- Rigor mortis, the stiffening of muscles after death, occurs because ATP is depleted. What is the specific molecular mechanism responsible for this stiffness?
Answer: Myosin heads cannot detach from actin binding sites without a new molecule of ATP binding to them.
ATP has two critical roles in the cross-bridge cycle. Its hydrolysis powers the stroke, but its binding is required to cause the detachment of the myosin head from the actin filament. In rigor mortis, ATP is no longer produced, so myosin heads remain locked onto the actin filaments in the state they were in when ATP ran out, causing stiffness. While A is true (calcium pumps are ATP-dependent), the direct cause of the stiffness is the failure of detachment, not just formation. C is incorrect; the power stroke may have already occurred. D is an event at the synapse and is not the primary cause of stiffness within the muscle fibre.
- A certain drug acts by enhancing the activity of the Ca²⁺-ATPase pumps on the sarcoplasmic reticulum membrane. What would be the likely effect of this drug on muscle contraction?
Answer: The muscle would relax more quickly after a contraction.
Muscle relaxation occurs when calcium ions are actively transported back into the sarcoplasmic reticulum by Ca²⁺-ATPase pumps. This removes calcium from the sarcoplasm, allowing troponin and tropomyosin to once again block the actin binding sites. By enhancing the activity of these pumps, the drug would speed up the rate of calcium reuptake, leading to a faster cessation of cross-bridge cycling and thus a more rapid relaxation phase.
- Which statement accurately describes the changes in sarcomere banding patterns during an isotonic muscle contraction?
Answer: The I band and H zone both shorten, while the A band remains constant in length.
During contraction, the thin (actin) filaments slide over the thick (myosin) filaments. The A band represents the full length of the thick filaments, which does not change. The I band (region of only thin filaments) and the H zone (region of only thick filaments in the center) both decrease in width as the filaments overlap more. The Z lines, which anchor the thin filaments, are pulled closer together. Distractor A is a key misconception; the A band's length is constant. Distractor C incorrectly states the A band shortens. Distractor D incorrectly states the I band widens; it shortens.
- An athlete's muscles are contracting isometrically, meaning the muscle generates force without changing length. Which statement best describes the activity at the sarcomere level during this type of contraction?
Answer: Cross-bridges are rapidly cycling, but the external force is equal to the force generated, so no filament sliding occurs.
Isometric contraction involves force generation without a change in muscle length. At the molecular level, this means the cross-bridge cycle (attachment, power stroke, detachment, re-cocking) is active and consuming ATP. However, the force generated by the cycling cross-bridges is equal to the load (external force), so the thin filaments cannot slide and the sarcomeres do not shorten. Distractor A is incorrect because force generation requires cross-bridges. Distractor C describes the initial phase before movement, but in a sustained isometric contraction, there is no net shortening. Distractor D is incorrect as holding a position isometrically requires significant ATP expenditure.
- Which event directly triggers the 'power stroke' during the sliding filament mechanism of muscle contraction?
Answer: The release of inorganic phosphate (Pi) from the myosin head.
The sequence is as follows: 1) ATP is hydrolyzed, energizing the myosin head. 2) The energized head binds to actin, forming a cross-bridge. 3) The release of the inorganic phosphate (Pi) that was generated during hydrolysis is the immediate trigger for the power stroke, where the myosin head pivots and pulls the actin filament. The release of ADP occurs after the power stroke. A causes detachment. B precedes the power stroke. D allows B to happen but does not directly trigger the stroke itself.
- During a muscle contraction, which of the following describes the state of a myosin head immediately after it hydrolyses ATP but before it binds to actin?
Answer: It is in a high-energy, 'cocked' position, containing ADP and inorganic phosphate (Pi).
The hydrolysis of ATP (ATP → ADP + Pi) provides the energy that 'cocks' the myosin head into a high-energy conformation. At this stage, the products of hydrolysis (ADP and Pi) are still attached. The head is now ready to bind to an exposed site on the actin filament. Distractor A describes the state after the power stroke and before ATP binds. Distractor C describes the state at the end of the power stroke. Distractor D describes the state just prior to detachment.
- During muscle relaxation, what is the primary energy-dependent process that must occur?
Answer: The active transport of Ca²⁺ from the sarcoplasm back into the sarcoplasmic reticulum.
Relaxation is an active process that requires ATP. The key step is the removal of Ca²⁺ from the sarcoplasm. This is accomplished by Ca²⁺-ATPase pumps in the membrane of the sarcoplasmic reticulum, which actively transport Ca²⁺ back into the SR against its concentration gradient. This requires ATP. While C and D also use ATP and are part of the overall process, the removal of calcium (A) is the direct trigger for relaxation as it allows the troponin-tropomyosin complex to re-block the actin binding sites. B is enzymatic and does not directly consume ATP.
