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.