Understanding the physiology of muscle contraction is essential for B.Pharm students. This focused review explains skeletal, cardiac, and smooth muscle mechanisms, emphasizing the sliding filament theory, excitation–contraction coupling, and cross-bridge cycling. Key molecular players—actin, myosin, troponin, tropomyosin, ATP, Ca2+, ryanodine and DHP receptors, and SERCA—are discussed with clinical and pharmacological relevance, including neuromuscular transmission, muscle fibre types, fatigue, and drugs affecting the neuromuscular junction. Grasping length–tension and force–velocity relationships, energy systems (ATP, creatine phosphate, glycolysis, oxidative phosphorylation), and regulatory feedback (spindles, Golgi tendon) will prepare you for applied therapeutics. Now let’s test your knowledge with 30 MCQs on this topic.
Q1. Which pair of proteins primarily interact during the sliding filament mechanism of skeletal muscle contraction?
- Actin and myosin filaments sliding past each other
- Troponin and tropomyosin generating force
- DHP receptor and ryanodine receptor coupling
- SERCA and calsequestrin releasing calcium
Correct Answer: Actin and myosin filaments sliding past each other
Q2. What is the immediate effect of ATP binding to the myosin head in the cross-bridge cycle?
- Initiates the power stroke
- Causes detachment of myosin from actin
- Triggers calcium release from the SR
- Phosphorylates myosin light chains
Correct Answer: Causes detachment of myosin from actin
Q3. During skeletal muscle activation, calcium binds to which protein to permit actin–myosin interaction?
- Tropomyosin
- Troponin C
- Myosin light chain phosphatase
- Calsequestrin
Correct Answer: Troponin C
Q4. In skeletal muscle excitation–contraction coupling, which structure directly triggers calcium release from the sarcoplasmic reticulum?
- L-type (DHP) receptor mechanically coupling to ryanodine receptor
- Voltage-gated sodium channels causing calcium influx
- Acetylcholinesterase activation at the motor endplate
- SERCA pump opening to release stored calcium
Correct Answer: L-type (DHP) receptor mechanically coupling to ryanodine receptor
Q5. Which pump is primarily responsible for resequestering Ca2+ into the sarcoplasmic reticulum during muscle relaxation?
- Na+/K+ ATPase
- SERCA (SR Ca2+-ATPase)
- Voltage-gated Ca2+ channel
- Ryanodine receptor
Correct Answer: SERCA (SR Ca2+-ATPase)
Q6. What neurotransmitter is released at the neuromuscular junction to initiate skeletal muscle contraction?
- Norepinephrine
- Acetylcholine
- Glutamate
- Dopamine
Correct Answer: Acetylcholine
Q7. The nicotinic acetylcholine receptor at the motor endplate is best described as which type of receptor?
- G protein–coupled receptor
- Tyrosine kinase receptor
- Ligand-gated cation channel
- Voltage-gated sodium channel
Correct Answer: Ligand-gated cation channel
Q8. Botulinum toxin produces muscle weakness by which mechanism?
- Blocking postsynaptic nicotinic receptors competitively
- Inhibiting acetylcholine release by cleaving SNARE proteins
- Antagonizing DHP receptors on T-tubules
- Preventing calcium uptake into the SR
Correct Answer: Inhibiting acetylcholine release by cleaving SNARE proteins
Q9. Succinylcholine acts as a neuromuscular blocker by which mechanism?
- Non-depolarizing competitive antagonism at nicotinic receptors
- Depolarizing agonist that causes persistent end-plate depolarization
- Inhibition of acetylcholinesterase increasing ACh levels
- Blocking voltage-gated sodium channels in motor neurons
Correct Answer: Depolarizing agonist that causes persistent end-plate depolarization
Q10. Rigor mortis after death arises mainly because of which biochemical change?
- Excess ATP production causing hypercontraction
- Depletion of ATP preventing detachment of myosin from actin
- Overactivation of SERCA leading to calcium overload
- Continuous acetylcholine release at the motor endplate
Correct Answer: Depletion of ATP preventing detachment of myosin from actin
Q11. Which muscle fibre type has the highest resistance to fatigue and abundant mitochondria?
- Type IIb (fast glycolytic)
- Type IIx (fast intermediate)
- Type IIa (fast oxidative-glycolytic)
- Type I (slow oxidative)
Correct Answer: Type I (slow oxidative)
Q12. What is the primary role of creatine phosphate in muscle cells during the first seconds of intense activity?
- Generate lactate to buffer pH
- Rapidly regenerate ATP from ADP
- Transport oxygen to myoglobin
- Activate sarcomeric calcium channels
Correct Answer: Rapidly regenerate ATP from ADP
Q13. The optimal sarcomere length for maximal active tension generation in human skeletal muscle is approximately:
- 0.6–0.8 μm
- 1.0–1.2 μm
- 2.0–2.2 μm
- 3.5–4.0 μm
Correct Answer: 2.0–2.2 μm
Q14. According to the force–velocity relationship, what happens to contraction velocity as the external load increases?
