Creatine Uptake, Bioavailability, and Efficacy - We've Gotten it all Wrong and Low Serum Creatine Levels are Better!?

Creatine Uptake, Bioavailability, and Efficacy - We've Gotten it all Wrong and Low Serum Creatine Levels are Better!?

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If you put some faith into the marketing campaigns of supp producers, there's a creatine for everyone: one to get lean, one to get strong and one to get big and buffed... bullocks!

It has been a while since I've discussed the bioavailability of different forms of creatine. On various supplement sites, the notion that there was one form of creatine that was significantly more bioavailable and would thus allow you to 'load' muscle phosphocreatine (PCr) faster and more efficiently is obviously still a matter of constant debate... a debate of which the latest study by Ralf Jäger et al. (2016) indicates that it may argue based on a fundamentally flawed premise, i.e. that higher serum levels of creatine after the ingestion of a given product would signify an increased efficacy in terms of performance / strength / size gains.

How come? Well, the previously mentioned, as of yet unpublished data from a study by Ralf Jäger, Martin Purpura, and Roger C Harris did not just confirm the results of previous studies, which indicate that glucose (75g) and alpha lipoic acid (ALA | 200mg) will increase the bioavailability of creatine, i.e. "the proportion of a drug or other substance [in this case creatine] that enters the circulation when introduced into the body" (Merriam-Webster.com), it also indicates that the practically relevant predictor of creatine's efficacy is - assuming equal dosing and complete absorption - not a high, but rather a low level of creatine in the blood.

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What? Let me explain: Initially, it may be worth pointing out that we are talking about a small scale study the results of which have not yet been published in the peer-reviewed journal. In that study, Jäger et al. aimed to compare the effects of ingesting tricreatine citrate (5g, TCrC),

• in combination with 75g of glucose and 200mg of alpha-lipoic acid, or
• without the former bioavailability enhancers.

on only six subjects. These three men and three women (35.5+/-14.5 yrs, 172.5+/-12.2 cm, 75.3+/-9.0 kg), who were all healthy, normal-weight and non-vegetarian and thus not, with creatine being a deficiency nutrient in vegetarians, extraordinarily susceptible to creatine supplementation (Burke. 2003), participated in two testing sessions during which they received the previously explained two treatments (the powdered supplements were simply dissolved in 450 ml of water).

Adding carbohydrates or cinnamon to creatine may well increase its uptake to the muscle. What it does not do, however, is to enhance creatine's efficacy - at least not in a 2015 3-week creatine loading study Islam et al. conducted in 25 recreational gymrats.

What's the increased absorption worth? If we rely on a a recent study by Islam, et al. (2015) the answer is (unfortunately) nothing. In their 2015 study, the scientists from the Wilfrid Laurier University and the University of Lethbridge in Canada found no (=zero) significant differences in anaerobic power, strength, and endurance when creatine was administered solo, with the same 70 g carbohydrate (CHO) that were used in Jäger et al. (2016), or 500 mg cinnamon extract (CIN), of which the authors believed that its proven ability to improve insulin sensitivity and up-regulate glucose transport in skeletal muscle would likewise enhance the uptake of creatine in the muscle and thus make it more effective.

With their cross-over after the initial test and a 7 day break between the tests, the scientists would have been able to compare the effect of adding glucose and alpha lipoic acid to the tricreatine citrate (Creapure™ Citrate, AlzChem, Trostberg, Germany | 65% w/w creatine) on an individual level. Corresponding data, however, is not (yet?) available. Instead, we get the likewise interesting statistical averages (see Figure 1):

Figure 1: Mean plasma creatine concentration over 8 hours following ingestion of 5g tricreatine citrate (TCrC) and 5g tricreatine citrate + 75g glucose + 200mg alpha-lipoic acid (TCrC+Glu+ALA | Jäger. 2016).

And these data present a quite intriguing result. More specifically, they indicate that the increase in peak concentration and the area under the curve (indicative of the total amount of creatine that appeared in the blood of the subjects) were significantly lower in the TCrC+Glu+ALA group in comparison to TCrC (75.3%, p<0.05, and 82.2% respectively).

Less creatine in the blood with sugar + ALA? That's bad, right? No that's good!

Just as the likewise lower 0.5 and 1h plasma concentrations of creatine, in the TCrC+Glu+ALA group (in comparison to TCrC), these reductions do not indicate a reduced efficacy of the supplement. On the contrary! The significantly elevated mean 8h urinary creatine elimination in the control group (TCrC | 26.5 ± 13.9% of the dose administered  vs. 17.2 ± 13.0% for TCrC+Glu+Ala) rather indicates that the addition of glucose and ALA "enhanced rate of creatine uptake into the muscle" - as previous studies indicate probably due to the presence of raised insulin (by glucose) and / or an increased insulin sensitivity (by ALA / Koszalka. 1972; Steenge. 1998; Pittas. 2010).

