Neuromuscular System & Skeletal Muscle Tension

Skeletal muscle cannot develop tension without neural stimulation.
- Muscular and nervous systems often referenced jointly as the neuromuscular system.
Key influencers of tension generation:
- Neural signals (action potentials) originating in the nervous system.
- Intrinsic contractile properties of individual muscle fibres.
- The architectural arrangement of those fibres inside the whole muscle.

Motor neuron: A nerve cell controlling skeletal muscle (voluntary).
Motor unit = one motor neuron + all muscle fibres it innervates.
- Functional unit of the neuromuscular system.
Motor-unit size depends on muscle function:
- Small, precise muscles (eye, finger) → motor neuron supplies $\approx$ $100$ fibres.
- Large, force-producing muscles (hip) → up to $\approx$ $2000$ fibres per neuron.
Neuron anatomy recap:
- Cell body (soma).
- Axon conducts impulses from soma to muscle fibres.
- Near the fibres, axon splits into axon terminals → each terminal contacts one fibre.

Neuromuscular junction: Synapse between axon terminal and muscle fibre membrane (sarcolemma).
- Gap = synaptic cleft; filled with interstitial fluid.
Sequence during excitation:
1. Action potential reaches axon terminal.
2. Terminal releases neurotransmitter acetylcholine (ACh) into cleft.
3. ACh binds sarcolemma receptors → membrane permeability rises.
4. Ion flux: $\text{Na}^+$ enters, $\text{K}^+$ exits; net $\text{Na}^+$ influx greater → depolarization.
5. Depolarization triggers a muscle-fibre action potential → contraction cascade begins.

Immediate ATP requirements met via:
- Glucose (stored as glycogen) catabolism.
- Phosphocreatine (PCr) shuttling high-energy phosphate to ADP.
Energy ultimately powers myosin–actin interaction.

Structural unit = sarcomere (Z-line to Z-line).
- Contains actin (thin) & myosin (thick) filaments.
Calcium ions (Ca $^{2+}$ ) released into fibre → bind regulatory proteins on actin → expose binding sites.
Myosin heads (cross-bridges):
1. Attach to exposed actin sites.
2. Pivot → pull actin toward sarcomere centre.
3. Detach, re-cock, and reattach in a cyclic fashion.
Sliding of actin over myosin shortens sarcomere → visible contraction.

Variation achieved by number & frequency of action potentials (APs) along motor neuron.
- Low AP frequency → slow, gentle contraction.
- High AP frequency → rapid, forceful contraction.
All-or-None Principle (at motor-unit level):
- If an AP reaches threshold, every fibre in the unit contracts with max tension.
Whole-muscle maximal tension needs recruitment of multiple motor units.
Tetanus: Sustained, maximal tension when APs arrive at very high frequency.
Twitch profile (most motor units): quick max-tension rise then relaxation.

After AP ceases:
- $\text{Na}^+$ pumped back into extracellular fluid.
- $\text{Ca}^{2+}$ actively re-sequestered into sarcoplasmic reticulum.
- Myosin releases actin; filaments slide back → fibre lengthens to resting state.

Two broad categories:
1. Slow-twitch (Type I) fibres.
2. Fast-twitch (Type II) fibres.
- Sub-types:
  - Type IIa (intermediate speed/fatigue).
  - Type IIb (classic fast, quickest-to-fatigue).
    - Contract in $\approx$ $\frac{1}{7}$ the time required by Type I fibres → rapid but fatigue-prone.
Each motor unit contains only one fibre type, yet most whole muscles mix Types I & II.
- Distribution ratios vary by muscle & individual.
Practical implication: Athletes may excel in endurance (Type I rich) vs power/speed (Type II rich) events due to fibre composition + training.

Links to prior nervous-system lectures: neuron structure/function, action-potential propagation, synaptic transmission.
Application examples:
- Eye & finger dexterity attributable to small motor units.
- Hip extensor strength due to large motor units.
- Athletic talent scouting may consider fibre-type distribution.
Ethical/Practical note: Awareness of genetic fibre composition can guide personalised training yet should not limit opportunity or foster discrimination.