Muscle Contraction (Excitation-Contraction Coupling)
Calcium-dependent actin-myosin sliding mechanism generating muscle force.
Overview
In skeletal muscle, motor neuron action potentials release ACh at the neuromuscular junction, depolarizing the sarcolemma. Depolarization spreads through T-tubules and activates voltage-sensing DHPR, which opens RyR1 on the SR, releasing Ca²⁺. Ca²⁺ binds troponin C, causing conformational changes that move tropomyosin and expose myosin-binding sites on actin. Myosin heads undergo a power stroke cycle (ATP hydrolysis → binding → power stroke → release). Relaxation occurs when Ca²⁺ is pumped back into the SR by SERCA.
Cellular Location
Sarcomere (skeletal/cardiac muscle), cytoplasm (smooth muscle)
Clinical Significance
Malignant hyperthermia = RyR1 mutation; heart failure involves SERCA dysfunction; muscular dystrophies affect structural proteins; dantrolene blocks RyR1 for MH treatment.