Final answer:
Myosin II generates force for sarcomere contraction by pulling on actin filaments, a process powered by ATP and governed by the sliding filament model of contraction. This action is unidirectional, resulting in shortening of the sarcomere; it does not facilitate sarcomere extension, which occurs during muscle relaxation.
Step-by-step explanation:
Myosin II in a sarcomere can produce force only for that sarcomere's contraction and not for that sarcomere's extension because of the specific way that muscle contraction occurs at the molecular level. The process, known as the sliding filament model of contraction, includes the thick and thin filaments sliding past one another as the myosin heads pull on the actin filaments causing the sarcomere to shorten. This cross-bridge cycling is powered by the hydrolysis of ATP which provides the energy necessary for the myosin heads to bind to, pull, and then release the actin filaments in a repetitive cycle that results in muscle contraction. The number of cross-bridges that can form between the actin and myosin, which determines the tension produced by the muscle fiber, depends on their overlap within the sarcomere—this is the essence of the length-tension relationship.
The sliding filament theory explains that myosin can only generate force in one direction as it pulls the actin filaments towards the middle of the sarcomere (the M line); it cannot push them to extend the sarcomere due to the unidirectional nature of the power stroke. Thus, sarcomere extension is not caused by myosin but instead occurs when the muscle relaxes and the external forces stretch the muscle back to its resting state.