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Principles of Human Physiology - Chapter 12a

Principles of Human Physiology

Chapter Overview

  • Muscle Physiology (Chapter 12a) by Cindy L. Stanfield, Sixth Edition, 2017
  • Focuses on the structure and function of muscle, specifically skeletal muscle.

Chapter Outline

  • 12.1 Skeletal Muscle Structure
  • 12.2 The Mechanism of Force Generation in Muscle

Learning Outcomes

  • Identify major structural features of a skeletal muscle cell and their functional relationships.
  • Describe the crossbridge cycle and connect it to the sliding-filament model of muscle contraction.

12.1 Skeletal Muscle Structure

  • Skeletal Muscles

    • Attach to two or more bones via tendons; exceptions include:
    • Facial muscles attach to skin.
    • Laryngeal muscles attach to cartilage.
    • Sphincter muscles can also connect to other muscles.
  • Connective Tissues in Skeletal Muscles

    • Epimysium: Connective tissue surrounding the entire muscle, continuous with tendons.
    • Perimysium: Connective tissue that divides the muscle into fascicles, containing hundreds to thousands of myofibers.
    • Endomysium: Connective tissue that surrounds individual muscle fibers.

Structure at the Cellular Level

  • Components of a Muscle Fiber (Myofiber)

    • Sarcolemma: Plasma membrane of the muscle fiber.
    • Transverse Tubules (T Tubules): Extensions that help transmit electrical impulses throughout the muscle.
    • Multinucleated: Myofibers contain multiple nuclei along their length.
    • Sarcoplasm: Cytoplasm of the muscle fiber, rich in organelles.
  • Mitochondria: Muscle fibers contain many mitochondria to support high energy demands.

  • Myofibrils: Bundles of protein filaments that are crucial for contraction.

Structure at the Molecular Level

  • Myofibrils: Composed of thick and thin filaments responsible for muscle contraction.
    • Contractile Proteins
    • Myosin: Thick filament that provides force during contraction.
    • Actin: Thin filament that interacts with myosin to facilitate contraction.
  • Striated Appearance: Visible striations due to the arrangement of filaments in skeletal and cardiac muscle.
  • Sarcomeres: Basic functional unit of muscle, composed of arrangement of actin and myosin filaments.

Structure of a Sarcomere

  • A Band:

    • Contains myosin with overlap from actin; appears as a dark band.
    • H Zone:
    • Myosin presence without overlap from actin; lighter region within the A band.
    • M Line:
    • Structure that anchors myosin and runs perpendicular to the long axis of the muscle.
  • I Band:

    • Region solely containing actin filaments; appears as a light band.
    • Z Line:
    • Anchors actin filaments and aligns adjacent sarcomeres.

Contractile Proteins in Detail

  • Myosin:
    • Thick myofilament with:
    • Tails directed toward the M line.
    • Heads directed toward the I band, containing binding sites for actin and ATP.
  • Actin:
    • Composed of G actin (globular) and F actin (fibrous), forming a double helical structure anchored at the Z line.

Regulatory Proteins

  • Tropomyosin:
    • Covers myosin binding sites on actin, preventing contraction.
  • Troponin:
    • Complex of three proteins, attaches to actin and tropomyosin, and binds Ca²⁺ reversibly, regulating muscle contraction.

Structural Protein

  • Titin:
    • A large structural protein that anchors thick filaments between M line and Z line, providing support and elasticity to the sarcomere.

12.2 The Mechanism of Force Generation in Muscle

  • Sliding Filament Model:
    • Theory explaining muscle contraction as the sliding of actin past myosin, leading to muscle shortening (sarcomeres shorten).
  • Changes during Contraction:
    • A band: remains unchanged.
    • I band: shortens.
    • H zone: shortens.

The Crossbridge Cycle: Generation of Force

  • Involves cyclical forming and breaking of links between actin and myosin during contraction, regulated by ATP hydrolysis.
  • Myosin heads undergo conformational changes, pivoting back and forth, causing muscle contraction.

Steps of the Crossbridge Cycle

  1. Binding: Myosin head attaches to actin, with ATP and inorganic phosphate (Pi) present.
  2. Power Stroke:
    • Pi release triggers the pulling of actin toward the center of the sarcomere, which is referred to as the power stroke.
  3. Release:
    • ADP is released, reforming the low-energy rigor state of myosin.
  4. Cocking:
    • New ATP binds to the myosin head, allowing it to detach from actin.
  5. ATP Hydrolysis:
    • ATP is hydrolyzed, returning myosin to a high-energy state, prepared for another cycle.

Analogy for Crossbridge Cycle

  • Rowing a Boat:
    • The myosin head acts as an oar.
    • The linking of myosin head to actin is similar to the oar contacting the water.
    • The sequence of movement mimics the repetitive nature of rowing with power strokes and repositioning the oar out of the water.

Excitation of the Myofiber

  • Role of the Neuromuscular Junction:
    • Each somatic motor neuron innervates multiple myofibers; however, each myofiber receives input from only one motor neuron.

Structure of the Neuromuscular Junction

  • Presynaptic Cell: Somatic motor neuron releasing acetylcholine (ACh).
  • Postsynaptic Cell: Myofiber with ACh receptors and motor end plate containing cation channels.

End-Plate Potential (EPP)

  • Represents a graded potential that induces a muscle cell action potential in response to motor neuron action potentials.

Excitation-Contraction Coupling

  • Process transitioning from excitation of the myofiber to the initiation of the crossbridge cycle.
  • Involves:
    • Release of Ca²⁺ from the sarcoplasmic reticulum.
    • Binding of Ca²⁺ to troponin, resulting in tropomyosin shifting to expose myosin-binding sites on actin.

Steps Throughout Excitation-Contraction Coupling

  1. Relaxed State: Without Ca²⁺, troponin holds tropomyosin over myosin-binding sites, preventing crossbridge formation.
  2. Contraction Initiation: Ca²⁺ ions bind to troponin, leading to a shift in tropomyosin, exposing myosin-binding sites, allowing crossbridge cycling.
  3. Ca²⁺ Release Mechanism:
    • Action potential in the muscle cell propagates to T tubules, activating voltage-gated DHP receptors, causing mechanically gated ryanodine receptors to open Ca²⁺ channels in the sarcoplasmic reticulum.

Relaxation of the Myofiber

  • Termination of contraction occurs when stimulation from the somatic motor neuron ceases:
    • Ca²⁺ must be released from troponin.
    • Ca²⁺-ATPase actively transports Ca²⁺ back into the lumen of the sarcoplasmic reticulum, leading to a shift of tropomyosin back to block myosin-binding sites, resulting in muscle fiber relaxation.