The crossbridge cycle is a series of events that occur during muscle contraction, allowing for the interaction between actin and myosin filaments. Here’s a detailed description of the events, starting with the binding of calcium ions (Ca++) to troponin:
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Calcium Binding: When a muscle fiber is stimulated by a nerve impulse, calcium ions (Ca++) are released from the sarcoplasmic reticulum into the cytoplasm of the muscle cell.
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Troponin and Tropomyosin Shift: The increase in Ca++ concentration leads to the binding of calcium ions to troponin, a protein complex associated with the actin filament. When Ca++ binds to troponin, it causes a conformational change that moves tropomyosin, a regulatory protein that normally blocks the myosin binding sites on actin. This movement exposes the binding sites on the actin filament.
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Crossbridge Formation: With the binding sites on actin exposed, the energized myosin heads (which have previously hydrolyzed ATP to ADP and inorganic phosphate) can now attach to the exposed binding sites on the actin filaments, forming crossbridges.
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Power Stroke: Once the myosin heads bind to the actin, they undergo a conformational change and pull the actin filament toward the center of the sarcomere in a movement known as the power stroke. During this process, the myosin heads release ADP and inorganic phosphate, which were previously bound to them, and this release triggers the stroke.
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Detachment of Myosin: After the power stroke, a new molecule of ATP binds to the myosin head. This binding causes a change in the shape of myosin, reducing its affinity for actin, and leading to the detachment of the myosin head from the actin filament.
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Re-cocking of Myosin Head: The hydrolysis of ATP into ADP and inorganic phosphate occurs while the myosin head is detached. This energy released from ATP hydrolysis is used to re-cock the myosin head into its energized position, ready for another cycle.
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Repeat Cycle: If Ca++ levels remain elevated, the myosin head can bind to another actin site, and the cycle repeats, resulting in continued contraction of the muscle fiber.
As long as adequate Ca++ and ATP are available, the crossbridge cycle can continue, leading to muscle contraction until the signal for contraction stops, Ca++ is pumped back into the sarcoplasmic reticulum, and tropomyosin covers the actin binding sites again.