Comment on Facebook!

Probiotics under urgently needed scrutiny - This is the first study to test for antibiotic resistances and to highlight the discrepan- cy between label claims and the actual number of live bacteria in supplements.

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Figure 1: Petri dishes from the antibiotic test (top). If the antibiotics still worked on the bacteria in the probiotics, they all should be dead. As you can see (in the graph, as well), that's by no means the case (Wong. 2015).

• Even probiotics that help weight loss, could transfer antibiotic resistances.

  Probiotics of all batches of products were resistant towards vancomycin.
• Several batches of probiotics from four different brands were also resistant towards streptomycin, aztreonam, gentamycin and / or ciprofloxacin antibiotics (this includes the US and Austrian products, i.e. Cn and Bn, respectively)
• The fifth brand showed a unique resistance towards gentamycin, strepto- mycin and ciprofloxacin antibiotics. 

Figure 2: Non-strain specific essay that evaluated the number of live bacteria in the products. The products from producers Bi, Bg, and L didn't just contain significantly less living bacteria than the manufacturers claim, the number is even so low that it is absolutely certain that they are 100% useless. The good news may be that the low dose supplements from the Austria(BN) and USA (CN) contained either more or at least roughly the amount of bacteria on the label (Wong. 2015).

The "live bacteria"-problem can be solved by eating probiotic foods like yogurt. The problem with potential antibiotic resistances, on the other hand, is rampant with foods, too. Even meat (especially chicken) and allegedly extra-healthy products like veggies from the farmers market may be tainted (the latter due to natural fertilizers of animal origin aka slurry).

Bottom line: The transfer of genes that could make bad gut bugs resistant to antibiotic is only a possibility, but it's one with literally fatal consequences. If bacterial strains in your gut have become resistant to antibiotics and you end up - for whatever reason - with an infection, i.e. a rapid multiplication of these bacteria, you could probably find yourself in the emergency room ... or worse.

In conjunction with the proven lack of viable bacteria in the five products from the US, Malaysia and Austria this study casts a shadow on a class of supplements with rapidly increasing sales - a shadow that becomes even darker if you remember my previous warning that we know literally nothing about the far-reaching interactions between the billion of different bacteria in our gut to even know the "good" from the "bad" guys | Comment on Facebook!

• Wong, Aloysius, et al. "Detection of antibiotic resistance in probiotics of dietary supplements." Nutrition journal 14.1 (2015): 1-6.

Want to maximize net protein retention? Order another one... another steak ;-)

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Table 1: Overview of the macronutrient intake during the 4-day run-in and the actual experiment (Kim. 2015b)

• exercise did not significantly affect protein kinetics and blood chemistry, while 
• feeding, in general, resulted in a positive net protein balance at both levels of protein intake,

Figure 1: It's the decrease in protein breakdown, not the marginal increase in protein synthesis that makes the difference between the net protein balance after the high and medium protein meals (Kim. 2015b).

Figure 2: The analysis of the inter-group differences in EAAs, glucose and insulin suggest that the difference is meadiated mainly by the increase in serum EAAs and not a "side effect" of increased, highly anticatabolic (Fukagawa. 1985) insulin.

Bottom line: When it comes to interpreting the results, two things are important. Firstly, it is worth mentioning that the previously described decrease in protein breakdown was achieved in response to a greater increase in plasma EAAs (p<0.01) - not in response to increased insulin levels (inter-group differences were non-significant over time). That's important because it means that you wouldn't see the same effect by simply adding more insulinogenic carbs to the meal in order to increase the levels of one of the most powerful inhibitors of protein breakdown: insulin (Fukagawa. 1985)!

Sounds great, right? More helps more! True, there's yet (a) the previously hinted at problem that we can't tell if what the scientists measured was muscle or splachnic protein. Furthermore, the results of the study are (b) valid only if the protein comes from slow-digesting meat. From previous research, I discussed in detail back in 2013, already, we know that the ingestion of similarly high amounts of fast digesting proteins, like whey, does not inhibit, but rather trigger an increase in protein breakdown and gluconeogenesis that uses the ingested protein as a substrate. Now, that doesn't mean that using too much whey protein will cost you muscle mass. What it does mean, though, is that you'll be "Protein Wheysting" if you mistakenly believe that the results of Kim's study apply with a very slow digesting protein source apply turbo-proteins, as well.

So what's the verdict?  Don't economize on protein, but don't fool yourself to believe that with protein more is always always better. Maybe I should also remind you that when you're dieting a high protein intake can yield better results than a very high one and that's a conclusion from a metabolic ward study | Tell me and others what you think on Facebook!

• Fukagawa, N. K., et al. "Insulin-mediated reduction of whole body protein breakdown. Dose-response effects on leucine metabolism in postabsorptive men." Journal of Clinical Investigation 76.6 (1985): 2306.
• Kim, Il-Young, et al. "Quantity of dietary protein intake, but not pattern of intake, affects net protein balance primarily through differences in protein synthesis in older adults." American Journal of Physiology-Endocrinology and Metabolism 308.1 (2015): E21-E28.
• Kim, et al. "The anabolic response to a meal containing different amounts of protein is not limited by the maximal stimulation of protein synthesis in healthy young adults." Am J Physiol Endocrinol Metab (November 3, 2015b). doi:10.1152/ajpendo.00365.2015.

Will slimming down from a 120 cm to a 60 cm waist always ruin your metabolic rate and set you up for weight regain or can high GI protect you from yoyoing?

# Women appear to be particularly prone to # metabolic damage - more on # female fat loss:

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Figure 1: Overview of the key parameters of the study design and dietary composition (Karl. 2015).

Metabolic Damage in Biggest Losers: Will Diet & Intense Exercise Make You Fat, While Surgery Will Make You Lean? Plus: How to Avoid or Even Correct Diet-Induced REE Reductions | more

"Phase 1 was a 5-week weight maintenance phase in which weight maintenance energy needs were determined by adjusting provided energy intake to maintain stable weight. Mean Phase 1 energy intake was 12.2 MJ/day with 48% energy provided as carbohydrate, 16% as protein, and 36% as fat. Following Phase 1, participants were randomized by the study statistician to their Phase 2 dietary assignment using computer-generated randomization. The four diets differed in carbohydrate content (55%, ModCarb or 70%, HighCarb of total energy) and dietary GI (less than 60, LowGI or 80, HighGI), and were provided for 12 weeks at 67% of the weight maintenance energy intake determined in Phase 1. 

Participants were allowed to increase their energy intake during Phase 2 by requesting additional, randomization-appropriate foods from the metabolic kitchen if too hungry to be adherent. Phase 3 was a 5-week weight maintenance phase during which food was provided according to randomization. Energy intake during Phase 3 was prescribed to support weight maintenance at the new, lower body weight, and was predicted from body weight and energy intake measured at the end of Phase 2, with adjustment for self-reported physical activity. Phase 4 was a 12- month follow-up period during which participants selected and pre pared their own meals after being provided with instructions on fol lowing the diet to which they were randomized" (Karl. 2015)

Figure 2: (A) Weight loss and (B) percentage of total weight loss attributable to fat mass and fat free mass while consuming provided-food diets differing in glycemic index (GI) and percent energy from carbohydrate (55%, ModCarb and 70%, HighCarb) for 17 weeks (n = 79). Values are mean 6 SEM. Weight loss analyzed by repeated measures ANCOVA, body composition by two-factor ANOVA. a,bMain effect of time; asignificant decrease from baseline (P < 0.001), bsignificant difference from Phase 2 end (P < 0.001). No diet effects (main effects or interactions) for any comparisons. GI, glycemic index; HighCarb, 70% energy from carbohydrate; ModCarb, 55% energy from carbohydrate (Karl. 2015).

Figure 3: Measured resting metabolic rate as a function of predicted metabolic rate (Karl. 2015). Note: If there was no "metabolic damage", the solid line which represents the ideal body-weight dependent decline of energy expenditure and the dashed line which represents the actual ratio of the measured to the predicted RMR should be congruent.

Figure 4: Changes in body composition (absolute value in kg) after 20 weeks and after weight loss phase 2 (Karl. 2015).

Bottom line: As Karl et al. point out, "neither low-GI relative to high-GI diets nor moderate-carbohydrate relative to high-carbohydrate diets showed differences with respect to effects on changes in body composition or resting metabolism during weight loss when confounding dietary factors were tightly controlled in a study providing all food for 22 weeks" (Karl. 2015).

This does not just go against the mainstream assumption that low GI and/or low(er) carbohydrate diets facilitate weight loss, fat loss and weight maintenance (see data in Figure 4 for an overview of these parameters, it also contradicts the initially mentioned broscientific assumption that carbohydrates, in general, and high GI carbs, in particular, have a protective effect against the unexpected diet-induced reduction of basal energy expenditure many people know as "metabolic damage". If there's anything of which the study at hand suggests that it could protect you from such unexpectedly large decrease in RMR, it's not high GI carby, but rather an already high(er) baseline RMR (see Figure 3).

