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Sabtu, 05 Maret 2016

Recent Studies Cast Shadow Over High Dose BCAA Intake: Increased Protein Wasting, Lower Brain Serotonin and More

To guzzle BCAAs all day or not - is that still a question or is the answer settled with the publication of two recent studies?
From previous SuppVersity articles about BCAA you will know that I don't buy into the hype supplement producers generate about the muscle-building and/or muscle-protective effects of high dose BCAA- or leucine-only supplementation.

One of the previously mentioned issues with BCAAs are their putative ill effects on neurotransmitter levels in the brain - effects that had only been observed in rodents, though. Now, a recent study in pigs, who are a much better model of human metabolism (even much better than most apes | Miller. 1987), is fueling the concerns about the pro-depression effects of high dose leucine supplementation.
Learn more about amino acid and BCAA supplements at the SuppVersity

Peri-WO BCAA Blunt Fat Loss

Whey + C Kicks BCAA Ass

Alanyl-Glutamine is it any good?

Glutamine Insted of CHO?

GLU as Intra-Workout BV?

BCAAs deplete neurotransmitters
The corresponding study  (Wessels. 2016), which happens to have been sponsored by the BCAA producer Ajinomoto (quite ironic, isn't it?), sought to elucidate the response of high leucine diets on the activity of the BCAA metabolizing enzyme branched-chain keto acid dehydrogenase complex (BCKDH) and subsequent changes in the concentrations of free amino acids and amino acid derivates in several tissues, including the brain.

