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Chapter 9 – Skeletal Muscle Tissue Study Notes

Types of Muscle Tissue

  • Skeletal Muscle Tissue
  • Cardiac Muscle Tissue
  • Smooth Muscle Tissue
  • Figure 9.1 illustrates microscopic/structural differences.

Functions of Skeletal Muscle Tissue

  • Produce skeletal movement (voluntary locomotion, facial expression, respiration).
  • Maintain posture & body position (continuous low-level contractions counteract gravity).
  • Support soft tissues (e.g., abdominal wall supports visceral organs).
  • Guard body entrances & exits (orbicularis oris, sphincters of digestive & urinary tracts).
  • Maintain body temperature (shivering thermogenesis; ~85 % of resting heat is muscular).
  • Provide nutrient reserves (breakdown of contractile proteins releases amino acids for glucose synthesis in starvation).

Skeletal Muscle Connective Tissues

  • Skeletal muscle = bundle of fibers wrapped in 3 concentric CT layers.
  • Epimysium ("on muscle")
    • Dense collagen layer encircling entire muscle; separates it from surrounding organs/tissues.
  • Perimysium ("around")
    • Fibrous layer partitioning muscle into fascicles.
    • Contains blood vessels & nerves; collagen + elastin.
  • Endomysium ("inside")
    • Delicate CT around each individual fiber; loose connections among adjacent fibers.
    • Houses capillaries, myosatellite (stem) cells, and axons controlling the fiber.
  • Collagen fibers of all three layers merge beyond muscle to form:
    • Bundled cord = tendon → attaches muscle to bone (periosteum) & fibers embed into bone matrix.
    • Broad sheet = aponeurosis → anchors muscle to multiple bones/muscles.

Skeletal Muscle Fiber Anatomy

  • Muscle fiber = very long (up to 30 cm) multinucleate syncytium formed by myoblast fusion; nuclei located peripherally beneath sarcolemma.
  • Cytoplasm = sarcoplasm; plasma membrane = sarcolemma.
  • Filled with hundreds–thousands of myofibrils (1–2 µm diameter) extending full fiber length and causing visible striations.
  • Myofibrils composed of repeating contractile units (sarcomeres) built from myofilaments:
    • Thin filament: mostly actin.
    • Thick filament: myosin.
  • Abundant mitochondria positioned between myofibrils supply ATP.

Myofibrils and Sarcomeres

  • ~10{,}000 sarcomeres per myofibril; resting length ≈ 2\,\mu m.
  • Z lines: boundary; composed of actinins linking adjacent thin filaments.
  • M line: center of sarcomere; proteins stabilize thick filaments.
  • A band: length of thick filaments; includes H band (thick only) & zone of overlap (thin + thick interdigitate).
  • I band: thin filaments only; spans two sarcomeres.
  • Striation pattern results from alternating A & I bands.

Sarcoplasmic Reticulum and Calcium Handling

  • Sarcoplasmic reticulum (SR) = modified smooth ER forming tubular network around each myofibril.
  • Enlarged sacs (terminal cisternae) flank each T-tubule; one T-tubule + two cisternae = triad (critical for rapid Ca²⁺ release).
  • SR actively transports Ca²⁺ from cytosol → lumen; [Ca²⁺]_SR ≈ 40{,}000 × cytosolic level (free + protein-bound).
  • Action potential (AP) on T-tubule → SR permeability change → Ca²⁺ floods cytosol initiating contraction.

Thin and Thick Filaments

  • Thin filament composition:
    • F-actin (two twisted rows of G-actin monomers).
    • Each G-actin has an active site binding myosin.
    • Nebulin spans filament length, acts as scaffold.
    • Tropomyosin covers active sites at rest.
    • Troponin complex binds tropomyosin & Ca²⁺; Ca²⁺ binding → conformational shift exposing active sites.
  • Thick filament composition:
    • ~300 myosin molecules; each myosin has long tail + hinged bi-lobed head (ATPase).
    • Heads project toward thin filaments forming cross-bridges.
    • Core elastic protein titin anchors thick filament to Z line, resists overstretching & aids recoil.

Sliding Filament Theory

  • Contraction = thin filaments slide toward M line past thick filaments → sarcomere shortens.
  • A band length constant; I band & H band narrow/disappear; Z lines drawn closer.
  • Figure 9.4-3 shows rest vs contracted sarcomere.

Excitable Plasma Membranes and Membrane Potentials

  • All cells polarized; in neurons & skeletal muscle, resting potential ≈ -70\,\text{mV}.
  • Charge contributors:
    • ECF: Na^+, Cl^- (positive & negative).
    • Cytosol: K^+ (positive) + large impermeant proteins (negative).
  • Plasma membrane = selectively permeable; leak channels favor K^+ efflux & limited Na^+ influx.
  • Voltage-gated channels open/close with membrane potential changes; sequence of openings constitutes an action potential.

Neuromuscular Junction (NMJ)

  • Single NMJ per muscle fiber; motor neuron may innervate many fibers (motor unit).
  • Components:
    • Synaptic terminal: vesicles containing acetylcholine (ACh).
    • Synaptic cleft (≈50 nm gap) with ACh + acetylcholinesterase (AChE).
    • Motor end plate: sarcolemma region with junctional folds → ↑ACh receptors + AChE.
  • Events:
  1. AP arrives at axon terminal.
  2. Voltage-gated Ca^{2+} channels → vesicle fusion → ACh exocytosis.
  3. ACh diffuses & binds receptors → Na^+ influx → end-plate potential.
  4. ACh removed via diffusion or hydrolysis by AChE.

