Muscle Physiology and Contraction Practice Questions
20 free Muscle Physiology and Contraction practice questions for the USMLE Step 1. Tap an option to answer — you get instant feedback, the correct answer, and a detailed explanation for every question.
Which structure is the basic contractile unit of skeletal muscle that shortens during contraction?
- A Motor unit
- B Myofibril
- C Sarcomere
- D Myofilament
Correct answer: Sarcomere
The sarcomere — the segment between two Z-discs — is the functional unit that shortens when muscle contracts, as thin (actin) and thick (myosin) filaments slide past each other.
According to the sliding filament theory, which of the following occurs during muscle contraction?
- A Thick myosin filaments shorten
- B Thin actin filaments shorten
- C Thin filaments slide past thick ones
- D Both thick and thin filaments shorten
Correct answer: Thin filaments slide past thick ones
Muscle contraction occurs by actin (thin) filaments sliding past myosin (thick) filaments — the filaments themselves remain same length; the sliding shortens the sarcomere.
Which zone or band of the sarcomere remains constant in length during contraction, according to the sliding filament model?
- A I band
- B H zone
- C A band
- D Distance between Z-discs
Correct answer: A band
The A band — the region containing the full length of the thick filaments — remains constant during contraction; shortening is due to movement of thin filaments past thick ones.
What triggers calcium release from the sarcoplasmic reticulum in skeletal muscle during excitation–contraction coupling?
- A Binding of ATP to the myosin head
- B Binding of acetylcholine to actin
- C T-tubule depolarization activating DHPR–RyR coupling
- D Passive diffusion of Ca²⁺ from extracellular fluid
Correct answer: T-tubule depolarization activating DHPR–RyR coupling
An action potential spreads along the sarcolemma and T-tubules; voltage-sensing dihydropyridine receptors (DHPR) activate ryanodine receptors (RyR) on the SR, causing Ca²⁺ release — the key step in excitation–contraction coupling.
In the absence of sufficient intracellular calcium, muscle contraction cannot proceed because:
- A Myosin heads are unable to hydrolyze ATP
- B ATP cannot bind to the myosin head
- C Tropomyosin still blocks actin's myosin-binding sites
- D The sarcoplasmic reticulum cannot refill with calcium
Correct answer: Tropomyosin still blocks actin's myosin-binding sites
Without Ca²⁺, tropomyosin remains in a position that blocks myosin-binding sites on actin — preventing cross-bridge formation and thus muscle contraction.
Which process describes the repeated attachment, pivoting (power stroke), detachment, and re-cocking of myosin heads during muscle contraction?
- A Calcium cycling
- B Cross-bridge cycle
- C Sliding filament shift
- D Excitation–contraction coupling
Correct answer: Cross-bridge cycle
The cross-bridge cycle is the molecular mechanism of contraction — myosin heads cyclically bind to actin, undergo a power stroke using ATP, detach, and re-attach, driving filament sliding.
Which energy molecule is directly hydrolyzed by myosin ATPase to power muscle contraction and cross-bridge cycling?
- A GTP
- B ATP
- C Creatine phosphate
- D cAMP
Correct answer: ATP
ATP is hydrolyzed by the myosin ATPase on the myosin head, providing the energy required for the power stroke and detachment in each cross-bridge cycle.
What structural arrangement at the neuromuscular junction ensures that one motor neuron can control multiple muscle fibers simultaneously?
- A Multiple neuromuscular junctions per muscle fiber
- B Many-to-one innervation (many neurons → one fiber)
- C One-to-many innervation (one neuron → many fibers)
- D Electrical synapses between fibers
Correct answer: One-to-many innervation (one neuron → many fibers)
In a motor unit, one somatic motor neuron branches to innervate many muscle fibers, allowing those fibers to contract simultaneously in a coordinated fashion.
Which of the following correctly describes the sequence of events in excitation–contraction coupling in skeletal muscle, from membrane excitation to force generation?
- A ACh release → SR Ca²⁺ reuptake → T-tubule repolarization → cross-bridge cycling
- B Action potential → T-tubule depolarization → Ca²⁺ release → cross-bridge cycling
- C Cross-bridge cycling → Ca²⁺ release → T-tubule depolarization → action potential
- D ATP hydrolysis → membrane excitation → Ca²⁺ release → filament sliding
Correct answer: Action potential → T-tubule depolarization → Ca²⁺ release → cross-bridge cycling
The correct sequence: motor neuron triggers action potential → AP travels along sarcolemma and T-tubules → depolarization activates DHPR-RyR → SR releases Ca²⁺ → Ca²⁺ binds troponin → cross-bridge cycling begins.
During muscle relaxation after a contraction, which mechanism primarily reduces cytosolic Ca²⁺ concentration to stop contraction?
- A Calcium freely diffuses out into the extracellular space
- B SERCA pumps Ca²⁺ into the sarcoplasmic reticulum
- C Myosin hydrolyzes more ATP to absorb the Ca²⁺
- D Troponin is enzymatically degraded
Correct answer: SERCA pumps Ca²⁺ into the sarcoplasmic reticulum
Relaxation requires removal of Ca²⁺ from the cytosol; the sarcoplasmic/endoplasmic reticulum Ca²⁺-ATPase (SERCA) actively pumps Ca²⁺ back into the SR, ending cross-bridge formation.