Figure 2: The study on creatine + glucose and creatine + cinammon by Islam et al. (red box) is not the only one that shows that the increased deposition of creatine in the muscle doesn't give you athletic advantages. The exact same results have been observed in an 8-week study comparing 70 g of a dextrose placebo (PL), 5 g creatine/70 g of dextrose (CRD) or 3.5 g creatine/900 mg fenugreek extract (CRF) by Taylor et al. (2011)

Why's this study relevant? Well, the answer should be obvious. The few allegedly 'advanced creatine products' on the market that actually have scientific back-up of their efficacy often refer to studies showing increases in plasma creatine of which the study at hand shows that they are no valid predictor of the actual efficacy of the supplement. The latter obviously depends on muscle creatine uptake, not serum peak levels or AUC. Don't be a fool, though: This does not mean that lower serum levels after ingestion were automatically better. After all, those lower levels of creatine in the blood may well be a mere result of an impaired / incomplete absorption in the gut.

Confusing? Well, let's summarize: By measuring the creatine level in the blood and the excretion of creatine in urine, Jäger et al. were able to refute the (ostensibly) logical assumption that higher serum creatine levels would indicate an improved efficacy. What they did not prove conclusively, however, is that the creatine levels in the muscle were in fact significantly higher (no biopsies) and, most importantly, that this makes a performance difference. The latter has after all been refuted in previous studies, such as Islam et al. (2015 | see red box and Figure 2). The hunt for the "best form" of creatine will thus probably go on, albeit with different experimental means, i.e. either the measurement of serum and urinary creatine as it was done in the study at hand or (even better) the direct assessment of muscle creatine stores and the actual performance benefits | Comment!

References:

• Burke, Darren G., et al. "Effect of creatine and weight training on muscle creatine and performance in vegetarians." Medicine and science in sports and exercise 35.11 (2003): 1946-1955.
• Jäger, Ralf, Martin Purpura and Roger C Harris. "Reduction of Plasma Creatine Concentrations as an Indicator of Improved Bioavailability." Upublished data from privatt conversation (2016).
• Koszalka, Thomas R., and Carole L. Andrew. "Effect of insulin on the uptake of creatine-1-14C by skeletal muscle in normal and X-irradiated rats." Experimental Biology and Medicine 139.4 (1972): 1265-1271.
• Pittas, G., et al. "Optimization of insulin-mediated creatine retention during creatine feeding in humans." Journal of sports sciences 28.1 (2010): 67-74.
• Steenge, G. R., et al. "Stimulatory effect of insulin on creatine accumulation in human skeletal muscle." American Journal of Physiology-Endocrinology And Metabolism 275.6 (1998): E974-E979.
• Taylor, Lem, et al. "Effects of combined creatine plus fenugreek extract vs. creatine plus carbohydrate supplementation on resistance training adaptations." Journal of sports science & medicine 10.2 (2011): 254.

Nigella Sativa Quadruples Fat Loss Success: 8% vs. 2% Rel. Body Fat Reduction in 8 Weeks With NS Before Every Meal

Nigella Sativa Quadruples Fat Loss Success: 8% vs. 2% Rel. Body Fat Reduction in 8 Weeks With NS Before Every Meal

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Nigella sativa is not well known in the West.

You may remember the SuppVersity special on Nigella sativa from January 2015. A special, in which beneficial metabolic effects of nigella sativa aka black cumin were only one item on a long list of health benefits, of which many had unfortunately been observe in rodent studies.

With a recent study from the Tabriz University of Medical Sciences, there's now evidence for humans that the fat loss benefits of the oil from nigella sativa are real - at least when it is ingested before meals by dieting overweight individuals.

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We are talking about a double-blind, placebo-controlled, randomized, clinical trial, with 50 obese women. The participants were randomly divided into an NS oil group (n=25) and a placebo
group (n=25). All subjects received the same standardized diet, the scientists describe as follows:

"All the participants received a moderate fat, nutrient-balanced reduction diet. A dietician designed an individual diet by using the Mifflin equation to determine resting energy expenditure (Namazi et al., 2015). After adding the estimated physical activity coefficient (based on International physical activity questionnaire) and thermic effect of food coefficient (1.1), 500 kcal from the amount of total required daily energy calculated for each subject was subtracted. The resulting diet was composed of 15% protein, 55% carbohydrates, and 30% fat. A 24-hour dietary recall (one weekend day and two weekdays) was applied for assessing the level of patients’ compliance with the diet" (Mahdavi. 2016).

