The Right Nutrition for Muscle Growth

Macros to Boost mTOR and Protein Synthesis

By Michael J. Rudolph, Ph.D.

Nutrition may be the most important component of an athlete or bodybuilder’s training protocol, allowing the athlete to maximize anabolic potential.

I know what you may be thinking – here’s just one more article reiterating the fact that protein consumption is essential for muscle growth. Well, rest assured that’s not what this article is about. On the contrary, the central focus of this article highlights the important functions that specific macronutrients carry out in order to stimulate the all-important nutrient-sensing molecule mTOR. Furthermore, how mTOR regulates muscle protein turnover in response to a vast array of nutritional stimuli directing protein synthesis in muscle cells and optimizing muscle growth and strength during times of energy surplus. 

Macronutrients for Greater Muscle Mass

Protein turnover in the muscle cell is a complex process that encompasses both protein synthesis and protein breakdown of existing muscle protein. Increasing muscle mass requires a greater amount of muscle protein synthesis along with reduced muscle protein breakdown.  Consuming the right macronutrients will profoundly enhance muscle protein synthesis and diminish muscle protein degradation, promoting greater muscle mass and strength.¹ More specifically, certain macronutrients achieve greater muscle protein synthesis by activating the extremely important nutrient-sensing molecule mTOR. Upon activation, mTOR stimulates muscle protein synthesis and inhibits muscle protein breakdown – therefore increasing muscle mass.

Essential Amino Acids Activate mTOR

Several scientific studies have drawn attention to mTOR being activated by the essential amino acids, especially leucine. Walker et al.² demonstrated in humans that ingesting essential amino acids shortly after working out increased mTOR activity – leading to greater post-workout muscle protein synthesis by an additional two hours, as compared to an exercised group that was not fed essential amino acids. Interestingly, this study also confirmed that consuming greater amounts of essential amino acids, with the effect leveling off at 10 grams per day, increased the cellular stockpile of amino acids. The increased concentration of essential amino acids within the muscle cell stimulates the insulin-signaling pathway, thus activating mTOR – which cranks up protein synthesis.

In a second investigation, Wilson et al.³ presented evidence supporting the idea put forth by Walker et al. that increased levels of essential amino acids stimulate muscle protein synthesis. Wilson et al. demonstrated this by showing that mice fed essential amino acids plus carbohydrate have significantly greater muscle protein synthesis, as compared to mice fed essential amino acids alone. Given that carbohydrates are the preferred energy source for muscle cells, carbohydrate consumption will diminish the utilization of amino acids as an energy source – consequently, generating a greater amount of available essential amino acids and enhancing muscle protein synthesis.

Interestingly, the preferential use of carbohydrate by the muscle cell generates cellular energy (ATP). AMPK, the cell’s energy-sensing gauge, will be turned off by ATP production. In view of the fact that active AMPK inhibits mTOR, turning AMPK off will also stimulate mTOR activity.

In a separate investigation, Pasiakos et al.⁴ showed that human consumption of the essential amino acid leucine immediately after exercise specifically enhances muscle protein synthesis by 33 percent. 

Fatty Acids Enhance Insulin Pathway Signaling

Long-chain omega-3 fatty acids stimulate muscle protein synthesis by activating mTOR. Research by Gingras et al.⁵ presented long-chain omega-3 fatty acids as specific activators of mTOR and muscle protein synthesis via the insulin signaling pathway. This study established that long-chain omega-3 fatty acids enhance the insulin-mTOR-protein synthesis-signaling pathway by diminishing whole-body inflammation, which has been shown to cause insulin insensitivity.⁶ Furthermore, the researchers showed that consumption of long-chain omega-3 fatty acids produced an increase in amino acid incorporation into muscle protein synthesis by 108 percent.

High-Fat Diets Reduce Protein Synthesis

As certain macronutrients stimulate mTOR activity and muscle protein synthesis, other macronutrients inhibit mTOR signaling and muscle protein synthesis. A study by Rivas et al.⁷ confirms that consuming a high-fat diet triggers insulin insensitivity, yielding diminished mTOR signaling and muscle protein synthesis. mTOR inhibition stems from negative feedback within the insulin signaling pathway. Chronic consumption of a high-fat diet overactivates mTOR, which in turn heavily activates the molecule S6K. A hyperactive S6K produces inactivating signals within the insulin-signaling cascade, thus diminishing sensitivity to insulin along with mTOR activation and protein synthesis.