And what does that tell us? Right! Since a high predicted RMR is a function of (a) being male, (b) being tall, and (c) being muscular, all three attributes may protect you from diet-induced "metabolic damage" | Let me know your thoughts and comment on Facebook!

• Danforth Jr, Elliot, et al. "Dietary-induced alterations in thyroid hormone metabolism during overnutrition." Journal of Clinical Investigation 64.5 (1979): 1336.
• Karl, J. Philip, et al. "Effects of carbohydrate quantity and glycemic index on resting metabolic rate and body composition during weight loss." Obesity 23.11 (2015): 2190-2198.
• Mariash, C. N., et al. "Synergism of thyroid hormone and high carbohydrate diet in the induction of lipogenic enzymes in the rat. Mechanisms and implications." Journal of Clinical Investigation 65.5 (1980): 1126.
• Serog, P., et al. "Effects of slimming and composition of diets on VO2 and thyroid hormones in healthy subjects." The American journal of clinical nutrition 35.1 (1982): 24-35.
• Ullrich, Irma H., Philip J. Peters, and M. J. Albrink. "Effect of low-carbohydrate diets high in either fat or protein on thyroid function, plasma insulin, glucose, and triglycerides in healthy young adults." Journal of the American College of Nutrition 4.4 (1985): 451-459.

15 min in the AM, 15 in the PM = Win? For many of you that may sound laughable, but according to a recent study from the University of Copenhagen it is at least as effective as three "mammoth" workouts-sessions per week.

No single workout routine works forever. Periodize to make continuous progress!

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Table 1: Description of the two different training regimen (Kilen. 2015) | *To minimize the potential negative effect of concurrent cardio + strength training, MI performed 2 days of strength (Mon and + Tue) and 1 day of cardio training (Wed) in odd weeks, and 1 day of strength (Mon) and 2 days of cardio training (Tue + Wed) in even weeks.

• Strength training consisted of leg exercises (deadlifts, lunges, step-ups, and 1 leg squats), with 1–2 warm-up sets and 2–3 target sets of 8RM, and upper-body exercises (pullups, dips, weighted push-ups, and 1 arm rows), with 1–2 warm-up sets and 2–3 target sets of 5RM. For progression, the exercises were adjusted using extra loading (sandbags in 1-kg steps) if the subjects were able to accomplish more repetitions than prescribed. If the subjects were not able to perform the number of repetitions prescribed, they performed as many as they could in proper form and finished the set conducting only the eccentric phase of the exercise. 
• High-intensity cardiovascular training (HIIT) consisted of running for 2 and 4 minutes at an average speed of 15.1 and 14.5 km/h, respectively, which elicited ;90% maximal heart rate during exercise. Micro training performed two 4-minute run intervals in the morning with 3 minutes of rest in between and four 2-minute run intervals in the afternoon with 1 minute of rest in between. Classical training performed three 4-minute and six 2-minute run intervals in the same training session with the same rest as MI in between. The training volume was evaluated and the only significant difference was running distance during 2-minute and 4-minute intervals, where MI ran significantly further than CL in each interval. 
• Muscle endurance training consisted of three 5-minute exercise sessions involving 5 different exercises performed continuously for 30 seconds with 30-second rest periods. Micro training conducted 3 sessions; the first was “easy,” the second “hard,” and the third “very hard.” Classical training conducted 9 sessions in the same order, starting over with “easy” on the fourth and seventh sessions. The exercises were weighted lunges (with a 20-kg sandbag); push-ups; shuttle runs; abdominal exercises ([a] regular sit-ups from a supine position with knees bent at 908, fists in contact with the ears and the lumbar arch supported by a folded towel, and [b] diagonal sit-ups from a horizontal supine position, outstretched hand to opposite raised foot, alternating); and back exercises ([a] back extensions on an incline bench and [b] kettlebell swings in a standing position). 

Figure 1: Relative pre- vs. post changes in all measures performance markers (calculated based on Kilen. 2015).

• Increases in shuttle run performance were observed in both group, albeit with a higher significance as far as the pre- vs. post-difference is concerned in the classical training (CL) vs. micro training (MI) group (MI: 1,373 +/- 133 m vs. 1,498 +/- 126 m, p < 0.05; CL: 1,074 6 213 m vs. 1,451 6 202 m, p , 0.001).
• Significant improvements in peak oxygen uptake (3,744 6 +/- 615 mL/min vs. 3,963 +/- 753 mL/min | p < 0.05), maximal voluntary isometric (MVC) force of the knee extensors (646 +/- 135 N vs. 659 +/- 209 N | p < 0.001), MVC of the finger flexors (408 +/- 109 N vs. 441 +/- 131 N, p < 0.05), and the maximal number of lunges performed in 2 minutes (65 +/- 3 vs. 73 +/- 2, p , 0.001), however, were seen only in the micro = high frequency training group.

"similar training adaptations can be obtained with short, frequent exercise sessions or longer, less frequent sessions where the total volume of weekly training performed is the same" (Kilen. 2015)

Figure 2: Neither the in-group nor the inter-group changes in body composition did reach statistical significance (calculated base on Kilen. 2015). At least in my humble opinion, though, they are still interesting.

Speaking of what people will deem relevant: We haven't addressed the changes in body composition yet. Why's that? Well, if we go by statistical significance, there were none. If we go by %-ages, though, the increase in lean and decrease in fat mass in the micro training, as well as the opposite trends in the classical training group add to the non-significant evidence that it may make sense to train more frequent and that - when all is said and done - total volume may eventually not be the only thing that matters... I mean, if you look at the data in Figure 2 it would - in defiance of the statistical insignificance of the changes - still seem as if the previously mentioned fitness model was right: For him or her, for whom improves body composition are the primary goal, his / her frequent AM/PM training regimen does in fact appear to be the training model of choice | Comment!

• Kilen, Anders, et al. "Adaptations to Short, Frequent Sessions of Endurance and Strength Training Are Similar to Longer, Less Frequent Exercise Sessions When the Total Volume Is the Same." The Journal of Strength & Conditioning Research 29 (2015): S46-S51.

Gut health is "all the rage", lately. So even if it's true that this may be one of the most culpably neglected areas of research in the past century, we should still be careful not to hype the effect of the gut on your physique and health too much.

You can learn more about the gut & your health at the SuppVersity

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• Cheesy! Casein keeps your trigs in check - Due to the interaction between elevated postprandial triglyceride levels, insulin resistance and cardiovascular disease, the results of the previously mentioned study by Mariotti et al. (2015) may be of interest not just for all of us. After all, the proposed mechanism of which the authors, scientists from the AgroParisTech speculate that it is a direct result of the same

  "solubility of casein and its precipitation that forms a gel in the stomach [which have long been] known to influence its rate of absorption and postprandial protein metabolism in the context of regular, low-energy meals" (Mariotti. 2015),

  as the marked effect on the chylomicron kinetics and decrease in postprandial TGs, a risk factor for cardiovascular disease, the French scientists observed in the study at hand.
  

  Figure 1: Area under the curve for triglycerides (did respond), amino acids (didn't respond) and glucose (didn't respond) in 10 overweight subjects after consuming isocaloric high-energy meals with 15% of the energy from protein in form of casein (CAS), whey protein (WHE) or alpha-lactalbumin enriched whey (LAC | Mariotti. 2015)

  As you can see in Figure 1, the proteins which made up exactly 15% of the total energy content of the high-fat meal that was fed to 10 healthy overweight men with an elevated waist circumference (>94 cm) did not affect the subjects' postprandial plasma glucose, amino acids, insulin, or nonesterified fatty acid levels (which would, by the way, suggest that ingesting whey or an alpha-lactalbumin enriched whey protein with a meal ruins its amino acid absorption advantage). The study outcome that did differ, though were the postprandial triglycerides (TGs) levels, where the provision of casein lead to a highly significant 22% (+/- 10%) reduction in the 6-h area under the curve.

• As the authors point out, similar trends were shown for plasma chylomicrons [apolipoprotein (apo)B-48; P < 0.05], yet not for the postprandial oxidative stress (plasma hydroperoxides and malondialdehyde), endothelial dysfunction (salbutamol-induced changes in pulse contour analysis), or low-grade inflammation. This is also why it is as of yet only a logical, but hitherto unsupported hypothesis that consuming casein (micellar casein, not regular sodium or calcium caseinates) would also reduce one's cardiovascular disease risk. Eventually, it does yet appear to be the more reasonable adjunct to a full meal anyway - the purpose of the latter is after all to keep you satiated for a long time; and that's where casein is unquestionably a better choice than whey.
• Probiotics - 0.5% body fat reduction, and a 2.68 cm² reduction in subcutaneous fat area are not much, but they occurred in the absence of diet and exercise - If the trend continued and the 120 nondiabetic and overweight subjects Jung et al. divided into two groups: There was the probiotic group with 60 individuals who consumed 2 g of powder of two probiotic strains, L. curvatus HY7601 and L. plantarum KY1032, each at 2.5 × 109 cfu, twice a day. And there was the and a placebo group, likewise 60 individuals, who consumed the same amount of powder that did not contain any probiotics.
  

