PY3.1-12 | Nerve and Muscle Physiology — Gate Quiz

Correct! Type Aα fibres (also called Group Ia afferents from muscle spindles) are the largest myelinated fibres (12–20 μm diameter) with the fastest conduction velocity (70–120 m/s). They carry proprioceptive information from primary endings of muscle spindles.

Key concept: Nerve fibre classification — Aα (Ia/Ib, proprioception, motor): 70–120 m/s; Aβ (II, touch/pressure): 30–70 m/s; Aδ (III, pain/temp, fast pain): 5–30 m/s; C fibres (IV, slow pain, autonomic): 0.5–2 m/s. Myelination and diameter determine velocity.

Incorrect. The fastest nerve fibres are Type Aα (Ia afferents, diameter 12–20 μm, velocity 70–120 m/s) carrying muscle spindle proprioception.

Correct! During the absolute refractory period, voltage-gated Na⁺ channels are in the inactivated state. No stimulus, however strong, can open them to generate another action potential. This period corresponds to the Na⁺ channel inactivation gate being closed.

Key concept: Absolute refractory period (ARP) = Na⁺ channel inactivation (corresponds to depolarisation + early repolarisation). Relative refractory period = K⁺ channels still open (hyperpolarised), requires supranormal stimulus. ARP sets maximum firing frequency (~1000 Hz) and ensures unidirectional AP propagation.

Incorrect. During the absolute refractory period, Na⁺ channels are inactivated — no stimulus can trigger another action potential. Only during the relative refractory period can a stronger-than-normal stimulus succeed.

Correct! Acetylcholine (ACh) is released from motor nerve terminals at the neuromuscular junction. It binds to nicotinic ACh receptors (nAChR) on the motor end plate, triggering an end-plate potential and muscle contraction.

Key concept: NMJ transmitter = Acetylcholine → nicotinic receptor (ionotropic, ligand-gated Na⁺/K⁺ channel) → end-plate potential → action potential → muscle contraction. Blocked by: tubocurarine (competitive), succinylcholine (depolarising). ACh broken down by acetylcholinesterase.

Incorrect. Acetylcholine is the neurotransmitter at the neuromuscular junction. It acts on nicotinic receptors on the motor end plate.

Correct! Ca²⁺ binds to troponin C (the calcium-binding subunit of the troponin complex). This causes a conformational change that moves tropomyosin away from myosin-binding sites on actin, allowing cross-bridge formation and contraction.

Key concept: Skeletal muscle regulation is troponin-mediated. Troponin complex: TnC (Ca²⁺ binding), TnI (inhibitory), TnT (tropomyosin binding). In smooth/cardiac muscle, Ca²⁺ also activates calmodulin → myosin light chain kinase → myosin phosphorylation.

Incorrect. In skeletal muscle, Ca²⁺ binds to troponin C → shifts tropomyosin → exposes actin binding sites for myosin. (Myosin light chain phosphorylation is the mechanism in smooth muscle.)

Correct! Type I (slow-twitch, "red") fibres are rich in myoglobin and mitochondria, use oxidative phosphorylation, and are highly fatigue-resistant. They are ideal for sustained, low-intensity activity (posture, marathon running).

Key concept: Type I (slow-twitch, red): oxidative, fatigue-resistant, postural/endurance. Type IIa (fast-twitch oxidative): moderate speed and endurance. Type IIb/IIx (fast-twitch glycolytic, white): fast, strong, fatigue quickly. Athletes can shift IIb→IIa with endurance training.

Incorrect. Type I (slow-twitch) fibres are red, myoglobin-rich, oxidative, and fatigue-resistant. Type II (fast-twitch) fibres are white, glycolytic, and fatigue quickly.

Correct! Myasthenia gravis is an autoimmune disease caused by IgG antibodies against post-synaptic nicotinic ACh receptors (nAChR). Receptor destruction reduces end-plate potentials, causing fatigable weakness that worsens with activity.

Key concept: Myasthenia gravis = post-synaptic anti-nAChR antibodies → fatigable weakness. Lambert-Eaton myasthenic syndrome = pre-synaptic anti-VGCC antibodies → weakness improves with repeated activity. Treat MG with acetylcholinesterase inhibitors (pyridostigmine) + immunosuppression.

Incorrect. Myasthenia gravis is caused by autoantibodies against post-synaptic nicotinic ACh receptors (nAChR). Lambert-Eaton syndrome (Ca²⁺ channel antibodies) is the presynaptic variant.

Correct! At stimulation frequencies >50 Hz, individual twitches fuse completely because sarcoplasmic Ca²⁺ does not return to baseline between stimuli. The result is complete (fused) tetanus — a smooth, sustained maximum-force contraction.

Key concept: Summation and tetanus — single stimulus = twitch; increasing frequency → summation → incomplete tetanus (oscillations visible, ~15–50 Hz) → complete tetanus (smooth, fused, >50 Hz). Most voluntary movements use partial tetanus (motor unit firing at 10–50 Hz). Normal muscle never reaches complete tetanus involuntarily.

Incorrect. At high frequency stimulation (>50 Hz), individual twitches fully fuse, giving complete tetanus. At lower frequencies (15–50 Hz), incomplete tetanus with visible oscillations occurs.

Correct! A sarcomere is defined as the region between two successive Z lines (Z discs). It contains one complete A band (thick myosin filaments) flanked by two half I bands (thin actin filaments). During contraction, the Z lines are pulled closer together.

Key concept: Sarcomere = Z line to Z line. Contents: I band (actin only, gets shorter during contraction), A band (myosin + actin overlap, fixed width), H zone (myosin only, disappears during contraction), M line (myosin attachment, centre of A band). During contraction: I band and H zone shorten; A band stays constant.

Incorrect. The sarcomere is defined as the unit between two consecutive Z lines (Z discs). It contains the A band (with M line at centre) and half I bands at each end.

Correct! Local anaesthetics (lignocaine, bupivacaine) work by entering axons (especially when firing frequently) and blocking voltage-gated Na⁺ channels preferentially in their inactivated state. This prevents depolarisation and blocks action potential conduction.

Key concept: Local anaesthetics — use-dependent block (more effective in actively firing fibres). Mechanism: enter axon as uncharged base → ionise intracellularly → block Na⁺ channel from inside (inactivated state). Order of block: small unmyelinated C > small Aδ > large Aα. Pain blocked before motor function.

Incorrect. Lignocaine blocks voltage-gated Na⁺ channels (preferentially in the inactivated state), preventing Na⁺ influx and action potential generation/propagation.

Correct! AP arrival → depolarisation → voltage-gated Ca²⁺ channels open → Ca²⁺ influx → SNARE protein-mediated vesicle fusion → exocytosis of neurotransmitter → diffuses across synapse → binds post-synaptic receptors.

Key concept: Ca²⁺ is the trigger for neurotransmitter release. Voltage-gated Ca²⁺ channels (N-type at NMJ, P/Q-type in CNS) open. SNARE proteins (synaptobrevin, SNAP-25, syntaxin) mediate vesicle-membrane fusion. Botulinum toxin cleaves SNARE proteins, blocking ACh release. Ca²⁺ channel blockers prevent neurotransmission.

Incorrect. The sequence is: AP depolarises terminal → voltage-gated Ca²⁺ channels open → Ca²⁺ influx → vesicle fusion (via SNARE proteins) → NT release → receptor binding.