The diet was supplemented with either nigella sativa (NS) oil soft gel capsules (3g/day) with one capsule a 1g being taken 30 minutes before meals or a sunflower oil (SF) placebo capsules for eight weeks, total.

Does timing matter and what about the seeds? While it is difficult to tell, whether the effects would vanish if the oil was timed differently (i.e. not 30 minutes before meals), the mix of active ingredients, including thymoquinone (TQ), thymol, nigellone, nigellicine, alpha-hederin, unsaturated fatty acids, vitamins (B1, B3, B6, E) and minerals (Fe, Zn, Cu) may in fact have to be present in the digestive tract before / during a meal. It is similarly questionable, whether simply eating the seeds will have the same effect. If we assume that they don't "got through" (soaking, grinding or chewing them may help), they should. After all, the seeds contain the same (if not more) of the active ingredients as the oil - even if they are probably less concentrated.

To assess the success of the intervention, the scientists analyzed their subjects' BMI, and anthoprometric indices (body fat by bio-impedance), serum levels of insulin, adiponectin, peroxisome proliferator-activated receptor γ (PPAR-γ) and insulin sensitivity in obese women. Secondary outcomes were effects of NS oil supplementation with a low-calorie diet on liver enzymes and other health parameters. Dietary intake and physical activity were controlled.

Figure 1: Changes in body composition during the 8-week study in the treatment and placebo group (Mahdavi. 2016).

The first somewhat surprising result of the study is that all 50 participants completed the trial - an observation that suggests that both the diet and the consumption of the oil weren't difficult to adhere to. Accordingly, it is not surprising that all women lost a significant amount of boy weight. Especially in terms of body fat, however, the benefits differed according to treatment: While the NS oil group lost -3.6% of their total body fat mass (that's a relative reduction of ~8%), the control group lost only -0.8% (a relative reduction of ~2% | note: I used the values from the table in FT and not the questionable percentages the scientists provide in the abstract, which are even higher, but not in line with the recorded absolute changes in body fat).

These benefits went hand in hand with significantly more pronounced improvements in basal insulin levels, which were reduced by -29.3% in the treatment group and by only -8.6% in the placebo group. In conjunction with the +87.5% vs. 39.4% increase in adiponectin levels, and a significantly higher relative visceral fat loss, it is save to conclude that the addition of nigella sativa did also affect the subject's metabolic disease risk significantly.

Reader Question: Are Black Seeds (Nigella Sativa), Their Oil, Ointments & More Good For Me? What do the Studies Say?

Bottom line: Black cumin or Nigella sativa has been used in traditional oriental medicine as a weight loss aid for centuries. With the study at hand and similar studies in rodents, we are now finally able to confirm what has been "best practice" elsewhere forever.

With that being said, you cannot expect weight / fat loss miracles. No weight loss without dieting, no dieting without effort... taking black cumin oil as weight loss support may accelerate the progress, but eventually it's the energy reduced diet that had the women shed 8% of their superfluous body fat in 8 weeks, not the Nigella sativa oil | Agreed? If not, leave a comment on FB!

References:

• Mahdavi, Reza, et al. "Changes of body composition and circulating adipokines in response to Nigella sativa oil with a calorie restricted diet in obese women." Journal of Herbal Medicine (2016).
• Namazi, Nazli, et al. "Oxidative Stress Responses to Nigella sativa Oil Concurrent with a Low‐Calorie Diet in Obese Women: A Randomized, Double‐Blind Controlled Clinical Trial." Phytotherapy Research 29.11 (2015): 1722-1728.

Minimal Amounts of Fish Peptide Hydrolysate Double Fat Loss Compared to Whey Isolate on Energy Restricted Diet

Minimal Amounts of Fish Peptide Hydrolysate Double Fat Loss Compared to Whey Isolate on Energy Restricted Diet

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I certainly recommend eating fish. Whether I will be recommending fish hydrolysate supplements in the future, however, will have to be determined when additional studies with different baseline diets will have been published.

You may remember that I've written about fish protein hydrolysates / peptides before. Unlike today's article, however, previous articles dealt with the effects of fish protein in rodents. Intrigued by in vitro and animal studies showing that fish-derived peptides demonstrated antihypertensive (Hatanaka. 2009; Kim. 2012; Li. 2012; Ngo. 2011), antioxidant (Nazeer. 2012; Najafian. 2012), immunomodulating effects (Duarte. 2006), reparative properties in the intestine (Fitzgerald. 2005; Marchbank. 2008), and effects in reducing plasma cholesterol and triglycerides levels (Möller. 2008), a group of Italian researchers decided to investigated the effect of Slimpro(R), a supplement containing commercially available fish protein hydrolysate from blue whiting (Micromesistius poutassou), on body composition and on stimulating cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1) secretion in 120, overweight, non-obese (25 kg/m² < BMI < 30 kg/m²), male (25%) and female (75%) subjects aged 18 - 55 year.