- What is the primary role of acetylcholinesterase at the neuromuscular junction?
Answer: To break down acetylcholine in the synaptic cleft, terminating the signal for contraction.
Acetylcholinesterase is an enzyme located in the synaptic cleft. Its function is to rapidly hydrolyze acetylcholine into acetate and choline. This breakdown removes the neurotransmitter from the cleft, preventing it from continuously binding to its receptors and allowing the muscle fibre to relax after the initial stimulus. Without this enzyme, a single nerve impulse would cause a prolonged, uncontrolled contraction. The other options describe the roles of other components: the action potential (A), acetylcholine itself (B), and reuptake transporters (D), which are not the primary mechanism for ACh removal here.
- If a skeletal muscle fibre were treated with a substance that allows Ca²⁺ to enter the sarcoplasm but also blocks the ATPase site on myosin, what would be the result?
Answer: The myosin heads would be unable to bind to actin because they could not be energized.
The ATPase site on myosin is where ATP binds and is hydrolyzed. This hydrolysis (ATP -> ADP + Pi) is essential for 'cocking' the myosin head into a high-energy state, which is a prerequisite for it to bind to actin. If this site is blocked, ATP cannot be hydrolyzed, and the myosin heads will remain in a low-energy state, unable to initiate cross-bridge formation, even if Ca²⁺ has exposed the binding sites on actin. Therefore, no contraction would occur. Distractor A is incorrect because the power stroke also depends on events at this site. D is incorrect as the Ca²⁺-troponin interaction is unaffected.
- A researcher prepares an experimental solution containing isolated myofibrils, an abundance of Ca²⁺ ions, and a modified, non-hydrolyzable analogue of ATP. What is the expected outcome when this solution is applied to the myofibrils?
Answer: No contraction occurs because the energy for the power stroke cannot be released from the ATP analogue.
Contraction requires two key events involving ATP: hydrolysis to energize the myosin head, and binding to release it. A non-hydrolyzable ATP analogue can bind to the myosin head, causing it to detach from actin (if it was already attached). However, it cannot be hydrolyzed to provide the energy to 'cock' the myosin head for the power stroke. Therefore, even with calcium present to expose binding sites, the sliding of filaments cannot be initiated. C is incorrect because detachment requires prior attachment, and D is incorrect because the binding of myosin to actin is not directly dependent on hydrolysis, but the power stroke is.
- Which of the following correctly orders the sequence of events that couple excitation of a muscle fibre to its contraction?
Answer: Acetylcholine binding → Action potential in T-tubules → Ca²⁺ release from SR → Troponin binds Ca²⁺
The correct sequence begins at the neuromuscular junction and proceeds into the cell. 1) Acetylcholine binds to receptors on the sarcolemma, initiating an action potential. 2) The action potential propagates down the T-tubules. 3) This triggers the release of Ca²⁺ from the sarcoplasmic reticulum (SR). 4) The released Ca²⁺ binds to troponin, which is the next step leading to contraction. All other options present an incorrect sequence of these key events.
- The generation of a graded response in a whole skeletal muscle, such as lifting a light object versus a heavy one, is primarily achieved by which mechanism?
Answer: Varying the number of motor units that are activated within the muscle.
A single muscle fibre contracts in an 'all-or-nothing' fashion in response to a stimulus above its threshold. The central nervous system controls the total force produced by a whole muscle by varying the number of motor units (a motor neuron and all the muscle fibres it innervates) that are recruited. Activating more motor units generates more force. This is known as motor unit recruitment. The other options are incorrect as the cellular-level responses (A, B, D) are not typically graded in this manner for a single stimulus.
- A toxin is discovered that irreversibly binds to and blocks voltage-gated calcium channels on the axon terminal of a motor neuron. What would be the most immediate consequence for the neuromuscular junction and the associated muscle fibre?
Answer: Acetylcholine (ACh) would not be released into the synaptic cleft, preventing muscle fibre stimulation.
The influx of calcium ions through voltage-gated channels at the axon terminal is the direct trigger for the exocytosis of vesicles containing acetylcholine. If these channels are blocked, ACh cannot be released, and the signal to contract is never transmitted to the muscle fibre. Distractor B describes an effect related to issues with acetylcholinesterase. Distractor C describes an event within the muscle fibre, which would not occur because the initial signal (ACh) is absent. Distractor D is incorrect because the action potential propagates via sodium and potassium channels along the axon; the toxin affects only the terminal.
