Fasted vs. Fed Cardio for Fat Loss: Which is Better?

Fasted vs. Fed Cardio for Fat Loss: Which is Better?

Rationale for fasted cardio for fat loss

A common strategy among those competing in aesthetic sports (e.g. bodybuilders, fitness competitors etc.) and those competing in weight class sports (e.g. boxing, wrestling, judo etc.) is to perform cardiovascular exercise after an overnight fast, waiting until after the exercise bout to consume breakfast. The basic premise for this practise is that low levels of glycogen (and/or glycogen depletion during the exercise bout itself) and insulin, shift energy utilisation away from carbohydrate for fuel, thereby allowing greater mobilisation of stored fat that can be used for fuel (fat oxidation).

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Science vs. Broscience: a matter of economy?

Science vs. Broscience: a matter of economy?

Many of you will have heard the term broscience thrown around over social media and have a gist of what the term stands for. Everyone who has been involved in the pursuit of muscle gain and/or fat loss would have been guilty of broscience at least once in their lives; I certainly have. As such, the purpose of this article is to try and sum up the differences between science and broscience. In doing so, it will hopefully convince you that some of the things you’re currently doing in order to reach your body composition goals are pointless or ‘bro’. The elimination of these unnecessary practices will therefore make your life easier with respect to attaining whatever goal(s) you may have. To keep this article short, and because I’m a nutritionist, this article will focus primarily on aspects of nutrition, as opposed to the training side of things.

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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.


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.


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.


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.


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.


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.

Guest Post: The nuts and bolts of nutrition and neurotransmission (by Matt Jones)


Neurotransmitter’ appears to be the buzz word of the moment; the belief being that nutrition can have a significant affect on the appearance of blood and brain neurotransmitters themselves, a substantial body of evidence supports this notion (Wurtman & Fernstrom, 1974; Growdon & Wurtman, 1977, 1980; Gelenberg, Wojcik & Growdon, 1980). Such evidence has given rise to a spate of theories, generally all of the ‘Broscience’ ilk, a number of which originate from Charles Poliquin’s ideologies. The Meat & Nut breakfast is his most infamous nutrition and neurotransmission tale. While I personally also see the benefits of the inclusion of meat and nuts at breakfast, Poliquin has vastly over exaggerated the impact this meal has on your brain neurotransmitters and thus the subsequent actions and emotions. Here we’ll critique the current evidence regarding nutrition and neurotransmission and hopefully dispel any of the Poliquin myths along the way.

Science talk, a neurotransmitter is a chemical signal which allows transmission of signals from one neuron to another, across a synapse; in English that basically means it’s a vehicle which allows messages to be transported from one nerve to another. Neurotransmissions allow, and control muscle fibre contraction, bodily actions, emotions and feelings. The most significant neurotransmitters in the human body are acetylcholine, norepinepherine, dopamine, GABA, glutamate, serotonin and endorphin.


Neurotransmitters and cognitive function

Serotonin is a known sleep inducing agent (Hartman & Spinweber, 1979), and human research has suggested serotonin reduces subjective alertness, objective performance, and increases feelings of relaxation and lethargy (Spring, 1984). Dopamine on the other hand is associated with pleasurable reward, behaviour, cognition, mood, memory, movement, attention and learning. Acetylcholine has a number of physiological functions, and is a widely distributed excitatory neurotransmitter that in the central nervous system is involved in wakefulness, attentiveness and memory. Interestingly, Alzheimers disease is characterised by a significant reduction in acetylcholine concentration and function (Francis, 2005), highlighting its importance in human performance.

Neurotransmitters and nutrition

The primary neurotransmitters are synthesized from the amino acids, tyrosine and tryptophan. The rates at which these neurotransmitters are synthesized depends upon the availability of the amino acid precursor; where tryptophan is the precursor of serotonin, and tyrosine is the precursor of dopamine and norepinepherine (Wurtman et al. 1980); this link was made in the 70’s and early 80’s when evidence from rat studies became available. The administration of a single dose of tryptophan elevated brain tryptophan levels, and thus the levels of serotonin and its major metabolite 5-hydroxyindole acetic acid (5-HTP). The administration of tyrosine similarly elevated brain tyrosine levels, and thus catecholamine synthesis increased in the central nervous system (CNS), while the consumption of lecithin or choline (found in fat) increases brain choline levels and neuronal acetylcholine synthesis (Wurtman & Fernstrom, 1975).


