- During a vigorous muscle contraction, which of the following changes occurs within the sarcomere?
Answer: The distance between Z-lines decreases as the H-zone narrows.
According to the sliding filament theory, the myofilaments (actin and myosin) slide past each other but do not change length. This sliding action pulls the Z-lines closer together, thus shortening the sarcomere. As actin filaments slide inwards towards the M-line, the I-band (containing only actin) and the H-zone (containing only myosin) both narrow. The A-band, which represents the full length of the myosin filament, does not change length.
- A researcher is studying a mutation in skeletal muscle where the voltage-gated Ca²⁺ channels in the axon terminal of motor neurons are non-functional. Which process would be most immediately inhibited?
Answer: The exocytosis of acetylcholine into the synaptic cleft.
The arrival of an action potential at the axon terminal depolarizes the membrane, opening voltage-gated Ca²⁺ channels. The influx of Ca²⁺ into the axon terminal is the direct trigger for the fusion of synaptic vesicles with the presynaptic membrane and the subsequent release (exocytosis) of acetylcholine. If these channels are non-functional, acetylcholine will not be released, and the entire process of muscle stimulation will be halted at this point.
- During muscle contraction, the length of the A-band remains constant. What is the most accurate explanation for this observation?
Answer: The A-band corresponds to the full length of the myosin filament, which does not change its length.
The A-band (anisotropic band) is defined by the length of the thick (myosin) filaments. The sliding filament theory states that the filaments slide past one another, but the filaments themselves do not shorten. Since the myosin filaments do not change length during contraction, the A-band, which represents their span, remains constant in width. A is incorrect because the A-band is primarily myosin. C is incorrect as the H-zone narrows, not widens. D is incorrect as actin, not the A-band itself, is anchored to the Z-lines.
- The T-tubule system is essential for coordinated muscle contraction because it:
Answer: allows for the rapid propagation of an action potential deep into the muscle fibre.
T-tubules (transverse tubules) are invaginations of the sarcolemma that penetrate deep into the muscle cell, surrounding each myofibril. Their function is to carry the action potential from the cell surface to the interior. This ensures that the signal to contract reaches the sarcoplasmic reticulum throughout the entire muscle fibre nearly simultaneously, leading to a coordinated release of calcium and a uniform contraction.
- What is the primary role of the calcium pumps (Ca²⁺-ATPase) located on the membrane of the sarcoplasmic reticulum?
Answer: To actively transport Ca²⁺ from the sarcoplasm back into the sarcoplasmic reticulum.
For a muscle to relax, the concentration of calcium ions in the sarcoplasm must be lowered. The Ca²⁺-ATPase pumps on the sarcoplasmic reticulum (SR) membrane use energy from ATP to actively transport Ca²⁺ against its concentration gradient from the sarcoplasm back into the SR. This allows tropomyosin to once again block the myosin-binding sites on actin, ending the contraction. Ca²⁺ release (A) occurs through voltage-gated channels, not pumps.
- The energy for the 'cocking' or re-energizing of the myosin head into its high-energy conformation is directly provided by which event?
Answer: The hydrolysis of ATP into ADP and Pi.
After a myosin head has completed a power stroke and detached from actin (by binding a new ATP), it must be re-energized for the next cycle. This re-energizing process, often called 'cocking' the head, is powered by the hydrolysis of the newly bound ATP into ADP and Pi. The energy released from this hydrolysis is stored in the myosin head, putting it in a high-energy conformation, ready to bind to actin again.
- Which of the following comparisons between the events at the neuromuscular junction and events within the sarcomere is correct?
Answer: Both processes are initiated by a depolarization event, but the ion channels involved are different.
Both processes are triggered by action potentials (depolarization events). However, at the axon terminal, depolarization opens voltage-gated Ca²⁺ channels. At the sarcolemma, depolarization is initiated by ligand-gated Na⁺ channels (ACh receptors) and propagated by voltage-gated Na⁺ channels. This makes the ion channels involved different. A is incorrect; the power stroke is powered by ADP+Pi release, while detachment needs ATP. B is incorrect; calcium, not sodium, triggers the movement of tropomyosin (via troponin). D is incorrect; acetylcholine does not enter the muscle cell.
- A chemical agent is introduced that increases the permeability of the sarcoplasmic reticulum membrane to Ca²⁺, causing a continuous leak of Ca²⁺ into the sarcoplasm. Assuming sufficient ATP is available, what would be the state of the muscle fibres?
Answer: A state of sustained contraction or spastic paralysis.
