BCAAs for Bodybuilders: Just the Science (Part 3)

Firstly, I’d like to apologise for my lack of activity on my blog. I have been extremely busy over the past few weeks and was lucky enough to have Matt Jones of Nutrition Condition to fill my shoes and post a couple of guest articles. As his content has been well received, you can expect to see future posts from him here.

Today, I aim to tie up the article series looking at BCAA supplementation and its effects on body composition. Before moving onto part 3, I first want to quote the summary from part 2, as it will set the stage for this post:

  • The amount of muscle mass a person has depends on the long-term relationship between muscle protein breakdown and synthesis.

  • A threshold amount of leucine of 2-3 g (~ roughly 0.05g/kg body weight) is thought to exist, with no apparent further stimulation of MPS with higher intakes.

  • This would translate to 25-37.5 g of leucine-rich protein sources.

  • Yes, you can absorb more than 30g of protein in one sitting!

  • Due to the apparent refractory nature of MPS, it would seem that eating meals spaced every 3/4-6 hours apart would optimise MPS within a 24-hour period.

  • However, it appears that there is more to muscle gain than frequently stimulating MPS; the reasons being as follows:

  1. A recommendation for higher daily amounts of protein than is likely to ‘max’ out MPS.
  2. Concept of the anabolic drive and hidden signaling pathways involved in protein turnover and AA oxidation.
  3. Real-world observations of excellent improvements in muscle mass despite theoretically ‘too high/too low’ meal frequencies.
  1. Apparent lack of effects on LBM whilst dieting with reduced meal frequencies (i.e. 1-2 meals per day).
  • It therefore seems that total protein intake is the most important variable, and how this intake is distributed, impacts body composition to a lesser degree.
  • For this reason, I don’t see any reason for meal frequency to be higher than the typical 3-4 meals per day for most people seeking optimal rates of muscle gain.
  • Though it is unknown whether moving to the ‘optimal frequency’ would be of benefit, it seems unlikely in the real world; and if so, it may only benefit the elite physique athlete looking for that 1-2% over their competition. Likewise, eating less than twice per day may compromise rates of muscle gain, however, no solid data exist to be make definitive conclusions.

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Whole proteins vs. free form amino acids: between-meal dosing

Having mentioned the practise of consuming free-form amino acids such as leucine and BCAAs on top of an existing sufficiency of protein in part 1, it is now time to get to the main point of this article and discuss the more theoretical uses of BCAAs. Having nicely set the stage by taking a look at the topic of meal frequency, the information that follows will hopefully make a bit more sense.

It was Dr. Layne Norton who originally popularised the notion of consuming free-form amino acids (e.g. BCAA) between meals. In recent years, several others have latched on to this concept and recommended their own protocols, such as dosing leucine between meals, on top of meals, between exercise sets etc.; I’m still waiting for someone to recommend snorting pure leucine!

If you remember from part 2, I talked about the refractory phenomenon associated with MPS, which has been explained by the ‘protein stat hypothesis’. It is argued that because free-form BCAAs aren't protein-bound within the matrix of the food, they are more quickly absorbed than intact proteins such as whey. It is further argued that because of this protein stat hypothesis - which indicates that an extracellular membrane-bound sensor is influenced by relative changes in amino acid concentrations as opposed to absolute concentrations - whole proteins don’t elicit a rapid rise and subsequent fall in amino acid levels, unlike their free-form counterparts. As such, Norton has advised that a BCAA mix containing 2-3g leucine (with our without additional carbohydrates – as the time course of MPS somewhat reflects plasma insulin levels) should be consumed between meals spaced 4-6 hours apart, with the aim of circumventing this refractory phenomenon associated with protein synthesis in response to the first meal. Theoretically, blunting the decrease in MPS (with a BCAA/BCAA-CHO mixture), which may occur a couple hours following the first meal, would lead to increased muscle hypertrophy over time.

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Is there any data to support this theory?