Most of these studies were on rats, using a single dose of the precursor, although similar effects have been seen following the consumption of dietary sources. The consumption of a single protein-free high-carbohydrate meal elevated brain tryptophan levels. Similarly the consumption of a single 40% protein meal accelerated brain catecholamine synthesis through increased availability of tyrosine (Wurtman & Fernstrom, 1975). A minimal change of delta 0.07 in the tryptophan to large neutral amino acid ratio is required to influence mood following protein consumption, so a considerable shift in the ratio is required to have an effect on subsequent cognition (Fernstrom, 1994).

These early observations clearly demonstrate that serotonin and catecholamine neurotransmitters are under specific dietary control, so in that regards Poliquin is correct. The acute effects of a high-carbohydrate protein-free meal, typical of most children’s and a vast majority of westerner societies breakfast (think cereals) do induce marked increases in serotonin synthesis, and thus may result in increased feelings of lethargy; however, is the absolute avoidance of carbohydrate justifiable based on the current evidence?

It appears not. Interestingly, the addition of protein to that otherwise protein-free high-carbohydrate meal suppressed the increases in brain tryptophan and serotonin (Wurtman & Fernstrom, 1975), because protein contributes to the blood plasma considerably larger amounts of the other neutral amino acids (e.g., BCAA’s, phenylalanine) than of tryptophan. Tryptophan and other large neutral amino acids, most notably the BCAA’s leucine, isoleucine and valine share and compete for uptake along the specific transport mechanism across the blood brain barrier (Maughan, 2000). Therefore brain 5-HTP synthesis will increase when there is an increase in the ratio of free tryptophan to BCAA’s in the blood (Chaouloff et al. 1986), thus explaining why the addition of protein to an otherwise protein-free high-carbohydrate meal can suppress serotonin synthesis.

Just to confirm, this theory has also been confirmed in humans. Using 20 men, Lieberman et al. (1985) administered single oral doses of tryptophan (50 mg/kg) and tyrosine (100 mg/kg) in a double-blind, crossover study. Tryptophan increased subjective fatigue and decreased self-ratings of vigour and alertness, but did not impair performance on any of the tests. Tyrosine produced no effects in our young population compared with placebo, but did decrease reaction time relative to tryptophan. The authors concluded that tryptophan has significant sedative-like properties, but unlike other sedatives may not impair performance in a series of cognitive tests. Now being critical, it’s extremely unlikely – probably impossible in fact – you’d ever consume 50 mg/kg tryptophan in a single dose from a dietary source, thus wouldn’t necessarily have to worry about the negative mental effects of tryptophan consumption.

charles_poliquin_on_food_15931_7So Poliquin, who strongly advocates the avoidance of carbohydrate at breakfast time has no science to back up such claims. The truth is the brain neurotransmitters are influenced by the ratio of free tryptophan to large neutral BCAA’s (Fischer et al. 2002), so a mixed meal that will maintain a balance in that ratio is adequate. Further an increase in the ratio of free tryptophan to large neutral amino acids following a high-carbohydrate meal is reversible through the addition of a protein to that meal.

An intricate study by Fischer et al. (2002) examined the cognitive effects of isoenergetic meals consisting of three carbohydrate ratios, a carbohydrate rich meal (4:1), a balanced meal (1:1), and a protein rich meal (1:4) in 15 healthy subjects. Not surprising, attention and decision times were improved in the first hour with the high carbohydrate meal, owing to the greater rise in glucose metabolism. But during the first hour it was both the balanced and higher protein meals that resulted in improved performance. Further, overall reaction times in a central task were fastest after the balanced or high protein meal, thus suggesting a high protein meal or a balanced meal seems to result in better overall cognitive performance. Although the results also revealed participants subjective measures of ‘tasty’ and ‘pleasant’ were greater in the balanced meal than in the high protein meal, which suggests this would be the most effective in a practical sense.


The mechanisms

Now, from reading the above it may appear that carbohydrates contain significant amounts of tryptophan, thus increase free tryptophan concentrations after ingestion, thus increasing tryptophan uptake and stimulating serotonin synthesis. However, this is not the case. For the sake of dispelling Poliquins breakfast argument let’s take oats for example, the amino acid profile of 100g oats indicates a tryptophan concentration of 234 mg, compared to 694 mg isoleucine, 1284 mg leucine, and 937 mg valine, which collectively make up the BCAA’s. So a high carbohydrate breakfast doesn’t contain that much tryptophan and yet accelerates serotonin synthesis through an increase in tryptophan uptake by the brain, how does that work?