Figure 1: Brian tryptophan and serotonin levels in response to diets containing normal or two- (white) and four-fold (grey bar) elevated amounts of leucine (Wessels. 2016).
What the scientists found was a significant decrease in brain tryptophan with twice and a significant reduction of both brain tryptohan and serotonin levels with four times the regular amount of leucine in the piglets' diets (that's 1% vs. 2% vs. 4%). Bad news!? Well, 4% leucine in the diet are a very high amount with questionable practical implications. Even though the study confirms the potentially negative effects of the tryptophan blocking effects of leucine and BCAAs in general, the good think is that it assigns a relatively high number to the required dosage to see effects - whether lower doses would suffice to mess with all three BCAAs, as they were used by Choi et al. (2013), remains elusive, though.
In vivo comparison of the central action of isoleucine, valine, and leucine on glucose kinetics during pancreatic insulin clamps (Arrieta-Cruz. 2016).
It's not all bad news: While the potentially depression promoting effects of high dose leucine and the anti-anabolic / pro-catabolic effects of BCAA supplementa-tion in rodents are bad news, another recent study from the Mexican Ministry of Health supports the previously discussed anti-diabetic effects of isoleucine and sug-gests that valine may have similar effects. In view of the fact that the putative mechanism, for the increased glucose infusion rate (GIR | see Figure on the left) is an increased inhibitory effect of insulin on endogenous glucose production (EGP), not an increase in peripheral glucose utilization, it is yet questionable how relevant the results of Arrieta-Cruz' recent study in diet-induced o-bese rats are for athletes / healthy individuals for whom exuberant glycolysis / gluconeogenesis isn't a problem.
While it obviously depends on the severity of your BCAA addiction, whether the Wessels study is bad news for you, it is it is unfortunately too early to rejoice: More potentially bad news for BCAA junkies comes from a recent study by Milan Holecek et al. (2016) whose efforts to prove that diets containing extra BCAAs (valine, leucine, and isoleucine | HVLID), or a high(er) content of leucine (HLD) would have beneficial effects on the protein balance of rats in a two months study produced results neither the scientists nor I would have expected: In high doses BCAAs make your body waste protein!
Figure 2: BCAA content of the standard (SLD), high BCAA (HVLID) and high leucine (HLD) diets (Holecek. 2016).
Needless to say that this result is in diametrical contrast to what the scientists expected. Not only did Holecek et al. fail to demonstrate the expected positive effects of the chronic consumption of a BCAA- / leucine-enriched diet on protein balance in skeletal muscle. The results of their latest study actually "indicate rather negative effects from a leucine-enriched diet" (Holecek. 2015).
But BCAAs are muscle-builders how can leucine & co ruin protein synthesis? A reliable answer to this question has unfortunately yet not been found, but the results of the Holecek study suggest that an overabundance of BCAAs triggers an overexpression of the BCAA degrading enzyme BCKA dehydrogenase and the subsequent conversion of BCAAs to BCAA keto acids and / or eventually alanine or glutamine which are then (ab-)used as energy source by the liver (cf. modified figure from Holeček. 2001)
Instead of reducing the breakdown of protein, Holecek et al. found that a BCAA- or leucine-enriched diet tends to increase not just the breakdown of BCAAs, as well as the production of branch-chain keto acids (BCKA), alanine and glutamine and their utilization in visceral organs, it also impaired the rodent's protein synthetic response to a meal in postabsorptive state - particularly in fast-twitch (white) muscles.
Figure 3: Fractional rate of protein synthesis. Means ± SE, p < 0.05. *compared to the corresponding control (SLD or SLD + S); # compared to the corresponding fed group; † HLD (HLD + S) group vs. HVLID (HVLID + S) group (Holecek. 2016).
In spite of the fact that this increase in protein wastefulness, as I would call it, is bad news and the exact opposite of what the shiny BCAA ads and product write-ups promise, a significant loss in muscle weight was only observed in the soleus and ext. digitorum longus of the rodents in the high BCAA, but not the high leucine group. Accordingly, the study sheds a whole new light on the usefulness of BCAAs as 'muscle builders' or 'muscle protectors' and may, as Holecek et al. rightly point out...
"[...] explain the discrepancy between the protein anabolic effects of BCAA or leucine on muscles that were reported under in vitro conditions and/or shortly after BCAA intake and their reduced or lack of effects following chronic administration" (Holecek. 2016).
With the present study being conducted in healthy rodents without any of the condition that lead to muscle wasting (e.g. disorders like diabetes, or natural processes like aging) and in the absence of the stimulatory effect of exercise on signalling pathways that activate protein synthesis, future studies will have to determine, whether the ill effects on protein synthesis and increases in protein breakdown are (a) even more severe in muscle-wasting disorders, the elderly, and / or during endurance exercise, and how (b) the effects are modified by resistance training.
Figure 4: The previously not discussed ill (BCAA) and beneficial (leucine) effects of different levels of said amino acids on the HDL to LDL ratio of the rodents in the Holecek study should be taken into account, as well.
Bottom line: While the main outcomes of the two studies I discussed in detail in today's SuppVersity article do in fact cast a dark shadow on the health and performance benefits of BCAAs, it's not all bad news. Why's that? Here's why: (A) the Wessels study suggests that the amount of BCAAs that is required to produce practically significant reductions in brain serotonin is very high; (B) the significant reduction in the LDL/HDL ratio Holecek observed in the high leucine group of their study (Figure 4) and the lack of visible effects on actual muscle mass in the same group put the relevance of the increased protein breakdown in response to (at least) high dose leucine into perspective; and (C) there's still the Arrieta-Cruz study which shows that even isoleucine and valine of which the Holecek study draws a rather negative image, can have benefits - at least in the obese | Comment!
References:
  • Arrieta-Cruz, Isabel, Ya Su, and Roger Gutiérrez-Juárez. "Suppression of Endogenous Glucose Production by Isoleucine and Valine and Impact of Diet Composition." Nutrients 8.2 (2016): 79.
  • Choi S, Disilvio B, Fernstrom MH, Fernstrom JD. Oral branched-chain amino acid supplements that reduce brain serotonin during exercise in rats also lower brain catecholamines. Amino Acids. 2013 Aug 1. [Epub ahead of print] 
  • FAO (Food and Agriculture Organization of the United Nations. "Food and nutrition in numbers." Rome, 2014; Food and Agriculture Organization of the United Nations.
  • Holeček, Milan. "The BCAA–BCKA cycle: its relation to alanine and glutamine synthesis and protein balance." Nutrition 17.1 (2001): 70.
  • Holeček, Milan, et al. "Alterations in protein and amino acid metabolism in rats fed a branched-chain amino acid-or leucine-enriched diet during postprandial and postabsorptive states." Nutrition & metabolism 13.1 (2016): 1.
  • Miller, E. R., and D. E. Ullrey. "The pig as a model for human nutrition." Annual review of nutrition 7.1 (1987): 361-382.
  • Wessels, et al. "Branched-Chain Amino Acid Degradation and Modify Serotonin and Ketone Body Concentrations in a Pig Model." PLoS ONE 11.3 (2016).

Minggu, 17 Januari 2016

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

"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).
Learn more about amino acid and BCAA supplements at the SuppVersity

Glutamine Helps W/ Diabetes

Whey + C Kicks BCAA Ass

Alanyl-Glutamine is it any good?