There are two main pieces of data used to support this hypothesis. The first is the already cited amino acid infusion data by Bohe et al. (2001). Secondly, Norton uses the study by Paddon-Jones et al. (2005) to justify his between-meal dosing strategy. In this trial, the authors compared the effects of supplement containing 30g of carbohydrate and 15g of essential amino acids (EAA) ingested between meals (consisting of 23.4g PRO, 126.6g CHO, 4g FAT) spaced five hours apart, with ingesting nothing between meals. The authors found that the supplement group experienced a greater overall anabolic response (nitrogen balance and fractional muscle protein synthesis) compared with the control group. This is all well and good but the problem with these findings are that the supplement group consumed 45g extra EAA (equivalent to 90g of whey or roughly 20g BCAA) and 90g extra carbohydrate than the control group. Furthermore, since total protein intake in the experimental group was 109g compared to 64 in the control group, what we’re actually comparing is an adequate intake (1.25g/kg) with an intake below the RDA of 0.8g/kg (0.74g/kg). As such, it is extremely unsurprising that a sufficient protein intake plus extra carbs is potentially more anabolic than an insufficient protein intake.

Ultimately, the practise of ingesting BCAAs between meals is largely based on amino acid infusion data - that doesn’t accurately represent oral protein ingestion – and a heavily flawed piece of research by Paddon-Jones et al. (2005). As such, between-meal dosing is an extremely optimistic strategy, based on questionable theoretical evidence. For such a strategy to prove its worth, I’d like to see a between-meal dosing strategy set up around a sufficient protein intake, in trained individuals undergoing a structured resistance programme with body composition endpoints. Will we ever see this data? I doubt it, but I can always dream! But unless it happens, I wouldn’t recommend it to my clients.

Moreover, as discussed in my last article, given the apparent lack of difference in body composition with a decent protein intake spread over 3-4 meals compared with six meals, it is highly unlikely that a slight extension of MPS with a given meal will make any meaningful differences in terms of muscle mass accrual; it almost certainly wouldn’t make a difference in terms of maintenance of muscle mass.

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BCAAs and fat loss?

As you recall from part 2, reducing meal frequency doesn’t seem to affect muscle mass retention as long as sufficient protein is being consumed. This is why intermittent fasting (LeanGains style) works very well for those looking to lose fat and retain muscle. In fact, an interesting review by Varaday (2011) concluded that intermittent calorie restriction (ICR) is just as effective as daily calorie restriction (DCR) at promoting fat and weight loss, though ICR may be more effective for retaining lean mass. However, before the intermittent fasting crowd gets too excited, it is worth remembering that the majority of the ICR studies used bioelectrical impedance (BIA) as a measure of body composition. Anyone familiar with BIA knows that it’s inaccurate at the best of times.

Therefore, it appears that an optimal meal frequency whilst dieting is the one you can best stick to. Because of this, attempting to increase the number of stimulations in MPS, or extend this process, during dieting seems a futile one.

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What about their caloric efficiency?

Given that BCAAs are the only amino acids that stimulate protein synthesis, another rationale for the use of BCAAs whilst dieting is due to their greater caloric economy in comparison to whole protein sources. In other words, if your aim were to get 3g of leucine in a given meal, ingesting whole protein food such as whey would require about 25g (100kcal), whereas 6g (24kcal) of BCAAs would provide the same amount of leucine.

By the same logic, if things were only as simple as getting enough leucine to max out MPS at each meal (~4-6g of most brands of BCAAs), we would theoretically only need 24-36g of BCAAs per day to cover protein requirements. However, it’s no use having leucine to initiate protein synthesis if there is no protein (i.e. other amino acids) to actually carry on this process. What will basically happen is that things will short circuit, meaning that MPS may begin but then stop soon after. A quote from a review by Balage & Dardevet (2010) on the topic sums this up nicely:

“There is some evidence that long-term leucine availability is sufficient to improve muscle mass or performance during exercise training. However, it needs to be associated with other amino acids to be efficient (for example, through leucine-rich proteins).”

This wouldn’t seem to be a problem for the between-meal dosing of BCAAs since there are already other amino acids in circulation. The aim of this strategy isn't to stimulate MPS using BCAAs by themselves; rather, it is to extend MPS.

