Mechanism of Muscle Contraction
Muscle contraction is crucial for movement, and it is explained by the sliding filament theory. This theory proposes that muscle fibers contract through the sliding motion of thin (actin) filaments over thick (myosin) filaments.
Process of Contraction:
- Initiation: The process is initiated by a neural signal from the central nervous system (CNS) traveling through a motor neuron to the junction known as the neuromuscular junction or motor-end plate.
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When the signal reaches this junction, it stimulates the release of a neurotransmitter called Acetylcholine.
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Action Potential: The release of Acetylcholine generates an action potential in the sarcolemma (muscle cell membrane) which quickly spreads throughout the muscle fiber.
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Calcium Release: The action potential causes the sarcoplasmic reticulum (specialized endoplasmic reticulum in muscle cells) to release calcium ions (Ca²⁺) into the sarcoplasm (muscle cell cytoplasm).
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Tropomyosin and Troponin Interaction: The increase in calcium ions interacts with troponin, a protein associated with the actin filaments, leading to the exposure of active sites on actin that allow myosin to bind.
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Cross-Bridge Formation: The myosin heads, energized by ATP hydrolysis, bind to the exposed active sites on actin, forming a cross-bridge.
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Sliding Mechanism: The myosin head pulls the actin filaments toward the center of the sarcomere (the functional unit of muscle), resulting in muscle contraction. The myosin head returns to a relaxed state after releasing ADP and inorganic phosphate (Pi), and a new ATP molecule binds to the myosin head, breaking the cross-bridge.
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Relaxation: As Ca²⁺ ions are pumped back into the sarcoplasmic reticulum, the actin sites are re-masked by tropomyosin, leading the muscle to relax back to its original length.
This cycle continues as long as calcium ions remain high in concentration, allowing for muscle contractions until fatigue occurs, often characterized by the accumulation of lactic acid.