- In the context of the neuromuscular junction, what is the role of the sarcolemma immediately surrounding the axon terminal (the motor end plate)?
Answer: It contains ligand-gated ion channels that open in response to acetylcholine.
The motor end plate is the specialized region of the muscle fibre's plasma membrane (sarcolemma) that lies opposite the axon terminal. Its membrane is highly folded and contains a high density of ligand-gated sodium channels that are specifically acetylcholine receptors. When ACh binds, these channels open, causing a local depolarization (end-plate potential) that can trigger a full action potential in the muscle fibre. A and D describe the axon terminal. C describes the sarcoplasmic reticulum.
- A genetic mutation results in a troponin molecule that cannot change its conformation upon binding Ca²⁺. How would this mutation affect muscle function?
Answer: Muscle contraction would be prevented because tropomyosin would fail to move from the actin binding sites.
The role of the troponin-tropomyosin complex is to regulate the availability of myosin-binding sites on actin. Ca²⁺ binds to troponin, which then changes shape and pulls the associated tropomyosin strand away from the binding sites. If troponin cannot change shape, it cannot move tropomyosin, regardless of calcium concentration. The binding sites on actin would remain blocked, preventing cross-bridge formation and thus muscle contraction.
- Which comparison between the H zone and the I band of a sarcomere is correct when the muscle fibre is fully relaxed?
Answer: The H zone contains only thick filaments, while the I band contains only thin filaments.
By definition, the H zone is the central region of the A band that contains only thick filaments (myosin). The I band is the region that contains only thin filaments (actin) and is bisected by the Z line. During contraction, both regions shorten as the degree of filament overlap increases. Distractor A incorrectly describes the H zone's composition. Distractor C incorrectly describes the composition of both. Distractor D incorrectly describes the I band; its length is not defined by the thick filament (that would be the A band).
- The protein dystrophin links actin filaments to a complex of proteins in the sarcolemma. In Duchenne muscular dystrophy, this protein is absent. Which of the following consequences is most likely to result from the absence of dystrophin?
Answer: Structural instability of the sarcolemma, leading to damage during muscle contraction.
Dystrophin acts as a molecular shock absorber, anchoring the contractile apparatus (actin) to the cell membrane (sarcolemma) and the extracellular matrix. This connection helps to distribute the forces generated during contraction and maintains the structural integrity of the sarcolemma. Without dystrophin, the sarcolemma becomes fragile and is easily damaged by the stress of contraction, leading to cell death and the progressive muscle weakness characteristic of the disease. The other options describe processes that are not directly dependent on dystrophin.
- Which of the following describes the relationship between T-tubules, the sarcoplasmic reticulum (SR), and the initiation of muscle contraction?
Answer: T-tubules are invaginations of the sarcolemma that transmit action potentials deep into the fibre, adjacent to the SR.
T-tubules (transverse tubules) are deep invaginations of the sarcolemma (the cell membrane) that penetrate into the muscle cell's interior. They run alongside the terminal cisternae of the sarcoplasmic reticulum. This arrangement, called a triad, ensures that an action potential travelling along the sarcolemma can quickly be transmitted deep within the fibre, triggering the voltage-sensitive proteins that cause the adjacent SR to release its stored Ca²⁺. A is incorrect as the SR stores Ca²⁺. B reverses the roles of the T-tubules and SR. D is functionally and structurally incorrect.
- Which of the following events is the most direct consequence of an action potential propagating down the T-tubules of a skeletal muscle fibre?
Answer: The opening of voltage-gated Ca²⁺ release channels in the membrane of the sarcoplasmic reticulum.
The process of excitation-contraction coupling involves the action potential traveling from the sarcolemma down the T-tubules. This electrical signal directly triggers the opening of calcium release channels in the adjacent sarcoplasmic reticulum, causing Ca²⁺ to flood the sarcoplasm. Distractor A is incorrect because calcium binds to troponin, not tropomyosin. Distractor C is a part of the cross-bridge cycle that happens after calcium is released. Distractor D is the event that initiates the action potential at the neuromuscular junction, so it precedes the T-tubule event.
- What is the structural and functional significance of the Z line within a myofibril?
Answer: It is a protein disc that defines the boundary of a sarcomere and serves as an anchor point for thin filaments.
The Z line (or Z disc) is a dense protein structure that forms the lateral boundary of each sarcomere. The thin filaments (actin) are directly attached to the Z line and extend towards the center of the sarcomere. During contraction, the Z lines are pulled closer together as the thin filaments slide over the thick filaments. Distractor A describes the M line. Distractor C describes the zone of overlap within the A band. Distractor D describes the protein titin.
