IB Biology Quiz: Apply Muscle And Motility
20 questions · exam conditions
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Apply Muscle And MotilityQuestion 1 of 20

The T-tubule system is essential for coordinated muscle contraction because it:

stores and releases the calcium ions required for contraction.
forms the Z-lines that anchor the thin filaments in the sarcomere.
allows for the rapid propagation of an action potential deep into the muscle fibre.
contains the enzyme acetylcholinesterase to terminate the signal for contraction.
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IB Biology Quiz

IB Biology Quiz: Apply Muscle And Motility

Practice Apply Muscle And Motility in IB Biology with focused quiz questions that help you check what you know, review explanations, and build confidence with test-style prompts.

What this quiz covers

This quiz focuses on Apply Muscle And Motility, giving you a quick way to practice the rules, question types, and explanations that matter most for IB Biology.

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Try each quiz question before looking at the correct answer. Use the explanations to review missed ideas, then come back to similar questions until the pattern feels familiar.

All questions

Question 1

The T-tubule system is essential for coordinated muscle contraction because it:

  1. stores and releases the calcium ions required for contraction.
  2. forms the Z-lines that anchor the thin filaments in the sarcomere.
  3. allows for the rapid propagation of an action potential deep into the muscle fibre. (correct answer)
  4. contains the enzyme acetylcholinesterase to terminate the signal for contraction.
Explanation: 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.

Question 2

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?

  1. The propagation of the action potential along the sarcolemma.
  2. The exocytosis of acetylcholine into the synaptic cleft. (correct answer)
  3. The binding of acetylcholine to receptors on the motor end plate.
  4. The reuptake of calcium ions into the sarcoplasmic reticulum.
Explanation: 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.

Question 3

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?

  1. The motor neuron releases progressively larger amounts of acetylcholine with each action potential.
  2. The muscle fibre does not have time to fully relax between stimuli, as calcium levels remain elevated in the sarcoplasm. (correct answer)
  3. All available ATP in the muscle fibre is consumed, locking the myosin heads onto the actin filaments.
  4. Successive action potentials recruit more and more muscle fibres within the motor unit to contract.
Explanation: 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.

Question 4

The energy for the 'cocking' or re-energizing of the myosin head into its high-energy conformation is directly provided by which event?

  1. The binding of a new ATP molecule.
  2. The release of ADP and inorganic phosphate (Pi).
  3. The binding of calcium ions to the myosin head.
  4. The hydrolysis of ATP into ADP and Pi. (correct answer)
Explanation: 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.

Question 5

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?

  1. A state of sustained contraction or spastic paralysis. (correct answer)
  2. Flaccid paralysis, as the muscle cannot be stimulated.
  3. Rigor mortis, as all cross-bridges would be permanently locked.
  4. Normal function, as Ca²⁺ pumps would compensate for the leak.
Explanation: 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.

Question 6

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?

  1. The sarcoplasmic reticulum would be unable to release calcium ions into the sarcoplasm. (correct answer)
  2. Acetylcholinesterase would be unable to break down acetylcholine in the synaptic cleft.
  3. Myosin heads would remain permanently attached to actin filaments, causing muscle rigidity.
  4. The presynaptic terminal would be prevented from releasing acetylcholine upon arrival of an action potential.
Explanation: 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.

Question 7

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?

  1. It increases the number of functional acetylcholine receptors on the motor end plate.
  2. It increases the amount of acetylcholine released from the motor neuron.
  3. It prevents the breakdown of acetylcholine, increasing its concentration in the synaptic cleft. (correct answer)
  4. It directly stimulates the sarcoplasmic reticulum to release calcium ions, bypassing the receptors.
Explanation: 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).

Question 8

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?

  1. Maximum tension would be generated because all myosin heads are available to bind.
  2. No tension could be generated because cross-bridges cannot form. (correct answer)
  3. Tension would be generated, but it would be very low due to steric hindrance.
  4. The muscle would be stuck in a contracted state due to constant Ca²⁺ release.
Explanation: 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.

Question 9

Which sequence correctly outlines the events following the arrival of a nerve impulse at a motor end plate?

  1. Acetylcholine release → T-tubule depolarization → Ca²⁺ release from SR → Troponin binds Ca²⁺ → Cross-bridge formation (correct answer)
  2. Ca²⁺ release from SR → Acetylcholine release → T-tubule depolarization → Troponin binds Ca²⁺ → Cross-bridge formation
  3. T-tubule depolarization → Acetylcholine release → Troponin binds Ca²⁺ → Ca²⁺ release from SR → Cross-bridge formation
  4. Acetylcholine release → Cross-bridge formation → Troponin binds Ca²⁺ → T-tubule depolarization → Ca²⁺ release from SR
Explanation: 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.

