Practice question

Muscle relaxation requires rapid removal of activating calcium signal and restoration of inhibitory thin filament state to prevent ATP waste. During excitation depolarization opens dihydropyridine receptors coupled to ryanodine receptors of sarcoplasmic reticulum flooding sarcoplasm with calcium that binds troponin C or calmodulin initiating cross bridge cycling. For relaxation three mechanisms lower cytosolic calcium efficiently: sarcoplasmic reticulum Ca ATPase SERCA a P type pump hydrolyzing one ATP to transport two calcium ions into lumen against concentration gradient, plasma membrane Ca ATPase PMCA and sodium calcium exchanger NCX extruding calcium to extracellular space, and cytosolic calcium buffers like parvalbumin and calsequestrin transiently binding calcium. As free calcium falls below about 300 nM calcium dissociates from troponin C tropomyosin returns to blocked B position and myosin light chain phosphatase dephosphorylates smooth muscle myosin heads. Myosin heads can bind ATP and detach but cannot reattach strongly tension decays sarcomeres return to resting length passively by elastic titin and connective tissue forces.