Anatomy and Physiology - Muscular System

Overview

Muscle tissue converts chemical energy to force and movement. Core ideas include excitation–contraction coupling, sarcomere mechanics, fiber types, and motor unit recruitment.

Tissue types and structure

• Skeletal: striated, multinucleate, voluntary; organized into myofibrils with repeating sarcomeres (Z‑line to Z‑line).
• Cardiac: striated, branching cells, intercalated discs (desmosomes, fascia adherens, gap junctions); intrinsic pacemaking.
• Smooth: non‑striated; dense bodies; slow, economical cross‑bridge cycling; tone and latch states.

Sarcomere mechanics

• Bands/Zones: A band (myosin length), I band (actin only), H zone (myosin only), M line, Z discs. Contraction shortens I band and H zone; A band stays constant.
• Cross‑bridge cycle: myosin‑ATP detaches → ATP hydrolysis cocks head → cross‑bridge forms (Ca²⁺/troponin unblocks sites) → power stroke releases Pi → ADP leaves; rigor when ATP absent.
• Length–tension: optimal overlap yields maximal active force; too short (actin overlap) or too long (poor overlap) reduces force.
• Force–velocity: concentric force falls as velocity rises; eccentric contractions produce higher force at lower metabolic cost.

Excitation–contraction (EC) coupling

• Skeletal: motor neuron AP → ACh at NMJ → end‑plate potential → muscle AP → T‑tubule DHP receptor → ryanodine receptor (RyR1) Ca²⁺ release from SR → troponin C binds Ca²⁺ → tropomyosin shift → cross‑bridges.
• Relaxation: SERCA pumps resequester Ca²⁺; calsequestrin buffers; acetylcholinesterase clears ACh.
• Cardiac (contrast): Ca²⁺‑induced Ca²⁺ release (L‑type channels → RyR2); graded by extracellular Ca²⁺; β‑adrenergic modulation.

Energetics and fatigue

• Immediate: ATP/PCr (phosphagen system). Short‑term: anaerobic glycolysis; lactate production. Long‑term: oxidative phosphorylation.
• Fatigue mechanisms: central (drive), peripheral (ion gradients, metabolites, cross‑bridge kinetics); fiber‑type specific.

Fiber types and motor units

• Type I (slow oxidative): high mitochondria/myoglobin, fatigue‑resistant, low power.
• Type IIa (fast oxidative‑glycolytic): intermediate.
• Type IIx (fast glycolytic): high power, quick fatigue. Training shifts IIx↔IIa; genetics constrain proportions.
• Motor unit recruitment: size principle (Type I → IIa → IIx) as force demand rises; asynchronous firing smooths force.

Clinical correlations (survey depth)

• NMJ: myasthenia gravis (AChR antibodies) → fatiguable weakness; botulinum toxin blocks ACh release.
• Myopathies vs neuropathies: proximal weakness (myopathy) vs distal and denervation signs (neuropathy); CK elevated in myopathy.

Worked micro‑examples

1. Length–tension

• Predict force change when a sarcomere is stretched 20% beyond optimal—reduced cross‑bridge overlap → lower active force despite lower passive tension.

2. Force–velocity

• At a given load, explain why eccentric lowering permits higher force than concentric lifting (cross‑bridge detachment kinetics and elastic components).

3. NMJ pharmacology

• AChE inhibitor transiently improves MG strength by prolonging ACh; excessive inhibitor causes cholinergic toxicity (weakness with muscarinic signs).

Pitfalls

• Confusing which bands change length during contraction.
• Attributing skeletal EC coupling to extracellular Ca²⁺ influx (it is SR‑driven via RyR1–DHP coupling).
• Ignoring passive elastic elements (titin) in length–tension reasoning.

Practice prompts

• Draw a labeled sarcomere and annotate changes from rest → contraction.
• Compare fiber type properties and predict marathon vs sprint advantages.
• Outline skeletal vs cardiac EC coupling differences and β‑adrenergic effects.

References

• SciOly Wiki – Anatomy & Physiology (Muscular system)
• OpenStax Anatomy & Physiology (Muscle tissue)