Question 10

Which statement correctly distinguishes the roles of troponin and tropomyosin in skeletal muscle contraction?

  1. Tropomyosin binds to calcium ions, which causes troponin to slide away from the actin binding sites.
  2. Troponin binds to myosin heads, while tropomyosin covers the binding sites on actin.
  3. Tropomyosin is a long filament that blocks myosin-binding sites, and troponin is a complex that moves it upon binding Ca²⁺. (correct answer)
  4. Troponin is directly attached to the Z-line, while tropomyosin is a component of the thick filament.
Explanation: 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.

Question 11

During a vigorous muscle contraction, which of the following changes occurs within the sarcomere?

  1. The A-band shortens as the myosin filaments contract.
  2. The I-band widens as actin filaments slide away from the M-line.
  3. The distance between Z-lines decreases as the H-zone narrows. (correct answer)
  4. The lengths of both actin and myosin filaments decrease.
Explanation: 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.

Question 12

What is the direct function of ATP binding to the myosin head during the cross-bridge cycle?

  1. To provide the energy for the power stroke that moves the actin filament.
  2. To cause the detachment of the myosin head from the actin binding site. (correct answer)
  3. To trigger the conformational change in troponin that exposes actin binding sites.
  4. To energize the myosin head, moving it into the high-energy 'cocked' position.
Explanation: 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.

Question 13

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?

  1. The release of calcium ions from the sarcoplasmic reticulum.
  2. The hydrolysis of ATP to energize the myosin heads.
  3. The binding of myosin heads to the active sites on actin.
  4. The detachment of myosin heads from actin filaments. (correct answer)
Explanation: 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.

Question 14

Which of the following events must occur before the myosin head can perform the power stroke?

  1. A new molecule of ATP binds to the myosin head.
  2. The myosin head detaches from the actin filament.
  3. ADP and inorganic phosphate are released from the myosin head.
  4. Calcium ions bind to troponin, and the myosin head binds to actin. (correct answer)
Explanation: 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.

Question 15

What is the primary role of the calcium pumps (Ca²⁺-ATPase) located on the membrane of the sarcoplasmic reticulum?

  1. To release Ca²⁺ into the sarcoplasm in response to an action potential.
  2. To actively transport Ca²⁺ from the sarcoplasm back into the sarcoplasmic reticulum. (correct answer)
  3. To pump Ca²⁺ out of the muscle fibre and into the extracellular fluid.
  4. To hydrolyze ATP, providing energy directly for the movement of tropomyosin.
Explanation: 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.

Question 16

In the process of neuromuscular transmission, what event is directly responsible for the depolarization of the sarcolemma at the motor end plate?

  1. The influx of Ca²⁺ ions into the axon terminal.
  2. The breakdown of acetylcholine by acetylcholinesterase.
  3. The influx of Na⁺ ions through ligand-gated ion channels. (correct answer)
  4. The propagation of the action potential along the T-tubules.
Explanation: 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.

Question 17

Which of the following comparisons between the events at the neuromuscular junction and events within the sarcomere is correct?

  1. ATP is required for acetylcholine release at the junction, while ATP is required for the power stroke in the sarcomere.
  2. Calcium ions trigger exocytosis at the junction, while sodium ions trigger the movement of tropomyosin in the sarcomere.
  3. Acetylcholine directly binds to troponin in the sarcomere after diffusing from the junction.
  4. Both processes are initiated by a depolarization event, but the ion channels involved are different. (correct answer)
Explanation: 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.

Question 18

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?

  1. Muscles will be in a constant state of contraction because myosin cannot detach from actin.
  2. Muscles will be unable to contract because tropomyosin will continuously block myosin-binding sites. (correct answer)
  3. Contraction will occur, but it will be weak because fewer cross-bridges can be formed.
  4. Acetylcholine release at the neuromuscular junction will be inhibited, preventing stimulation.
Explanation: 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.

Question 19

During muscle contraction, the length of the A-band remains constant. What is the most accurate explanation for this observation?

  1. The A-band corresponds to the full length of the myosin filament, which does not change its length. (correct answer)
  2. The A-band represents the length of the actin filaments, which do not shorten during contraction.
  3. The A-band shortens, but this is compensated by the widening of the H-zone.
  4. The A-band is anchored to the Z-lines, which move closer but do not affect the band's width.
Explanation: 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.

Question 20

A hypothetical drug prevents the hydrolysis of ATP to ADP and Pi by myosin ATPase. How would this affect the cross-bridge cycle?

  1. Myosin heads would be unable to detach from the actin filaments.
  2. Myosin heads would bind to actin but would be unable to perform the power stroke.
  3. Myosin heads would detach from actin but could not be 're-cocked' for the next cycle. (correct answer)
  4. Tropomyosin would remain permanently bound to actin, preventing any cross-bridge formation.
Explanation: 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.