Glutamine Insted of CHO?

GLU as Intra-Workout BV?

BCAAs deplete neurotransmitters
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.

Rabu, 21 Oktober 2015

Low Grade Metabolic Acidosis May Eat Away Your Bones and Blow Up Your Belly Via Empowering Glucocorticoids!

The way we eat and live is not just obesogenic it is also acidogenic... or is the former just a consequence of the latter? 
I've written about the nasty effects of low grade metabolic acidosis which include calcium loss and brittle bones, nitrogen / protein loss and decreased protein synthesis, impaired growth hormone and IGF-1 production and more in a 2013 SuppVersity Science Round-Up (read it).

For you, as a SuppVersity veteran who's read this and related articles, it should thus not be surprising that scientists from the German Aerospace Center in Cologne were now able to establish a new, mechanistic link between the "long-term ingestion of habitually acidifying western diets may constitute an independent risk factor for bone degradation and cardiometabolic diseases" (Buehlmeier. 2015).

As Judith Buehlmeier and her colleagues point out, we have long been aware of the ill effects of low-grade metabolic acidosis (LGMA), as induced by high dietary acid load or sodium chloride (NaCl) intake and a lack of alkaline foods and nutrients in the average Western diet. What has hitherto not been fully elucidated is the underlying mechanisms, which is not as simple as the dissolving tooth in a glass of coke would suggest.
You can learn more about bicarbonate and pH-buffers at the SuppVersity

The Hazards of Acidosis

Build Bigger Legs W/ Bicarbonate

HIIT it Hard W/ NaCHO3

Creatine + BA = Perfect Match

Bicarb Buffers Creatine

Alkalosis Boosts Muscle Activity
In their latest study, the researchers from the German Aerospace Center in Cologne and their colleagues from the Universities of Bonn and Heidelberg do now present the first convincing evidence that the previously cited catabolic / anti-anabolic effects of chronic low-grade acidosis (LGMA) are triggered by interactions of the acid–base balance with the metabolism of glucocorticoids (GC). In said, study, the researchers "aimed to investigate GC activity/metabolism under alkaline supplementation and NaCl-induced LGMA" in eight young, healthy, normal-weight men who participated in two crossover designed interventional studies.
Figure 1: Correcting a diet-induced low grade metabolic acidosis with K-bicarbonate reduces the nitrogen loss of 750mg - 1000mg per day (per 60kg BW) in post- menopausal women in a prev. study (Frassetto. 1997)
  • In Study A, two 10-day high NaCl diet (32 g/d) periods were conducted, one supplemented with 90 mmol KHCO3/day.
     
  • In Study B, participants received a high and a low NaCl diet (31 vs. 3 g/day), each for 14 days. During low NaCl, the diet was moderately acidified by replacement of a bicarbonate-rich mineral water (consumed during high NaCl) with a non-alkalizing drinking water. 
In repeatedly collected 24-h urine samples, potentially bioactive GCs (urinary-free cortisol / free cortisone), as well as tetrahydrocortisol (THF), 5a-THF, and tetrahydrocortisone (THE), were analyzed.
Even Low Grade Acidosis Will Increase Your Diabetes Risk | learn more!
Beware! It does not take much to mess you up! A quantitative analysis of the data from the study at hand shows that even increases of dietary acid loads in the magnitude of only 30 mEq/d, which drive the renal net acid excretion into a range that is commonly seen in people on the standard Western diet (60–70 mEq/d), suffice to affect glucocorticoid activity in ways that may ruin your bone, heart and muscle health. In that, the main offenders are grains, not meats. Grains contribute an estimated 38% to the net acid load of the avg. Westerner (Sebastian. 2002).
A brief glimpse at the glucocorticoid levels in the urine of the subjects (see Figure 2) shows that with supplementation of 90 mmol KHCO3, the marker of total adrenal GC secretion dropped (p = 0.047) and potentially bioactive-free GCs were reduced (p = 0.003).
Figure 2: aily adrenal cortisol secretion as indexed by the sum of excretion rates of the 3 major urinary glucocorticoid (GC) metabolites tetrahydrocortisol, 5a-tetrahydrocortisol, and tetrahydrocortisone (THF + aTHF + THE) as well as excretions of potentially bioactive-free GCs (UFF + UFE | Buehlmeier. 2015)
This is particularly interesting if we also take into account that in Study B, the GC secretion and potentially bioactivefree GCs did not exhibit the expected fall with NaCl-reduction as net acid excretion was raised by 30 mEq/d. In conjunction study A + B do thus underline the important role of alkalizing agents like bicarbonate or potassium - irrespective of the total intake of NaCl, of which the study at hand confirms that it is part of the problem. Its ill effects, however, appear to be mediated mainly, if not exclusively, via the acidifying effects of chloride.
Bottom line: As the authors point out, their study is the first to provide convincing evidence that the ill effects of chronic low-grade metabolic acidosis are mediated via enhanced glucocorticoid activity and secretion. In that, the pro-acidic effects of NaCl, as well as the lack of alkalizing foods and nutrients in the Western diet are the main motors of dietary induced glucocorticoid elevations.

