Remember that troponin, tropomyosin, and calcium are not involved in the detachment of myosin head from actin; they are involved in the attachment of myosin head to actin. The molecule required for muscle relaxation (detachment of myosin head from actin) is ATP. After muscle contraction, a molecule of ATP binds to the myosin head and signals it to detach from the active site on actin.  After detachment, myosin head converts the ATP to ADP and inorganic phosphate and the cycle of muscle contraction and muscle relaxation continues.

The theory that describes the movement of actin and myosin is the sliding filament theory. This theory proposes that the myosin filaments slide relative to the actin filaments and shorten the length of sarcomere. A sarcomere is the basic unit of muscle; therefore, when myosin filaments shorten the length of the sarcomere, the muscle contracts. 

Cross-bridge theory is not an actual theory. A cross-bridge is a term used to describe the linkage between actin and myosin. Endosymbiotic theory states that mitochondria and chloroplasts were originally prokaryotes that evolved by forming a symbiotic relationship with eukaryotic cells. This explains why mitochondria and chloroplasts have their own unique DNA. Finally, the Central Dogma theory describes the flow of genetic information in a living organism. It states that genetic information is transferred through the processes of replication, transcription, and translation.

Smaller motor units are activated first during muscular contraction. If more force is needed, larger motor units will be recruited in order to provide the necessary force.

During a contraction, smaller motor units are typically fired first, followed by larger units in order to have a smooth, controlled movement. Movements that require fine, controlled motion, such as the muscles of the fingers, will be composed of smaller motor units.

The neurotransmitter associated with skeletal muscle is acetylcholine, not epinephrine. A single action potential may initiate contraction of a motor unit, but the neuron must continue to fire in order to sustain the contraction.

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.