Recent Perspectives Regarding the Role of Dietary Protein for the Promotion of Muscle Hypertrophy with Resistance Exercise Training

Abstract

Skeletal muscle supports locomotion and serves as the largest site of postprandial glucose disposal; thus it is a critical organ for physical and metabolic health. Skeletal muscle mass is regulated by the processes of muscle protein synthesis (MPS) and muscle protein breakdown (MPB), both of which are sensitive to external loading and aminoacidemia. Hyperaminoacidemia results in a robust but transient increase in rates of MPS and a mild suppression of MPB. Resistance exercise potentiates the aminoacidemia-induced rise in MPS that, when repeated over time, results in gradual radial growth of skeletal muscle (i.e., hypertrophy). Factors that affect MPS include both quantity and composition of the amino acid source. Specifically, MPS is stimulated in a dose-responsive manner and the primary amino acid agonist of this process is leucine. MPB also appears to be regulated in part by protein intake, which can exert a suppressive effect on MPB. At high protein doses the suppression of MPB may interfere with skeletal muscle adaptation following resistance exercise. In this review, we examine recent advancements in our understanding of how protein ingestion impacts skeletal muscle growth following resistance exercise in young adults during energy balance and energy restriction. We also provide practical recommendations for exercisers who wish to maximize the hypertrophic response of skeletal muscle during resistance exercise training.

Keywords: amino acids; energy balance; energy restriction; muscle hypertrophy; protein turnover; resistance exercise; skeletal muscle.

Figure 1

Simplified overview of whole body oral protein utilization at rest. Of the protein ingested, approximately 50% is extracted by splanchnic tissues before entering peripheral circulation. Interestingly, only ~10% of the ingested protein is utilized for skeletal muscle protein synthesis while the rest is catabolized.

Figure 2

Whey protein ingestion-induced increase in MPS in young men, percent change from 0 g. (A) At rest, consumption of 10 g or 20 g of protein results in a rise of 19% and 52% respectively from 0g. Consumption of 40 g of whey protein does not result in superior stimulation of MPS beyond consumption of 20 g; (B) Following resistance exercise, consumption of 20 g of protein increases MPS almost twice as much as consumption of 10 g, while consumption of 40 g of whey protein results in a small stimulation of MPS over and above that seen at 20 g indicating there are diminishing returns in terms of stimulation of MPS above 20 g. Data redrawn from Witard et al. [35], however, similar data are reported by MacNaughton et al. [38], and Moore et al. [36].