  Figure 2: Changes in body composition according to waist measurement and CT scans - All values are relative changes in waist and fat area measure from week 0 to week 12 (Jung. 2015).

  Both groups were advised to take their supplements immediately after breakfast and dinner, but only the probiotic group saw relevant improvements in body fat at slow) pace - albeit a pace at which it would take them "only" 5 years to finally make it into healthy body fat zones.

Probiotics under urgently needed scrutiny: Many Probiotics Contain Antibiotic Resistant Bacteria. Plus: Number of Live Bacteria is up to 95% Below Label Claims | Learn more.

Prebiotic supplements are not created equal! You may remember my recent article on (a) antibiotic resistances in supplemental probiotics and (b) the lack of viable bacteria in the different supplements the researchers analyzed. It should be obvious that these results mean that even though the study at hand appears to suggest that everyone should take probiotics, further research is needed before we can say which of the many pills on the market this should be... ah, and by the way. It is still not clear whether the same bacteria that are benefical for the obese are anywhere close to beneficial for lean athletic individuals. Rather than general recommendations, I expect the future of probiotic supple-ments to be individual (based on diet and metabolic data).

• Ok, that's painfully slow, but given the fact that the food intake of both groups didn't differ significantly, it is still noteworthy that the 2 g of probiotic powder which contained contained 0.1 g of L. curvatus HY7601, 0.1 g of L. plantarum KY1032, 1.24 g of crystalline cellulose, 0.5 g of lactose, and 0.06 g of blueberry-flavouring agent made the subjects lose significant amounts of body fat, while their peers who received 2 g of a placebo powder that contained 1.34 g of crystalline cellulose, 0.6 g of lactose, and 0.06 g of blueberry-flavouring agent kept gaining.
  

  Figure 3: The provision of the probiotic supplement did also trigger significant improvements in the above markers of cardiovascular disease risk - if it's not the small fat loss, it would thus be the potential CVD risk reduction that makes the use of probiotic supplements attractive especially for overweight individuals (Jung. 2015).

  In conjunction with the likewise statistically significant beneficial effects on health markers like LDL oxidation and LDL particle size which indicate significant improvements in cardiovascular disease risk, this is still the first non-sponsored study (the study was financed by Korean Ministry of Science) that shows that supplementing with commercially available probiotics in man may actually produce health-relevant beneficial effects.

Probiotics aren't for the overweight and obese, only. A recently discussed study, for example, showed that a patented multi-strain probiotic will reduce the fat gain on a 4-week "bulk" by more than 50% - and that's in twenty young men who consumed an extra 1,000kcal per day | more.

You are kidding me, right? No, I am not. I know that neither casein nor probiotics appear to be game-changers, but eventually you will have to understand that the one trick, supplement or modification of your lifestyle cannot correct the 10,000 mistakes you have or even are still making. Losing fat and getting healthy is about taking one baby step at a time; and the studies by Mariotti et al. and Jung et al. describe two promising ways of taking another of these steps.

In that it would be great if we knew for sure how both of them work on a mechanistic (molecular) level. As of now, the only thing that appears to be certain, though, is that they act at the level of the gut. One by affecting the digestive process, the other by modifying the make-up of the intestinal microbiome of which more and more studies appear to suggest that it may not be triggering, but at least perpetuating the ill health effects of obesity | Comment!

• Jung, Saem, et al. "Supplementation with two probiotic strains, Lactobacillus curvatus HY7601 and Lactobacillus plantarum KY1032, reduced body adiposity and Lp-PLA 2 activity in overweight subjects." Journal of Functional Foods 19 (2015): 744-752.
• Laugesen, Murray, and R. B. Elliott. "Ischaemic heart disease, Type 1 diabetes, and cow milk A1 β-casein." (2003).
• Mariotti, François, et al. "Casein Compared with Whey Proteins Affects the Organization of Dietary Fat during Digestion and Attenuates the Postprandial Triglyceride Response to a Mixed High-Fat Meal in Healthy, Overweight Men." The Journal of nutrition (2015): jn216812.
• McLachlan, C. N. S. "β-Casein A 1, ischaemic heart disease mortality, and other illnesses." Medical Hypotheses 56.2 (2001): 262-272.

Diabetes is a disease that is currently often only managed, not treated and that despite the fact that scientists know ways to send T2DM it into remission.

Educate yourself @ www.suppversity.com do battle or avoid T2DM

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"[i]ntensive lifestyle intervention is also superior to conventional treatment for inducing remission of type 2 diabetes, with remission rates of type 2 diabetes between 10 and 15 % at 1 year of follow-up" (Esposito. 2015), 

Table 1: Factors associated with weight loss maintenance and weight regain after intentional weight loss according to a literature review (Elfhag & Rössner. 2005)

Figure 1: If you look at the relatively low number of subjects who weren't able to maintain at least 50% of their weight loss, it should become obvious that at least within the first year RYGB surgery is not as black as it is painted by some critics (Cooper. 2015).

• Food urges is associated with a 5.1x increased risk of weight regain.
• Not feeling that the surgery has improved ones life is linked to a 21.5x increased risk.
• Alcohol or drug use is associated with a 12.74x increased risk.

After sign. weight loss beta-cells can be "resurrected". Meaning they will undergo a process of apoptosis, death and regeneration (Su. 2015).

But isn't the damage already done? While the damage is done, recent research clearly indicates that once the excess weight and with it the chronic hyperglycaemia, hyperlipidaemia and/or cytokines are gone, the damaged beta-cells "undergo the process of rebirth, which involves apoptosis evasion, regeneration and improved beta-cell function" (Su. 2015). While Su et al. point out that the research is not far enough to copy the effects with a drug, it is yet far enough to say that weight loss surgery works and that's what matters, no?

Figure 2: The amount of overweight lost is the only significant predictor of remission of remission of type 2 diabetes mellitus (T2DM) after gastric bypass in a cohort of 177 patients with T2DM who had undergone Roux-en-Y gastric bypass from 1993 to 2003 had 5-year follow-up data available (Chikunguwo. 2010).

1. "Metabolic damage" may make it harder, but not impossible for "reduced obese" individuals to stay lean | learn more

   All forms of weight loss surgery lead to caloric restriction, weight loss, decrease in fat mass and improvement in T2DM. 
2. Improvements in glucose metabolism and insulin resistance following bariatric surgery result in the short-term from decreased stimulation of the entero-insular axis by decreased caloric intake. 
3. In the long-term by decreased fat mass and resulting changes in release of adipocytokines. 

Figure 3: If a given life-style intervention facilitates high enough rates of fat loss, remission to tolerable HbA1c levels (see dashed line in small graph) occurs in more than half of the subjects (Ades. 2015).

Type II diabetes is treatable! That's the good news. The bad news is that the only treatment that doesn't require the same efforts people were not willing to go through in the years over which they acquired one extra-pound of body fat after the other is bariatric surgery. And even here, only those who are really willing to make a change have a good chance of reversing type II diabetes.

An alternative, in form of an intense diet + exercise lifestyle intervention exists; and while it may take longer to work, remission rates should border zero for all of those who understand that they cannot return to their previous diet and activity levels. Now I will leave it up to you to decide whether that's a good or bad news on "World Diabetes Day" | Let me and others know what you think and comment!

• Ades, Philip A., et al. "Remission of recently diagnosed type 2 diabetes mellitus with weight loss and exercise." Journal of cardiopulmonary rehabilitation and prevention 35.3 (2015): 193-197.
• Chikunguwo, Silas M., et al. "Analysis of factors associated with durable remission of diabetes after Roux-en-Y gastric bypass." Surgery for Obesity and Related Diseases 6.3 (2010): 254-259.
• Cooper, Timothy C., et al. "Trends in weight regain following roux-en-Y gastric bypass (RYGB) bariatric surgery." Obesity surgery (2015): 1-8.
• Elfhag, K., and S. Rössner. "Who succeeds in maintaining weight loss? A conceptual review of factors associated with weight loss maintenance and weight regain." Obesity reviews 6.1 (2005): 67-85.
• Esposito, Katherine, et al. "Remission of type 2 diabetes: is bariatric surgery ready for prime time?." Endocrine 48.2 (2015): 417-421.
• Gregg, Edward W., et al. "Association of an intensive lifestyle intervention with remission of type 2 diabetes." Jama 308.23 (2012): 2489-2496.
• Gumbs, Andrew A., Irvin M. Modlin, and Garth H. Ballantyne. "Changes in insulin resistance following bariatric surgery: role of caloric restriction and weight loss." Obesity surgery 15.4 (2005): 462-473.
• Malandrucco, Ilaria, et al. "Very-low-calorie diet: a quick therapeutic tool to improve β cell function in morbidly obese patients with type 2 diabetes." The American journal of clinical nutrition 95.3 (2012): 609-613.
• Su, Yinjie, Yanling Zhao, and Chaojun Zhang. "Bariatric surgery: beta cells in type 2 diabetes remission." Diabetes/metabolism research and reviews (2015).