Although the carbohydrate meal itself doesn’t contain much tryptophan, the insulin that is secreted following the carbohydrate meal results in a decrease in plasma levels of the large neutral amino acids (tyrosine, phenylalanine, BCAA’s and methionine) that would ordinarily compete with tryptophan for uptake by the brain. Tryptophan then crosses the blood-brain barrier and is converted to serotonin (Spring, 1984).

So it’s not actually the carbohydrate that causes the problem, it’s the insulin response to that carbohydrate that is the issue.


Innovative idea

The following is a novel thought that stemmed from logic and my intuition: looking at the insulin index created by Holt et al. (1997) beef, the food advocated by Poliquin in his infamous meat and nut breakfast comes in at an insulin area under the curve of 7910 ± 2193 pmol.min.L and grain bread, a food demonized by Poliquin in fear of it frying your brain cells comes in at 6659 ± 837 pmol.min.L. The insulin index clearly indicates beef is more insulinogenic than most forms of carbohydrate, therefore suggesting that the net effect in regards neurotransmitter synthesis of a high-protein carbohydrate-free meal may be similar to that of a mixed meal. The greater insulin response to beef consumption will lead to a reduction in the BCAA’s and other neutral amino acids, leaving free tryptophan to be taken up by the brain; interestingly 100g steak contains more tryptophan than the same portion of oats (288 mg).

Logic and intuition suggests this could be true, although a number of rat studies have disproved the hypothesis, where Rouch et al. (1998) revealed a high protein diet significantly reduced serotonin concentrations for 2-hours, Wurtman & Fernstrom (1975) reported similar findings. Interestingly, the reduction in serotonin following protein feeding is thought to be among the reasons why protein is more satiating that carbohydrate.

Finally, Poliquins suggestion that the first meal of the day dictates that whole days brain neurotransmitters. We’ll start with a rat study from 1995; Fernstrom & Fernstrom studied the brain tryptophan concentrations and serotonin synthesis rates of fasted rats fed a high-carbohydrate meal followed 2-hours later by a protein-containing meal. They demonstrated that when the high-carbohydrate meal was fed first, brain tryptophan concentrations increased as did serotonin synthesis, and these changes were reversed at 4-hours if the second meal contained protein. Interestingly they go on to conclude, and I quote: “brain tryptophan concentrations and serotonin synthesis are thus responsive to the sequential ingestion of protein and carbohydrate meals if there is a sufficient interval between meals”. Similarly, Rouch et al. (2003) reported the plasma ratio of free tryptophan to large neutral amino acids was increased by a carbohydrate meal, and remained high for 2-hours, a subsequent casein (protein) meal reversed this change. Interestingly, a first casein meal reduced the ratio, and was not increased again by a subsequent carbohydrate meal. These findings actually favour Poliquins suggestions, although the weight of the evidence doesn’t, again supporting my belief of a mixed meal consumption.

From a human perspective the reversible nature of neurotransmitter synthesis is supported by the central fatigue hypothesis, which predicts that the ingestion of BCAA’s during exercise will raise plasma BCAA concentration and hence reduce transport of free tryptophan into the brain; subsequently reducing the formation of serotonin and alleviating sensations of fatigue and therefore improve endurance performance (Gleeson et al. 2005). This hypothesis lacks support, although does highlight the obvious reversible nature of neurotransmitter synthesis.


Conclusion and recommendations

My recommendation based on this evidence is that a single macronutrient meal can have a significant impact on the brain neurotransmitters, where a protein-free high-carbohydrate meal can increase serotonin synthesis, and thus increase feelings of fatigue just as Poliquin suggests. Although alternatively, a high-protein high-fat carbohydrate-free meal can increase catecholamine synthesis. Granted you would favour catecholamine synthesis, but with your daily macronutrient requirements in mind, combined with the fact that eating single macronutrient meals would be extremely tasteless and boring it would be more appropriate to consume mixed meals than to focus on meals free from certain macronutrients in fear of a surge of sleep inducing neurotransmitters.

In conclusion the promotion of carbohydrate free, high-protein breakfasts is largely unsubstantiated. A mixed meal consisting of meat, carbohydrate (both starchy and fibrous) and fat (possibly nuts) is adequate, and in a practical sense is optimal.


