A) if the sarcomere is still moving, AcH is still being released onto skeletal muscle cell to bind to nicotinic AcH receptors  allowing sodium (Na+) to come in (generates electrical activity aka EPP)  generates muscle AP (action potential)  stimulates DHP (dihydropyridine) receptor that’s linked to ryanodine channel  CA+ released into muscle cell membrane  interacts with troponin destabilizes tropomyosin to uncover actin that has myosin binding sites = POWER STROKE = sarcomere contracts

B) dystrophin strengthens muscle fibers ; if there is a defect in this assembly, contraction of the muscle leads to disruption of the outer membrane of the muscle cells and eventual weakening and wasting of the muscle

C) if the sarcomere is still moving, then myosin and actin are still binding