The sliding filament model explains the molecular basis by which muscular contraction occurs. During muscular contraction, thin filaments within the sarcomere of a myofibril are pulled towards the center of the sarcomere (called the H zone) by the thick filaments. In the process, the sarcomeric length shortens and the myofibril shortens. As a result, the muscle contracts (see Figure 8.11). Steps in the process include the following:

1. Muscular contraction is initiated by a signal from the nervous system.

2. The nervous system causes release of calcium from the sarcoplasmic reticulum.

3. Calcium release causes thick filaments of the cocked headpiece of a myosin filament (thick filament) to bind to a site on actin, forming a tight cross-bridged binding. In the absence of calcium from the sarcoplasmic reticulum, access of the headpiece to the thin filament is blocked by tropomyosin and the troponins (I, C, and T) (Figure 8.13). Calcium binding by troponin C causes a rearrangement of the troponin-tropomyosin-actin complex, allowing actin-myosin cross-bridges to form.

4. Release of phosphate and ADP from a previously hydrolyzed ATP on the thick filament causes it to perform a "power stroke", pulling the thin filament (actin) in towards the center of the sarcomere.

5. The binding of ATP causes the cross-bridge between actin and myosin to be broken and the myosin headpiece to remain in the low energy configuration. In the absence of calcium, the actin can slide back past the myosin to the original relaxed position.

6. ATP is hydrolyzed, but not released by the myosin headpiece, causing the myosin headpiece to assume the cocked position.

7. When the stimulation from the nervous system ceases, calcium is taken up again by the sarcoplasmic reticulum.

8. The resulting decrease in calcium concentration causes the thin filament to slide back past the thick filament and the muscle to relax.