Chaouloff et al. (1986)

Fernstrom & Fernstrom (1995)

Fernstrom et al. (1994)

Fischer et al. (2002)

Francis (2005)

Gelenberg et al. (1980)

Gleeson et al. (2005)

Growdon & Wurtman (1977)

Hartman & Spinweber (1979)

Holt et al. (1997)

Lieberman et al. (1985)

Maughan (2000)

Rouch et al. (1998)

Rouch et al. (2003)

Spring et al. (1984)

Wurtman, R., & Fernstrom, J. (1974). Nutrition and the Brain. Scientific American, 230, 84- 91.

Wurtman & Fernstrom (1975)

Wurtman et al. (1980)


UnknownBio: Matt holds a BSc (Honours) degree in Sport & Exercise Science, an MSc in Nutrition Science. Through his own Performance Nutrition business, Nutrition Condition, he delivers frequent Health & Wellbeing Workshops to corporate and personal clients advising on how best to develop a sound, scientifically structured nutrition programme free from fads and marketing bias. Nutrition Condition also delivers Performance Nutrition services to professional athletes.

Matt can be contacted on or at

For regular updates follow Matt on Twitter @mattNCUK.

Protein requirements for people who will never settle for being average

With over 50 years of research, we are still debating over how much protein you actually need for given types of exercise (i.e. weight training vs. endurance training etc.). On the conservative side of protein intakes we tend to have the mainstream nutritionists who maintain the idea that athletes don’t need to consume protein in excess of the recommendations outlined for non-athletes. On the other side of the argument are the athletes and bodybuilders themselves who have for several decades maintained the idea that they need to consume greater amounts of protein than the average person.

As research exists for both sides of the argument, scientists tend to have mixed views on how much protein a person actually needs, whether they are sedentary, in training or a professional athlete.

In this article I will address the popular, yet often misunderstood, topic of protein requirements. I will examine the research from both sides of the argument, as well as what I’ve seen work in practise, and present my own recommendations.

The basics of protein metabolism

The amount of muscle tissue in the human body remains fairly stable over time. However these tissues are undergoing a continuous process of breakdown and resynthesis; these processes are referred to as protein turnover.

The amount of muscle mass a person has depends on the long-term relationship between muscle protein breakdown and synthesis. For example, if muscleprotein synthesis exceeds breakdown, there will be an increase in the amount of that protein.

Protein turnover is mediated by severalfactors including hormones (testosterone, growth hormone, thyroid, insulin, glucagon & cortisol), caloric intake, amino acid/protein availability and training. The largest factors that influence skeletal muscle metabolism are eating and training.

Eating a meal

Theprimary factors influencing protein breakdown and synthesis following the consumption of a meal are the concentrations of insulin andamino acids in the blood. With regards to protein synthesis, the essential amino acid (EAA) content of a meal plays a significant role in promoting synthesis; insulin plays a smaller role. In a more direct role, insulin increases amino acid transport into skeletal muscle. Assuming sufficient amino acids are available, only small elevations in insulin are required to maximally stimulate protein synthesis. Regarding protein breakdown, consuming a meal would appear to decrease protein breakdown by increased amino acid availability as well as the presence of insulin.

The take home message here is that insulin combined with increased amino acid availability, results in net protein gain. This may lead one to assume that the simple act of eating a load of protein will lead to gains in muscle mass. However, this isn’t the case due to a process called diurnal cycling, whereby net protein synthesis following a meal is matched by an increased protein breakdown when food is not being consumed. So the more protein someone eats and the more they store in the day, the more they break down at night. This process is thought to provide amino acids from the ingested food more evenly over a 24-hour period.

The effects of training

In untrained people diurnal cycling tends to keep the body at a stable amount of muscle mass. However, when exercise is introduced, it basically “forces” the body to store more protein (assuming sufficient protein and overall caloric intake that is).

The type of training dictates how dietary protein is used to synthesise new proteins in the body. Following weight training both protein synthesis and breakdown are increased, though breakdown is stimulated to a greater degree, meaning that the body is likely to be in a catabolic state following weight training. The provision of protein/calories around the workout will shift the body into an anabolic state “forcing the body to store protein at a higher level (increase muscle mass).

In contrast, endurance exercise results in a different effect on skeletal muscle. Instead of increasing the size of contractile proteins, it mainly stimulates the synthesis of mitochondrial enzymes within the muscle, contributing to an increase in energy production (oxidative capacity) during such activity.


