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

anti-catabolic BCAA catabolism citrulline glutamine lean mass lose fat peri-workout post-workout pre-workout supplementation supplements XTend

"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.

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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.

Fructose May Help Control Post-Exercise Cravings - Almost 30% Reduced Desire to Eat After 1h Low-Intensity "Cardio"

Fructose May Help Control Post-Exercise Cravings - Almost 30% Reduced Desire to Eat After 1h Low-Intensity "Cardio"

appetite breakfast exercise fructose health hiking hunger lose fat pre-workout walking

About to go for a walk? Have fructose for breakfast to keep the hunger at bay.

I know very well that fructose is the nutritional boogyman of the 21st century, but avoiding it altogether is about as unwarranted as consuming it by the pound is unhealthy. A recent study from the Department of Health and Physical Education at the Hong Kong Institute of Education and the Department of Sports Science and Physical Education at the Chinese University of Hong Kong does now show a new, hitherto unknown, or at least under-appreciated effect of fructose: The ingestion of a fructose containing, albeit not fructose only (not tested, though) breakfast will significantly reduce the desire to eat that will usually rise sharply after a 60 minute bout of "cardio" training in form of walking at 50% of one's individual VO2max.

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As a SuppVersity reader you will know that low-intensity cardio, much more than HIT or HIIT (learn more), will trigger significant increases in hunger and one's desire to eat. To ameliorate this effect, you could - that's at least what the aforementioned study shows - simply replace part of the starchy or high GI carbs of your breakfast with high fructose fruits and/or other fructose containing food items.... that's at least - as  previously mentioned - what the study at hand suggests; a study in which Hong Kong researchers compared the effects of three isocaloric breakfasts with identical amounts of carbs (1.0 g/kg body weight) from different food sources with different GIs (41, 39, and 72) and fructose contents on the appetite scores of ten healthy young male volunteers (21.7 ± 1.5 yr, 20.9 ± 1.1 kg/m²) who had to rate different aspects of appetite every 30 min during the 2-hr postprandial period after the meal, as well as during the 1-hr recovery period that followed the 1h of brisk walking (46% VO2max) all subjects had do perform 2h after consuming the standardized breakfasts.

"Three isocaloric meals were used in the present study. [...] Briefly, all meals had similar macronutrients and provided 1.0 g∙kg−1 body weight CHO for each participant. The LGI meal was composed of cooked spaghetti, egg, and full-fat milk. The LGIF meal comprised rice vermicelli, egg, ham, and fructose. The HGI meal involved rice vermicelli, egg, ham, and glucose. In the LGIF and HGI meals, approximately 25% of energy was derived from the fructose or glucose beverage (nearly 25 g for a 60 kg person). The calculated GI values for the LGI, LGIF, and HGI breakfasts were 41, 39, and 72, respectively. All meals were freshly prepared in the morning of each main trial, and the preparation procedure was standardized."

As you can see in Figure 1 the three test-meals initially had very similar effects on the subjects' appetite ratings, i.e. their desire to eat, hunger, fullness, and perceived ability to eat.

Figure 1: Appetite Sub-Score. b: P < 0.05 vs. LGIF. LGI: Low-GI meal without fructose; LGIF: Low-GI meal including fructose beverage; HGI: High-GI meal (Sun. 2015).

Only the 25% fructose meal, however, kept the rapid increase (or decrease in the case of fullness) in all four parameters after the 1h of brisk walking (Rec-X in Figure 1) at bay. That's quite an interesting observation, even though one could argue that the study cannot serve as a definite litmus test, because it lacks a post-exercise test-meal where the practical significance of the reduced appetite scores was measured against the reduction in food intake in the fructose group.

But isn't fructose the appetite increasing, liver clogging devil? While it may be the devil in the books of a couple of researchers who have nothing else to publish, the specific effect of fructose on appetite are far from being proven to be good or bad. (Rodin. 1990 & 1991). While it appears as if the isolated consumption of high amounts of free fructose has negative effects on appetite control (Lowette. 2015); and still, there's  no debating that fructose has the general ability to blunt food intake compared to an isocaloric amount of glucose in healthy individuals, as it has been shown by Rodin in 1991 (see Figure on the left).

Irrespective of the previously mentioned methodological short-coming, it is, as the authors highlight, quite striking that "the increased fructose content in LGIF breakfast suppressed the appetite score, compared with isocaloric HGI and LGI breakfast" (Sun. 2015). Previously, scientists often argued that the satiety promoting effect of fructose must be mediated by the lower GI and correspondingly lower insulin spikes as well as reduced glucose excursions after fructose vs. glucose containing meals. The data in Figure 2, however, tells us that neither the insulin spikes (Figure 2, right) nor the glucose excursions (Figure 2, left) differed significantly between the LGI (low GI) and the LGIF (low GI + fructose) meals over the relevant last part of the study period - an observation which does by the way also show us that "[w]hen exercise is included as a co-intervention strategy, the effect of GI on appetite may be highly complex" (Sun. 2015) and in most cases relatively irrelevant.

