Physiology
Muscular Contraction
Sliding filament theory — actin, myosin, calcium, and ATP at work
Muscle contraction is the ATP-powered shortening of cells via the sliding filament mechanism (Huxley & Hanson, Huxley & Niedergerke, 1954). Skeletal muscle fibers contain myofibrils built from sarcomeres — the contractile unit between Z-discs (~2-3 μm long at rest). Within each sarcomere, thin filaments (actin, with troponin/tropomyosin) interdigitate with thick filaments (myosin). Calcium release from sarcoplasmic reticulum (triggered by depolarization via the T-tubule and dihydropyridine-ryanodine receptor coupling) shifts tropomyosin off actin's myosin-binding sites. Myosin heads bind, swing (power stroke), and detach in cycles powered by ATP hydrolysis. Cross-bridge cycle: ~50 ms per stroke, ~10 nm displacement. Cardiac muscle uses the same machinery with calcium-induced calcium release. Pathology — Duchenne muscular dystrophy, malignant hyperthermia, myasthenia gravis — disrupts specific links.
- Sarcomere length~2-3 μm at rest
- Myosin power stroke~10 nm per stroke
- Cross-bridge cycle~50 ms (fast fibers)
- Calcium sourceSarcoplasmic reticulum (SERCA pump back)
- Resting calcium~10⁻⁷ M; rises to ~10⁻⁵ M during contraction
- Skeletal muscle mass (adult male)~30-40% of body weight
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Why muscle contraction matters
- Movement. Skeletal muscle generates locomotion and posture.
- Cardiac function. Same machinery powers the heart.
- Breathing. Diaphragm and intercostals — failure means ventilation.
- Vascular tone. Smooth muscle controls BP and blood distribution.
- Drug targets. Beta-blockers, succinylcholine, dantrolene, calcium channel blockers.
- Anesthesia. Neuromuscular blockers depend on this biology.
- Disease. Muscular dystrophies, MG, MH, statin myopathy.
Common misconceptions
- Muscles push. They only pull (shorten); pushing requires antagonist muscles.
- Filaments shorten during contraction. They slide; A-band length is constant.
- ATP is for contraction only. Required for relaxation too (myosin detachment, SERCA pumping).
- More calcium = stronger contraction. Saturating calcium reaches a force ceiling; further increase is pathologic (MH).
- Lactic acid causes muscle soreness. DOMS is microtears and inflammation; lactate clears within hours.
- Smooth muscle uses troponin. Uses calmodulin-MLCK; no troponin.
Frequently asked questions
What is the sliding filament theory?
Sarcomere shortens not by filaments shortening but by thin (actin) filaments sliding past thick (myosin) filaments. A-band (myosin length) is constant; I-band and H-zone shrink; Z-discs move closer. Driven by myosin heads attaching to actin, swinging ~10 nm (power stroke), detaching, and re-cocking — like rowers pulling along a rope. Each myosin head cycles independently; coordinated cycling generates force and shortening.
What's the cross-bridge cycle?
Four steps. (1) ATP binds myosin → myosin detaches from actin. (2) ATP hydrolyzed to ADP + Pi → myosin head cocks (90°). (3) Myosin binds actin (when calcium has exposed binding site) → Pi released. (4) Power stroke — myosin head rotates ~45°, pulling actin ~10 nm; ADP released. Cycle repeats while ATP and calcium present. Rigor mortis: ATP depletion locks myosin to actin (no detachment without ATP) — bodies stiffen 2-6 hr post mortem until proteolysis breaks bonds (24-72 hr).
How does calcium trigger contraction?
Action potential travels along sarcolemma into T-tubules. Voltage-gated dihydropyridine receptors (L-type Ca²⁺ channels) sense depolarization and mechanically couple (in skeletal) or activate (in cardiac via Ca-induced Ca-release) ryanodine receptors on the SR, releasing stored Ca²⁺. Ca²⁺ binds troponin C → conformational shift moves tropomyosin off actin's myosin-binding sites. Relaxation requires SERCA pumping Ca²⁺ back into SR (ATP-dependent) and Ca²⁺ removal from cytosol via NCX. Phospholamban regulates SERCA in cardiac muscle.
How do muscle fiber types differ?
Type I (slow oxidative, "red") — high mitochondria, myoglobin, capillaries; uses oxidative phosphorylation; fatigue-resistant; postural muscles, marathon runners. Type IIa (fast oxidative-glycolytic) — moderately fast, fatigue-resistant. Type IIx (fast glycolytic, "white") — rapid, powerful, fatigues quickly; sprinters. Determined by myosin heavy chain isoform (MYH7 in I, MYH2 in IIa, MYH1 in IIx) and metabolic enzymes. Composition is partly genetic, modifiable by training. Aging selectively atrophies type II — sarcopenia.
What's the difference between cardiac and skeletal muscle?
Skeletal: voluntary, multinucleated cells, long cylindrical fibers, neuromuscular junction triggers, T-tubule at A-I junction. Cardiac: involuntary, single/binucleated cells joined by intercalated discs (gap junctions for electrical continuity, desmosomes for mechanical), branched, intrinsic pacemaker (SA node), CICR mechanism, plateau action potential ~300 ms (long refractory prevents tetanus), T-tubule at Z-disc. Smooth: thin/thick filaments not striated; calmodulin-MLCK (not troponin); slow, sustained contraction; visceral.
What's a motor unit?
One alpha motor neuron + all muscle fibers it innervates. Size ranges from ~5 fibers per neuron (extraocular muscles, fine control) to ~2000 (gastrocnemius, gross power). All fibers in a unit are the same fiber type. Force gradation by recruitment (small slow units first — Henneman size principle) and rate coding (firing frequency 5-50 Hz). Tetanus — at ~30+ Hz, individual twitches summate into smooth sustained contraction.
What are common muscle disorders?
Duchenne muscular dystrophy: X-linked dystrophin loss; progressive proximal weakness from age 2-3; loss of ambulation by 12; cardiac/respiratory death by 20-30 (now extended). Myasthenia gravis: autoantibodies vs nicotinic AChR at NMJ; fatiguable weakness, ptosis, diplopia. Malignant hyperthermia: RYR1 mutation; volatile anesthetics or succinylcholine trigger uncontrolled SR Ca release; rigidity, hyperthermia, rhabdomyolysis; treat with dantrolene. Statins: rare myopathy/rhabdomyolysis.