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Unlike the product that was used may suggest, the study was not sponsored by the supplement company. The authors received neither funding nor other external support and they also declare that they don't have a conflict of interest that may be related to patents or direct involvements in the industry. I guess it's important to point that out, even though fact that the scientists chose whey, i.e. an actually relevant control, instead of carbohydrates or just plain water, may have given away the lack of sponsorship, anyways.

Two weeks before the study started, subjects were asked to fill in an alimentary diary reporting their food preferences. A mild hypocaloric ( 300 kcal/day) diet was elaborated for each subject by a dietitian based on subject’s food preferences and habits as reported in the alimentary diary.

Figure 1: The low protein content of the diet is - as highlighted in the annotations to this graphical illustration of the macronutrient composition of the test diets - problematic, to say the least.

Approximately, 55% of energy intake was from carbohydrates, 25% from lipids, and the remaining 20% from proteins. Part of these 20% of protein were either 1.4g and 2.8g of fish protein or 1.4g of whey protein isolate as a control (I just assume that the dosage was 1.4g, because there was only one whey group), which were consumed in form of a flavored shake according to the following protocol:

"Both the active (one dose treatment arm) and the placebo products were taken as follows: ‘dilute the content of one sachet in a large glass of cool water (200 ml). Shake or stir with a spoon. Consume within 10 30 min before the main meal’. In the case of two-dose treatment arm, one sachet of the active product was taken 30 min before lunch and one sachet 30 min before dinner" (Nobile. 2016).

To be able to tell what could be responsible for advantages or disadvantages of the two treatments, the scientists assessed more than just body weight, fat mass (DXA scans), and safety of use as well as the secondary efficacy endpoints, extracellular water, and the circumference of waist, hips, and thighs. They also checked the CCK and GLP-1 levels in their subjects' blood. This is relevant, because this is how the fish hydrolysate is advertised on the manufacturers website:

"Taken daily before meals, Slimpro® increases the production of CCK and GLP-1 in the body, thus amplifying messages associated with a decrease of food intake. Promising results were reported from in vivo et in vitro trials of these molecules that may control food intake. Scientists have described this ingredient as a direct action on the hunger process" (Nobile. 2015).

As it is usually the case in studies like this, some patients were "lost". In this case, we're talking about a total count of eleven subjects who did not reappear for the follow-up check (One subject in the one-dose treatment arm, four subjects in the twodose treatment arm, and six subjects in the placebo treatment arm discontinued intervention because they were no longer interested to participate in the study). The results of the other subjects are plotted in Figure 2:

Figure 2: Changes in body composition after 45 and 90 days of dieting w/ the specific supplements (Nobile. 2016).

As you can see, double-dosing had astonishingly little effect on the subjects' ability to lose body fat. That's in contrast to switching from fish protein hydrolysate to whey protein isolate, which produced measurably, but not statistically reduced rates of fat loss and waist reductions.

Figure 3: Blood biomarker levels. (a) CCK blood levels and (b) GLP-1 blood levels. Intragroup (vs. D0) statistical analysis is reported upon the bars of the histogram. The lines report the intergroup (vs. placebo) statistical analysis. Statistical analysis is reported as follows: *p < 0.05, **p < 0.01, and ***p < 0.001. Data are mean +/- SE (Nobile. 2016).

And guess what: Even though the bars don't look like it, the asterisks over the bars tell you that these differences may be caused by the same differential expression of the satiety hormones CCK and GLP-1 in the fish hydrolysate vs. whey protein group that has been observed with other control protein in previous studies and is boldly advertised on the producer's website.

Great! Let's eat more fish... It stands out of question that the former is actually a very good idea (assuming you make the right fish choices). I have to warn you, though: Firstly, the fish protein consumed in the study at hand came from fish, but just like whey protein and milk, fish and fish protein hydrolysates will also have different effects.

Is Wild Caught Fish Always the Better Choice? With Sign. More N3 and Less Pollutants?  Learn more!

