PHSI 208 Lecture Notes - Lecture 21: Muscle Hypertrophy, Myosatellite Cell, Muscle Atrophy
Document Summary
There is a constant remodeling of muscle mass. Changing rates of contractile protein synthesis and degradation, regulated by pathways that are influenced by mechanical stress, physical activity, availability of nutrients, growth factors and age: constant turnover of actin and myosin proteins. Igf-1 pathway leads to muscle growth while myostatin pathway leads to muscle atrophy. Increasing muscle mass: protein synthesis > protein degradation. *satellite cells remain in quiescent state outside the sarcolemma until activated. Hypertrophy of muscle is driven by myotrauma or physical exertion. E. g. lifting weights causes damage to the myofibers sarcolemma begins to break down. Damaged muscle fibers leak atp and recruits immune cells satellite cells gets activated. In response to an injury, satellite cells become activated and proliferate. Then the satellite cells fuse to the muscle fibers and donate their nuclei: a reason why skeletal muscles are multinucleated (constantly receiving nuclei from satellite cells) The addition of more nuclei increases their ability to synthesize actin and myosin proteins.
