BIOL 2040 – Lecture 5 Part 1 Notes (Skeletal Muscle Physiology)

Introduction to Vertebrate Muscle Tissue and Classification

Muscle is the single largest tissue category in the vertebrate body. It appears in three histological/functional forms that are further subdivided by the presence/absence of striations and by degree of voluntary neural control.

  1. Skeletal muscle – the bulk of the muscular system; striated, voluntarily controlled & multinucleated.

  2. Cardiac muscle – restricted to the myocardium; striated but involuntary (to be covered in Ch. 8).

  3. Smooth muscle – non-striated, involuntary layers in the walls of hollow organs or tubes (covered in Part 2).

Controlled contraction underlies purposeful whole-body locomotion, manipulation of external objects, propulsion or emptying of luminal contents, postural support, thermogenesis, and even communicative facial expression.

Standard Terminology

• Greek/Latin combining forms help decode text-book vocabulary: “myo-/mys-” = muscle, “sarco-” = flesh.
• Sarcolemma is the excitable plasma membrane; sarcoplasm is the cytoplasm rich in glycogen, myoglobin, mitochondria.
• The individual skeletal muscle cell is called a muscle fibre (length ≈ entire muscle, diameter ≈ 10–100 µm).

Gross Structure of a Skeletal Muscle

Muscle is hierarchically wrapped in connective tissue:

  • Endomysium – delicate areolar sheath around each fibre.

  • Perimysium – fibrous envelope around a bundle of fibres = a fascicle.

  • Epimysium – dense irregular coat around the whole muscle; fuses with deep fascia, periosteum, or becomes a cord-like tendon / sheet-like aponeurosis.
    Tendons cross rugged bony projections, economise space, and transmit force to the skeleton.

Microscopic Anatomy: Myofibrils, Filaments, and the Sarcomere

• ~80 % of the fibre’s volume is occupied by thousands of parallel myofibrils.
• Each myofibril is a linear series (~10 000) of contractile compartments called sarcomeres (Z-line ↔ Z-line).
• Sarcomeric banding: dark A band (thick ± thin overlap), light I band (thin only), central H zone (thick only), M line (support proteins), Z discs (α-actinin plates anchoring thin filaments and titin).
• Hexagonal lattice – each thick filament surrounded by six thin filaments.

Thick (Myosin) Filament

≈300 myosin-II molecules: double-headed cross-bridges with ATPase & actin-binding sites; tails align toward the centre, heads face outward. Titin anchors the stack to M line and acts as a molecular spring ensuring alignment.

Thin Filament

Helical F-actin backbone + regulatory proteins:

  • Tropomyosin – rod-shaped dimer that blocks myosin-binding grooves on actin in relaxed state.

  • Troponin – trimer (TnT-binds tropomyosin, TnI-inhibitory to actin, TnC-binds \mathrm{Ca^{2+}}).
    When \mathrm{[Ca^{2+}]_{cyto}} rises, Ca²⁺→TnC → conformational shift → tropomyosin rolls off → cross-bridge cycling commences.

Membrane Systems: T-Tubules & Sarcoplasmic Reticulum

Invaginations of sarcolemma form transverse tubules (T-tubules) that penetrate at A-I junctions and triad with two SR terminal cisternae.
• SR is a specialised smooth ER storing \mathrm{Ca^{2+}} during rest.
• An arriving action potential (AP) travels along sarcolemma → dives into T-tubule → voltage-sensitive \mathrm{DHP} receptors mechanically open adjacent SR \mathrm{RyR} Ca²⁺-release channels → Ca²⁺ floods sarcoplasm (excitation–contraction coupling).

Sliding Filament Theory (Cross-Bridge Cycle)

  1. Energised myosin head (ATP → ADP + Pi) attaches to exposed actin site (cross-bridge).

  2. Pi release triggers the power-stroke: head pivots, pulling thin filament ≈10 nm toward M line.

  3. New ATP binds → myosin detaches (rigor link broken).

  4. ATP hydrolysis re-cocks head. Cycle repeats if \mathrm{Ca^{2+}} ≥ threshold and ATP present. Coordinated rowing shortens every sarcomere → fibre → whole muscle.

The latent period (≈1–2 ms) separates AP end from visible tension because electromechanical coupling, Ca²⁺ diffusion, and slack take-up of series-elastic components precede force output.

Relaxation

AP ceases → ACh hydrolysed by acetylcholinesterase, SR \mathrm{Ca^{2+}}-ATPase (SERCA) pumps reclaim Ca²⁺ → troponin–tropomyosin re-blocks → passive recoil + antagonist stretch returns fibre length. All within a few 10⁻³ s.

Rigor Mortis (Applied Example)

Post-mortem membrane failure allows extracellular & SR Ca²⁺ influx; myosin heads already loaded with ATP bind to actin, but ATP synthesis stops, so detachment cannot occur → muscles lock ≈3–12 h after death until proteolysis.