Excitation–Contraction (E-C) Coupling

  1. AP propagates across sarcolemma & into T-tubules.
  2. Triad senses voltage change, SR releases Ca²⁺.
  3. Ca²⁺ binds troponin → tropomyosin shifts → active sites uncovered.
  4. Contraction cycle (Fig. 9.7):
    • Attach: energized myosin head (ADP + P) binds actin → cross-bridge.
    • Pivot: power stroke → ADP + P released; sarcomere shortens.
    • Detach: ATP binds myosin → head releases from actin.
    • Reactivate: ATP hydrolysis re-cocks head.
  5. Cycle repeats while Ca²⁺ & ATP present.
  6. When APs cease → SR re-sequesters Ca²⁺ (active transport) → troponin–tropomyosin re-cover sites → relaxation.

Tension Production in Muscle Fibers

  • Force depends on number of simultaneously cycling cross-bridges, governed by sarcomere length (length-tension relationship).
  • Optimal length (≈2.0–2.2\,\mu m): maximal overlap → peak tension.
    • >130 % length → overlap ↓ → fewer bridges → tension ↓ to zero when no overlap.
    • <75 % length → filaments collide with Z lines → cannot shorten further.

Muscle Tension Development (Twitch Patterns)

  • Twitch = single stimulus–contraction–relaxation event.
  • Treppe: stimuli delivered just after relaxation; successive peaks staircase ↑ (first 30–50 stimuli) due to Ca²⁺ accumulation.
  • Wave summation: new stimulus before relaxation ends → tensions add.
    • Leads to incomplete tetanus: fluctuation around near-max tension.
    • At very high frequency, complete tetanus: no relaxation, Ca²⁺ stays high, maximum tension; rare physiologically.

Motor Units and Recruitment

  • Motor unit = one motor neuron + all fibers it controls.
    • Size correlates with precision: ocular muscles (4–6 fibers/unit) vs gastrocnemius (1000–2000).
  • Recruitment:
    • Small, low-force units activated first; progressively larger/faster units added → smooth force ramp.
  • Asynchronous motor-unit summation: during sub-maximal sustained contraction, units cycle on/off to delay fatigue → constant muscle tone.

Muscle Tone

  • Background, involuntary activation of motor units producing resting tension.
  • Functions in posture & joint stabilization.
  • Elevated tone increases basal metabolic rate (heat production & energy consumption even at rest).

Isotonic vs Isometric Contractions

  • Isotonic (constant tension, length changes):
    • Concentric: tension > load → muscle shortens (e.g., lifting/curling).
    • Eccentric: tension < load → muscle lengthens while contracting (lowering weight).
  • Isometric (constant length, tension < load):
    • No macroscopic length change; elastic elements stretch; maintains posture, stabilizes joints.

Energy Production in Muscles

  • Immediate ATP: free ATP (~1 sec) + creatine phosphate (CP) (~15 sec).
    • ADP + CP \rightarrow ATP + C.
  • Glycolysis (anaerobic, cytosol):
    • Each glucose → 2 \; ATP + 2 pyruvate; rapid but inefficient; by-product lactic acid lowers pH.
  • Aerobic metabolism (mitochondria):
    • Each pyruvate → 17 \; ATP via citric acid cycle + ETC; supplies 95 % ATP at rest/mod activity.
  • Energy state scenarios:
    • Rest: low ATP demand; fatty acids+glucose oxidized; surplus ATP builds CP & glycogen.
    • Moderate exercise: ATP demand ↑; mitochondria meet need; glycogen broken to glucose; no lactate accumulation.
    • Peak activity: ATP demand enormous; O₂ insufficient → glycolysis predominates → lactate + H⁺ accumulate, pH drops, fatigue ensues.

Muscle Fatigue and Recovery

  • Fatigue = inability to maintain power output.
    • Major cause: pH decline (lactic acidosis) → ↓Ca²⁺–troponin binding + enzyme inhibition.
  • Under low O₂: glycolysis supplies ATP quickly but depletes glycogen within 1–2 min, yields only 4–6 % energy from glucose, raises temperature & sweating.
  • Recovery / Cori cycle:
    • 70–80 % lactate transported to liver → converted to pyruvate → glucose → glycogen; 20–30 % directly oxidized by mitochondria.
    • Requires O₂ & ATP; leads to oxygen debt (excess post-exercise O₂ consumption, EPOC).

Skeletal Muscle Fiber Types

  • Fast (Type II-B/X):
    • Peak tension <0.01 s; large diameter; densely packed myofibrils; large glycogen; few mitochondria; powerful but fatigue rapidly; anaerobic ATP.
  • Slow (Type I):
    • ½ diameter of fast; 3× slower twitch; abundant mitochondria, myoglobin, capillaries; primarily aerobic ATP; sustain contractions; dark red color.
  • (Note: Intermediate Type II-A not detailed in transcript but exists—fastish with more endurance).

Muscle Adaptations and Clinical Conditions

  • Hypertrophy:
    • ↑ myofilaments, ↑ myofibril size, ↑ mitochondria, ↑ glycogen & glycolytic enzymes; due to repeated exhaustive stimulation; enhanced by anabolic steroids.
  • Atrophy:
    • ↓ size, tone, power after prolonged inactivity (casting, denervation); initially reversible, extended atrophy → fiber loss.
  • Polio: viral destruction of motor neurons → paralysis.
  • Tetanus: Clostridium tetani toxin blocks inhibitory interneurons → unchecked motor neuron firing → sustained contraction; thrives in low-O₂ wounds; 40–60 % mortality without vaccination.
  • Botulism: C. botulinum toxin prevents ACh release → flaccid paralysis; foodborne.
  • Myasthenia gravis: autoimmune loss of ACh receptors → progressive weakness.
  • Rigor mortis: begins 2–7 h post-mortem as ATP depleted → myosin remains bound to actin; ends 1–6 days later with protein decomposition.