regulation of skeletal muscle contraction by action potential

Definition

Target type: biologicalprocess

Any action potential process that regulates skeletal muscle contraction. [GOC:cjm, GOC:obol]

The regulation of skeletal muscle contraction by action potentials is a complex and intricate process involving several key players and steps. Here’s a detailed breakdown:

1. **Action Potential Arrival**: The process begins with an action potential arriving at the neuromuscular junction, the point of contact between a motor neuron and a muscle fiber.

2. **Neurotransmitter Release**: The action potential triggers the release of acetylcholine (ACh), a neurotransmitter, from the motor neuron's synaptic vesicles into the synaptic cleft, the gap between the neuron and the muscle fiber.

3. **ACh Binding**: ACh diffuses across the synaptic cleft and binds to receptors on the muscle fiber's sarcolemma, the plasma membrane of the muscle cell.

4. **Depolarization**: Binding of ACh to its receptors triggers the opening of sodium channels in the sarcolemma, allowing sodium ions (Na+) to flow into the muscle fiber. This influx of Na+ causes depolarization, a change in the membrane potential of the muscle fiber.

5. **Action Potential Propagation**: Depolarization of the sarcolemma initiates an action potential that travels along the muscle fiber's surface and into the T-tubules, a network of invaginations of the sarcolemma that extend deep into the muscle fiber.

6. **Calcium Release**: The action potential reaching the T-tubules triggers the release of calcium ions (Ca2+) from the sarcoplasmic reticulum (SR), a network of intracellular membranes responsible for storing and releasing Ca2+.

7. **Calcium Binding**: The released Ca2+ binds to troponin, a protein complex associated with the thin filament (actin) of the sarcomere, the basic contractile unit of the muscle fiber.

8. **Tropomyosin Shift**: Binding of Ca2+ to troponin causes a conformational change in tropomyosin, another protein associated with the thin filament. This shift exposes the myosin-binding sites on the actin filaments.

9. **Cross-Bridge Formation**: With the myosin-binding sites exposed, myosin heads, the globular protein projections from the thick filament (myosin), can bind to actin, forming cross-bridges.

10. **Power Stroke**: The binding of myosin to actin triggers the power stroke, a conformational change in the myosin head that pulls the thin filament past the thick filament, shortening the sarcomere and generating muscle force.

11. **ATP Hydrolysis**: The myosin head then detaches from actin, hydrolyzing ATP to ADP and inorganic phosphate (Pi). This energy is used to reposition the myosin head for another binding cycle.

12. **Muscle Relaxation**: The cycle of cross-bridge formation, power stroke, and detachment continues as long as Ca2+ remains bound to troponin. When the action potential ceases, Ca2+ is actively pumped back into the SR, reducing the Ca2+ concentration in the sarcoplasm. As Ca2+ detaches from troponin, tropomyosin shifts back, covering the myosin-binding sites on actin. This prevents further cross-bridge formation, allowing the muscle to relax.

13. **ACh Breakdown**: Acetylcholinesterase, an enzyme present in the synaptic cleft, rapidly breaks down ACh into acetate and choline. This ensures that ACh's effect on the muscle fiber is brief and controlled.

In summary, the regulation of skeletal muscle contraction by action potentials involves a complex interplay of electrical and chemical events, resulting in the coordinated interaction of proteins within the sarcomere, ultimately leading to muscle contraction and relaxation.'
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Proteins (1)

Compounds (30)