Which band(s) of the sarcomere shorten during contraction as thin and thick filaments slide past each other?
- A A band only
- B I band and H zone
- C Z disc width
- D M line length
Correct answer: I band and H zone
During contraction, the I band (only thin filaments) and H zone (only thick filaments) decrease as thin filaments slide toward the center; A band remains constant.
Which structure in the muscle fiber ensures rapid propagation of action potentials into the interior of the fiber to trigger Ca²⁺ release from the SR?
- A Sarcoplasmic reticulum
- B Transverse tubules
- C Mitochondria
- D Endomysium
Correct answer: Transverse tubules
T-tubules are invaginations of the sarcolemma that carry the action potential deep into the muscle fiber, coupling membrane excitation to Ca²⁺ release from the sarcoplasmic reticulum.
In isometric muscle contraction, which of the following is true?
- A Muscle shortens and lifts an external load
- B Muscle lengthens as it actively contracts
- C Muscle length is unchanged as tension rises
- D The muscle's filaments physically elongate
Correct answer: Muscle length is unchanged as tension rises
In isometric contraction the muscle generates tension without changing its overall length; the filaments attempt to slide but the external load prevents shortening.
Which statement about smooth muscle contraction is correct compared to skeletal muscle contraction?
- A Smooth muscle completely lacks the proteins actin and myosin
- B Smooth muscle uses a sliding-filament mechanism but with different regulation
- C Smooth muscle can contract without requiring any ATP
- D Smooth muscle is organized into sarcomeres with Z-discs
Correct answer: Smooth muscle uses a sliding-filament mechanism but with different regulation
Smooth muscle contracts through a sliding-filament mechanism involving actin and myosin, but regulation differs (calcium-calmodulin, MLCK), and smooth muscle lacks sarcomeres/Z-discs.
Which protein complex undergoes a conformational shift upon Ca²⁺ binding to expose the myosin-binding sites on actin?
- A Myosin heavy chain
- B Titin
- C Troponin-tropomyosin complex
- D Nebulin
Correct answer: Troponin-tropomyosin complex
When Ca²⁺ binds to troponin C, the troponin–tropomyosin complex changes shape, moving tropomyosin away from actin’s myosin-binding sites, allowing cross-bridge formation.
What is the effect of a deficit in ATP availability (e.g., ischemia) on muscle contraction and relaxation?
- A Enhanced contraction and rapid relaxation
- B Contraction occurs but relaxation is impaired
- C Muscle relaxes more quickly than normal
- D There is no impact on muscle mechanics
Correct answer: Contraction occurs but relaxation is impaired
Without ATP, myosin heads cannot detach from actin, so cross-bridges stay locked, producing sustained contraction (rigor) and impaired relaxation; relaxation requires ATP for cross-bridge detachment and Ca²⁺ reuptake.
How does an increase in intracellular Ca²⁺ concentration lead to force generation in muscle fibers?
- A By hyperpolarizing the muscle sarcolemma
- B By directly increasing cellular ATP synthesis
- C By shifting troponin–tropomyosin to expose actin's binding sites
- D By fragmenting the thick myosin filaments
Correct answer: By shifting troponin–tropomyosin to expose actin's binding sites
Elevated Ca²⁺ binds to troponin, shifting troponin–tropomyosin and unmasking actin binding sites; myosin heads can then bind actin and perform the power stroke, generating force.
Which of the following best describes “summation” of contractions in skeletal muscle physiology?
- A More Ca²⁺ is released with each action potential
- B Recruitment of additional motor units only
- C Successive stimuli prevent full relaxation, boosting tension
- D Switching from slow-twitch to fast-twitch fibers
Correct answer: Successive stimuli prevent full relaxation, boosting tension
When stimuli arrive in rapid succession before the muscle fully relaxes, cytosolic Ca²⁺ stays elevated and successive contractions build on one another, so summation increases the overall tension.
Which structural protein in muscle fibers contributes to elasticity and returns stretched sarcomeres to resting length after contraction or stretch?
- A Actin
- B Myosin
- C Titin
- D Tropomyosin
Correct answer: Titin
Titin spans from the Z-disc to the M-line and acts as a molecular spring, contributing to the passive elasticity of muscle and restoring sarcomere length after stretch or contraction.
During prolonged, repeated contractions (fatigue), which factor contributes to decreased force generation in muscle fibers?
- A Excessive release of Ca²⁺ from the SR
- B Build-up of metabolic byproducts and reduced ATP
- C Increased troponin Ca²⁺ sensitivity
- D Enhanced rate of filament sliding
Correct answer: Build-up of metabolic byproducts and reduced ATP
With repeated contraction, ATP depletion and the accumulation of metabolites impair cross-bridge cycling and calcium handling, leading to muscle fatigue and reduced force generation.