However, like a complete protein, it also appears that an EAA mixture may optimise MPS. As such, consuming sufficient whole protein the majority of the time and then replacing around-workout whey protein with BCAAs may also have the intended benefit (i.e. optimal MPS stimulation) but with greater caloric efficiency. For example, whey contains roughly 25% BCAA, so assuming someone consumes 30g of whey protein pre and post training, this would amount to 60g of whey (240kcal), whereas isolated BCAAs will account for 15g total (60 kcal), a saving of 180kcal per workout day. If this person trained four times per week, this would be a saving of 720kcal per week, just over 100 kcal per day.

However, I honestly can’t see why someone would want to save calories by reducing protein intake in the first place, never mind go to all that effort just to save themselves 100kcal per day. The same reduction could be achieved by sticking with whey and reducing fat by 11g or carbohydrate by 25g per day, or a combination of the two. Not only will this save you money, you’ll get as much BCAA as well as all the other essential and non-essential amino acids (which may impart added benefit). You’ll also get the

I don't know about you but I'd prefer more to a meal than this whilst dieting.

potentially therapeutic compounds contained in whey such as immunoglobins and lactoferrin, as well potentially anabolic properties of whey independent of its constituent amino acids. Finally, you’ll likely experience greater satiety with whey compared to isolated BCAAs (something that would benefit dieters). In clinical research, BCAAs have been used to stimulate appetite in populations at risk for muscle wasting. The mechanism to explain why this is the case involves BCAAs competing with tryptophan for entry into the brain, thereby reducing the production of a satiating neurotransmitter, serotonin.  As such, it is ironic that the same supplement many take for dieting purposes may actually make dieting a more difficult experience than it needs to be. Conversely, the satiating effects of whey protein are well documented.

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Conclusions & Practical Recommendations

In summary, form part 1 of this article series, I discussed BCAA supplementation on top of a pre-existing sufficiency of protein and came to the conclusion that BCAAs would seem to make little, if any, difference in terms of muscle gain. In part 2, the stage was set for the current article in where I discussed the issue of meal frequency, the conclusion of which is outlined at the beginning of this article.

In this final instalment, we dug deeper into the more theoretical arguments for BCCA supplementation. Specifically,  the claims behind the between-meal dosing of BCAAs and how this might positively impact on muscle hypertrophy were examined, as well as their potential benefits whilst dieting.

The protocol advised by Layne Norton involves using doses of BCAAs likely to maximally stimulate MPS (~4-6g) in between meals spaced 4-6 hours apart. However, this strategy is largely based on amino acid infusion data and a deeply flawed study with highly predictable findings. Therefore, the practise of between-meal BCAA doing is essentially a hypothesis (that extending MPS slightly will lead to greater gains in strength/hypertrophy over time) based on a hypothesis (that such dosing protocols will actually extend MPS  under more realistic dietary conditions) based on a hypothesis (that the protein stat hypothesis holds true), thus extremely optimistic.

In terms of muscle retention whilst dieting, the frequency of protein ingestion doesn’t seem to make a difference as long as sufficient total protein is being consumed, meaning that between-meal dosing is irrelevant under dieting scenarios, at least in terms of optimising MPS on a meal-per-meal basis. As such, the caloric economy of BCAAs is their main attraction for dieters. However, at best, this tactic will save you a few calories, possibly at the expense of hunger, other beneficial properties associated with complete protein sources and money. It is much less hassle, cheaper, and potentially more beneficial to cut calories from either fat or carbohydrate.

Layne Norton may indeed be ahead of the game when it comes to his suggested BCAA protocol taken between meals separated by 4-6 hours. However, when compared to a sufficient protein intake (2.5-3g/kg) spread over the typical 3-4 meals (as suggested in part 2), I can’t see how this tactic could be much more beneficial, if at all. To quote Alan Aragon speaking about Layne Norton about the very topic:

“it’s crucial to realize that [Layne’s BCAA protocol] might be miniscule and not worth the effort or expense for non-competitive populations. In repeated personal communication, he has admitted to me that this tactic is done in attempt to clinch a very small edge to win. As a top-level, drug-free competitor, it’s justifiable to exploit all hypothetical nutritional means within reason in order to conjure the last bit of potential.”

