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Skeletal muscle

Resistance training and subsequent consumption of a protein-rich meal promotes muscle hypertrophy and gains in muscle strength by stimulating myofibrillar muscle protein synthesis (MPS) and inhibiting muscle protein breakdown (MPB). The stimulation of muscle protein synthesis by resistance training occurs via phosphorylation of the mechanistic target of rapamycin (mTOR) and subsequent activation of mTORC1, which leads to protein biosynthesis in cellular ribosomes via phosphorylation of mTORC1's immediate targets (the p70S6 kinase and the translation repressor protein 4EBP1). The suppression of muscle protein breakdown following food consumption occurs primarily via increases in plasma insulin. Similarly, increased muscle protein synthesis (via activation of mTORC1) and suppressed muscle protein breakdown (via insulin-independent mechanisms) has also been shown to occur following ingestion of β-hydroxy β-methylbutyric acid.

Aerobic exercise induces mitochondrial biogenesis and an increased capacity for oxidative phosphorylation in the mitochondria of skeletal muscle, which is one mechanism by which aerobic exercise enhances submaximal endurance performance. These effects occur via an exercise-induced increase in the intracellular AMP: ATP ratio, thereby triggering the activation of AMP-activated protein kinase (AMPK) which subsequently phosphorylates peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α), the master regulator of mitochondrial biogenesis.