What is probably way more important, however, is the relative protein deficiency of the subjects. With only 20% of the diet being protein, the study participants hovered around at the meager level of the RDA. Since the effects of 1.4g of fish protein hydrolysate you throw on top of a low protein diet are probably very different from those of the same amount of fish protein consumed alongside 2g/kg of dietary and supplemental protein, I wouldn't guarantee and in fact even doubt that you would see a similar almost 100% increase in fat loss while dieting - and still,  the CCK and GLP-1 boosting effects of fish protein hydrolysates are intriguing | Comment on Facebook!

References:

• Duarte, Jairo, et al. "Immunomodulating capacity of commercial fish protein hydrolysate for diet supplementation." Immunobiology 211.5 (2006): 341-350.
• Hatanaka, Akimasa, et al. "Isolation and identification of antihypertensive peptides from antarctic krill tail meat hydrolysate." Journal of food science 74.4 (2009): H116-H120.
• Kim, Se-Kwon, Dai-Hung Ngo, and Thanh-Sang Vo. "Marine fish-derived bioactive peptides as potential antihypertensive agents." Adv Food Nutr Res 65 (2012): 249-260.
• Li, Ying, et al. "Purification of a novel angiotensin I-converting enzyme (ACE) inhibitory peptide with an antihypertensive effect from loach (Misgurnus anguillicaudatus)." Journal of agricultural and food chemistry 60.5 (2012): 1320-1325.
• Marchbank, T., et al. "Clinical trial: protective effect of a commercial fish protein hydrolysate against indomethacin (NSAID)‐induced small intestinal injury." Alimentary pharmacology & therapeutics 28.6 (2008): 799-804.
• Möller, Niels Peter, et al. "Bioactive peptides and proteins from foods: indication for health effects." European journal of nutrition 47.4 (2008): 171-182.
• Nazeer, R. A., NS Sampath Kumar, and R. Jai Ganesh. "In vitro and in vivo studies on the antioxidant activity of fish peptide isolated from the croaker (Otolithes ruber) muscle protein hydrolysate." Peptides 35.2 (2012): 261-268.
• Najafian, L., and Abd Salam Babji. "A review of fish-derived antioxidant and antimicrobial peptides: their production, assessment, and applications." Peptides 33.1 (2012): 178-185.
• Ngo, Dai-Hung, et al. "Free radical scavenging and angiotensin-I converting enzyme inhibitory peptides from Pacific cod (Gadus macrocephalus) skin gelatin." International journal of biological macromolecules 49.5 (2011): 1110-1116.

Peri-Workout BCAA + Glutamine + Citrulline Consumption Blunts Muscle & Fat Loss Compared to Powerade Placebo

Peri-Workout BCAA + Glutamine + Citrulline Consumption Blunts Muscle & Fat Loss Compared to Powerade Placebo

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"Shed the fat, keep the muscle!" That's a promise you will find not literally, but analogously in every ad for BCAAs, but do they actually do that? Help you shed fat and retain muscle? Scientific prove to support this claim is, as of yet, missing.

With BCAAs it is just as it is with 99.9% of the supplements: Ads and product labels are full of scientifically unproven claims. One of these unproven claims is that the consumption of branched-chain amino acids would protect you from losing muscle while you're dieting ... the problem with this notion is - as sound as it may seem in view of the mTOR promoting effects of leucine, there's no study which would prove that guzzling BCAAs all day will in promote fat and blunt lean mass losses when you're cutting.... or I should say "as of now, there was no study...", right? After all, there's this new study by Dudgeon et al.'s the abstract of which tells us that "BCAA supplementation in trained individuals performing resistance training while on a hypocaloric diet can maintain lean mass and preserve skeletal muscle performance while losing fat mass" (Dudgeon. 2015).

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As we are going to see after taking a look at the design and results of Dudgeon's single-blind study in seventeen resistance-trained males (21–28 years of age) on hypocaloric diets, this is yet a potentially misleading conclusion. Not because it was wrong, but rather because it omits an observation that could be of paramount importance to dieters who have the free choice between the two treatments, the subjects of the study were randomly assigned to, namely...

• 14g of Xtend (BCAA) before after workouts or
• 14 g Powerade (CHO) before and after workouts

The supplements were consumed for a total study time of 8 weeks during which all subjects trained four times per week according to a standardized workout program and consumed a diet that was programmed (but not controlled) to contain roughly 35% less energy than the subjects required on workout days and approximately 10% less energy than required on off-days.