As such, unless you are a physique competitor in search of that extra 1-2% (if it exists), it may be feasible to experiment with such tactics in the effort to gain an advantage. For the rest of us (>99.99 of people) looking to get in better shape, I see little point in supplementing with BCAAs. Instead, I’d urge you to save your money and invest in what delivers. That is, consume a sufficient amount (2.5-3g/kg) of high quality protein that will put you in good stead for making solid gains in the gym, whilst constantly hitting other macronutrient targets across a range of minimally processed foods. From there spread this intake evenly over the typical 3-4 meals, with two of these protein-containing meals placed within windows 90-120 minutes prior to and after weight training. If you have difficulty in reaching such intakes with solid proteins, opt for a decent whey protein concentrate or isolate in order to make up the difference. Speaking of weight training, focus on adding manageable weight in the main compound movements. Not only will this save you money, you will surpass the vast majority of people who use isolated BCAA supplements.

An Objective look at Biosignature Modulation: Part 2

In part one, I discussed the theory behind BioSignature Modulation. Today we will look at the practical side of things, and how we can go about losing stubborn body fat.

Practical issues regarding Biosig

Even if the theory behind Biosig did hold up, there are still some major limitations regarding its methodology.  Trainers/coaches etc. undergo a five-day, lecture-based course in order to become certified. Oddly, certification is guaranteed, as there are no examinations to filter out competent individuals from hopeless ones. While it would appear relatively straightforward, to become consistent and accurate with skinfold calipers takes quite a bit of practise. Practitioners often need to perform hundreds of skinfold measurements across dozens of subjects in order for their results to approach acceptable levels of validity and reliability. However, there is no evidence that Biosig practitioners abide by stringent methodology to ensure accurate and reliable measurements.

For example, in thisYouTube video, Mike Bystol – the owner/director of Strength and Conditioning at Poliquin Performance Center Chicago - is conducting a Biosig consultation on a female client. The regurgitation of Poliquin’s nonsense notwithstanding, he commits several errors in measuring her skinfold sites. Firstly, he only takes one measurement for each site. Standard practice is to take at least two measurements in order to produce two values within a very close range (i.e. 2 mm). Secondly, he failed to mark his subject up with a washable pen in order to determine the exact locations where he will take each skinfold measurement. A distance of as little as 1 cm deviation around a skin fold site is enough to produce significantly different values from trial to trial. Without standardised skinfold locations (such as those outlined by ISAK) and the consistent measurements of such sites via marking up the subject with a tape measure and washable pen, the measurement is utterly useless. For example, simply taking a skinfold measurement where the triceps are located is a complete waste of time. The only positive I can see from the video is that he appears to be using the research standard Harpenden skin fold callipers.

Why does BioSignature Modulation work?

When questioned about its efficacy, supporters of Biosig will turn to real world observations and say, “it works”. When they refer to it working, they invariably mean that skinfold measurements are generally decreasing, thus indicating that their client is losing body fat. These reductions in skinfold thickness will allow the Biosig practitioner to tell their client that they have reduced their skinfold measurements due to positive hormonal changes associated with their dietary, exercise and lifestyle prescriptions.

In fact, any half decent exercise and nutrition program will cause fat loss in a typical subject. Although improvements in body composition (i.e. increased muscle mass and decrease in fat mass), generally improve hormonal profiles (e.g. increased testosterone and decreased oestrogen), the only reason why a client would lose body fat (as assessed via reductions in skinfold thickness) is due to anenergy deficit (i.e. calories consumed were less than calories expended) brought about by the diet and exercise program, not because of some useless supplement, fancy routine or abstinence of carbohydrates.

Because of this apparent ‘masking’ of cause and effect, the trainer can tell their client what they want with regards to why ‘it worked’. As the client would be paying over the odds for this special Biosig service, they can be assured that the trainer will undoubtedly say it was due to this, not thermodynamics.

