As muscle contracts, the overlap between the thin and thick filaments increases, decreasing the length of the sarcomere—the contractile unit of the muscle—using energy in the form of ATP. At the molecular level, this is a cyclic, multistep process that involves binding and hydrolysis of ATP, and movement of actin by myosin.
When ATP, that is attached to the myosin head, is hydrolyzed to ADP, myosin moves into a high energy state bound to actin, creating a cross-bridge. When ADP is released, the myosin head moves to a low energy state, moving actin toward the center of the sarcomere. Binding of a new ATP molecule dissociates myosin from actin. When this ATP is hydrolyzed, the myosin head will bind to actin, this time on a portion of actin closer to the end of the sarcomere. Regulatory proteins troponin and tropomyosin, along with calcium, work together to control the myosin-actin interaction. When troponin binds to calcium, tropomyosin is moved away from the myosin-binding site on actin, allowing myosin and actin to interact and muscle contraction to occur.
As a regulator of muscle contraction, calcium concentration is very closely controlled in muscle fibers. Muscle fibers are in close contact with motor neurons. Action potentials in motor neurons cause the release of the neurotransmitter acetylcholine in the vicinity of muscle fibers. This generates an action potential (depolarization) in the muscle cell, that is carried along the plasma membrane and through invaginations of the plasma membrane called transverse, or T-tubules.
T-tubules run deep into the muscle and are adjacent to specialized endoplasmic reticulum organelles called sarcoplasmic reticulum, or SR. Calcium sequestered inside the SR is released when voltage-gated ion channels (ion channels that open and close based on local charges) open in response to depolarization, allowing calcium ions to enter the cytoplasm, and muscles to contract.
When signaling from motor neurons stops, relaxation of the muscle begins as calcium is pumped back into the SR, decreasing the cytoplasmic levels of calcium and replenishing the SR calcium stores in preparation for the next contraction.
Healthy muscle can contract but diseased muscle often loses this ability. Diseases like myasthenia gravis prevent motor neuron stimulation of muscle which results in muscle atrophy and a decrease in muscle mass. Amyotrophic lateral sclerosis (ALS or Lou Gehrig’s disease) causes motor neurons to degenerate, which similarly leads to muscle degeneration and atrophy.
