How is skeletal muscle contraction initiated and sustained?

Skeletal muscle contraction consists of two stages. The first is the initiation by the nervous system and the events leading up to myofibril interactions. The second is the actual shortening of sarcomeres, which requires both the presence of Calcium and ATP.

The contraction of skeletal muscle cells is under voluntary control by the nervous system. Motor neurons from the spinal cord terminate at the neuromuscular junction – a structure that acts as a specialised synapse. These nerve cells release the neurotransmitter acetylcholine onto nicotinic receptors. Acetylcholine binding to its receptors causes an efflux of potassium (K+) and influx of sodium (Na+) through an ion channel. These ions cause changes in membrane potential in the same way as action potentials do in nerve cells. However, muscle cells are structured differently and possess specialised T-tubules that descend deep into the cell. T-tubules allow for these changes at the membrane to be passed deeper into the cell, and transmitted to a structure called the sarcoplasmic reticulum (SR). The SR is a storage of Calcium (Ca++), and when stimulated releases this Ca++, which is necessary to allow myofibrils to interact. These steps initiate muscle contraction.

Calcium released from the SR binds to a protein called tropomyosin. This protein normally blocks sites on actin that bind myosin heads during contraction. Adding Ca++ causes a change of shape that reveals these binding sites and allows contraction to begin. Muscle contraction consists of cycling between relaxed state, cocked state, and the power stroke, which depends upon ATP hydrolysis. Provided ATP and Ca++ remain at high enough concentration then the muscle contraction will be sustained.