With all being said, my comments still don't fully explain the heart of the problem, and the main reason why people buy into Biosig: ‘stubborn body fat’.

How do you get rid of ‘stubborn’ body fat?

As I’ve hopefully convinced you of the vast limitations of BioSignature Modulation, I want to quickly explain how body fat is actually lost. To lose fat in general, net fat oxidation (fat burning) has to exceed fat storage; this is accomplished by creating an energy deficit either via exercise, diet or both. In order to oxidise fat, it first must be mobilised from the fat tissue and transported to the muscle or the liver so that it can be used for energy.

As mentioned in the previous article, stubborn fat is typically located in hips and thighs for women and lower abdominals for men. The reason why stubborn fat is stubborn has a lot to do with adrenoreceptors and blood flow. All hormones work through specific receptors. The catecholamines (epinephrine and norepinephrine AKA adrenaline and noradrenaline) work through adrenoreceptors (which are found all over the body, including fat cells). There are two main classes of adrenoreceptors: alpha and beta receptors. While there are two key alpha receptors (alpha 1 and 2) and four main beta receptors (beta 1-4), the only ones we will concern ourselves here with are alpha-2 and beta-2 adrenoreceptors.

When catecholamines bind to these beta adrenoreceptors, they promote fat mobilisation, and when they bind to the alpha adrenoreceptors, they decrease fat mobilisation. Stubborn fat cells contain a higher ratio of alpha-2 to beta-2 receptors, making it difficult to mobilise fat from these areas, preventing the transportation of fat to various tissues to be used for energy. It is worth noting that insulin pretty much always wins over catecholamines with regards to lipolysis, in that modest elevations of insulin will inhibit fat mobilisation, even in the presence of high levels of catecholamines.

An additional reason stubborn fat is stubborn is due to a lack of blood flow. With limited blood flow,free fatty acids (FFAs) can’t be transported away from the fat tissue to other tissues for burning. Similar to FFA mobilisation, fat tissue blood flow is also largely controlled by adrenoreceptor levels, with increased alpha adrenoreceptor activity inhibiting blood flow and increased beta adrenoreceptor activity increasing it.

This explains why this stubborn fat is only lost as we reach low body fat levels, and why fat with large amounts of blood flow (e.g. visceral fat) and that containing higher amounts of beta to alpha adrenoreceptores (e.g. that of the arms, upper back, detls etc.) generally comes off first.

In order to actually get rid of this stubborn body fat, we have to manipulate the adrenoreceptors by up-regulating the activity of beta receptors and down-regulate the activity of alpha receptors, as well as increasing blood flow to stubborn fat cells. We can increase catecholamine levels as well as blood flow to these tissues via aerobic exercise and the modulation of insulin levels via carbohydrate restriction. At the same time, we can supplement with oral yohimbe (an alpha-2 adredoreceptor antagonist) in order to inhibit the activity of the alpha receptors and increase FFA mobilisation. Lyle McDonald discusses such methods of eliminating fat in extreme detail in one of his books: The Stubborn Fat Solution.

Conclusions

Despite anecdotal reports of Biosig’s success, due to the complete lack of scientific evidence to support Poliquin’s methods, as well as the overreliance on physiologically inaccurate ideas, it is extremely difficult to see any value in this protocol. While I don’t doubt that a Biosig trainer can get you results (albeit at a very high price), the results wouldn’t be due to Biosig, rather, just a decent enough exercise and nutritional regime. The whole concept of Biosig combines unsubstantiated hokum and the glorification of the method of tracking changes in skinfold thickness, with one apparent goal: to fatten Poliquin’s wallet by ripping off trainers as well as their clients. A slapdash certification process as well the heavy reliance on his supplement line evidences this.

My advice to a trainee would be to save their money and continue with a structured nutrition and exercise regime and attempt to cross the bridge of stubborn fat if and when they come to it. If you suspect that you might have a problem hormonally, get your doctor to arrange for you to get a blood test. Unlike Biosig, this will actually show you your hormonal profile, as opposed to attempting to guess it, as well as being free of course!