Final answer:
Calcium ions will continue to stimulate muscle contraction as long as the ryanodine receptor channel is open. This increases the interaction between myosin and actin filaments, leading to muscle fiber shortening. Relaxation occurs when signals from motor neurons cease, causing calcium to be reabsorbed into the sarcoplasmic reticulum.
Step-by-step explanation:
As long as the ryanodine receptor channel on the sarcoplasmic reticulum remains open, calcium ions (Ca++) will continue to flood the sarcoplasm, which is the cytoplasm in muscle cells. This influx of Ca++ stimulates muscle fibers to contract by binding to troponin, leading to the unshielding of actin-binding sites and allowing actin and myosin filaments to form cross-bridges.
Consequently, contraction is sustained as long as there is sufficient ATP to drive the cross-bridge cycling, which is the molecular mechanism where myosin heads pull on actin filaments, causing the muscle fiber to shorten. Muscle contraction will continue until the signaling from the motor neuron ends, which leads to the repolarization of the membrane, closing the calcium channels in the sarcoplasmic reticulum, and resulting in calcium being actively pumped back into the SR, causing the muscle to relax.
Muscle relaxation occurs when the motor neuron stops releasing acetylcholine (ACh), leading to repolarization and the closing of the calcium gates in the sarcoplasmic reticulum. ATP-dependent pumps then move Ca++ out of the sarcoplasm back into the SR, causing the muscle fibers to lose tension and relax.