The body's largest metabolic organ. Skeletal muscle is 40 percent of body mass — every step a burst of ATP turnover, every training block a remodeling of its fuel machinery.
Multinucleated fibers built from sarcomeres — actin and myosin filaments ratcheting under calcium control. Fiber types set the metabolic character: type I oxidative and fatigue-resistant, type II glycolytic and fast. Creatine phosphate buffers the first seconds of ATP demand; glycogen carries the next; blood glucose and fatty acids feed the oxidative engines beyond — beta oxidation for the long haul.
Metabolic Pathways
Immediate system: phosphocreatine donates its phosphate to ADP — seconds of maximal power.
Glycogenolysis and glycolysis fuel the first minutes, lactate as output and shuttle fuel.
Oxidative metabolism sustains endurance: fatty acids dominant, glucose rationed for the brain.
Regulation
Recruitment order: motor units fire small-to-large — the size principle matches force to demand.
Insulin-dependent glucose uptake via GLUT4, enhanced by contraction independently — exercise as its own insulin.
Training remodels enzyme profiles and mitochondrial density in weeks.
Interactions
Amino-acid export in fasting: muscle releases alanine for hepatic gluconeogenesis — the glucose-alanine cycle.
Myokines signal to fat and brain — muscle as endocrine organ.
Its heat output is the body's furnace in cold.
Clinical Relevance
Muscular dystrophies: structural protein failure — dystrophin the classic.
Rhabdomyolysis dumps myoglobin into blood — crush injury and statin risk.
Sarcopenia and disuse atrophy are the clinical poles of too little demand.
Delayed-onset muscle soreness tracks eccentric work — lengthening under load — not absolute force.
Training doubles mitochondrial density in weeks; detraining unbuilds it almost as fast.