After the myosin head has attached to the actin filament, a power stroke occurs, which causes the "sliding filament theory" (contraction).This process occurs in a cycle as long as two conditions are present: calcium must be available to bind to troponin, revealing the binding sites on actin, and ATP must be available for the movement of the myosin head. When an individual is no longer alive, calcium is no longer sequestered and remains available to bind to troponin, revealing the binding sites. This would allow continued normal contraction, but is not the cause of sustained contraction seen in rigor mortis. After death, cellular metabolism no longer produces ATP, and stores of ATP are quickly depleted. This results in a break in the contraction cycle. ATP is necessary to detach the myosin head from the actin filament. Without ATP present, the myosin head remains bound and the contraction is sustained. The depletion of ATP is thus the cause of rigor mortis, causing stiffness due to myosin's inability to detach from actin.

Calcium is released from the sarcoplasmic reticulum and binds to troponin. At rest, troponin interacts with tropomyosin to block the active sites on actin, preventing myosin from binding. When calcium binds troponin, it causes a conformational change in tropomyosin. This allows the myosin heads to bind to the actin active sites, initiating the contraction process. ATP is used to cause the dissociation of the myosin head from the actin filament, and is not involved in initiating actin-myosin interaction.

Acetylcholine (ACh) is released from neurons at the neuromuscular junction. Once ACh binds to its receptor in the muscle T-tubule, the sarcolemma is depolarized and calcium can be released from the sarcoplasmic reticulum, triggering muscle contraction.

The force of a muscle contraction can be manipulated in several ways. When a muscle is stimulated by an action potential, all fibers within a given motor unit are activated together. Increasing the number of motor units will increase the percentage of the muscle mass that is contracting, increasing the force. Increasing the size of the motor units will have the same effect. Increasing the number of action potentials will allow for sustained contraction.

Action potentials themselves are all-or-nothing; they either happen or they do not. There is no such thing as a large or small action potential. Several action potentials can arrive simultaneously, causing a summation effect, but the size of an action potential on its own cannot affect the force of a muscle contraction.

The T-tubules are responsible for propagating action potentials deep down into muscle fibers, allowing for a uniform and coordinated contraction. The T-tubules are invaginations of the sarcolemma, the specialized cell membrane of muscle cells. T-tubules run adjacent to the sarcoplasmic reticulum, triggering calcium release as the tubule is depolarized. The sarcoplasmic reticulum stores calcium, while the extracellular matrix provides structural support for cells.

Motor neurons are responsible for the stimulation of muscle. Pathways traveling away from the central nervous system to the body are considered to be efferent, where pathways going from the body into the central nervous system are afferent.

All sensory signals are afferent and all motor signals are efferent. Sensory input causes stimulation of various sensors and receptors, which carry the signal to the central nervous system for processing. The central nervous system interprets the signal and generates a response, which is then sent to the appropriate muscle groups.

An action potential sent to the muscles of the hand would follow an efferent pathway (away from the central nervous system) through motor neurons.

It is important to remember that neurons and muscle cells both depolarize in an "all or nothing" response, meaning that the action potential is not a graded process. As such, neurons cannot produce a larger or smaller depolarizing charge in the muscle.

Instead, the strength of a neurological action potential or muscle contraction is determined by the frequency of signal firing. The strength of each individual action potential or signal cannot be changed, and remains constant; however, frequent stimulation to the same area can activate more motor units and cause a larger total contraction.

When muscle contraction occurs, a calcium ion binds to troponin to move tropomyosin off of the myosin binding site on actin. ATP then is hydrolyzed to release the myosin head from actin.

The neuromuscular junction is where the nerve fibers directly connect to the muscle to deliver signals from the brain to the muscle tissue.  "Cross bridge" refers to the linkage of actin and myosin filaments. The other answers sound similar, but are incorrect.

The troponin-tropomyosin complex wraps around actin when the muscle fiber is inactive, blocking all myosin-binding sites. When Ca²⁺ is released it binds to troponin, inducing a change in tropomyosin, which shifts its position to expose the myosin-binding sites on the actin filament.

Calcium does not bind any of the other listed answer choices.

This question requires us to know the ATP binding cycle associated with muscle contraction. I is true; binding of ATP causes myosin to release actin. When there is no ATP present, the myosin remains bound and the muscle becomes stiff (rigor mortis). II is false; actin does not bind ATP. III is also false; ATP is converted to ADP when the myosin head goes from the contracted position to the relaxed position, not the other way around.