The sarcoplasmic reticulum is responsible for the storage of calcium ions that are used in muscle contraction. Prior to a contraction, an action potential will reach the sarcoplasmic reticulum, making it permeable to calcium ions. At the end of the contraction, the sarcoplasmic reticulum will actively pump calcium ions back into its lumen.

The sarcoplasmic reticulum is not involved in protein synthesis.

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.

The question states that the sarcoplasmic reticulum is a specialized endoplasmic reticulum. This means that the structures that make up the sarcoplasmic reticulum must be similar to the endoplasmic reticulum. Recall that both endoplasmic reticulum (rough and smooth) are made up of a network of tubules. Similarly, both structures contain vesicles that transport processed molecules to a target location (proteins in rough endoplasmic reticulum and lipids in smooth endoplasmic reticulum); therefore, the sarcoplasmic reticulum must contain vesicles and a network of tubules.

The sarcoplasmic reticulum does not contain digestive enzymes, nor does the endoplasmic reticulum. Digestive enzymes are usually found in degradative organelles, such as lysosomes.

The main function of the sarcoplasmic reticulum is to store and release calcium ions. Calcium ions released into the cytoplasm of a muscle cell activate troponin. Activated troponin removes tropomyosin from actin, which opens up the myosin active site on actin. Myosin head binds to actin, which causes muscle contraction. 

The sarcoplasmic reticulum does not play a role in releasing calcium ions into synapses during action potential propagation. The calcium ions in synapses are released via vesicles in the presynaptic neuron; therefore, an abnormal sarcoplasmic reticulum will not stop the release of calcium ions in neuronal synapses.

The sarcoplasmic reticulum is an organelle that closely resembles the smooth endoplasmic reticulum. They are structurally similar, but have very different functions. The main function of the sarcoplasmic reticulum is to store and release calcium, whereas the smooth endoplasmic reticulum functions in lipid synthesis.

Muscle contraction is usually initiated by an action potential. The first step in muscle contraction is the release of calcium ions from the sarcoplasmic reticulum; therefore, a change in membrane potential (action potential) will stimulate the sarcoplasmic reticulum to become more permeable to calcium ions. Once stimulated, the sarcoplasmic reticulum releases calcium ions into the cytoplasm, where the calcium ions interact with troponin and remove tropomyosin from actin. This sequence allows for myosin to bind actin and shorten the sarcomere, resulting in contraction.

The sarcoplasmic reticulum is actually found in all three types of muscle cells: smooth muscle, cardiac muscle, and skeletal muscle. Recall that skeletal muscles are voluntary, whereas smooth and cardiac muscles are involuntary; therefore, sarcoplasmic reticulum is found in both voluntary and involuntary muscles.

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.