Inactivity amplifies the ill effect of glucocorticoids on muscle loss by up to 213% (Ferrando. 1999).
These elevations are - in spite of being still in the physiological range - significant enough to compromise bone quality (Bedford. 2010; Shi. 2015), cardiometabolic health & diabetes (Prodam. 2013; Qi, 2007), and protein turnover (Frassetto. 1997 | see Figure 1; Buehlmeier. 2012), and appear to be particularly unfavorable under conditions of physical inactivity (Ferrando. 1999 | see Figure on the right). Reason enough for the authors to conclude that "[a]ccordingly, higher dietary acid loads may, in the long run, constitute an independent GC-driven musculoskeletal and cardiometabolic risk factor related with western dietary habits" (Buehlmeier. 2015) | Comment!
References:
  • Bedford, Jennifer L., and Susan I. Barr. "The relationship between 24-h urinary cortisol and bone in healthy young women." International journal of behavioral medicine 17.3 (2010): 207-215.
  • Buehlmeier, Judith, et al. "Alkaline salts to counteract bone resorption and protein wasting induced by high salt intake: results of a randomized controlled trial." The Journal of Clinical Endocrinology & Metabolism 97.12 (2012): 4789-4797.
  • Ferrando, Arny A., et al. "Inactivity Amplifies the Catabolic Response of Skeletal Muscle to Cortisol 1." The Journal Of Clinical Endocrinology & Metabolism 84.10 (1999): 3515-3521.
  • Frassetto, L., R. Curtis Morris Jr, and A. Sebastian. "Potassium bicarbonate reduces urinary nitrogen excretion in postmenopausal women." The Journal of Clinical Endocrinology & Metabolism 82.1 (1997): 254-259.
  • Qi, Dake, and Brian Rodrigues. "Glucocorticoids produce whole body insulin resistance with changes in cardiac metabolism." American Journal of Physiology-Endocrinology and Metabolism 292.3 (2007): E654-E667.
  • Prodam, Flavia, et al. "High-end normal adrenocorticotropic hormone and cortisol levels are associated with specific cardiovascular risk factors in pediatric obesity: a cross-sectional study." BMC medicine 11.1 (2013): 44.
  • Sebastian, Anthony, et al. "Estimation of the net acid load of the diet of ancestral preagricultural Homo sapiens and their hominid ancestors." The American journal of clinical nutrition 76.6 (2002): 1308-1316.
  • Shi, Lijie, et al. "Higher glucocorticoid secretion in the physiological range is associated with lower bone strength at the proximal radius in healthy children: importance of protein intake adjustment." Journal of Bone and Mineral Research 30.2 (2015): 240-248.

Senin, 19 Oktober 2015

Load Carrying Cardio Doesn't Affect Muscle Protein Flux While Intra-Workout EAA Reduces Protein Breakdown and Bumps Nitrogen Balance From Zero to Plus 50µmol/kg/h

While this picture shows loaded cardio in its most beautiful form, the study investigated loaded cardio on the treadmill and compared it (for questionable reasons) to non-loaded cardio on a stationary bike and guess what: Both burn the same amount of muscle - NET: Zero!
Carrying a (heavy) load during cardio? Sounds dumb? Well, that's however, how the real world looks like. Not just soldiers who are carrying armor and a heavy backpack in the field, but also hikers will attest to the fact that doing "cardio" with a weight on your shoulders or elsewhere is more natural than running around in the park with your mobile and ear-plugs as the only load you're carrying on top of your ultra-light runners clothing.

