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.

In a typical muscle cell, tropomyosin is bound to an active site on actin. This prevents muscle contraction because the myosin head cannot bind to actin active site. Muscle contraction is initiated when the sarcoplasmic reticulum releases calcium ions into the cytoplasm of the muscle cell. Calcium ions bind to and activate troponin. Activated troponin molecules subsequently remove tropomyosin from the active site on actin. This allows muscle contraction to occur because the myosin head can now bind to the active site on actin and initiate a power stroke to shorten the sarcomere.

An individual with depleted calcium ions in his sarcoplasmic reticulum will not activate troponin and, therefore, will have reduced muscle tone and strength.

The question states that muscle cramps occur because myosin heads remain attached to the active site on actin; therefore, you are looking for a molecule that is responsible for the detachment of the myosin head from actin. Recall that binding of ATP to the myosin head releases the myosin head from the actin binding site. This allows tropomyosin to re-attach to actin and causes the muscle to relax. The ATP that is bound to the myosin head dissociates into ADP and inorganic phosphate, allowing the myosin head to enter its high-energy state and prepare for another contractile stroke. Once tropomyosin is released again from the actin filament, the ADP and inorganic phosphate on the myosin head are released, the myosin head attaches to actin, and the cycle continues.

Calcium is essential for muscle contraction because it allows for the removal of tropomyosin from the actin binding sites. Depletion of calcium, however, would cause the actin sites to be blocked, preventing contraction from occurring (as opposed to the sustained contraction of a muscle cramp). Depleted sodium may result in fewer action potentials at the neuromuscular junction. This would also inhibit muscle contraction, rather than sustain it. Muscular microtears can occur during exercise, but are unrelated to muscle cramps.

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.

The sarcoplasmic reticulum, an organelle unique to muscle cells, sequesters calcium when the muscle is at rest. This calcium is released into the cytosol during stimulation, and is an integral part of contraction. The affected individual probably has a leaky sarcoplasmic reticulum, allowing the release of calcium into the cytosol and resulting in abnormally high levels of intracellular ion.

Ribosomes are used during protein synthesis and not related to muscle contraction. The nucleus also is not involved in muscle contraction. The Golgi body is involved in modification and packaging of proteins, and also not involved in muscle contraction. Mitochondria are responsible for producing ATP. While ATP is an important part of the contraction process, and mitochondria are abundant in muscle cells, a defect in the mitochondria would not directly cause an increase in intracellular calcium.

The sarcoplasmic reticulum is the specialized organelle of the muscle cells that allows for calcium to be sequestered. Once calcium is released into the cytoplasm it interacts with troponin and tropomyosin, allowing myosin and actin to bind and cause contraction. Calcium must be sequestrated to allow for the myosin-actin bridges to be broken and reset for future contraction.

The sarcolemma is the muscle cell membrane. The T-tubules permeate the muscle cell to allow for propagation of the stimulating action potential to all parts to the cell. The sarcomeres are the contractile units of the muscle cell.

Calcium plays a huge role in the regulation of muscle contraction. Without the presence of calcium, the myosin binding sites on the actin filaments are blocked by tropomyosin and muscle contraction cannot occur. Stimulation from the nervous system causes a chain reaction that releases large stores of calcium from the sarcoplasmic reticulum to regulate muscle contraction.

Sodium ions play an essential role in initiating the chain reaction that eventually leads to calcium release, but is not stored in the sarcoplasmic reticulum. Potassium plays a role in regulating membrane potential, but also is not stored in the sarcoplasmic reticulum. Protons are essential to mitochondrial function and play a crucial role in myocyte metabolism, but are not linked to the sarcoplasmic reticulum or contractile function.

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.

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.

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.