In the strict sense, this is actually no "BCAA study": Some of you may already have realized that the "BCAA supplement" the scientists used, i.e. Scivation XTend, is not really a "BCAA only" supplement. Next to only 7 grams of BCAAs per 14g of powder the subjects ingested before and after the workout, it also contains 1 g citrulline and 2.5 g glutamine and obviously a hell lot of flavorings, fillers and what not. Now, while the latter are not of any importance, both of the former have been heralded as muscle protectors, as well, with citrulline probably having the more convincing scientific data to back it up (it appears to act similar to leucine, by the way | Moinard. 2007; Faure. 2012; Ventura. 2013) outside of scenarios with extremely high glucocorticoid levels where glutamine unquestionably helps (Hickson. 1995 & 1997; Salehian. 2006). It is thus in my humble opinion at least highly imprecise to conclude that the provision of 2x7g of BCAA ameliorated the the fat to muscle loss ratio during the 8-week study.

Now you may be rightly asking yourselves why I am so vague with respect to the energy deficit. Well, everything we learn from the full text of the study is that all subjects were "provided an individualized caloric restricted diet based on individual data (body mass, body composition, resting metabolic rate, etc.)" (Dudgeon. 2015) - a diet the scientists describe as follows:

Table 1: W/ the Harris-Benedict equation you calculate the basal metabolic rate and multiply it with a factor (multiplier) that describes your activity level best to arrive at the "real" estimated energy requirements.

"The caloric-restricted diet was designed as an 8 week “cut diet” for reducing body fat, and used a modified carbohydrate-restricted diet approach (percent of total calories for workout days were 30 % carbohydrates, 35 % protein and 35 % fat and for off days were 25 % carbohydrates, 40 % protein and 35 % fat). Each individual’s daily caloric and macronutrient intake was determined using the Harris Benedict formula with an activity factor of 1.35 (lightly active individual engaging in light exercise 1–3 days/week) for workout days and 1.125 (sedentary individual) for off days" (Dudgeon. 2015).

Since the Harris-Benedict formula is only a really rough estimate of how much energy you actually need, my previous estimations of the energy deficit are as "accurate" as I can possibly be. The 1604kcal that are printed in red bold letters on top of the exemplary meal plan in Figure 2, however, suggest that the deficit on the off days was significantly larger. After all, the subjects' mean weight was >80kg and their daily energy requirements should thus be at least 2,000kcal - even on off days (and the table in which the macronutrient composition is listed actually says that the mean intake was 2046 and 2264kcal/day for the BCAA and CHO group respectively).

Table 2: Sample dietary card for a subject during an off, non-workout, day (Dudgeon. 2015).

In view of the fact that the response I got from the authors to an email in which I asked about the exact kcal deficit only referred me to the previously cited passage about the activity factors, I guess it is futile to further speculate about the energy deficit, of which I would still like to add that it was probably higher in the heavier and taller BCAA group. Why? Well, the BCAA group had plans with 2456 and 2046 kcal on workout and off days, the CHO group on the other hand were fed 2717 and 2264 kcal... Whatever, let's get to the more relevant, but not less confusing changes in body weight, lean mass and fat mass the researchers report for the BCAA and CHO groups:

Figure 1: Pre and post absolute mean body weight, body fat and lean body mass values before and after the 8-week intervention; * p < 0.05 for the difference within groups (no difference between groups | Dudgeon. 2015)

-0.1 kg and -2.3 kg of body weight, +0.4 kg and -0.9 kg of lean mass and 0.6 kg and 1.4 kg fat mass in the BCAA and CHO groups respectively - that's in line with the previously cited conclusion. The BCAA supplement blunted the small loss of lean mass in the CHO group, but if we look at the complete dataset, a somewhat different image emerges; one in which the two classic markers of body composition, namely the relative amount of body fat (aka "body fat percentage") and the lean mass as percentage of the total mass changed in a way that favors CHO over BCAA supplements:

Figure 2: Pre vs. post values for body fat % and lean mass %, the two parameters you would classically use to assess body composition (instead of absolute lean and fat mass); pre-to-post change on top of the post-bars (Dudgeon. 2015).

Now, I am not saying that the consumption of the BCAA (+citrulline + glutamine) supplement did not blunt the loss of lean mass - it obviously did. What I want you to keep in mind, though, is the fact that the consumption of 14g of BCAAs before and after workouts appears to suffocated any dieting efforts - after all, the subjects lost a practically irrelevant (and for whatever reason allegedly statistical significant) amount of 600g body fat; that's in contrast to the 1.4 kg of fat mass the subjects in the control group lost; and that's a practically relevant insight, even if this fat loss was allegedly statistically non-significant, because  it implies that BCAAs practically blunt fat loss.

