From Barbells to Brawns: The Physiology of Resistance Exercise and Skeletal Muscle Growth

A complex network of biochemical pathways carries out the process of muscle regeneration/growth following resistance exercise. The initial inflammatory response following muscle damage is primarily mediated by the nuclear factor κ -light-chain-enhancer of activated B cells (NF-κ B), cyclooxygenase enzymes, and prostaglandins. Muscle damage also stimulates the activation, proliferation, differentiation, migration, and fusion of satellite cells onto damaged myofibers, resulting in myofibrillar hypertrophy. The progression of the myogenic lineage is predominantly coordinated by the wingless/integrated family of glycoproteins which engages in crosstalk with NF-κ B and the mitogen-activated protein kinase (MAPK)/extracellular signaling-regulated kinase network. The MAPK cascade is essential for mechanotransduction, the process of converting mechanical stimuli into biochemical responses such as accelerated protein synthesis and satellite cell activation. Muscle protein synthesis is primarily governed by the insulin-like growth factor 1/phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin pathway. Several calcium-dependent pathways are also integrated into the process of myogenesis and influence skeletal muscle plasticity. These dynamic interactions are part of the anabolic priming by resistance exercise effect, which defines resistance exercise as an acute catabolic event that potentiates multiple downstream anabolic pathways. Plateaus in muscle growth are attributed to deteriorating inflammatory signaling with repeated bouts of muscle damage as well as increasing thresholds for continuous adaptations, which ultimately become unreachable beyond a certain point. The physiological ceiling of skeletal muscle mass is also credited to myostatin. However, recent discoveries suggest the role of myostatin is not limited to preventing excessive skeletal muscle hypertrophy.