Muscle relaxation occurs when the muscle fibers return to their original length, dissipating the contraction-associated tension. It starts when the motor neuron terminal ceases the release of acetylcholine vesicles. In the synaptic cleft, the enzyme acetylcholinesterase breaks down the remaining acetylcholine molecules into choline and acetic acid. This results in membrane repolarization, inhibiting a new muscle action potential. In the absence of an action potential, the sarcoplasmic reticulum closes the calcium-release channels and actively pumps the accumulated calcium ions back from the sarcoplasm using calcium ATPase pumps. As calcium ion concentration in the sarcoplasm decreases, it induces a conformational change in troponin bound to the actin filaments. As a result, troponin molecules pull the tropomyosin molecules to block the myosin binding sites on actin filaments. Simultaneously, ATP binding on the myosin heads deactivates the cross-bridges between myosin and actin. After deactivation, the ATP-bound myosin heads reorient away from the actin filaments, preventing sarcomere contraction. As a result, the sarcomere tension is released, and the muscle fiber relaxes passively.