Single-Fibre Mechanical Events

• Twitch: response to a single AP (phases—latent, contraction, relaxation). Insufficient for useful work.
• Summation: \ge 2 APs arrive before complete relaxation (≥8–12 Hz); residual Ca²⁺ + elastic preload elevate tension.
• Tetanus: fused maximal tension at ≥100 Hz; 3–4× twitch force.

Length–Tension Relationship

Maximal active tension at optimal length l0 (physiological resting length ≈l0). Deviations shorten (<70 % l_0) or overstretch (>130 % l_0) reduce cross-bridge overlap. In vivo joints seldom permit >±30 % change.

Force–Velocity Curves

Concentric (shortening) contractions show inverse force–velocity (Hill’s equation). Eccentric (lengthening) show direct relation—greater load accelerates lengthening; explains delayed-onset muscle soreness (DOMS).

Whole-Muscle Mechanics

Muscles are organised into motor units (MU): one α-motor neuron + all fibres it innervates (intermingled). Precision muscles (ocular, hand) have ≈10–50 fibres per MU; powerful antigravity muscles >1000 fibres per MU.

Grading muscle force

  1. Recruitment – progressive activation of additional MUs (size principle: type I → type IIa → type IIx).

  2. Frequency modulation – AP rate within active fibres (temporal summation → tetanus).
    Asynchronous MU cycling sustains submaximal posture, delaying fatigue.

Contraction Types

  • Isotonic – constant load, fibre length changes (dynamic): concentric vs eccentric.

  • Isometric – tension rises but length fixed (static), useful in posture or immovable loads.

  • Real movements blend static/dynamic phases.

Energetics and Fatigue

Three ATP-dependent steps: (1) myosin power-stroke, (2) cross-bridge detachment, (3) SR Ca²⁺ re-uptake. ATP is regenerated by phosphagen (creatine-P), anaerobic glycolysis, or aerobic oxidative phosphorylation.

Fatigue safeguards energy homeostasis; multifactorial: elevated ADP/Pi, pH drop (lactic acid), extracellular \mathrm{K^+}, central drive decline, rare neuromuscular synaptic depletion.

Fibre-Type Spectrum (within one MU all same type)

  1. Slow-oxidative (Type I) – small diameter, high mitochondria/capillaries, myoglobin-rich (red), low ATPase; fatigue-resistant.

  2. Fast-oxidative-glycolytic (Type IIa) – intermediate.

  3. Fast-glycolytic (Type IIx) – large, pale (low myoglobin), high glycogen & glycolytic enzymes, powerful but fatigue-prone.

Genetic distribution shaped by function (postural back muscles bias Type I; biceps/eye muscles bias Type IIx). Training can interconvert IIa ↔ IIx, enlarge fibre diameter (hypertrophy), or enhance oxidative capacity (mitochondria, capillarity). Disuse or denervation leads to atrophy. Muscle stem-cell (satellite cell) activation provides limited repair.

Proprioceptive Afferents & Reflex Control

• Muscle spindle (intrafusal fibres) – senses length/velocity, innervated by γ-motor neurons & primary (Ia) + secondary (II) afferents; mediates stretch (myotatic) reflex for posture.
• Golgi tendon organ – Ib afferents intertwined in tendon collagen; monitors tension, triggers inverse myotatic reflex to protect against excessive force. Conscious perception correlates with tension, not length.

Neural Hierarchy of Motor Control

  1. Spinal afferent input → segmental reflexes.

  2. Primary motor cortex (corticospinal/pyramidal) → fine voluntary control.

  3. Brainstem multineuronal (extrapyramidal) pathways → posture, locomotion.
    Cerebellum, basal nuclei, premotor regions act indirectly. Lesions cause: spastic or flaccid paralysis, hemiplegia, tetraplegia/paraplegia, ataxia, etc.

Pathophysiological and Clinical Notes

• Tetanus (disease) vs physiological tetanus – do not confuse.
• Spasticity arises from lost inhibition (e.g., upper motor neuron lesion).
• Rigor mortis is transient because proteolytic degradation eventually frees actin–myosin.

Ethical & Practical Connections

Understanding muscle mechanics guides rehabilitation, athletic conditioning, ergonomics, and management of neuromuscular disorders. Appreciation of copyright/IP cautions against unauthorised dissemination of teaching material.

Key Numerical Benchmarks & Equations

• Twitch summation threshold ≈ 8\;\text{Hz}.
• Maximal physiological tetanus ≈ 100\;\text{Hz}.
• Optimal sarcomere length l0 yields peak tension; functional range 0.7l0 \text{–} 1.3l_0 still delivers ≥½ maximal force.
• Relative force in fused tetanus ≈ 3–4× single twitch.
• Rigor onset ~3–4 h, peaks ≈12 h post-mortem.

A compact expression of Hill’s concentric force-velocity curve: \bigl(F + a\bigr)(v + b) = (F0 + a)\,b, where F = force, v = shortening velocity, F0 = isometric max force, a, b = constants.