With that being said, it is actually quite astonishing that Stefan M. Pasiakos and colleagues from the Military Nutrition Division at the US Army Research Institute of Environmental Medicine in Natick are the first to take a look at the muscle anabolic and catabolic effects of regular (unloaded) and loaded cardio training in 40 free-living healthy, physically fit (peak oxygen uptake, VO2peak 40/60 mL/ kg/ min), adults (37 males and 3 females), normal weight men and women between the ages of 18–39 years.
HIIT is the ideal complement to classic "cardio" training!

Never Train To Burn Calories!

Tabata = 14.2kcal /min ≠ Fat Loss

30s Intervals + 2:1 Work/Rec.

Making HIIT a Hit Part I/II

Making HIIT a Hit Part II/II

HIIT Ain't For Everyone
In said study, the volunteers were then randomly assigned to one of four experimental groups, each
of whom performed a single 90 min exercise bout.
  • Two groups performed CE and the other two performed LC. 
  • One of each of the exercise groups received EAA drinks to consume during exercise, and the other groups received control (CON) drinks. 
To determine the effects on skeletal muscle, the subjects' individual muscle protein synthesism (MPS) was assessed during exercise and recovery and whole protein turnover was determined in recovery only. What may be a bit surprising in this context is the fact that a resting MPS measure was not included in the study. The authors, however, have a good argument to neglect this, when they say that (a) the MPS responses to endurance-type exercise (i.e.,as they relate to resting MPS) are well established and that (b) their ...
"[...] intent was not to determine temporal changes in MPS within an exercise mode (with or without EAA), but to examine MPS responses between LC and CE during exercise and recovery independently" (Pasiakos. 2015).
Another thing that was just like in any other study, though, was the standardization of diet and physical activity, the scientists describe as follows:
"Volunteers completed 3 d diet and activity records at baseline, and similar to our previous work (Pasiakos. 2011), these records were used to individually prescribe 7 d lead-in diets to maintain body weight and to limit the potential confounding effect of diet on outcome measures. Compliance was confirmed by 24 h dietary recalls conducted every two days during the lead-in phase (Food Processor SQL1, version 10, ESHA Research, Salem, OR) (Table 1). Volunteers were also instructed to maintain activity levels reported at baseline for the first five days of the lead-in phase. All resistive and endurance-type activity was prohibited 48 h before data collection to minimize any potential residual effects of previous exercise on protein turnover" (Pasiakos. 2015).
The actual news is however not the dietary standardization what you are (rightly) interested in is probably the exercise protocol which is - and I will get to that in the bottom line - not ideal: While the LC, i.e. the load carriage training, was performed by walking on a treadmill while wearing a weighted vest equivalent to 30% of baseline body mass, the CE, i.e. the control endurance exercise, was non-weight bearing and performed on a cycle ergometer (Lode, BV, Netherlands), of which the scientists say that they used it to "allow for comparisons with our previous studies" (Pasiakos. 2015).
Illustration 1: Graphical overview of the study design (Pasiakos. 2015) | EAA = 10g of EAAs, CON = non-nutritious control drink; LC = load carrying cardio on a treadmill, CE = control endurance exercise on a stationary bike.
What's unquestionable a strength of the study, though, was the fact that the baseline VO2peak and associated heart rates at maximal and submaximal levels were used to establish target exercise intensities for the LC and CE trials. In addition, speed and grade for LC and power (watts) for CE were adjusted to match the absolute exercise intensity (intended oxygen uptake was 2.4 L /m) and
to elicit a similar energy cost (intended energy expenditure was 1050 kcal /90 min) between
LC and CE. Lastly, ...
"[m]atching the intensity and energy cost was done to isolate the effects of the possible differences in mechanical force and contractile properties of LC and CE from the relative intensity and energy cost of the exercise bout [and a] familiarization trial was conducted to ensure the accuracy of the exercise prescription and the ability of the volunteer to complete the prescribed exercise bout" (Pasiakos. 2015).
As previously alluded to, the intra-workout beverage the subjects consumed was either a high EAA drink (10 g EAA: 0.7 g histidine, 0.7 g isoleucine, 3.6 g leucine, 1.2 g lysine, 0.3 g methionine, 1.4 g phenylalanine, 1.0 g threonine, and 1 g valine) or an identically looking placebo drink (non-nutritive).
Figure 1: Overview of protein fluxes (synthesis vs. breakdown and oxidation) and subsequent net protein balance in the four treatment groups, i.e. loaded and control cardio with and with out EAA (Pasiakos. 2015)
