20.8
Kruisbrugcyclus
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Q1: What triggers the myosin head to bind to actin during muscle contraction?
ATP hydrolysis converts the myosin head to a high energy state, enabling it to bind to actin and form a cross-bridge. This binding is controlled by regulatory proteins tropomyosin and troponin, which respond to calcium concentration. When troponin binds calcium, it moves tropomyosin away from the myosin binding site on actin, allowing the cross-bridge to form and muscle contraction to occur.
Q2: How does ATP release affect the myosin head during the cross-bridge cycle?
When ADP is released from the myosin head, it returns to a low energy state and pulls actin toward the sarcomere center. Binding of a new ATP molecule then dissociates the myosin head from actin. The next time the myosin head binds to actin, it attaches to a portion closer to the Z line, advancing the contraction cycle.
Q3: What role does calcium play in regulating muscle contraction?
Calcium is released from the sarcoplasmic reticulum in response to motor neuron signals and binds to troponin, a regulatory protein. This binding moves tropomyosin away from myosin binding sites on actin, allowing cross-bridges to form. When calcium is pumped back into the sarcoplasmic reticulum, muscle relaxation occurs as calcium concentration decreases in the cytoplasm.
Q4: How do motor neurons initiate the cascade that leads to muscle contraction?
Action potentials in motor neurons release acetylcholine, generating depolarization in muscle cells. This depolarization travels along the plasma membrane and through T-tubules, triggering voltage-gated ion channels in the sarcoplasmic reticulum to open. Calcium then floods the cytoplasm, binding to troponin and enabling the cross-bridge cycle to begin.
Q5: Why does the sarcomere length decrease during muscle contraction?
The sarcomere shortens because the overlap between thin and thick filaments increases. As myosin heads pull actin toward the sarcomere center through successive cross-bridge cycles powered by ATP hydrolysis, the distance between the Z lines decreases, reducing overall sarcomere length and producing muscle contraction.
Q6: What happens to muscle function when motor neuron signaling is disrupted?
Diseases like myasthenia gravis and amyotrophic lateral sclerosis (ALS) prevent or degrade motor neuron stimulation of muscle, resulting in muscle atrophy and loss of contractile ability. Without motor neuron signals, calcium cannot be released from the sarcoplasmic reticulum, preventing cross-bridge formation and muscle contraction.
Q7: How are tropomyosin and troponin coordinated to control cross-bridge formation?
Tropomyosin blocks myosin binding sites on actin until troponin binds calcium. When calcium is available, troponin undergoes a conformational change that moves tropomyosin away from the binding sites, exposing them for myosin attachment. This coordinated regulation ensures cross-bridges form only when calcium signals are present, controlling muscle contraction timing.