The recommended daily intake of protein

Challenging the RDA

According to thelatest dietary reference intake (DRI) in 2005, the amount of protein that all adults should consume on a daily basis (RDA) is 0.8 grams per kilogram of bodyweight (0.8g/kg). Based on nitrogen balance data, this intake is estimated to cover the basic needs of 97-98% of individuals. The authors of this report state that this intake is suitable for both sedentary individuals as well as endurance or strength athletes: “In view of the lack of compelling evidence to the contrary, no additional dietary protein is suggested for healthy adults undertaking resistance or endurance exercise.”

In contrast, the most recent scientific literature would recommend intakes from 1.2-2.2g/kg for strength and endurance trained athletes. Even for untrained individuals the RDA would seem insufficient for some individuals. For example, a 14 week study by Campbell and colleagues observed that subjects (55-77 years) consuming the RDA for protein (0.8g/kg) experienced significant muscle loss in the mid-thigh area, despite consuming calories to maintain bodyweight. Since this study was published in 2001, the authors of the latest DRI report had sufficient time to amend these recommendations based upon the most recent literature. Either sincere ignorance or laziness may account for this. In keeping with the latter, this may also explain why the RDA for protein hasn’t changed for several decades.

While the RDA may meet the need for the majority of sedentary individuals in energy balance, this amount is simply inadequate for strength and endurance athletes as well as for the elderly or dieting individuals, regardless of training status. Given the lower digestibility and inferior quality of many grain and legume (i.e. beans and nuts) proteins, vegetarians and vegans may need to consume protein in the excess of the RDA to compensate.


Protein requirements for strength and endurance athletes

An early review article by Lemon in 1991 recommended protein intakes of 1.2-1.4 g/kg for endurance athletes and 1.4-1.7 g/kg for strength/power athletes; for athletes competing in sports where a mix of these training methods is warranted (i.e. MMA, Rugby etc.), the upper limit recommended for strength athletes has been suggested to cover protein needs.

These increased requirements for endurance and strength athletes occur for different reasons. During intense aerobic activity (i.e. running or cycling) amino acids, namely the branched chain amino acids (BCAAs), have been shown to account for roughly 5-10% of total energy cost of the activity; this percentage may increase further when muscle glycogen is depleted. In contrast, amino acids provide little energy during strength training. Instead, the increased need for protein comes from the repair of damaged muscle tissue as well as the synthesis of new muscle proteins.

Lemon’s conclusions have since been criticised by Millward, mainly because of the inherent limitations associated with nitrogen balance (the technique used to deduce protein needs). Indeed, the errors associated with estimating nitrogen losses may accumulate and lead to an overestimation of true protein requirements. Additionally, nitrogen balance doesn’t consider the dynamic processes of protein turnover, rather, the amount of nitrogen going into the body (food and drink) minus nitrogen losses form the body (i.e. urine, faeces, sweat etc.).

Millward has also cited earlierwork suggesting that endurance training may actually lower protein requirements compared with untrained individuals, due to an adaptive downregulation increasing the re-use of amino acids. Indeed, in a widely cited study, it was demonstrated that nitrogen balance was negative at the start of an exercise training programme, but returned to equilibrium after a period of accommodation. This occurred despite a constant daily protein intake. Following the period of accommodation, no increase in protein intake was necessary to maintain a stable nitrogen balance.

However, while more recent research has suggested that this may be the case for individuals performing low intensity endurance exercise, endurance athletes (and the more serious recreational athletes) who perform many hours of high intensity exercise per week, would seem to benefit from higher intakes than their untrained counterparts. Furthermore, for the evidence suggesting an increased efficiency of amino acid re-use as protein intake decreases, nitrogen balance may be attained with a compromise in some physiologically relevant processes such as enzyme upregulation or capailliarisation following endurance training. It would therefore seem that while training may improve protein retention (thus achieving a neutral nitrogen balance), this might hinder potential performance enhancing adaptations associated with endurance exercise.

For athletes wishing to gain lean body mass, it has been shown that whole body and muscle protein synthesis rates are greater with increasing protein intakes. In one study, experienced weightlifters were fed either 1.2 or 2.1 g/kg of protein per day for six weeks. In the group that ingested the higher amount, gains in lean tissue mass increased significantly, whereas there was no change in the 1.2 g/kg group.