Interestingly enough, the latter, i.e. the 10 grams of EAA drink that was consumed in four small doses (i.e., 350 mg of phenylalanine and 900 mg of leucine per serving), over 90 min to minimize "any isotopic dilution that may have occurred if the EAA drink was consumed as a bolus" (Pasiakos. 2015) was the only treatment that made a difference to the protein flux parameters illustrated in Figure 1. In that it is worth mentioning the tthe difference in protein oxidation alone does not fully explain the conservation of skeletal muscle protein even if we assume that all the amino acids that were oxidized during the EAA supplementation trial came from the EAA supplement. This is curious in view of the lack of effect of BCAAs on exercise (learn more) induced protein breakdown and points with a finger to other EAAs as potential motors of this effect.
Figure 1: Protein synthesis. Mixed-muscle (A), myofibrillar (B), and sarcoplasmic (C) muscle protein synthesis (MPS) during exercise and mixed-muscle (D), myofibrillar (E), and sarcoplasmic (F) MPS in recovery from a 90 min, metabolically matched load carriage (LC) or conventional endurance (CE) exercise bout, with and without (control, CON) essential amino acid (EAA) supplementation. Data are mean ± SD, n = 10 per group. †Mode main effect; LC different than CE, P < 0.05. *Drink main effect; EAA different than CON, P < 0.05 (Pasiakos. 2015).
The fact that the loading didn't make a difference in either direction, i.e. that it did neither increase nor decrease the breakdown or synthesis of muscle protein may be surprising, but it's not the only result worth mentioning before we evaluate the results in the bottom line. In addition, it should be noted:
  1. The EAA-mediated decrease in muscle breakdown was complemented by both enhanced mixed-muscle and sarcoplasmic MPS during exercise.
  2. During the recovery phase, the mixed muscle and sarcoplasmic protein synthesis in response to loaded cardio training were higher than they were in the control group.
Of these results, finding #2 is of most interest as it puts the alleged uselessness of loaded cardio into perspectives. Muscles do after all grow during rest and if the muscle protein synthesis during the recovery phase is increased compared to the control non-loaded exercise this clearly suggests that loaded endurance exercise is more anabolic than non-loaded endurance exercise.
Yes! You can use whey or even regular milk protein, as well and benefit. Better don't eat a steak during your workout though. Learn more in this SV Classic  "23g of Dairy Protein + 5g of Leucine Turn Cardio Sessions Into Muscle Building Workouts"
So, loaded endurance exercise is not much, but a little better? Well, in this study it appears to be as if the former was the correct conclusion to be drawn. Generalizations, however, must be made with utmost care. Especially in view of the unfair comparison of walking on a treadmill with cycling on a bike, of which you could argue that it is naturally less anabolic than walking - irrespective of whether you're carrying an extra-load or not. Thus, the researchers have weakened the generalizability of their results by making the (imho unnecessary) decision to rely on a tried and proven method, i.e. cycling, only to (as I suspect) make it easier to standardize the workload in numbers. This, however, is bogus: I mean, you all have probably worked out for say 500kcal on an exercise bike and for 500kcal on a treadmill. Now tell me: What did you feel was more exhausting and had a subjectively significantly larger impact on your metabolism? You answer probably is 'treadmill'.

Eventually, the most practically relevant information you can draw from the study at hand are thus: (A) You can do both 90 minutes of loaded cardio on the treadmill and 90 minutes of classic cardio on an exercise bike without any muscle loss (at least from the exercised muscles) even if you consume only water (see net balance = 0 in Figure 2). (B) If you bring 10g of EAA and consume them over the course of your workout you may even hop off the treadmill or bike with a few micrograms extra muscle on your legs. And (C) if you chose the treadmill and loaded cardio this will trigger a better post-workout anabolic response than the bike. How meaningful all that is - in terms of gains, I mean - will yet have to be seen in future long(er)-term studies | Comment!
References:
  • Pasiakos, Stefan M., et al. "Leucine-enriched essential amino acid supplementation during moderate steady state exercise enhances postexercise muscle protein synthesis." The American journal of clinical nutrition 94.3 (2011): 809-818.
  • Pasiakos SM, McClung HL, Margolis LM, Murphy NE, Lin GG, Hydren JR, et al. "Human Muscle Protein Synthetic Responses during Weight-Bearing and Non-Weight-Bearing Exercise: A Comparative Study of Exercise Modes and Recovery Nutrition." PLoS ONE 10.10 (2015): Online only.