Ketogenic Diets Bad for Muscle Growth

Bodybuilders have tried to get shredded by implementing a ketogenic diet high in fat and low in carbohydrate – the idea being to force the body to burn fats rather than carbohydrates. With very little carbohydrate in the diet, the liver converts fat into ketone bodies – which were suspected to possess appetite-suppressant properties, thus facilitating caloric restriction and loss of body fat.

Regardless of whether ketogenic diets reduce body fat, they still may not be a productive approach to getting lean – as a study by McDaniel et al.⁸ reveals that ketogenic diets significantly diminish insulin function and mTOR activation of muscle protein synthesis. Intriguingly, this study also demonstrated that a high-fat diet supplemented with high protein partially mitigated the negative effects of ketogenic diets by improving mTOR signaling and muscle protein synthesis.

To further substantiate the idea that a ketogenic diet is deficient for muscle growth, Bielohuby et al.⁹ demonstrated that ketogenic diets also lead to growth hormone insensitivity within the liver. Growth hormone insensitivity leads to a lack of IGF-1 production by the liver, which in turn diminishes the insulin signaling and mTOR pathways – leading to diminished protein synthesis within muscle cells.

Maximize Your Anabolic Potential

In conclusion, nutritional supplementation approaches promoting the most efficient muscular adaptations to strength training appear to center around the correct delivery of the appropriate macronutrients to the muscle cell that modulate the activity of the all-important energy-sensing molecule mTOR. For instance, consuming simple carbohydrates during exercise will cause an insulin response, activating mTOR and protein synthesis. Yet more notably, simple carbohydrate consumption during exercise will have a glycogen-sparing influence within muscle cells. Stored glycogen has been shown to inhibit AMPK activity. Since AMPK inhibits mTOR function, AMPK inactivity will lead to mTOR activity. Likewise, the precisely timed consumption of specific essential amino acids after your workout will optimally stimulate the activity of mTOR and lead to greater muscle protein synthesis and muscle growth.

All things considered, nutrition may be the most important component of an athlete or bodybuilder’s training protocol, allowing the athlete to maximize anabolic potential.

For most of Michael Rudolph’s career he has been engrossed in the exercise world as either an athlete (he played college football at Hofstra University), personal trainer or as a research scientist (he earned a B.Sc. in Exercise Science at Hofstra University and a Ph.D. in Biochemistry and Molecular Biology from Stony Brook University). After earning his Ph.D., Michael investigated the molecular biological effects of exercise as a fellow at Harvard Medical School and Columbia University. That research contributed seminally to understanding the function of the incredibly important cellular energy sensor AMPK – leading to numerous publications in peer-reviewed journals including the journal Nature. Michael is currently a Senior Scientist working at the New York Structural Biology Center where he investigates the molecular nature of human illness and disease.

References:

1. Hawley JA, Gibala MJ, et al. J Sports Sci 2007; 25 Suppl 1, S115-124.

2. Walker DK, Dickinson JM, et al. Med Sci Sports Exerc 2011; 43(12), 2249-2258.

3. Wilson GJ, Layman DK, et al. Am J Physiol Endocrinol Metab 2011; 301(6), E1236-1242.

4. Pasiakos SM, McClung HL, et al. Am J Clin Nutr 2011; 94(3), 809-818.

5. Gingras AA, White PJ, et al. J Physiol 2007; 579(Pt 1), 269-284.

6. Olefsky JM and Glass CK. Annu Rev Physiol 2010; 72, 219-246.

7. Rivas DA, Yaspelkis BB, et al. J Endocrinol 2009; 202(3), 441-451.

8. McDaniel SS, Rensing NR, et al. Epilepsia 2011; 52(3), e7-11.

9. Bielohuby M, Sawitzky M, et al. Endocrinology 2011; 152(5), 1948-1960.

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