- Velocity increases proportionally with load
- Velocity remains constant regardless of load
- Velocity decreases as load increases
- Velocity becomes independent of cross-bridge cycling
Correct Answer: Velocity decreases as load increases
Q15. Continuous high-frequency stimulation of a motor nerve that produces a sustained maximal contraction is called:
- Single twitch
- Summation
- Tetanic contraction (tetanus)
- Treppe (staircase) effect
Correct Answer: Tetanic contraction (tetanus)
Q16. Henneman’s size principle of motor unit recruitment states that:
- Large fast units are recruited before small slow units
- All motor units are recruited simultaneously regardless of force
- Smaller, low-threshold motor units are recruited before larger ones
- Recruitment order is random and depends on fatigue
Correct Answer: Smaller, low-threshold motor units are recruited before larger ones
Q17. In smooth muscle, calcium activates contraction primarily by binding to:
- Troponin C to move tropomyosin
- Calmodulin, which activates myosin light chain kinase (MLCK)
- Ryanodine receptor to open L-type channels
- Actin to directly enhance cross-bridge cycling
Correct Answer: Calmodulin, which activates myosin light chain kinase (MLCK)
Q18. Which molecular event most directly triggers the power stroke during cross-bridge cycling?
- ATP binding to myosin
- Release of inorganic phosphate (Pi) from myosin
- Binding of calcium to troponin
- Phosphorylation of myosin light chain
Correct Answer: Release of inorganic phosphate (Pi) from myosin
Q19. Which drug acts by inhibiting the ryanodine receptor to reduce skeletal muscle calcium release and is used in malignant hyperthermia?
- Neostigmine
- Dantrolene
- Pancuronium
- Suxamethonium
Correct Answer: Dantrolene
Q20. The enzyme intrinsic to the myosin head that hydrolyzes ATP to provide energy for contraction is called:
- Actin ATPase
- Myosin ATPase
- Creatine kinase
- Phosphofructokinase
Correct Answer: Myosin ATPase
Q21. An isometric contraction is characterized by:
- Shortening of the muscle with constant tension
- Lengthening of the muscle under low load
- Tension development without change in muscle length
- Rapid oscillatory contractions producing heat
Correct Answer: Tension development without change in muscle length
Q22. The end-plate potential (EPP) is primarily generated by increased permeability to which ion through nicotinic receptors?
- Chloride (Cl−) influx only
- Sodium (Na+) influx leading to depolarization
- Potassium (K+) efflux only causing hyperpolarization
- Calcium (Ca2+) influx exclusively
Correct Answer: Sodium (Na+) influx leading to depolarization
Q23. A major contributor to peripheral muscle fatigue during intense exercise is:
- Excessive acetylcholinesterase activity at the NMJ
- Accumulation of inorganic phosphate (Pi) and H+ interfering with cross-bridge function
- Increased SERCA activity causing too rapid calcium reuptake
- Enhanced mitochondrial ATP generation preventing contraction
Correct Answer: Accumulation of inorganic phosphate (Pi) and H+ interfering with cross-bridge function
Q24. Which skeletal muscle fibre type is fast-contracting and has substantial oxidative capacity (endurance plus speed)?
- Type I (slow oxidative)
- Type IIa (fast oxidative–glycolytic)
- Type IIb (fast glycolytic)
- Type IIx (extremely slow)
Correct Answer: Type IIa (fast oxidative–glycolytic)
Q25. During active contraction which sarcomeric region shortens markedly?
- A band shortens considerably
- I band shortens and H zone narrows
- Myosin filaments disappear
- Z line length increases
Correct Answer: I band shortens and H zone narrows
Q26. Which enzyme in the synaptic cleft terminates acetylcholine action at the motor endplate?
- Monoamine oxidase
- Acetylcholinesterase
- Butyrylcholinesterase
- Choline acetyltransferase
Correct Answer: Acetylcholinesterase
Q27. The “treppe” or staircase phenomenon (increased force with repeated low-frequency stimulation) is mainly due to:
- Progressive muscle fibre atrophy
- Gradual increase in intracellular Ca2+ availability between twitches
- Inactivation of acetylcholinesterase
- Depletion of creatine phosphate stores
Correct Answer: Gradual increase in intracellular Ca2+ availability between twitches
Q28. At rest in skeletal muscle which protein physically blocks myosin-binding sites on actin?
- Troponin I
- Tropomyosin
- Calsequestrin
- Myosin-binding protein C
Correct Answer: Tropomyosin
Q29. Non-depolarizing neuromuscular blocking agents such as tubocurarine act by:
- Irreversibly inhibiting acetylcholinesterase
- Competitively blocking postsynaptic nicotinic receptors
- Acting as depolarizing agonists at the motor endplate
- Blocking voltage-gated calcium channels in presynaptic terminals
Correct Answer: Competitively blocking postsynaptic nicotinic receptors
Q30. In cardiac muscle, the initial increase in cytosolic Ca2+ that triggers contraction largely arises from:
- SERCA releasing stored calcium into the cytosol
- Calcium influx through L-type (dihydropyridine) channels that triggers SR release
- Direct binding of calcium to troponin I
- Extracellular calcium being pumped out by Na+/Ca2+ exchanger
Correct Answer: Calcium influx through L-type (dihydropyridine) channels that triggers SR release
I am a Registered Pharmacist under the Pharmacy Act, 1948, and the founder of PharmacyFreak.com. I hold a Bachelor of Pharmacy degree from Rungta College of Pharmaceutical Science and Research. With a strong academic foundation and practical knowledge, I am committed to providing accurate, easy-to-understand content to support pharmacy students and professionals. My aim is to make complex pharmaceutical concepts accessible and useful for real-world application.
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