These results clearly refute the notion that trained individuals don't need more protein than the average person. However, these results still give no idea what an optimal intake might be in this case; just that 2.1 is better than 1.2 g/kg of protein.

Despite the above study, not all evidence supports the idea of increasing amounts of ingested protein leading to greater muscle mass gains. A study by Tarnopolsky and colleagues examined nitrogen balance, body composition and urea excretion during a habitual 10-day period followed by an altered protein intake for 10 days. However, by virtue of slow rates of muscle mass gains, with an altered protein intake period of 10 days, it is unsurprising that there were no changes in lean body mass seen among individuals in this investigation. A further study by the same lead researcher indicated that a protein intake of 2.4 g/kg was not superior to that of 1.4 g/kg in terms of lean body mass gain, among trained strength athletes. However, given the short (a few weeks) study period, it is possible that muscle gain was occurring in the higher protein group, and that the change was too small to be measured with existing body composition techniques.

From a separate standpoint, it has also been argued that the debate over protein requirements is pointless in the first place since the majority of both strength and endurance athletes habitually consume amounts in excess of the recommendations outlined by Lemon. While this is generally true, some athletes, particularly female athletes, have been shown to consume inadequate amounts of protein.

Why all the conflicting viewpoints?

Since the original review article on protein requirements by Lemon in 1991, much data has since been published regarding the interaction of protein and exercise. However, despite these advances, more questions remain unanswered than have been solved. Limitations in research methodology certainly confound results (i.e. nitrogen balance). Participant selection, their adaptation to the protein intakes during their respective studies, training status, nutritional status and exercise intensity further contribute to the discrepant findings, which ultimately to lead to different interpretations. As mentioned previously, short study periods are also far from realistic in order to observe true lean body mass changes with differing protein intakes.

Perhaps the most logical interpretation of the research findings thus far comes from the authors Tipton & Wolfe. Probably their most important point is that athletes and coaches are not interested in the academic debates surrounding protein requirements, rather, they are interested in the specific amount of protein that will optimise athletic performance. This is where the research has often fallen short; instead of looking at performance endpoints following the ingestion of different amounts of protein, studies have tended to simply examine protein “requirements”. That is, the daily amount of protein that supports net protein balance, measured via nitrogen balance or examining leucine kinetics. Indeed, a protein intake that stimulates optimal physiological adaptation (i.e. capillary and enzyme upregulation, muscle hypertrophy and total oxidative capacity of the muscle) as well as immune surveillance, may be in excess of the current recommendations outlined for strength and endurance athletes. It is therefore important to distinguish the difference between a protein “need” of a given athlete, and the amount of protein that will stimulate maximal “adaptations” leading to optimal performance.

A further point the authors make surrounding protein requirements is that the definition of a protein requirement is context specific. For example, the amount of protein that an strength power lifter is to consume to maintain lean body mass will be different to that of a bodybuilder trying to gain lean body mass or that of a bodybuilder aiming to lose body fat while maintaining their muscle mass. The list goes on…

This article also highlights the fact that a daily protein intake of 2.5-3 g/kg for strength and power athletes is not harmful and would appear more than is necessary for protein synthesis, any excess would simply be oxidised. As a slight tangent, it is worth noting that some authors feel that increased oxidation may contribute to the anabolic drive of the body. Given the scant and limited duration data on performance/bodycomposition endpoints, erring on the side of too much rather than too little dietary protein may be the best approach for strength and/or hypertrophy. Perhaps the single greatest risk of ingesting too much protein is the displacement of other macronutrients, namely carbohydrate, which might hinder high intensity exercise. However, since intakes of ~6400 kcal have been reported in strength athletes, an intake of 2.5 g/kg would only account for 14% of their daily intake.

Since endurance athletes are typically less interested in gains in lean body mass, or body weight for that matter, the upper limit for protein consumption would be lower than that for strength/ power athletes. Tarnopolsky’s research group hasdemonstrated that protein intakes above 1.7 g/kg result in the excess being oxidised. Therefore, there appears to be no reason to suggest protein intakes above 2 g/kg for endurance athletes. Similar to the strength/power athletes, this intake is unlikely to impede on carbohydrate or fat intakes. For example, if an endurance athlete consumes 3000 kcal per day, an intake of 2 g/kg would only account for 18% of total intake. Endurance athletes typically consume more total energy that this anyway. As mentioned earlier, athletes competing in team sports (i.e. soccer, rugby, basketball etc.), whose training consists of both endurance and strength work, the lower intake recommended for strength athletes (2.5 g/kg) would be a good starting point. However if hypertrophy is required, they maybe should consider the upper limit of 3 g/kg.

