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How do dietary proteins and amino acids induce muscle hypertrophy?

This is an excerpt from Biochemistry Primer for Exercise Science-5th Edition by A. Russell Tupling,Peter M. Tiidus & Michael E. Houston.

Dietary Protein, Amino Acids, and Muscle Mass
Resistance training has long been known to induce muscle hypertrophy as well as increase muscle strength. Increased muscle hypertrophy results from an overall positive net protein balance (NPB), where muscle protein synthesis (MPS) exceeds muscle protein breakdown (MPB). The molecular regulation of MPS and MPB, both under basal conditions and in response to resistance training, is discussed in chapter 3. Reviews by Burd and colleagues (2009; 2019) covered research developments related to dietary intake of specific amino acids and proteins and to their timing relative to optimization of positive NPB. As previously noted, protein and amino acid turnover in skeletal muscle is dynamic and rapid. Following a meal, amino acids are absorbed into muscle and MPS exceeds MPB. Between meals, the reverse is true (see figure 8.12a). Generally, these two processes cancel each other out, and relatively little net gain or loss of muscle mass occurs. However, as depicted in figure 8.12b, resistance exercise stimulates MPS to the extent that a positive NPB is achieved. Feeding of protein also accentuates the MPS signal arising from resistance training, which can last for up to 48 h following a single bout of resistance exercise. Additional high-quality dietary protein intake is recommended, particularly for older adults, to enhance the promotion of MPS following exercise (Burd et al. 2019).

The timing, amino acid type, and protein source of the feedings that optimize MPS in conjunction with resistance exercise have been subjects of much research. Findings from these studies, as reviewed by Burd and colleagues (2009; 2019), indicate that the essential amino acids are necessary for the stimulation of MPS with optimal amounts obtained from approximately 20 g of complete proteins (or 8-9 g of essential amino acids). Ingestion of protein up to 2 h following resistance training is also much more potent in stimulating MPS than ingestion of protein prior to exercise (Fujita et al. 2009). Delaying of feeding beyond 2 h after exercise may also reduce the rate of training-induced MPS and muscle hypertrophy. Optimal protein synthesis may also be enhanced by regular smaller dietary protein intake multiple times during the day and before sleep rather than one or two large protein meals (McKendry and Phillips 2021). The BCAAs, particularly leucine, appear to be the most potent stimulators of MPS (Stokes et al. 2018).

Rapidly digested proteins, such as whey and soy, can quickly but transiently augment MPS following resistance training. Milk proteins, particularly whey, also promote greater net MPS following training than soy or casein proteins do. This is possibly due to whey protein’s high content of the BCAAs, particularly leucine, and its rapid digestion and absorption (Devries and Phillips 2015).

Ingesting proteins in large enough quantities also inhibits muscle NPB following resistance exercise by inhibiting MPB through insulin-dependent and insulin-independent mechanisms, thereby supporting muscle mass gains. However, codigestion of carbohydrate does not appear to have additive effects on these mechanisms (Stokes et al. 2018; McKendry and Phillips 2021). It should be noted that significant reductions in MPB and turnover via proteolysis through autophagy and ubiquitine-proteasomal systems are important in maintaining muscle quality, mass, and function since a decrease in clearance of damaged or misformed proteins has been shown to result in impairment of muscle mass and function (Stokes et al. 2018). Hence, a reasonable balance needs to be maintained to optimize muscle mass.



NEXT STAGE
Dietary Protein, BCAA, Resistance Exercise, and Optimization of Muscle Mass Gains in Older Adults
Ongoing research is being conducted on optimizing the effects of exercise and diet for regulating protein and amino-acid metabolism to maximize muscle hypertrophy, particularly for older adults, who lose significant amounts of muscle mass and strength as they age.

Muscle mass decline begins in the fourth decade of life and accelerates with aging. In addition to losing muscle mass, older adults exhibit a blunted response to dietary and resistance training stimulus of MPS. These physiological changes, combined with reduced overall physical activity and suboptimal diets, render older adults prone to significant loss of muscle mass (sarcopenia), frailty, and loss of physical functioning capacity. Numerous studies have examined quality and quantity of dietary protein supplementation, timing of protein intake, resistance training, and other factors related to limiting muscle mass loss and optimizing muscle mass gain in aging individuals.

Strength training in older adults is particularly dependent on timely postexercise provision of protein to optimize muscle mass gains. Young men and women appear not to differ appreciably in rates of postexercise MPS and in the effects of diet on MPS. This indicates that local muscle control factors may be more important in regulating muscle hypertrophy than circulating hormone levels. Although not seen in all studies (Tieland et al. 2012), older women may have greater impairment of MPS following protein feeding and resistance exercise than older men (Burd et al. 2009; 2019). This may be due to their loss of estrogen, which has been demonstrated to stimulate factors associated with muscle hypertrophy, such as satellite-cell activation and proliferation (Enns and Tiidus 2008; Pellegrino, Tiidus, and Vandenboom 2022).

Reviews by Morton and colleagues (2018) and Devries and Phillips (2015) have concluded that certain combinations of dietary protein supplementations and resistance training interventions will optimize MPS in older adults and thereby limit the onset of sarcopenia and frailty. This is in part due to the dietary practices of older individuals, which tend to contain suboptimal levels of protein intake and calories. Significant improvements in muscle strength and mass are possible even in frail older adults with appropriate protein supplementation and resistance training (Tieland et al. 2012). The following are important considerations when attempting to maximize muscle mass and strength in both male and female older adults with regular resistance training:

• Protein supplementation that elevates protein intake up to 1.6 g/kg of body weight will enhance MPS as well as muscle mass and strength gains when compared to controls without dietary protein supplementation and with lower total protein intakes. Note that these recommendations are about double what earlier dietary protein recommendations have been for adults.
• Providing protein supplementation, such that consumption up to 30-40 g of high-quality protein is regularly available with each meal throughout the day, will optimize protein absorption and availability to facilitate optimal protein synthesis. Since older adults tend to consume most of their protein with their evening meal and absorb dietary protein less efficiently than younger adults, this recommendation will provide a steady and optimum availability of amino acids for protein synthesis throughout the day. These levels of protein intake are important for older adults due to their blunted MPS response to dietary protein intakes. The same levels of MPS could be stimulated by half the protein supplements in younger adults.
• The inclusion of BCAA, particularly leucine in dietary protein supplements or the inclusion of milk, will enhance MPS beyond that seen with protein supplementation with less BCAA content. This is the same effect also seen in younger adults.
• Regular resistance training is much more potent than dietary protein supplementation alone in enhancing MPS and muscle mass gains; however, results are enhanced with their combination.

Thus, the optimal combinations of dietary protein and resistance training will enhance muscle mass and strength in older adults and limit the onset of sarcopenia, frailty, and loss of mobility.

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