![]() ![]() In the rested, fasted state, rates of MPB exceed those of MPS and thus skeletal muscle is in a state of negative net protein balance (Biolo et al., 1995b). What this work has shown us is that the size of human muscle mass is dictated by diurnal changes in rates of muscle protein synthesis (MPS) and muscle protein breakdown (MPB) (Phillips, 2004). As a result, considerable research using stable isotopic tracers has been conducted that has aimed to understand the biology of muscle protein turnover in response to various stimuli. Specifically, we will focus on how the manipulation of protein intake during the recovery period following RE augments the adaptive response.īeyond its role in locomotion, skeletal muscle is the largest site of postprandial glucose disposal, a large site of lipid oxidation, and a substantial contributor to resting metabolic rate (for review see Wolfe, 2006). It is the goal of this review to provide nutritional recommendations for optimal skeletal muscle adaptation. This review provides a brief overview of our current understanding of how RE and protein ingestion can influence gains in skeletal muscle mass in young, healthy individuals. In addition, RE variables such as frequency of sessions, time under tension, volume, and training status play roles in regulating MPS. ![]() The magnitude of the RE-induced increase in MPS is dictated by a variety of factors including: the dose of protein, source of protein, and possibly the distribution and timing of post-exercise protein ingestion. Performing resistance exercise (RE) followed by the consumption of protein results in an augmentation of MPS and, over time, can lead to muscle hypertrophy. In healthy humans, MPS is more sensitive (varying 4–5 times more than MPB) to changes in protein feeding and loading rendering it the primary locus determining gains in muscle mass. Skeletal muscle mass is regulated by a balance between muscle protein synthesis (MPS) and muscle protein breakdown (MPB). ![]()
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