PY3.1-12 | Nerve and Muscle Physiology — Summary & Reflection

REFLECT

Try these on yourself to connect the physiology to your own body:

1. Feel your resting membrane potential at work — pinch your skin. The sharp pain you felt was carried by Aδ fibres (fast pain, ~20 m/s). The dull ache that follows is carried by C fibres (slow pain, ~1 m/s). The two-pain experience is direct evidence of different fibre conduction velocities.

1. Observe summation and tetanus — extend your arm and make a fist as hard as you can. You're recruiting progressively larger motor units (size principle) and your motor neurons are firing at tetanic frequencies. Now relax slightly — you're reducing both recruitment and firing frequency.

1. Experience the three energy systems — sprint 100 metres (phosphocreatine: first 8 sec), then keep running hard for 2 minutes (anaerobic glycolysis: burning, lactic acid), then jog for 10 minutes (aerobic oxidation: steady, sustainable). Notice how your breathing stays elevated after you stop — that's EPOC (oxygen debt repayment).

1. Feel rigor — clench your fist tightly for 60 seconds. The stiffness and difficulty releasing is a tiny taste of what happens at the molecular level in rigor mortis — when ATP runs out and myosin heads can't detach from actin.

Now consider: A patient with Guillain-Barré syndrome (autoimmune demyelination of peripheral nerves) develops progressive ascending weakness. Using what you've learned, explain why: (a) distal muscles weaken before proximal ones, (b) nerve conduction velocity is reduced, (c) tendon reflexes are lost early, and (d) the patient may need ventilatory support.

KEY TAKEAWAYS

Key takeaways — your study checklist:

1. Neuron — soma + dendrites + axon. Types: multipolar, bipolar, unipolar. Supported by glia (Schwann cells, oligodendrocytes, astrocytes).
2. Resting membrane potential (-70 mV) — created by K+ leak channels, maintained by Na+/K+-ATPase. Nernst equation gives equilibrium potential for one ion; Goldman equation accounts for all ions.
3. Action potential — threshold (-55 mV) → Na+ channels open (depolarisation) → Na+ inactivation + K+ channels open (repolarisation) → hyperpolarisation → rest. All-or-none. Absolute and relative refractory periods.
4. Nerve fibre classification — Aα (fastest, 120 m/s, motor) → C (slowest, 0.5 m/s, pain). Myelination + diameter determine velocity. Saltatory conduction in myelinated fibres.
5. Synaptic transmission — chemical (Ca²+-dependent vesicle release, SNARE proteins, EPSP/IPSP, neurotransmitter removal) vs electrical (gap junctions). Spatial and temporal summation.
6. NMJ — ACh release → nicotinic receptors → EPP → muscle AP. Safety factor. AChE degrades ACh. Diseases: myasthenia gravis (anti-nAChR), Botox (blocks SNARE).
7. Skeletal muscle contraction — E-C coupling (T-tubule → DHPR → RyR1 → Ca²+ release) → Ca²+ binds troponin C → cross-bridge cycle (binding → power stroke → ATP detachment → re-cocking) → SERCA pumps Ca²+ back.
8. Muscle fibre types — Type I (slow, red, oxidative, endurance), Type IIa (fast, mixed), Type IIb (fast, white, glycolytic, powerful).
9. Muscle properties — twitch, summation, tetanus (unfused → fused). Length-tension curve (optimal at 2.2 μm sarcomere length). Motor unit recruitment (size principle).
10. Smooth muscle — calmodulin pathway (not troponin), latch mechanism, single-unit (gap junctions) vs multi-unit. No voluntary control.
11. Cardiac muscle — striated + involuntary, intercalated discs, CICR, long AP with plateau, CANNOT tetanise (long refractory period).
12. Energy metabolism — PCr (immediate, 8-10 s) → anaerobic glycolysis (10 s–2 min) → aerobic oxidation (>2 min). Oxygen debt = EPOC. Fatigue is multifactorial and protective.