Final answer:
Muscle relaxation in skeletal muscles occurs when the motor neuron stops releasing ACh at the NMJ, causing repolarization and resorption of Ca++ into the SR, preventing cross-bridge formation. Muscle spindles adjust muscle length during relaxation, and the intrinsic elasticity of the muscle aids in rebounding to a relaxed state.
Step-by-step explanation:
Relaxation in skeletal muscle fibers, and ultimately the entire muscle, commences when the motor neuron ceases the release of acetylcholine (ACh) into the synaptic cleft at the neuromuscular junction (NMJ). The absence of this chemical signal allows the muscle fiber to repolarize, which then causes calcium ion (Ca++) gates to close within the sarcoplasmic reticulum (SR).
Subsequently, ATP-dependent pumps move Ca++ from the sarcoplasm back into the SR, leading to the 'reshielding' of the actin-binding sites on the thin filaments. This "reshielding" prevents the formation of cross-bridges between the thin and the thick filaments, resulting in the muscle fiber losing tension and relaxing.
Furthermore, during muscle relaxation, the muscle spindle—a proprioceptive stretch receptor within the muscle—plays a role by adjusting muscle length to optimal levels which diminishes tension on stretch receptors and decreases the rate of action potential firing. Elasticity, characterized by the muscle's ability to stretch and rebound, also contributes to the muscle's relaxation when no new nerve signals are present to maintain contraction.
The period after a muscle twitch, named the relaxation phase, is when the tension within a muscle decreases. The sarcolemma, which is the plasma membrane of a skeletal muscle fiber, and the sarcomere, the longitudinally repeating unit of a muscle fiber, return to their original states with reduced tension.