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At the neuromuscular junction, acetylcholine triggers an action potential that spreads along the sarcolemma and down T-tubules, prompting Ca²⁺ release from the sarcoplasmic reticulum. Calcium binds troponin C, causing a conformational change that moves tropomyosin away from the myosin-binding sites on actin. With sites exposed, myosin heads—preloaded with ADP + Pi—bind actin, release Pi, and perform the power stroke, sliding filaments (shortening the sarcomere). ATP then binds myosin, detaching it from actin; ATP hydrolysis “cocks” the head for the next cycle. Therefore, B is correct. A reverses roles—ATP binding actually causes detachment, not site exposure. C conflates events; Pi release drives the stroke but does not open SR channels (that’s voltage-sensitive coupling via dihydropyridine/ryanodine receptors). D misidentifies the regulator; acetylcholine activates the sarcolemma but does not bind troponin. TEAS physiology often aligns structure to function: troponin-tropomyosin regulate access, Ca²⁺ is the molecular “on” switch, ATP coordinates detachment and re-cocking, and cross-bridge cycling produces force. Understanding each player’s role avoids distractors that swap steps or molecules.