Introduction
23. Excitation-Contraction Coupling in the Working Myocardium.Mechanics of cardiac contraction.
1. Overview of Excitation-Contraction (E-C) Coupling in Cardiac Muscle
Excitation-contraction (E-C) coupling in cardiac muscle is the process that links an action potential (electrical excitation) to muscle contraction.
Calcium-Induced Calcium Release (CICR): In cardiac muscle, small amounts of Ca²⁺ enter the cell during an action potential, triggering a larger release of Ca²⁺ from internal stores (sarcoplasmic reticulum, SR). This amplification is unique to cardiac muscle and essential for strong contraction.
2. Phases of the Cardiac Action Potential
Phase 0 (Depolarization):
The action potential begins with a rapid influx of Na⁺ through voltage-gated Na⁺ channels, causing cell depolarization. The action potential peaks at +30mV then Na+ gates close.
Phase 1 (Initial Repolarization):
Brief outward flow of K⁺ ions causes slight repolarization, setting the stage for Ca²⁺ influx.
Phase 2 (Plateau Phase):
L-type Ca²⁺ Channels Open: Ca²⁺ enters the cell, balancing K⁺ efflux. This plateau prolongs the action potential.
Significance: The plateau phase allows sustained Ca²⁺ influx, critical for prolonged contraction and effective pumping.
Ca2+ binds to troponin which moves the tropomyosin so that the binding site is exposed to myosin heads.
The myosin heads then perform the power-stroke and pulls the actin towards the center of the sarcomere. This is the contraction of the muscle
Phase 3 (Repolarization):
Ca²⁺ channels close, while K⁺ channels stay open, causing repolarization and returning the cell to resting potential.
Phase 4 (Resting Potential):
The Na⁺/K⁺ ATPase pump restores ion balance, expelling Na⁺ and bringing K⁺ back into the cell.
3. Calcium-Induced Calcium Release (CICR)
Ca²⁺ Entry via L-type Channels: Ca²⁺ enters through L-type Ca²⁺ channels in response to the action potential during the plateau phase.
Ryanodine Receptors (RyR2) on the SR: The incoming Ca²⁺ activates RyR2 on the SR, triggering the release of a larger quantity of Ca²⁺ into the cytoplasm.
Amplification of Signal: This release of Ca²⁺ from the SR amplifies the initial Ca²⁺ signal, providing enough Ca²⁺ for full contraction.
Termination: CICR stops when SR Ca²⁺ levels are depleted or L-type channels close, halting Ca²⁺ entry.
Mechanics of Cardiac Contraction
1. Length-Tension Relationship
Optimal Length: The heart muscle generates maximum force when fibers are stretched to an ideal length (length-tension relationship).
Physiological Relevance: This relationship ensures efficient pumping by optimizing cross-bridge overlap between actin and myosin.
2. Force-Velocity Relationship.
Effect of Afterload: As afterload (arterial resistance) increases, contraction velocity decreases.