No acute changes in blood glucose, but extreme changes in insulin levels. How can this trigger a reduction in glycated albumin - How's that possible?

Learn more about the effects of GABA & co at the SuppVersity

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Figure 1: Acute glucose (top) and insulin (bottom) response after single and repeated administration of 2g of GABA (left). Chronic effects of repeated dose-administration of GABA on glycated albumin (right | Li. 2015).

As a loyal SuppVersity reader you will know that I talked about the potential need to re-balance glucose levels and its paradoxically agitating effects in a 2013 episode of SHR, already.

So what's the verdict, then? Whether and for whom GABA can be useful tool to improve his or her blood glucose management is virtually impossible to tell based on the study at hand. In spite of the fact that the scientists observed only minor adverse events such as transient dizziness and a sore throat, a further reduction of glycated albumin levels is not necessary an advantage that's worth having elevated insulin and glucagon levels. The latter would after all promote the use of proteins or rather amino acids as substrate for gluconeogenesis, the process of which the scientists believe that it is responsible for the non-existent instantaneous glucose response in the study at hand, while the former, i.e. the increase in insulin levels, is well-known for its negative effects on fatty acid oxidation.

Overall, "the verdict" is thus that we need additional research in both, healthy and diabetic individuals to be able to tell for whom the benefits of chronic high(er) dose (3x2g per day) GABA supplementation outweigh potential side effects. If you asked me for an educated guess, though, I would say (pre-)diabetics benefit while the average individual sees either no relevant benefits or detrimental effects due to the repeated need to re-stabilize the blood sugar levels... a phenomenon of which I have by the way previously said and written that it may explain the paradoxically agitating effects the ingestion of GABA has on some individuals - most likely those with already low(ish) blood glucose levels | Comment on Facebook!

• Li, Junfeng, et al. "Study of GABA in Healthy Volunteers: Pharmacokinetics and Pharmacodynamics." Frontiers in Pharmacology 6 (2015): 260.
• Prud’homme, Gérald J., et al. "GABA protects human islet cells against the deleterious effects of immunosuppressive drugs and exerts immunoinhibitory effects alone." Transplantation 96.7 (2013): 616-623.
• Prud’homme, Gérald J., et al. "GABA protects pancreatic beta cells against apoptosis by increasing SIRT1 expression and activity." Biochemical and biophysical research communications 452.3 (2014): 649-654.
• Purwana, Indri, et al. "GABA promotes human β-cell proliferation and modulates glucose homeostasis." Diabetes 63.12 (2014): 4197-4205.
• Roohk, H. Vernon, and Asad R. Zaidi. "A review of glycated albumin as an intermediate glycation index for controlling diabetes." Journal of diabetes science and technology 2.6 (2008): 1114-1121.
• Soltani, Nepton, et al. "GABA exerts protective and regenerative effects on islet beta cells and reverses diabetes." Proceedings of the National Academy of Sciences 108.28 (2011): 11692-11697.
• Tian, Jide, et al. "γ-Aminobutyric acid inhibits T cell autoimmunity and the development of inflammatory responses in a mouse type 1 diabetes model." The Journal of Immunology 173.8 (2004): 5298-5304.
• Tian, Jide, et al. "Oral GABA treatment downregulates inflammatory responses in a mouse model of rheumatoid arthritis." Autoimmunity 44.6 (2011): 465-470.
• Tian, Jide, et al. "γ-Aminobutyric acid regulates both the survival and replication of human β-cells." diabetes 62.11 (2013): 3760-3765.
• Tian, Jide, et al. "Combined Therapy With GABA and Proinsulin/Alum Acts Synergistically to Restore Long-term Normoglycemia by Modulating T-Cell Autoimmunity and Promoting β-Cell Replication in Newly Diabetic NOD Mice." Diabetes 63.9 (2014): 3128-3134.

Should you freak out about a small increase in body weight in a small-scale rodent study that is attributed to the consumption of saccharin in yogurt?

You can learn more about sweeteners at the SuppVersity

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Figure 1: The forest plots of the practically most relevant data of individual and combined effect sizes for sustained intervention studies comparing the effects on body weight of sweeteners versus sugar (upper panel) and versus water (lower panel) shows that not a single long(er) term study found negative effects - the exact opposite is the case. Even compared to water the use of low-energy sweeteners (artificial or not) lead to measurable, yet not always significant decreases in body weight in human trials (Rogers. 2015).

"that the balance of evidence indicates that use of LES [low or no energy sweeteners] in place of sugar, in children and adults, leads to reduced EI and BW, and possibly also when compared with water" (Rogers. 2015 | my emphasis).

"[...] the present review of a large and systematically identified body of evidence from human intervention studies, with varying designs, settings and populations (including children and adults, males and females, and lean, overweight and obese groups), provide no support for that view. The question then is whether those hypotheses should be rejected or whether, as seems unlikely, the relevant human intervention studies are consistently flawed in a way that leads, in most cases, to exactly the opposite outcome" (Rogers. 2015)

Figure 2: Cumulative weight gain and total cumulative energy intake of (only) 16 male Wistar reds fed diets that were supplemented with either saccharin-sweetened or non-sweetened yogurt added (Foletto. 2015)

Table 1: In view of the fact that any existing negative effects of dietary sweeteners may well be compound-specific. It is certainly worth noting that saccharin is no longer used in modern sweetener formulations of sodas (Wikipedia. 2015)

Measurable weight increases are a common pattern in rodent studies particularly for the (today rarely used) artificial sweetener saccharin. It is thus well possible that any existing negative effects are compound-specific. For aspartame, for example, similar evidence is rare to non-existent.

Bottom line: In the absence of a proven theory about the mechanism that may trigger the increased weight gain and in view of the lack of health-relevant data (no information about the body composition of the rodents) and health-relevant side-effects you would usually see in response to pathologic weight gain (changes in insulin resistance, leptin or PYY), I can only refer you back to the quote from the latest meta-analysis of the effects of low- to no-energy-sweetener intake on food intake and weight gain in humans, which say that "the balance of evidence indicates that use of LES [low or no energy sweeteners] in place of sugar, in children and adults, leads to reduced EI and BW, and possibly also when compared with water" (Rogers. 2015).

Furthermore, more relevant evidence from human clinical trials supports the use of artificially sweetened foods as dieting aids (Sørensen. 2014 | learn more).

Whether that's enough to convince you that the unproven negative effects of saccharin on caloric expenditure or increases in the glucose transport mediated by gut sweet-receptors, of which Foletto et al. speculate that they may explain the results of their study, are relevant enough to avoid non-nutritive sweeteners altogether is now up to you. For me it's not enough... | Comment on Facebook!

• Foletto, Kelly Carraro, et al. "Sweet taste of saccharin induces weight gain without increasing caloric intake, not related to insulin-resistance in Wistar rats." Appetite (2015).
• Rogers, P. J., et al. "Does low-energy sweetener consumption affect energy intake and body weight? A systematic review, including meta-analyses, of the evidence from human and animal studies." International Journal of Obesity (2015).
• Sørensen, Lone B., et al. "Sucrose compared with artificial sweeteners: a clinical intervention study of effects on energy intake, appetite, and energy expenditure after 10 wk of supplementation in overweight subjects." The American journal of clinical nutrition (2014): ajcn-081554.

Tea catechins (which can also be found in black and jasmin tea | see Figure 3) can help you keep particularly unhealthy abdominal fat (Després. 2012) at bay.

You can learn more about green tea at the SuppVersity

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Figure 1: Macronutrient composition (in g an % of energy) of the non-energy reduced diets the subjects consumed; the values in the left pie chart represent a group average of all three intervention groups. Since the data is based on food records with photographs, it is probably more reliable than in your average diet study (Kobayashi. 2015).

Figure 2: Detailed analysis of the rel. change in fat area in the abdominal depot of the subjects (Kobayashi. 2015)

1. the low caffeine content of the beverage limits the bioavailability of EGCG & co (caffeine enhances its bioavailability | Nakagawa. 2009) and
2. the ingestion of the beverage with a meal has been shown to significantly reduce the bioavailability of green tea catechins in comparison to the fasted state (Chow. 2005).

1. Table 1: Catechin composition of the test beverages.

   the fat loss in the abdominal area was dose dependent - even if the differences between the low and high dose group did not reach statistical significance (for the exact catechin composition see Table 1 on the right) - and that 
2. roughly 50% of the benefits were lost within only 5 weeks when the subjects stopped consuming the green tea beverage, even though their diet didn't change at all (in fact, they consumed minimally less energy in the withdrawal phase from week 12-17).

Green tea forever, it is then!? Well, as usual we have to consider what limits the generalizability of the results. Firstly, we are dealing with a group of people who have more than a few pounds of extra-weight on their hips. An abdominal fat loss of 8% in 12 weeks is thus not impossible, but not exactly likely to be seen in someone who starts at a body fat percentage of 15% or less (which is half what the subjects in the study at hand began with).