Figure 2: Glucose and insulin response to the test meals; significant differences were observed for high GI (HGI) compared to the other meals and initially for the fructose meal, where the glucose levels increased slightly more rapidly than in the low GI (LGI) reference meal -  in spite of identical calculated GI values, by the way (Sun. 2015)

Previous studies show that even though exercise exerts the most profound effect on human energy expenditure, it seems that post-exercise energy intake is not affected by exercise itself (Blundell. 1999; Melzer. 2005). In that, a study by Stevenson et al appears to confirm the finding of the study at hand which is that there is no difference relevant appetite scores between HGI and LGI trials during the postprandial period if the time between breakfast and moderate intensity exercise is sufficiently long.

Figure 3: The appetite suppressing effects of fructose preloads in the absence of exercise have been known ever since Rodin's 1990 study on the effects of fructose vs. glucose and water preloads on food intakes (Rodin. 1990).

What's new with the present study, though, is that "eating an LGIF [25% fructose] breakfast resulted in decreased appetite scores compared with HGI breakfast and LGI breakfast [25% non-fructose carbs]" (Sun. 2015). This and the fact that this difference cannot be explained by the usual suspects, i.e. insulin and blood glucose levels leads Sun et al to emphasize that ...

"[t]he effect of fructose on appetite has been substantially investigated. Earlier studies have indicated that fructose beverages suppressed energy intake more than glucose beverages did (Rodin, 1990 and Rodin, 1991). The underlying mechanism has been attributed to the metabolism of fructose in the liver and the effect of insulin" (Sun. 2015).

In fact, scientists have previously speculated that fructose may affect appetite through slow and incomplete absorption. This effect, however, is eliminated when fructose is consumed with other CHOs (Anderson. 2003). As far as potential mechanisms are concerned, we are thus left with changes in satiety hormones and peptides like ghrelin, cholecystokinin, glucagon-like-peptide-1 and peptide-YY and/or direct or indirect effects on the gut-brain axis as potential mechanisms that would explain the results of Sun's study. Unfortunately, neither of these mechanism was assessed in their study.

Make you choice - cholesterol and regular sugar (left), or fat free and fructose-laden? In the end it all may not even matter. In spite of that, you shouldn't forget that fruit is not the enemy, isolated fructose in drinks is.

So, what's the verdict? I'd like to cite the original conclusion first, before adding my two cents: "It appears that fructose content in, rather than the GI of, a pre-exercise breakfast meals affect subjective appetite score during the recovery period after 1-hr of brisk walking" (Sun. 2015).

There's no doubt that this is right, but there are important qualifications with respect to the real-world significance of the results: Firstly, the absence of a post-recovery test meal, where the actual food intake would have been measured, is a major methodological problem of the study at hand. Even though changes in appetite of a similar magnitude will usually translate in changes in food intake, this is not a necessity. Therefore the actual food intake and the mechanism for the appetite suppression have to be elucidated in future trials.

In the mean time, I'd suggest you do your own test-run. If it works, fine. If not, you don't have to care about the results of follow-up studies, anyway. Why? Well, what works for the virtual average study participant does not necessarily have to work for you | Comment on Facebook!

References:

• Anderson, G. Harvey, and Dianne Woodend. "Effect of glycemic carbohydrates on short-term satiety and food intake." Nutrition Reviews 61.5 (2003): S17.
• Blundell, John E., and Neil A. King. "Physical activity and regulation of food intake: current evidence." Medicine and science in sports and exercise 31 (1999): S573-S583.
• Lowette, Katrien, et al. "Effects of high-fructose diets on central appetite signaling and cognitive function." Frontiers in nutrition 2 (2015).
• Melzer, Katarina, et al. "Effects of physical activity on food intake." Clinical nutrition 24.6 (2005): 885-895.
• Rodin, Judith. "Comparative effects of fructose, aspartame, glucose, and water preloads on calorie and macronutrient intake." The American journal of clinical nutrition 51.3 (1990): 428-435.
• Rodin, Judith. "Effects of pure sugar vs. mixed starch fructose loads on food intake." Appetite 17.3 (1991): 213-219.
• Sun, Feng-Hua, Stephen Heung-Sang Wong, and Zhi-Gang Liu. "Post-exercise appetite was affected by fructose content but not glycemic index of pre-exercise meals." Appetite 96 (2016): 481-486.