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
- Binding: Myosin head attaches to actin, with ATP and inorganic phosphate (Pi) present.
- Power Stroke:
- Pi release triggers the pulling of actin toward the center of the sarcomere, which is referred to as the power stroke.
- Release:
- ADP is released, reforming the low-energy rigor state of myosin.
- Cocking:
- New ATP binds to the myosin head, allowing it to detach from actin.
- 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
- Relaxed State: Without Ca²⁺, troponin holds tropomyosin over myosin-binding sites, preventing crossbridge formation.
- Contraction Initiation: Ca²⁺ ions bind to troponin, leading to a shift in tropomyosin, exposing myosin-binding sites, allowing crossbridge cycling.
- 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.