Figure 3: Catechin content (mg/10ml) of black, green and jasmine tea prepared from commercial tea w/ different infusion times (Bronner. 1998).

The second thing we have to keep in mind is the beverage itself. As you've previously read, it has been enhanced with catechins with a galloyl moiety (CGMs | EGCG, ECG, GCG, CG). Does this mean that you cannot achieve similar results if you simply drink green tea? Luckily, data from Bronner, et al. (1998) suggests otherwise. As you can see in Figure 3, it would take only 100 ml of commercially available freshly brewed (infusion time 3 min) green tea and even less black tea to achieve similar concentrations of EGCG and the other catechins with a galloyl moiety in your tea. Accordingly, the second obstacle to the gene- relizability of the study is actually irrelevant.

Third- and lastly, there's yet still the fast reversal of the effects which suggests that it is necessary to become a habitual tea drinker to see long-term / lasting benefits of green tea (or as the data in Figure 3 suggests even catechin containing tea in general) on your body weight and, more importantly, body fat you're carrying around | Comment on Facebook!

• Bronner, W. E., and G. R. Beecher. "Method for determining the content of catechins in tea infusions by high-performance liquid chromatography." Journal of Chromatography A 805.1 (1998): 137-142.
• Chow, HH Sherry, et al. "Effects of dosing condition on the oral bioavailability of green tea catechins after single-dose administration of Polyphenon E in healthy individuals." Clinical Cancer Research 11.12 (2005): 4627-4633.
• Després, Jean-Pierre. "Body fat distribution and risk of cardiovascular disease an update." Circulation 126.10 (2012): 1301-1313.
• Kobayashi, Makoto, et al. "Green tea beverages enriched with catechins with a galloyl moiety reduce body fat in moderately obese adults: a randomized double-blind placebo-controlled trial." Food & Function (2016).
• Nakagawa, Kiyotaka, et al. "Effects of co-administration of tea epigallocatechin-3-gallate (EGCG) and caffeine on absorption and metabolism of EGCG in humans." Bioscience, biotechnology, and biochemistry 73.9 (2009): 2014-2017.

Yes, I could have exploited the ambiguity and called this article "Training 'On Cycle', Done Right - Women See Much Better Results When Periodization is in Line W/ Their Period", but let's be honest: This is a science website and that's neither scientific, nor actually funny, is it?

Learn more about the (often ;-) small but significant difference at the SuppVersity

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Figure 1: Relative changes in lean mass (DXA data), measures power and strength (torque) in 59 trained women in response two weeks of frequent leg-training in the first or second two weeks of their estrous cycle (Wikström-Frisén. 2015).

• regular non-periodized training, i.e. three leg training workouts per week that consisted of leg presses and leg curls (3x sets @ 8-10RM, 1-2 minutes rest between sets; progressive increase of weight by 2-10% whenever the subjects could perform 3x10 reps with a given weight) 

Figure 2: Comparison of the relative changes in the periodization group (high frequency in the first two weeks of the menstrual / CC cycle) vs. control group (three workouts per week for 4 months | Wikström-Frisén. 2015).

SuppVersity Classic: Train Like a Woman: Common Misconceptions About Training & Eating for A Cover-Model Physique - An Interview With Sports Nutritionist & Strength Coach Orit Tsaitli | learn more

Bottom line: Before I try to put things into perspective, I should mention that the participants of the study who were recruited at local gyms, were not jut healthy, non-smokers and had regular menses, they were also experienced trainees. All of them had been doing leg presses and leg-curls for several months - in fact, on average for 3.5 years. Against that background, even non-statistical significant inter-group differences as they were observed between the periodization (5 per week, 1 per week) and the control group (3 per week) may be practically relevant, because they may help experienced trainees to break through plateaus.

With that being said, I personally think of this study as one study in a series of studies that will hopefully elucidate how women can adapt their training regimen to the repetitive changes in the hormonal milieu of their bodies.

If we are honest with ourselves, the fact that Wikström-Frisén's results come as a surprise to most of us is only further evidence of how wantonly exercise scientists and trainers, alike, have hitherto neglected the peculiarities of the female physiology and endocrinology | Comment on Facebook!

• Reis, E., U. Frick, and D. Schmidtbleicher. "Frequency variations of strength training sessions triggered by the phases of the menstrual cycle." International journal of sports medicine 16.8 (1995): 545-550.
• Wikström-Frisén, L., C. J. Boraxbekk, and K. Henriksson-Larsén. "Effects on power, strength and lean body mass of menstrual/oral contraceptive cycle based resistance training." The Journal of sports medicine and physical fitness (2015).

Deadlifts w/ bands as they were done in the Galpin study (original photo from Galpin's 2015 study | see below).

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• Deadlift with bands for power and speed - Galpin et al. (2015) investigated how using bands while deadlifting at different loads, namely 60 and 85% of one's individual 1RM, i.e. the maximal weight you can lift for exactly one perfect rep, would influence the power and velocity at which twelve trained men (age: 24.08 ± 2.35 years, height: 175.94 ± 5.38 cm, mass: 85.58 ± 12.49 kg) with deadlift 1 repetition maxima (1RM) of 188.64 ± 16.13 kg pulled the weight off the floor.
  
  The results of the study show that there were significant peak (yet not relative) power changes irrespective of whether only 15% of the total resistance (group B1) or 35% of the total resistance (group B1) came from the bands (vs. the actual weight).
  

  Figure 1: Relative changes in power and bar velocity (compared to training w/out bands = control); * denotes sign. difference to control, ** denotes significant difference to control and light bands (Galpin. 2015)

  The effect became even more pronounced and extended from peak to average power, when the subjects used the heavier (85% 1RM) weights. In this condition using bands lead to greater peak and relative power production and lowered the velocity significantly compared to the control condition in which the subjects lifted at the same total level of resistance, albeit without bands (all values in Figure 1 are relative differences).
  
  For trainees the data in Figure 1 could be highly relevant, because it indicates that heavy bands should be used, when "prescribing the deadlift for speed or power, but not maximal force" (Galpin. 2015). If that's not you, i.e. you're not training for speed and power, but e.g. for size, future long(er)-term studies will have to show whether using bands makes a difference with respect to this study training goal.
• Interval length, can you really pick whichever suits your best? Even though a recent study by Wesley Tucker et al. (2015) shows that the rate of perceived exertion, as well as the mean heart rate of 14 recreationally active and thus not exactly jacked males who participated in their latest study were identical on 4x4 and 16x1 high intensity interval protocols (i.e. 4 intervals à 4 minutes vs. 16 intervals a 1 minute | see Figure 2), seasoned SuppVersity readers will probably remember that previous studies showed highly relevant differences in the long(er) term effects which obviously cannot be measured in an acute phase study like the one at hand.
  

  Figure 2: Illustration of the two HIIT protocols, incl. warm-up and cool down on cycle ergometers. White boxes are intervals during which the subjects were supposed to exercise at 90% of their peak heart rate (during the 16x1 protocol this was not achieved by all study participants in the latter intervals, though | Tucker. 2015).

  To be more specific, previous studies on high intensity interval training suggested that athletes who want to increase their VO2 max benefit more from fewer longer intervals, while "Mr. and Mrs. Average" could be better off improving their body composition and metabolic rate with a higher number of short intervals (even as short as 15 seconds in the Tabata protocol). Against that background and in order to explain or contradict the previous findings, it may be worth to consider other study outcomes in Tucker et al. (2015). Study outcomes which did differ. The total energy expenditure, for example, was 19% higher during the 16x1 protocol (p < 0.001) which is in line with the previously referenced recommendation of short intervals for people who are trying to lose weight.
  

  Figure 3: VO2, heart rate, and energy expenditure during the two HIIT protocols (watch the units! I converted them to be able to put all data into the same graph | Tucker. 2015).

  The VO2 uptake, as well as the maximal heart rates, which could be of interest for endurance athletes, on the other hand, were higher in the 4x4 protocol - a finding that would likewise support the previously voiced recommendation that (endurance) athletes should torture themselves with long(er) intervals to trigger further adaptations in VO2max and heart rate at a given power output.
  
  Overall, the study at hand will thus not revolutionize your training, but if you haven't read the previous SuppVersity articles, you may still have gotten some new insights into how you may want to adapt your HIIT training in the future.
• Kettlebell or cycle ergometer? Which do you chose for your HIIT sessions? I've written about kettlebell swings as muscle builders before and I've also hinted at the possibility of using the "bells" for your HIIT workouts. Now, a recent study by Williams and Kraemer shows that

  "[kettlebell high intensity interval training aka] KB-HIIT may [even] be more attractive and sustainable than [sprint interval cycling aka] SIC and can be effective in stimulating cardiorespiratory and metabolic responses that could improve health and aerobic performance" (Williams. 2015).