A continuous leak of Ca²⁺ into the sarcoplasm would lead to persistently high intracellular Ca²⁺ levels. This would cause Ca²⁺ to continuously bind to troponin, keeping the actin binding sites exposed. With sufficient ATP, the myosin heads would continuously cycle through binding, pulling, and detaching, resulting in a state of sustained contraction (spasm or spastic paralysis). It is not flaccid paralysis (A) because the contraction mechanism is activated. It is not rigor mortis (C) because ATP is available for detachment. While pumps (D) would work harder, a significant leak would overwhelm them, preventing relaxation.
- Which sequence correctly outlines the events following the arrival of a nerve impulse at a motor end plate?
Answer: Acetylcholine release → T-tubule depolarization → Ca²⁺ release from SR → Troponin binds Ca²⁺ → Cross-bridge formation
The correct sequence begins at the synapse: a nerve impulse causes acetylcholine release. ACh binds to receptors, depolarizing the sarcolemma and the T-tubules. This depolarization triggers voltage-sensitive proteins linked to the sarcoplasmic reticulum (SR), causing the SR to release calcium ions. The released calcium then binds to troponin, which initiates the chain of events leading to cross-bridge formation and contraction. The other options present these events in an incorrect order.
- In the process of neuromuscular transmission, what event is directly responsible for the depolarization of the sarcolemma at the motor end plate?
Answer: The influx of Na⁺ ions through ligand-gated ion channels.
When acetylcholine binds to its receptors on the motor end plate, these receptors, which are ligand-gated ion channels, open. This allows a rapid influx of sodium ions (Na⁺) into the muscle cell, causing a localized depolarization known as the end-plate potential. If this potential reaches threshold, it triggers a full action potential that propagates along the sarcolemma. Ca²⁺ influx (A) triggers ACh release. ACh breakdown (B) terminates the signal. T-tubule propagation (D) happens after the initial depolarization.
- Which statement correctly distinguishes the roles of troponin and tropomyosin in skeletal muscle contraction?
Answer: Tropomyosin is a long filament that blocks myosin-binding sites, and troponin is a complex that moves it upon binding Ca²⁺.
Tropomyosin is a fibrous protein that lies in the groove of the actin filament, physically covering the myosin-binding sites in a relaxed muscle. Troponin is a globular protein complex attached to tropomyosin. When calcium ions bind to troponin, it undergoes a conformational change that pulls the attached tropomyosin away from the binding sites, allowing cross-bridges to form. A incorrectly swaps their roles. B is incorrect as troponin does not bind myosin heads. D incorrectly describes their locations.
- A genetic disease results in a non-functional form of troponin that cannot bind calcium ions. Which statement best predicts the effect on muscle contraction?
Answer: Muscles will be unable to contract because tropomyosin will continuously block myosin-binding sites.
The binding of calcium to troponin is the critical step that causes the troponin-tropomyosin complex to shift, exposing the myosin-binding sites on the actin filament. If troponin cannot bind calcium, this conformational change will not happen. As a result, tropomyosin will remain in its blocking position, preventing myosin heads from forming cross-bridges with actin, and thus preventing muscle contraction, even if the muscle fibre is stimulated and sarcoplasmic calcium levels rise.
- If a single motor neuron fires a series of action potentials at a very high frequency, the resulting muscle contraction is a smooth, sustained contraction known as fused tetanus. What is the cellular basis for this phenomenon?
Answer: The muscle fibre does not have time to fully relax between stimuli, as calcium levels remain elevated in the sarcoplasm.
Fused tetanus occurs when stimuli are so frequent that the sarcoplasmic reticulum cannot reabsorb Ca²⁺ ions fast enough between action potentials. This keeps the sarcoplasmic Ca²⁺ concentration continuously high, meaning troponin remains saturated, tropomyosin remains displaced, and cross-bridges can continuously cycle, producing a sustained, maximal contraction. A is incorrect; the amount of ACh released per action potential is relatively constant. C describes fatigue or rigor, not tetanus. D describes motor unit recruitment, which increases force, but tetanus is a property of a single fibre's response to high-frequency stimulation.
- A toxin is discovered that irreversibly binds to and blocks acetylcholine receptors on the motor end plate. Which of the following would be the most direct result of this toxin's action on skeletal muscle function?
Answer: The sarcoplasmic reticulum would be unable to release calcium ions into the sarcoplasm.
