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.

ATP (adenosine triphosphate) is the primary chemical that provides the power for muscle contraction. ADP (adenosine diphosphate) is the resulting chemical when ATP is expended. ATP is required for the cross-bridge cycle. Acetylcholine is a neurotransmitter used in muscle contraction, but does not provide a power source. Lactic acid results from anaerobic production of ATP.

The sarcoplasmic reticulum contains a large amount of Ca²⁺ ions. This calcium is released from the sarcoplasmic reticulum when an electrical signal is sent to the cell. This release of calcium allows for contraction.

The muscular system has a variety of functions. It helps regulate the temperature of the body by generating heat through contraction; this is why we shiver when we are cold. It helps push blood and lymph throughout the blood vessels via the action of smooth muscle, as well as cardiac muscle. Skeletal muscle also maintains body stability and aids in body movement. Calcium storage is not a main function of the skeletal system, although calcium is an important ion for muscular function.

Acetylcholine will stimulate sodium channels on the sarcolemma, which will consequently trigger the release of calcium ions from the sarcoplasmic reticulum. The calcium will then attach to troponin, which pulls tropomyosin away from the active site on actin. With the active site available, myosin heads are able to attach to the actin filament.

Troponin binds free calcium once it is released from the sarcoplasmic reticulum, causing a conformational change in tropomyosin. This change exposes the myosin binding site on actin, allowing for cross-bridge formation and contraction.