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Questions and Answers
What triggers the release of Ca2+ from the sarcoplasmic reticulum during excitation-contraction coupling?
What is the primary consequence of an action potential ending in a muscle fiber?
What prevents myosin heads from attaching to actin at low intracellular Ca2+ levels?
During the repolarization process in a muscle fiber, which ion's flow is primarily responsible?
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What is the overall process called that connects action potential generation to muscle contraction?
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What occurs immediately after an action potential is propagated along the sarcolemma?
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What role do T tubules play in muscle contraction?
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What is the relationship between the action potential and muscle contraction in terms of timing?
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What triggers the binding of Ca2+ to troponin during muscle contraction?
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What is the first step in the cross bridge cycle?
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Which process resumes after nervous stimulation ceases in muscle contraction?
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What happens during the 'working (power) stroke' in the cross bridge cycle?
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What leads to rigor mortis after death?
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Which statement accurately describes the role of ATP in the cross bridge cycle?
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How does the cocking of the myosin head contribute to muscle contraction?
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What occurs when calcium levels increase in muscle fibers?
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What is the role of acetylcholine (ACh) at the neuromuscular junction?
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During the depolarization phase of an action potential, which ion primarily enters the muscle cell?
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Which step follows the generation of the end plate potential in action potential generation?
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In excitation-contraction coupling, which process occurs first after calcium is released into the cytosol?
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What happens during the repolarization phase of an action potential?
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Myasthenia gravis affects muscle contraction primarily by targeting which aspect of neuromuscular transmission?
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Which event occurs immediately after the arrival of an action potential at the axon terminal of a motor neuron?
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Cross bridge cycling in muscle fibers primarily involves which of the following molecules?
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Study Notes
Muscle Contraction: Crossbridge Cycling
- Calcium binds to troponin when intracellular calcium concentration is high.
- Troponin changes shape causing tropomyosin to move away from myosin-binding sites on actin.
- Myosin heads can then attach to actin, forming a cross bridge.
- During contraction, sarcomere shortening occurs due to the repeated cycle of cross bridge formation, power stroke, cross bridge detachment, and cocking of myosin head.
Cross Bridge Cycle Steps
- Cross bridge formation: High-energy myosin head binds to actin's active site.
- Power stroke: Myosin head pivots, pulling the thin filament towards the center of the sarcomere (M line).
- Cross bridge detachment: ATP binds to myosin head, detaching the cross bridge.
- Cocking of myosin head: ATP hydrolysis provides energy to “cock” the myosin head back to its high-energy state, preparing for the next cycle.
Rigor Mortis
- Muscle stiffness begins 3-4 hours after death.
- Peak rigidity occurs around 12 hours after death.
- Increased intracellular calcium levels are caused by the cessation of ATP production, preventing calcium from being pumped back into the sarcoplasmic reticulum (SR).
- Cross bridge formation occurs due to the presence of calcium, but ATP is required for cross bridge detachment, leading to a constant state of contraction.
- Muscle remains contracted until muscle proteins break down, allowing myosin to detach from actin.
Action Potential and Muscle Contraction
- Action potentials (APs) propagate along the sarcolemma and into T tubules.
- Voltage-sensitive proteins in T tubules trigger the release of calcium from the sarcoplasmic reticulum, leading to muscle contraction.
Excitation-Contraction Coupling
- This process links the transmission of an action potential (excitation) along the sarcolemma to the sliding of myofilaments (contraction).
- Action potentials travel along the sarcolemma and into the T tubules, triggering calcium release from the SR.
- Calcium release leads to muscle contraction.
- The action potential ends before the contraction becomes visible, indicating a brief duration for the nerve impulse.
Neuromuscular Junction
- An action potential (AP) arrives at the axon terminal of a motor neuron.
- Voltage-gated calcium channels in the motor neuron open, allowing calcium to enter.
- This triggers the release of acetylcholine (ACh) into the synaptic cleft (the space between the motor neuron and muscle fiber).
- Acetylcholine diffuses across the synaptic cleft and binds to acetylcholine receptors (sodium channels) on the sarcolemma (muscle cell membrane).
- Acetylcholine binding opens the sodium channels, allowing sodium to enter the muscle fiber, generating an end-plate potential (a localized depolarization of the sarcolemma).
- Acetylcholinesterase, an enzyme, breaks down acetylcholine, terminating its effect.
Myasthenia Gravis
- An autoimmune disease where antibodies attack acetylcholine receptors, leading to a shortage of receptors.
- Symptoms include drooping eyelids, difficulty swallowing and talking, and generalized muscle weakness.
Action Potential Generation
- At rest, the sarcolemma is polarized, meaning there is a voltage difference across the membrane, with the inside of the cell being negative compared to the outside.
- Changes in electrical charges result in an action potential.
- Action potential generation occurs in three steps:
- Generation of the end-plate potential
- Depolarization
- Repolarization
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Description
This quiz explores the intricate process of muscle contraction through crossbridge cycling. It covers key mechanisms such as the role of calcium, the steps of the cross bridge cycle, and the physiological phenomenon of rigor mortis. Test your understanding of how muscles function at the molecular level.