ATP (adenosine triphosphate) is the primary chemical that provides the power for muscle contraction. ADP (adenosine diphosphate) is the resulting chemical when ATP is expended. ATP is required for the cross-bridge cycle. Acetylcholine is a neurotransmitter used in muscle contraction, but does not provide a power source. Lactic acid results from anaerobic production of ATP.

The sarcoplasmic reticulum contains a large amount of Ca²⁺ ions. This calcium is released from the sarcoplasmic reticulum when an electrical signal is sent to the cell. This release of calcium allows for contraction.

The muscular system has a variety of functions. It helps regulate the temperature of the body by generating heat through contraction; this is why we shiver when we are cold. It helps push blood and lymph throughout the blood vessels via the action of smooth muscle, as well as cardiac muscle. Skeletal muscle also maintains body stability and aids in body movement. Calcium storage is not a main function of the skeletal system, although calcium is an important ion for muscular function.

Acetylcholine will stimulate sodium channels on the sarcolemma, which will consequently trigger the release of calcium ions from the sarcoplasmic reticulum. The calcium will then attach to troponin, which pulls tropomyosin away from the active site on actin. With the active site available, myosin heads are able to attach to the actin filament.

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.

Small motor units, typically consisting of one nerve and a few muscle cells, are recruited first. As the muscle contracts for a longer period of time or is required to lift a heavier load, intermediate and large muscle motor units are recruited. As intermediate and large muscle motor units are recruited, more action potentials begin to fire, releasing more calcium from the sarcoplasmic reticulum and increasing the overall strength of the muscle contraction.

Before a contraction, calcium is released from the sarcoplasmic reticulum and attaches to troponin. Troponin will then remove tropomyosin from the active site on actin where myosin is able to attach.

If calcium is never pumped back into the sarcoplasmic reticulum, the active site on actin will stay exposed, which allows myosin to attach at all times.

Note that calcium is also responsible for initiating acetylcholine release from the neuron at the neuromuscular junction; however, this process involves extracellular calcium ions and is not linked to the sarcoplasmic reticulum.

During muscle contraction, the I-band, the H-zone, and the area between the Z-lines get decreased in length. The A-band remains in constant length. Overall, the sarcomere constricts in size, allowing the muscle to contract.

The sliding filament model of muscle contraction states that as the cross-bridge forms between actin and myosin, the myosin head bends (the power stroke), causing actin to move (slide) in the direction of the M-line. When all the actin filaments slide toward the M line like this, the muscle fiber contracts. Calcium is needed for the binding of myosin head to actin. ATP binding leads to the detachment of myosin head from actin. ATP hydrolysis is needed for the unbending of myosin head.

The mechanism for troponin and tropomyosin’s interaction with calcium is comparable to a bike chain with a lock and key. Tropomyosin is the “chain” that blocks the binding sites on actin from the myosin heads. The calcium ion acts like a key to “unlock” troponin and move tropomyosin off of actin’s binding sites. This allows myosin heads to bind to actin and complete their power stroke.