  The purpose of the study was - you probably already guessed it - to determine the effectiveness of a novel exercise protocol we developed for kettlebell high-intensity interval training (KB-HIIT) in comparison to the classic, standard sprint interval cycling (SIC) exercise protocol most people associate with equipment-based HIIT sessions. To this ends, the researchers from the Southeastern Louisiana University had eight "very active" young men (mean age 21.5 years; body fat 18.52 +/-3.04%, fat free mass 67.44 kg of a total weight of 82.95 kg) complete two 12-minute sessions of KB-HIIT and SIC in a counterbalanced fashion.

  Figure 4: Overview of the KB-HIIT workout (my illustration).

  "In the KB-HITT session [exercises see Figure 4, mean weight depending on exercise and subject 10-22 kg], 3 circuits of 4 exercises were performed using a Tabata regimen.

  
  

  In the SIC session, three 30-second sprints were performed, with 4 minutes of recovery in between the first 2 sprints and 2.5 minutes of recovery after the last sprint" (Williams. 2015)

  The study's within-subjects' design over multiple time points allowed Williams and Kraemer to compare the oxygen consumption, the respiratory exchange ratio (RER, a marker of the ratio of fat to carbohydrates that is used as fuel during the workout), the tidal volume (TV, the volume of air that is inspired or expired in a single breath during regular breathing), the breathing frequency (f), the subject's minute ventilation (VE), caloric expenditure rate (kcal/min), and their heart rate (HR) on an individual basis between the exercise protocols. In conjunction with the total caloric expenditure which was likewise measured / calculated and compared. The total amount of data the authors collected was thus quite large.
  

  Figure 5: Mean total energy expenditure in kcal during the KB and SIC sessions (Williams. 2015)

  Significant inter-group differences were found for VO2, RER, TV and total energy expenditure, with VO2 and total energy expenditure being higher and TV and RER being lower in the KB-HIIT compared with the cycle ergometer HIIT protocol. For f, VE, the energy expenditure per minute and the heart rate, there were no general inter-group differences, but "only" significant group × time interactions. Practically speaking, this means that they changed differently over the course of the whole protocol and are thus maybe relevant for certain athletes, yet not for the general public.
  
  Overall, the William's and Kraemer's study does therefore support the notion that doing kettlebell HIIT workouts is probably at least on par with the classic cycling HIIT sessions. In view of the increased total caloric expenditure and the lower RER, which signifies a significantly higher fat oxidation during the workout, it is even possible that KB-HIIT would be the better choice for dieters than doing HIIT on a cycle ergometer. Since there is no direct link between fat oxidation and/or energy expenditure during workouts and fat loss, however, long(er)-term studies are necessary to find out whether doing KB-HIIT is in fact more than a equivalent and for many of you maybe funnier alternative to doing HIIT on a cycle ergometer. 

Block Periodization - Training revolution or simple trick? This is what we have to ask ourselves in view of the results of a previously discussed study from 2014 | Read the full SV-Classic article here!

Bottom line: That's it for today; so I suggest you take what you learned, pack it in your gymbag and go and impress your bros at the gym ;-) I am just kiddin'... actually I hope that you can really use some of the information in today's installment of the SuppVersity Short News to make your workouts more productive, more enjoyable and/or simply more versatile.

Personally, I will probably give the KB-HIIT workout a try,... and that even though I expect it to be much harder than cycling which is something I am already used to. But hey, isn't that what training is all about? You have to challenge your body - even if that means conquering your weaker self.

I mean, we all know that as soon as you are staying within the cozy comfort zone of doing the same exercises with the same weights workout after workout your progress will stall; and unless you are one of those people who hit the gym to be able to talk to their athletic friends, that's certainly nothing you should aim for | Comment on Facebook!

Resting long enough to maximize your training volume could be the key to success, i.e. strength and size gains.

It would be interesting to see if rest periods should also be periodized!

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Figure 1: Previous studies found "conflicting" evidence. While Ahtiainen et al. found no effects of 2 vs. 5 minutes in trained, Buresh et al. found effects of 2 vs. 1 minutes rest in untrained subjects. With different subjects, different workouts and most importantly different rest times that were compared it is yet not exactly right to say that the studies contradict each other.

"[c]onsistent with generally accepted guidelines on the topic (Willardson. 2006), we hypothesized that short rest intervals would produce greater increases in muscle growth and local muscle endurance while long rest intervals would result in superior strength increases" (Schoenfeld. 2015).

Figure 2: Changes in markers of strength and strength endurance; * denotes significant pre- vs. post difference, # denotes significant inter-group difference (here in favor of long(er) rest periods | Schoenfeld. 2015).

• three leg exercises, i.e. barbell back squats, plate-loaded leg presses, and plate-loaded leg extensions), 
• two exercises for the anterior torso muscles, i.e. flat barbell presses and seated barbell military presses, and 
• two exercises for the posterior torso muscles, i.e. wide-grip plate-loaded lateral pulldowns, and plate-loaded seated cable rows

Figure 3: Changes in muscle thickness and corresponding effect sizes; * denotes significant pre- vs. post-changes, # denotes significant inter-group differences; overall it is obvious that there's a long(er) rest advantage (Schoenfeld. 2015).

So what's the verdict, then? At first sight it would appear as if the study at hand would totally refute the idea that shorter rest intervals, or I should clarify, rest intervals that are as short as 60s (*) should have a place in your training regimen altogether (*Schoenfeld, et al. rightly point out that Ahtiainen's result suggest that even 120s could have been enough time to rest - it is thus important to give precise recommendations for rest intervals, not something as arbitrary "short" vs. "long"). We should not forget, though, that even a thoroughly conducted study like the one at hand has its limits and definite conclusions should not be drawn hastily based on a single study result - even if it is, as in this case, corroborated by the results of Buresh et al (2009).

Figure 4: The total training volume in the long(er) rest period group (3 vs. 1 minutes of rest) was on average 15% higher. Due to the relatively high inter-individual differences and the relatively low number of participants (N=21) a statistically significant correlation between the weight lifted per week (total volume in kg as in the figure) and the surprisingly superior gains in the 3-min-rest group could not be established (based on Schoenfeld. 2015).

With that being said, a secondary outcome of the study provides a reasonable explanation for why both, the strength and the size gains benefited from long(er) rest intervals: The total training volume I've plotted in Figure 4. As Schoenfeld et al. point out, the latter has previously been suspected to mediate the effects of inter-set rest on strength and hypertrophy on total training volume and strength (Henselmans. 2014). A correlation between the visible differences in training load (see Figure 4) and the magnitude of training adaptations, however, could not be found in the study at hand. As the authors highlight, the reason for this lack of statistical significant correlations may yet be a simple lack of statistical power, so that one "cannot rule out the possibility that the greater training load achieved by the longer rest period group was responsible for the greater training adaptations" (Schoenfeld. 2015 | Buresh et al. found such an effect for the upper, yet not for the lower body).

Personally, I tend to believe that, with a higher number of subjects, a correlation between the total training volume that was on average 15% higher in the 3 vs. 1 minute rest group could have been established. This, in turn, would support the notion that long(er) rest periods - maybe, as Schoenfeld et al. suggest based on the data from Ahtiainen's study, at least 120s - are necessary to maximize the total training volume and thus the overall = strength and hypertrophy response to workouts. Whether that is true for all types of workouts (e.g. split- vs. full-body), all subject groups (e.g. people who are used to short rest periods vs. those who are not) as well as special athletic requirements (e.g. power vs. strength & hypertrophy) will have to be determined in future studies, however | Comment on Facebook!

• Ahtiainen, Juha P., et al. "Short vs. long rest period between the sets in hypertrophic resistance training: influence on muscle strength, size, and hormonal adaptations in trained men." The Journal of Strength & Conditioning Research 19.3 (2005): 572-582.
• Buresh, Robert, Kris Berg, and Jeffrey French. "The effect of resistive exercise rest interval on hormonal response, strength, and hypertrophy with training." The Journal of Strength & Conditioning Research 23.1 (2009): 62-71.
• Henselmans, Menno, and Brad J. Schoenfeld. "The Effect of Inter-Set Rest Intervals on Resistance Exercise-Induced Muscle Hypertrophy." Sports Medicine 44.12 (2014): 1635-1643.
• Schoenfeld, Brad J. "The mechanisms of muscle hypertrophy and their application to resistance training." The Journal of Strength & Conditioning Research 24.10 (2010): 2857-2872.
• Schoenfeld, et al. "Longer inter-set rest periods enhance muscle strength and hypertrophy in resistance trained men." Journal of Strength and Conditioning Research (2015): Publish Ahead of Print.
• Villanueva, Matthew G., Christianne Joy Lane, and E. Todd Schroeder. "Short rest interval lengths between sets optimally enhance body composition and performance with 8 weeks of strength resistance training in older men." European journal of applied physiology (2014): 1-14.
• Willardson, Jeffrey M. "A brief review: factors affecting the length of the rest interval between resistance exercise sets." The Journal of Strength & Conditioning Research 20.4 (2006): 978-984.