Whey + Casein - A Superior Post-Workout Shake that Kicks Every Amino Acid Product's Ass | read more

So what do we make of this study? Well, first of all, I would like to come back to something fundamental: This is yet another BCCA study that did not make the practically most relevant comparison of BCAAs and cheap (whey) protein protein supplements, in which BCAAs have hitherto always failed. In my humble opinion that's a problem, after all having a carbohydrate supplement as control in a dieting study is nice, but eventually not relevant for the average trainee who is probably not really considering extra-carbs when he's dieting.  What a real trainee would have been interested in, is whether BCAAs can prevent muscle catabolism to a significantly greater degree than the cheap whey protein he's using anyway...

... and maybe, whether the latter has a similar negative effect on fat loss as the BCAAs in the study at hand - which leads me to the actual take home message of the study, which is, as usually, not as straight forward as the conclusion of the abstract suggested. When all is said and done, the study at hand does after all suggest that someone who is approaching the single-digit body-fat zone, where every gram of muscle that is not lost counts, could benefit from the apparent lean mass protective effects of BCAA the scientists observed in the study at hand. It does yet also indicate that someone who's "making weight" for a competition should take a second look at the data in Figure 1 + 2 and acknowledge that taking a BCAA supplement may be the reason he will fail to achieve his weight loss goal. You don't believe that? Well, let's do some scientifically not exactly kosher extrapolations: If you manage to lose 10 kg in 10 weeks without BCAAs, for example, the data from the study at hand suggests that your weight loss "on BCAAs" over the course of those 10 weeks would be as meager as 434 grams ... whether that's in fact the case (I doubt it ;-) will have to be studied in future studies, just like the effect of BCAAs, citrulline and glutamine, alone and whether using your regular whey protein before and after the workout wouldn't have the exact same, or even better effects | Comment on Facebook!

References:

• Dudgeon, WD; Page Kelly, E; Scheett TP. "In a single-blind, matched group design: branched-chain amino acid supplementation and resistance training maintains lean body mass during a caloric restricted diet." Journal of the International Society of Sports Nutrition  (2016) 13:1.
• Faure, Cécile, et al. "Leucine and citrulline modulate muscle function in malnourished aged rats." Amino acids 42.4 (2012): 1425-1433.
• Moinard, Christophe, and Luc Cynober. "Citrulline: a new player in the control of nitrogen homeostasis." The Journal of nutrition 137.6 (2007): 1621S-1625S.
• Hickson, R. C., S. M. Czerwinski, and L. E. Wegrzyn. "Glutamine prevents downregulation of myosin heavy chain synthesis and muscle atrophy from glucocorticoids." American Journal of Physiology-Endocrinology and Metabolism 268.4 (1995): E730-E734.
• Hickson, Robert C., et al. "Protective effect of glutamine from glucocorticoid-induced muscle atrophy occurs without alterations in circulating insulin-like growth factor (IGF)-I and IGF-binding protein levels." Experimental Biology and Medicine 216.1 (1997): 65-71.
• Salehian, Behrouz, et al. "The effect of glutamine on prevention of glucocorticoid-induced skeletal muscle atrophy is associated with myostatin suppression." Metabolism 55.9 (2006): 1239-1247.
• Ventura, G., et al. "Effect of citrulline on muscle functions during moderate dietary restriction in healthy adult rats." Amino acids 45.5 (2013): 1123-1131.

Ashwagandha Boosts Size & Strength Increases, Augments Fat Loss & Recovery in 8-Week Resistance Training Study

Ashwagandha Boosts Size & Strength Increases, Augments Fat Loss & Recovery in 8-Week Resistance Training Study

adaptogens ashwagandha Body Fat build muscle lose fat resistance training supplementation supplements

Ashwaghanda may be for gymrats, too.

Ashwaganda is one of the supplements that has been around forever. While this would suggest that it works, the relatively low number of people who actually use it suggests otherwise and scientific evidence in form of peer-reviewed, non-sponsored studies that would allow us to draw a reliable conclusion with regard to its usefulness for athletes is rare... Well, actually there are only four studies on Withania somnifera, which is also known as Indian Ginseng or Winter Cherry, of which you could say that they are at least relevant to the topic - even though none of them was conducted in resistance trained / training individuals.

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There's a study by Raut, et al. that evaluated the "tolerability, safety, and activity of Ashwagandha (Withania Somnifera) in healthy volunteers" from 2012; a study by Sandhu, et al. in which the researchers probed the "effects of Withania somnifera (Ashwagandha) and Terminalia arjuna (Arjuna) on physical performance and cardiorespiratory endurance in healthy young adults" and found an increase in velocity [+3%], relative power [+9%] and VO2 max [+7%] in response to 500mg/day for 8 weeks; a study by Choudhary et al. (2015) which found both, increases in VO2max and quality of life of 50 "athletic" individuals in response to a commercial Ashwaghanda product that goes by the cryptic acronym KSM-66 Ashwagandha; as well as a study by Shenoy, et al. (2012) which found 11%, 16% 16% and 2% increases in time to exhaustion, VO2, metabolic equivalents (METs) and respiratory exchange ratio (RER), respectively (note: the benefits were sign. lower in female study participants, see Table 1), in response to the same amount, i.e. 500 mg/day, of an aqueous root extract of Ashwagandha that has been used by Sandhu et al. two years before.

