Memory tricks for how muscles contract

During contraction, actin (thin filaments) slide over myosin (thick filaments) — neither filament actually changes length. The sarcomere shortens because the Z lines at each end are pulled inward. Myosin heads (cross-bridges) bind actin → power stroke pulls actin toward center (M line) → myosin releases → cocks back → rebinds → repeats. This cycle requires ATP. I band and H zone shorten during contraction. A band stays the same. Z lines move closer together. The whole muscle shortens as millions of sarcomeres shorten in series and parallel.

The cross-bridge cycle generates the force of muscle contraction. Attach: myosin head (in low-energy state after power stroke) binds actin — rigor state. Release: ATP binds myosin → myosin releases actin (rigor mortis = no ATP, cross-bridges stuck). Power stroke: ATP hydrolysis (ADP + Pi) cocks myosin head to high-energy position → myosin rebinds actin → Pi released → power stroke — actin pulled ~10 nm toward M line. Cock back: ADP released → myosin returns to low-energy position. Cycle repeats as long as Ca2+ present and ATP available.

Motor neuron action potential → ACh released at NMJ → muscle action potential → travels along T-tubules deep into muscle → activates dihydropyridine receptors (voltage sensors) in T-tubule → open ryanodine receptors (RyR) on sarcoplasmic reticulum → Ca2+ floods out of SR into cytoplasm. Ca2+ binds troponin C → conformational change in troponin-tropomyosin complex → tropomyosin shifts → exposes myosin-binding sites on actin → cross-bridge cycle begins → contraction. Relaxation: Ca2+ pumped back into SR by SERCA pump (requires ATP) → tropomyosin covers actin sites → relaxation.

The NMJ is the synapse between a motor neuron and skeletal muscle fiber. Motor neuron AP → Ca2+ enters terminal → ACh vesicles fuse → ACh released into synaptic cleft → binds nicotinic ACh receptors (nAChR) on motor end plate → Na+ enters muscle → end-plate potential (EPP) → if large enough, triggers muscle AP → E-C coupling → contraction. ACh degraded by acetylcholinesterase (AChE) in cleft. Myasthenia gravis: autoimmune attack on nAChR → fewer receptors → weak EPP → muscle weakness (worse with use, improved by AChE inhibitors). Botulinum toxin blocks ACh release → flaccid paralysis.

Type I (slow-twitch, red): slow contraction, highly fatigue-resistant, aerobic metabolism, many mitochondria, high myoglobin (red color). Used for endurance — marathon runners, postural muscles. Type IIa (fast-twitch oxidative): fast, moderate fatigue resistance, both aerobic and anaerobic. Middle-distance athletes. Type IIx (fast-twitch glycolytic, white): fastest and most powerful, fatigue rapidly, anaerobic glycolysis, few mitochondria, low myoglobin (white). Used for sprinting, weightlifting. Fiber type determined by motor neuron — the neuron dictates fiber type. Training can shift IIx toward IIa but rarely I.

A motor unit = one motor neuron + all the muscle fibers it innervates. Force is graded by recruiting more motor units (spatial summation) and firing them faster (temporal summation — unfused tetanus → fused tetanus). Henneman's size principle: small motor neurons have lowest threshold → recruited first. As force needed increases, progressively larger motor neurons recruited. Small neurons = Type I fibers (fatigue-resistant). Large neurons = Type IIx (fast, powerful, fatigue quickly). This ordering means low-force tasks use only fatigue-resistant fibers, while max effort recruits all types. Explains why prolonged exertion eventually calls in fast-fatigue fibers.

Skeletal muscle: voluntary, striated, Ca2+ from SR only, no spontaneous activity, somatic motor control, fatiguable. Cardiac muscle: involuntary, striated, Ca2+ from SR AND extracellular (CICR — Ca2+-induced Ca2+ release), connected by intercalated discs with gap junctions (syncytium), pacemaker activity (SA node), cannot be tetanized (long refractory period). Smooth muscle: involuntary, non-striated (actin and myosin but no sarcomeres), Ca2+ from SR and extracellular, calmodulin activates myosin light chain kinase (not troponin), slow sustained contractions, can maintain tone indefinitely without fatigue.

Muscle fatigue is multifactorial. Inorganic phosphate (Pi) accumulates from ATP hydrolysis → directly inhibits myosin cross-bridge cycling → reduces force. Lactate (lactic acid) accumulates from anaerobic glycolysis → was believed to cause fatigue (now more nuanced — H+ and Pi more important). ATP depletion: at very high intensity, ATP can't be regenerated fast enough. K+ accumulates in T-tubules during repetitive firing → disrupts membrane potential → AP generation fails. Calcium handling: SR becomes unable to release or reuptake Ca2+ rapidly → less Ca2+ available for troponin. Central fatigue: brain reduces motor neuron firing to protect the body.

Skeletal muscle generates maximum force at optimal sarcomere length (2.0–2.2 μm) — where actin-myosin overlap is greatest, allowing maximum cross-bridge formation. Too short: actin filaments from both sides overlap each other + myosin hits Z lines → less force. Too long: actin and myosin barely overlap → fewer cross-bridges → less force. This is the physiological basis of Frank-Starling law in cardiac muscle — stretch within physiological range increases overlap → stronger contraction. Clinical relevance: muscles work best at resting length — joint positioning affects muscle strength (why grip strength varies with wrist angle).