Acetylcholine binding to its receptors on the motor end plate causes depolarization of the sarcolemma, which propagates down the T-tubules and triggers the release of Ca²⁺ from the sarcoplasmic reticulum. If these receptors are blocked, this entire cascade is prevented at its first step, meaning Ca²⁺ will not be released. B is incorrect because the toxin affects the postsynaptic receptors, not the enzyme in the cleft. C describes rigor mortis, which results from a lack of ATP, not a failure of initial stimulation. D is incorrect because the toxin acts on the postsynaptic membrane, not the presynaptic terminal's release mechanism.
- In a condition known as myasthenia gravis, antibodies block or destroy acetylcholine receptors. A drug used for treatment is pyridostigmine, which inhibits acetylcholinesterase. How would this drug help alleviate the symptoms?
Answer: It prevents the breakdown of acetylcholine, increasing its concentration in the synaptic cleft.
Acetylcholinesterase is the enzyme that breaks down acetylcholine (ACh) in the synaptic cleft. By inhibiting this enzyme, pyridostigmine allows ACh to remain in the cleft for a longer period and at a higher concentration. This increases the probability that the remaining functional receptors will be stimulated, compensating for the reduced number of receptors and improving muscle contraction. The drug does not create new receptors (A), increase ACh release (B), or bypass the neuromuscular junction (D).
- A hypothetical drug prevents the hydrolysis of ATP to ADP and Pi by myosin ATPase. How would this affect the cross-bridge cycle?
Answer: Myosin heads would detach from actin but could not be 're-cocked' for the next cycle.
The cycle is: 1) ATP binds, causing detachment. 2) ATP is hydrolysed, 'cocking' the myosin head. 3) Myosin binds to actin. 4) Power stroke occurs (ADP+Pi released). If hydrolysis (step 2) is blocked, the myosin head will still detach when ATP binds (step 1), but it cannot be re-energized or 'cocked' into the high-energy position. Therefore, it would be unable to bind to actin again to start a new power stroke. A is incorrect because ATP binding, not hydrolysis, causes detachment. B is incorrect because binding cannot occur without the head first being 'cocked'. D is unrelated to myosin's ATPase activity.
- Maximum tension is generated by a skeletal muscle fibre when there is optimal overlap between thick and thin filaments. What would happen if a sarcomere were stretched to the point where there was no overlap between actin and myosin filaments?
Answer: No tension could be generated because cross-bridges cannot form.
The generation of tension in a muscle fibre is entirely dependent on the formation of cross-bridges between myosin heads and actin filaments. If the sarcomere is overstretched to the point where the actin and myosin filaments no longer overlap, the myosin heads have nothing to bind to. Consequently, no cross-bridges can form, and no force can be generated upon stimulation.
- What is the direct function of ATP binding to the myosin head during the cross-bridge cycle?
Answer: To cause the detachment of the myosin head from the actin binding site.
The binding of a new ATP molecule to the myosin head is the specific event that causes it to release its grip on the actin filament, breaking the cross-bridge. The energy for the power stroke (A) comes from the release of ADP and Pi that were already bound. The conformational change in troponin (C) is caused by Ca²⁺ binding. The 'cocking' of the myosin head (D) is caused by the hydrolysis of ATP into ADP and Pi, which occurs after it has detached.
- Which of the following events must occur before the myosin head can perform the power stroke?
Answer: Calcium ions bind to troponin, and the myosin head binds to actin.
The power stroke is the action of the myosin head pivoting and pulling the actin filament. For this to happen, a cross-bridge must first be formed. Cross-bridge formation is only possible after calcium ions have bound to troponin, causing tropomyosin to move and expose the actin binding sites. Once exposed, the energized myosin head can bind to actin. The power stroke itself is driven by the release of ADP and Pi (C), which happens during the stroke, not before. ATP binding (A) causes detachment, which is the end of the previous cycle. Detachment (B) must happen before a new cycle can begin, but binding to actin is the immediate prerequisite for the power stroke.
- Rigor mortis, the stiffening of muscles after death, occurs because ATP is depleted. Which molecular event in the sliding filament theory is directly prevented by the absence of ATP?
Answer: The detachment of myosin heads from actin filaments.
In the cross-bridge cycle, the binding of a new ATP molecule to the myosin head is required for the head to detach from the actin filament. After death, ATP production ceases. Existing calcium leaks out, causing cross-bridges to form, but without new ATP, the myosin heads cannot detach. This locks the muscles in a contracted state, causing rigidity. A is incorrect; calcium actually leaks out of the SR after death. B and C are steps that would have occurred leading up to the final locked state.