Ashwaghanda may be for gymrats, too.

Read more about exercise-related studies at the SuppVersity

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Table 1: Mean percentage (%) difference of pre-post readings of forty male and female elite (elite here refers to the participation of the athlete in at least state-level events) Indian cyclists in response to 8 weeks on 500 mg of standardized aqueous root extract, which was obtained in the form of capsules from Dabur India Limited (Sandhu. 2012).

"prospective, double-blind, placebo-controlled parallel group study to measure the possible effects of ashwagandha extract on muscle strength/size, muscle recovery, testosterone level and body fat percentage" (Wankhede. 2015)

Figure 1: Overview of the study design as it is visualized in Wankhede et al. (2015)

"The resistance training program consisted of sets of exercises over major muscle groups in both the upper body and the lower body. [...] Each subject in both groups was asked to come to a training session every other day, with one rest day pe week, for three days per week. Every session began with a warm up consisting of five minutes of low-intensity aerobic exercise. The subjects were instructed to perform, for each set as many repetitions as they could until failure. The subjects were asked to go through the full range of motion and were demonstrated the proper technique for safe and effective weight lifting" (Wankhede. 2015).

Figure 2: Absolute increases in thigh, arm and chest size and reduction in body fat (%) over the course of the 8-week study; the figures above the bars denote the inter-group difference in %, * denotes significant differences (Wankhede. 2015).

Figure 3: Changes in 1RM (kg) strength and testosterone (ng/dL) over the course of the 8-week study; the figures above the bars denote the inter-group difference in %, * denotes significant differences (Wankhede. 2015).

"[...] the following limitations which should lead us to interpret the findings with some caution: the subjects are untrained and moderately young, the sample size of 50 is not large and the study period is of duration only 8 weeks" (Wankhede. 2015)

Sometimes lab values are deceiving - specifically if allegedly pathological elevations of kidney, liver and (heart) muscle enzymes (CK) are nothing but a perfectly physiological reaction to exercise | learn more!

So, what's the verdict, then? Yes, this is definitely the most exciting 'Ashwaghanda study', I've seen so far. Next to the limitations Wankhede et al. already discuss in the conclusion of their recently published paper in the Journal of the International Society of Sports Nutrition one should not forget, though, that the methods they chose to determine the body composition and state of recovery of their subjects were appropriate, but not optimal. While the former would have been more reliable if they had used a DXA scan, the latter would actually have to be tested via several post-workout strength tests and auxiliary tests and questionnaires as it was done, for example, by Kraemer et al. (2010).

Enough of the complaints, though. Let's be greatful we even have a study investigating the effects of Ashwagandha on resistance training. Plus, the increases in strength, muscle size (which would be similarly thwarted by cell swelling in both groups when it was tested 'only' two days after the last workout) and testosterone, alone, warrant the authors' already carefully worded conclusion that "ashwagandha supplementation may be useful in conjunction with a resistance training program" (Wankhede. 2015) - even if the underlying mechanism is still unknown and the hypotheses the authors list in the discussion, i.e. (a) increase in testosterone (too low to have significant effects | learn why), (b) decrease in the levels of cortisol (not measured + acute cortisol elevations are associated w/ lean mass gains in strength training individuals | West. 2012), (c) beneficial effects on mitochondrial health and reduced ATP breakdown (observed only in rodents that were exposed to toxins vs. exercise), and (d) antianxiety effects and promotion of focus and concentration that "may translate to better coordination and recruitment of muscles" (Wankhede. 2015), are as the word "hypothesis" implies only hypothetical, i.e. conjectural | Comment on Facebook!

• Choudhary, Bakhtiar, A. Shetty, and Deepak G. Langade. "Efficacy of Ashwagandha (Withania somnifera [L.] Dunal) in improving cardiorespiratory endurance in healthy athletic adults." AYU (An international quarterly journal of research in Ayurveda) 36.1 (2015): 63.
• Kyle, Ursula G., et al. "Bioelectrical impedance analysis—part II: utilization in clinical practice." Clinical nutrition 23.6 (2004): 1430-1453.
• Patel, Dhaval, Harisha C. Rudrappa, and Proshanta Majumder. "A comparative pharmacognostical, physicochemical, and heavy metal analysis on Ashwagandha root obtained from natural and polluted sources." International Journal of Green Pharmacy 9.1 (2015): 14.
• Raut, Ashwinikumar A., et al. "Exploratory study to evaluate tolerability, safety, and activity of Ashwagandha (Withania Somnifera) in healthy volunteers." Journal of Ayurveda and Integrative Medicine 3.3 (2012): 111.
• Sandhu, Jaspal Singh, et al. "Effects of Withania somnifera (Ashwagandha) and Terminalia arjuna (Arjuna) on physical performance and cardiorespiratory endurance in healthy young adults." International journal of Ayurveda research 1.3 (2010): 144.
• Shenoy, Shweta, et al. "Effects of eight-week supplementation of Ashwagandha on cardiorespiratory endurance in elite Indian cyclists." Journal of Ayurveda and integrative medicine 3.4 (2012): 209.
• Wankhede, Sachin, et al. "Examining the effect of Withania somnifera supplementation on muscle strength and recovery: a randomized controlled trial." Journal of the International Society of Sports Nutrition 12.1 (2015): 43.
• 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.

Even though, the study at hand confirms that NaHCO3 doesn't work for everyone previous studies show it's worth trying.

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

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• 0.3 g/kg body mass of sodium bicarbonate (SB | 4 trials) or
• alcium carbonate placebo (PL, 2 trials).

Figure 1: Line graphs for blood measurements (mean ± 1SD) at Baseline, Pre-exercise, Post-exercise and 5-min post-exercise. Panel A displays pH; Panel B displays bicarbonate; Panel C displays base excess; Panel D displays lactate. PL trials are represented by dashed lines and SB trials are represented by solid lines (de Araujo Dias. 2015).

Learn more about Serial Loading!

You have problem "stomaching" NaHCO3? If you feelm, like some of the subjects in the study nauseated or even get diarrhea when you ingest a large bolus of sodium bicarbonate at once, try the Serial Loading Protocol from Dreher's 2012 study I discussed in an older SuppVersity article about sodium bicarbonate. That should work even for the most sensitive tummies. That's still no guarantee that it'll work, though, and would - just as the study at hand shows it for the regular bolus administration require some experimentation.

Figure 2: Rel increase (%) in total work (figures over the bars indicate likelihood of relevant benefits and relative increase, e.g. for bar 4: "It's 93% likely that the 7% increase displays a real-world relevant performance increase) - left; Total work done during SB trial as function of total work done during PLA trial - right (de Araujo Dias. 201).

25g of Baking Soda Will Up Your Squat (+27%) & Bench Press (+6%) Within 60 Min | more

Bottom line: If you belong to the unlucky 33%, who were represented in the study at hand by the 5 subjects the scientists found who didn't benefit in any of the four sodium bicarbonate trials, you could probably still try the serial loading protocol and if that doesn't work either, simply accept that "SB may not always improve exercise" (de Araujo Dias. 2015).

On the flipside, though, you must not give up on baking soda if you didn't see improvements in your first trial, either. Eventually, the data from the study at hand also shows that even in those who benefit the benefit can sometimes be small or even non-existent.

As a trainer or trainee, you should thus keep in mind that sodium bicarbonate, baking soda or NaHCO3 must be taken on multiple occasions in order to categorize yourself or your clients into non-responders and potential responders and excellent responders | Comment on Facebook!

From a health perspective it may be good that green tea does not contain all-too much caffeine. From a fat loss perspective, it clearly lacks caffeine.

You can learn more about coffee at the SuppVersity

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Figure 1: Energy expenditure (kcal/h) and fat oxidation (g/day) measure before (at rest) and during (during SIE) the sprint interval exercise 10 and 55 minutes after the ingestion of caffeine + GTE or placebo (Jo. 2015).

"Sprint-Interval Exercise Protocol. The SIE protocol was performed on the Velotron DynaFit Pro cycle ergometer and comprised of four 30-second maximal effort intervals each separated by 5 minutes of low-intensity, constant workload cycling (Figure 2). First, the ergometer was properly adjusted for the subject. Adjustment specifications for each subject was recorded during their familiarization visit and repeated for all experimental trials. Subjects initiated the SIE protocol with a 5-minute interval of low-intensity cycling at a constant workload of 75W. Immediately after, subjects cycled with maximal effort for 30 seconds against an added resistance that is 7.5% of BW for males and 7.2% for females. These two intervals were repeated three additional times. After the last 30-second sprint interval, the subjects performed an additional low-intensity 75W interval plus an extra 3 minutes of cool-down at a constant workload of 30W. The total duration of the SIE protocol was 30 minutes" (Jo. 2015).

Figure 2: Illustration of the sprint interval exercise test performed 55 min after ingesting the supplement (Jo. 2015).

Did you know this SuppVersity Calssic? "Post-Workout Coffee Boosts Glycogen Repletion by Up to 30% and May Even Have Sign. Glucose Partitioning Effects | learn more!