To clarify, based on these data, I feel that daily protein intakes of 2.5-3 g/kg appear optimal for strength/power athletes as well as many team sport players, or any athlete that combines both strength/hypertrophy and endurance training. For drug fuelled athletes looking to maximize muscle gains, more protein than 3 g/kg may be required (intakes in excess of 4-5 g/kg have been reported anecdotally). However, this is beyond the scope of this article. For endurance athletes, where muscle hypertrophy is  generally undesired, daily protein intakes of 1.7- 2 g/kg have been suggested to maximise the adaptive response to such training.

Protein requirements when dieting

Given the significant protein sparing effect of energy intake, when athletes need to make weight, reduce unnecessary fat or when physique athletes need to prepare for a show or photo shoot, increasing protein above the recommendations outlined here are imperative to avoid muscle loss. As calories are reduced, the body retains less protein and more is used to supply energy (via gluconeogenesis); therefore, the body needs more.

It has been demonstrated that in overweight, non-trained individuals, protein intakes almost double that of the RDA (~1.5 g/kg) are required to maintain lean body mass losses during calorie restriction. Bodybuilders have successfully used this practice over the last 40 or so years by increasing habitual protein intakes by roughly 150% in the pursuit of rapid fat loss while maintaining muscle. However, for most performance athletes, such a drastic calorie reduction isn’t optimal. Instead, a more modest fat reduction is optimal for several reasons (perhaps, most importantly, as carbohydrate intake will suffer, thus hindering training performance).

Given the relatively high protein intakes recommended above, there would be little need to increase protein too much over the outlined recommendations. Without any scientific data to go by, the lower end of the protein intake should be replaced by the upper amount suggested. For endurance athletes, this would be an intake of 2 g/kg of protein per day. If fat loss is achieved in a preferable manner (i.e. gradually), these intakes will minimally impede of carbohydrate intake. Thus, the athlete is able to maintain performance to a degree, while consuming enough protein to cover all needs and minimising muscle loss. For physique athletes aiming to reach the limits of leanness (i.e. 3-5% body fat for men and 9-12% for women), then increasing protein intakes in excess of these recommendations, may limit muscle loss to a greater extent.


Summary and application

In summary, well it does appear that the RDA of 0.8g/kg of protein may be enough for most untrained individuals (assuming they are in nitrogen balance), this simply isn’t enough for some untrained populations (i.e. older or dieting individuals).

There is plenty of research highlighting that the RDA is indeed insufficient for trained individuals, with original protein intake recommendations of 1.2-1.4 g/kg for endurance athletes and 1.4-1.7 g/kg for strength/power athletes. However, given that research exists supporting both the consumption of more and less than these original recommendations, the debate over protein requirements is likely to continue for decades.

More importantly, coaches and athletes are less interested in these academic debates. They simply wish to know what intake will optimise performance. However, until more valid performance endpoint research is conducted, these questions will remain unanswered. Furthermore, given the methodological difficulties in carrying out such research, this won’t be any time soon. With that being said, there does appear to be sufficient research to draw out reasonable protein intake recommendations for athletes. This, combined with my personal observations in the field, I am able to outline some specific recommendations depending on your type of training and body composition goals (see table below).

Given that protein intakes at the higher ends of my recommendations are unlikely to have negative impacts on health and performance, the best approach may be to err on the side of consuming too much, as opposed to too little. The positive effects on body composition (i.e. fat loss and muscle gain) of higher protein diets compared to calorie-matched lower protein diets, would also support this notion.

Outlined below are the intakes that I ultimately recommend. These intakes should ensure optimal adaptations as well as allowing room for the consumption of other important macronutrients. For regular gym-goers, the lower end of the recommendations will suffice.

Athlete type


General intake

Dieting intake















Mixed sport







Although protein quantity would appear to be more important than quality, protein intake is certainly not the whole picture with regards to optimising body composition or performance. To finish off nicely, I’ll leave you with a final quote by Tipton and Wolfe:

“Current literature suggests that it may be too simplistic to rely on recommendations of a particular amount of protein per day. Acute studies suggest that for any given amount of protein, the metabolic response is dependent on other factors, including the timing of ingestion in relation to exercise and/or other nutrients, the composition of ingested amino acids and the type of protein”