After calcium in the sarcoplasmic reticulum is released by a stimulus, it binds to and alters the shape of troponin as well as removes tropomyosin from the binding sites. Cross-bridge cling continues until the calcium ions and ATP are no longer available.

To enable a muscle contraction, tropomyosin must change conformation, uncovering the myosin-binding site on an actin molecule and allowing cross-bridge formation. This can only happen in the presence of calcium, which is kept at extremely low concentrations in the sarcoplasm. If present, calcium ions bind to troponin, causing conformational changes in troponin that allow tropomyosin to move away from the myosin-binding sites on actin. Once the tropomyosin is removed, a cross-bridge can form between actin and myosin, triggering contraction. Cross-bridge cycling continues until Ca²⁺ ions and ATP are no longer available, and tropomyosin again covers the binding sites on actin. The concentration of calcium within muscle cells is controlled by the sarcoplasmic reticulum. Muscle contraction ends when calcium ions are pumped back into the sarcoplasmic reticulum, allowing the muscle cell to relax.

The concentration of calcium within muscle cells is controlled by the sarcoplasmic reticulum, a unique form of endoplasmic reticulum in the sarcoplasm. Muscle contraction ends when calcium ions are pumped back into the sarcoplasmic reticulum, allowing the muscle cell to relax. During stimulation of the muscle cell, the motor neuron releases the neurotransmitter acetylcholine, which then binds to a post-synaptic nicotinic acetylcholine receptor.

A change in the receptor conformation causes an action potential, activating voltage-gated L-type calcium channels, which are present in the plasma membrane. The inward flow of calcium from the L-type calcium channels activates ryanodine receptors to release calcium ions from the sarcoplasmic reticulum. This mechanism is called calcium-induced calcium release (CICR). It is not understood whether the physical opening of the L-type calcium channels or the presence of calcium causes the ryanodine receptors to open. The outflow of calcium allows the myosin heads access to the actin cross-bridge binding sites, permitting muscle contraction.

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Key Points

• Tropomyosin covers the actin binding sites, preventing myosin from forming cross-bridges while in a resting state.

• When calcium binds to troponin, the troponin changes shape, removing tropomyosin from the binding sites.

• The sarcoplasmic reticulum stores calcium ions, which it releases when a muscle cell is stimulated; the calcium ions then enable the cross-bridge muscle contraction cycle.

Key Terms

Tropomyosin: any of a family of muscle proteins that regulate the interaction of actin and myosin.

Troponin: a protein involved in muscle contraction; it occurs with tropomyosin in the thin filaments of muscle tissue.

Sarcoplasmic reticulum: s smooth endoplasmic reticulum found in smooth and striated muscle; it contains large stores of calcium, which it sequesters and then releases when the muscle cell is stimulated.