Mechanism of Muscle Contraction

The contraction of a skeletal muscle fibre is triggered by a signal originating in the central nervous system and is executed through a precisely ordered sequence of electrical, chemical and mechanical events.

A signal (nerve impulse) generated in the central nervous system travels along a motor neuron to a specialised junction with a muscle fibre called the neuromuscular junction, or motor end plate. At this junction, the arriving nerve impulse causes the release of a chemical neurotransmitter, acetylcholine, into the narrow gap between the neuron and the muscle fibre. Acetylcholine binds receptors on the sarcolemma (the muscle fibre's plasma membrane) and generates a new action potential in the muscle fibre itself.

This action potential spreads rapidly across the sarcolemma and travels inward along a system of membranous tubules, the T tubules (transverse tubules), which are in close contact with the sarcoplasmic reticulum running throughout the fibre. This electrical signal causes the sarcoplasmic reticulum to release its stored calcium ions (Ca2+) into the sarcoplasm surrounding the myofibrils.

The released calcium diffuses to the thin filaments and binds troponin C. This binding produces a conformational (shape) change in the troponin complex, and this change, transmitted through troponin, physically shifts the position of tropomyosin, uncovering the myosin-binding sites that were previously hidden along the actin filament.

With the binding sites exposed, the cross-bridge cycle begins. An ATP-energised (cocked) myosin head attaches to the newly exposed site on actin, forming a cross-bridge. The head then bends at its point of attachment to actin, in what is called the power stroke, dragging the thin filament a short distance towards the centre of the sarcomere; this releases the ADP and inorganic phosphate that had been produced from the previous ATP hydrolysis. A fresh molecule of ATP then binds the myosin head, and this binding (not its hydrolysis) is what causes the head to detach from actin. The newly bound ATP is then hydrolysed by the myosin head's own ATPase activity, and the energy released re-cocks the head back to its original high-energy position, ready to attach to a new site further along the actin filament and repeat the entire cycle. Each such cycle advances the thin filament only a small distance, so a useful, visible shortening of the whole sarcomere requires the cross-bridge cycle to repeat many times in rapid succession across many sarcomeres simultaneously.

This entire cycle of attachment, power stroke, detachment and re-cocking continues for as long as the nerve stimulus persists and calcium remains bound to troponin. When nervous stimulation stops, the calcium ions are actively pumped back into the sarcoplasmic reticulum, sarcoplasmic calcium falls, troponin releases calcium and returns to its resting shape, tropomyosin slides back to cover the myosin-binding sites, and the muscle fibre relaxes, with the sarcomere returning to its resting length. …