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).

With that being I should mention that several studies suggest that your source of Ashwaghanda may well determine its effects. So, any current and future contradictions in the literature may be related to the level of desirable and undesirable "active ingredients" in the tested extracts. Patel, et al., for example, report that 50% of the samples they analyzed in 2015 contained mercury (Hg) at levels "above the permissible limit". Reason enough for the researchers to conclude that the "consumption of drug (Ashwagandha) obtained from polluted areas may cause accumulated side effect as well as the toxic effect of the heavy metals, respectively" (Patel. 2015). In view of the fact that I assume that Wankhede et al. used an (a) heavy-metal free and (b) truly standardized extract with actual steroidal lactones (withanolides, withaferins), saponins and alkaloids like isopelletierine and anaferine in it, in their recent

"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)

in young men who participated in a standardized resistance training regimen, it is thus not totally impossible that the next best Ashwaghanda product from the internet will produce significantly different results. I guess you should keep that in mind if you plan to go shopping after reading this article. The product Wankhede, et al. used, by the way, was provided by Shri Kartikeya Pharma and Ixoreal BioMed and happened to be the same KSM-66 high-concentration root extract Choudhary et al. used in their likewise very recent study.

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

I don't want to waste your precious time with speculations, though. Let's talk about Wankhede's recent study, on 57 men (18-50 years), who were randomly allocated to either the treatment group, in which the subjects consumed 300 mg of ashwagandha root extract twice daily, or the control group, which received identically looking starch placebo capsules.

BIA and CK - not the best ways to measure body fat and recovery: What should be noted about these measurements, though, is the fact that body fat levels were measured via bio impedance (BIA) and the recovery was judged based on creatine kinase (CK) values. With BIA being susceptible to variations in hydration status and other sources interference (Kyle. 2004) and the CK-values showing extreme inter-individual variability (learn more), the validity of these outcomes remains somewhat questionable.

Both, the subjects who received the active treatment in form of 2x300 mg/day Ashwagandha, as well as those who received the placebo treatment, underwent identical 8-week resistance training programs; programs, the scientists describe as follows:

"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).

The workouts were periodized with increasing number of sets from 1-2 to 3. More specifically, the subjects performed barbell squats, the leg extensions, seated leg curls, machine chest presses, barbell chest presses, seated machine rows, one-arm dumbbel rows, machine biceps curls, dumbbel biceps curls, cable triceps press-downs, dumbbell shoulder presses, and the straight-arm pull-downs in the first two weeks and barbell squat (3 sets) the leg extension (3 sets), the leg curl (2 sets), one chest exercise (flat, incline or decline press or fly, cable cross over, 3 sets), one back exercise (rows, pull up, pull down or seated cable row, 3 sets), another chest exercise (3 sets) another back exercise (3 sets), one biceps exercise or one triceps exercise (curls or extensions, 3 sets), and one shoulder exercise (raises or presses, 3 sets) for the rest of the 8-week study.

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).

Significant inter-group differences were found for almost all of the measured variables: the size increases in the arms and chest, the change in body fat (remember, those are only BIA values), serum testosterone, and CK (remember, this is not a very reliable marker of exercise recovery), as well as the strength increase on the bench press and leg extension machine (1RM, each) differed significantly not just from pre- to post, but also from the supplement to the placebo group (see Figure 2, Figure 3).

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).

Against that background it seems certainly warranted that Wankhede et al. postulate that their study "confirms previous data regarding the adaptogenic properties of ashwagandha" and it also clearly "suggests it [Ashwaghanda supplementation] might be a useful adjunct to strength training" (Wankhede. 2015). The authors are yet also right, when they point out that their study has...

"[...] 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)

Accordingly, Wankhede et al. rightly demand that further "[r]esearch studying the possible beneficial effects of ashwagandha needs to be conducted", research that spans "longer periods of time" and includes "different populations including females and older adults of both genders" (Wankhede. 2015). In this regard, I would like to remind you that the previously discussed results Shenoy et al. published three years ago, in which the sex of the participants had a major impact on the study outcome, make studies comparing male to female resistance trainees particularly appealing - from a science perspective, obviously ;-)

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!

References:

• 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.