Bottom line: I admit, they certainly sound less exciting as the latest exotic herb from the rain-forest or a substance that is listed only under its funky chemical name on the label, but unlike your average "innovative breakthrough metabolic activator" caffeine and green tea will deliver. The 10% increase in metabolic rate and the accompanying increase in fat oxidation won't make you lose slabs of body fat, but the effects are pronounced enough to expect a measurable effect on the success of your next diet / cut. A cut, by the way, that will still require a significant reduction in energy intake, even if your energy expenditure and fat oxidation. So, don't be a fool and confuse a 10% increase in fat oxidation w/ a 10% increase in fat loss that occurs in the absence of dieting on an ad-libitum diet | Comment!

• Jo et al. "Dietary Caffeine And Polyphenol Supplementation Enhances Overall Metabolic Rate And Lipid Oxidation At Rest And After A Bout Of Sprint Interval Exercise." Journal of Strength & Conditioning Research: Post Acceptance: November 23, 2015. doi: 10.1519/JSC.0000000000001277

Hershey's 100% Cacao, soon also available at your local GNC? If you look at the results of the study at hand, it does appear likely that a regular "food item" can compete with sign. more expensive sport supplements.

You can learn more about chocolate and cacao at the SuppVersity

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Table 1: Nutritional profile of the cocoa "supplement", Hershey's 100% cacao powder (González-Garrido. 2015).

Figure 1: Rel. changes (%) of markers of lipid and protein per-oxidation and anti-oxidant defenses (González-Garrido. 2015).

So what? Now the obvious question is: "Couldn't this impair the adaptation to exercise?" This question cannot be answered based on an acute response study, but with the acute increases in exercise performance (Cooper test, see Figure 2) and in spite of the significant reductions in CK and LDH (see Figure 2), which are usually interpreted as markers of muscle damage, this appears generally unlikely - yet not impossible.

Figure 2: Copper test (test of physical fitness | more) performance and creatine kinase (CK | more) and lactate dehydro- genase (LDH) levels after the 12-minute Cooper test before and after 7-days of supplementing with ~21g/d of 100% cacao powder (González-Garrido. 2015).

On the other hand, it is important to note that only the increased Cooper test performance (Figure 2), but none of the other markers has at least a non-significant predictive value with respect to the possible long-term effects on exercise performance - an effect that will have to be tested in future longer-term studies. A conclusion that would go beyond the scientists' statement that they "have shown the potential that cocoa consumption has on endurance performance and its role in recovery from muscle damage in athletes" (González-Garrido. 2015) would thus be unwarranted... as unwarranted as any speculations about the underlying mechanisms: yes, it is likely that the high polyphenol content of 100% cacao is what does the trick, but to prove that we'd need a low polyphenol chocolate control we don't have. If you want to benefit, though, I highly suggest to pick a 100% cacao powder with a low degree of processing | Comment!

• Berry, Narelle M., et al. "Impact of cocoa flavanol consumption on blood pressure responsiveness to exercise." British Journal of Nutrition 103.10 (2010): 1480-1484.
• Davison, Glen, et al. "The effect of acute pre-exercise dark chocolate consumption on plasma antioxidant status, oxidative stress and immunoendocrine responses to prolonged exercise." European journal of nutrition 51.1 (2012): 69-79.
• González-Garrido, et al. "An association of cocoa consumption with improved physical fitness and decreased muscle damage and oxidative stress in athletes." The Journal of Sports Medicine and Physical Fitness (2015): Epub ahead of pring Dec 02, 2015.

Low carb, or fat? Left or right?  Which one should you chose and why? Shall you go by your body weight, your insulin sensitivity or your personal food preferences?

You can learn more about improving your body composition at the SuppVersity

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Figure 1: Weight loss (kg) after 6 months on the respective in insulin resistant and sensitive subjects (Gardner. 2015).

Figure 2: Proportions of carbohydrates, fats, and proteins for each diet at baseline, 3 months, and 6 months (Gardner. 2015).

Figure 3: Fiber, added sugar and saturated fat intake in g/1000kcal (Gardner. 2015).

Figure 4: Changes in LDL-C, HDL-C, Trigs and fasting glucose after 3 & 6 months (Gardner. 2015).

Figure 5: Changes in the prevalence of metabolic syndrome after 3 and 6 months (Gardner. 2015).

Bottom Line: So, it doesn't matter how you diet as long as you diet? Well, as previously pointed out, the absolute weight-loss values in Figure 1 appear to confirm the hypothesis that "low carb" is for the sick, while "low fat" for the healthy overweight individuals.

The significant intra-group differences, however, tell us that whether you are or aren't insulin resistant is not the only determinant of your response to the different diets. Especially for healthy individuals experimentation and finding what suits you, your lifestyle and sports best does therefore still appear to be the way to go.

In those with pre-existing metabolic syndrome (which is more than just insulin resistance, by the way), the generally higher relative reduction in MetSyn prevalence Gardner et al. observed in their study (Figure 5) do yet appear to confirm the general trend towards low-carbohydrate diets for people with serious metabolic issue; and maybe that's actually the main take-home message of a study that must be seen as a first attempt to identify one of the variables that determine whether an individual thrives on a low carb, a low fat or maybe just a completely balanced diet | Comment!

• Gardner, et al. "Weight Loss on Low-Fat vs. Low-Carbohydrate Diets by Insulin Resistance Status Among Overweight Adults and Adults with Obesity: A Randomized Pilot Trial" Obesity (2015): Ahead of print.
• Mansoor, et al. "Effects of low-carbohydrate diets v. low-fat diets on body weight and cardiovascular risk factors: a meta-analysis of randomised controlled trials." British Journal of Nutrition (2015): First view article.

The results of a Wingate test cannot be translated 1:1 to any sports.

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

Bicarbonate Works for Most(!) Athletes

Figure 1: Subject allocation.

Yes, the washout period could be a problem: With only nine participants you have to do crossover study, but in view of the results of previous studies (McKenna. 1999), which report washout times of 4 weeks, the scientists would have been on the safer side if they had planned for a washout of 28, not just 7 days. Now you may argue that not all subjects started "on" creatine, so that the residual effect could average out. The problem, however, is that the significance of the results of a study with only nine participants gets impaired with every subject who was in a creatine group before being randomly assigned to one of the placebo + X groups, so that the researchers would have had to order all the creatine conditions last, not one first and the other last, as it is depicted in Figure 1 and described in the full text of the study.

• In general, the coingestion provided "small meaningful improvements on indices of mechanical power output (W)" (Griffen. 2015) 
• The previously mentioned advantage was yet only seen when comparing sodium bicarbonate (ES = 0.28–0.41) with the combination treatment; a similar beneficial effect was not seen compared to creatine alone

This does obviously mean that the addition of bicarbonate to creatine did not result in meaningful increases in power output in this particular exercise test.

Figure 2: The only relevant advantage of combining both creatine and bicarbonate was seen for the total work done (orange bars, see orange arrow); this however is also among the most relevant measures for real athletes (Griffin. 2015).

What it did do and that's what we actually take bicarbonate for is to "provided a small meaningful improvement in total work (J; ES = 0.24) compared with creatine" (Griffin. 2015) - or, in other words, anyone who does not just one, but several all-out sprints (and that's almost every athlete) will see a small but meaningful performance increase, one that may make the difference between victory and defeat (see Figure 1, orange bars).

The increase in PGC-1a expression you get if you do HIIT w/ sodium bicarbonate and the correspondingly increased stimulus for mitochondrial biogenenesis is a hitherto often overlooked benefit of "baking soda" supplementation | learn more

Disappointing? I would not say so, which significant improvements in response to both supplements and a potential "game changing" increase in the total work the subjects were able to perform on the cycle ergometer during the repeated Wingate tests, both supplements have proven their efficacy and the potential benefits of combining them. Benefits the Griffin et al rightly call "small", but "meaningful" in the conclusion to their recently published paper.

The fact that these benefits may not be as exorbitant as some of you may have hoped for does not imply that the combination of creatine and bicarbonate supplements is useless. In view of the overall small study size (low number of subjects even for a crossover study), the problem with the washout and the specificity of the exercise - who knows what the results in the gym or on a football field would have looked like, thus, future studies are warranted | Comment!

• Barber, James J., et al. "Effects of combined creatine and sodium bicarbonate supplementation on repeated sprint performance in trained men." The Journal of Strength & Conditioning Research 27.1 (2013): 252-258.
• Griffen, C., et al. "Effects of Creatine and Sodium Bicarbonate Co-Ingestion on Multiple Indices of Mechanical Power Output During Repeated Wingate Tests in Trained Men." International Journal of Sport Nutrition and Exercise Metabolism, 2015, 25, 298-306.
• McKenna, Michael J., et al. "Creatine supplementation increases muscle total creatine but not maximal intermittent exercise performance." Journal of Applied Physiology 87.6 (1999): 2244-2252.