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M04.03.07 Contraction of cardiac muscle
The contraction of cardiac muscle is a vital process that ensures the efficient pumping of blood throughout the body. This section provides a detailed exploration of the mechanisms involved in cardiac muscle contraction, supported by tables, side notes, and key points to memorize.
Overview of Cardiac Muscle Contraction
Cardiac muscle contraction involves a coordinated sequence of electrical and mechanical events that result in the heart’s rhythmic beating. The process is initiated by electrical impulses, leading to the shortening of cardiac muscle fibers and subsequent ejection of blood from the heart chambers.
Key Phases of Cardiac Muscle Contraction
- Depolarization
- Plateau Phase
- Repolarization
- Excitation-Contraction Coupling
| Phase | Description | Key Points to Memorize |
|---|---|---|
| Depolarization | Rapid influx of Na+ ions through voltage-gated Na+ channels | Initiates action potential |
| Plateau Phase | Slow influx of Ca2+ ions through L-type Ca2+ channels; K+ efflux | Prolongs contraction, prevents tetany |
| Repolarization | Efflux of K+ ions through voltage-gated K+ channels | Restores resting membrane potential |
| Excitation-Contraction Coupling | Calcium influx triggers calcium release from sarcoplasmic reticulum, leading to muscle contraction | Links electrical signal to mechanical contraction |
Mechanisms of Contraction
Excitation-Contraction Coupling:
- Initiation: Action potential triggers the opening of voltage-gated calcium channels.
- Calcium-Induced Calcium Release (CICR): Calcium entry through L-type channels activates ryanodine receptors on the sarcoplasmic reticulum (SR), releasing more calcium into the cytoplasm.
- Cross-Bridge Cycling: Increased intracellular calcium binds to troponin, causing conformational changes in tropomyosin and exposing myosin-binding sites on actin filaments. Myosin heads attach to actin, performing power strokes that shorten the sarcomere.
Relaxation:
- Calcium Reuptake: Calcium is actively pumped back into the SR by SERCA (sarcoplasmic/endoplasmic reticulum calcium ATPase) and extruded from the cell by the Na+/calcium exchanger and plasma membrane calcium ATPase.
- Troponin-Tropomyosin Complex: As calcium levels fall, calcium dissociates from troponin, allowing tropomyosin to cover myosin-binding sites on actin, leading to muscle relaxation.
Table: Excitation-Contraction Coupling in Cardiac Muscle
| Step | Description |
|---|---|
| 1. Action Potential Arrival | Electrical signal reaches the cardiac muscle cell membrane (sarcolemma). |
| 2. Calcium Influx | Voltage-gated calcium channels open, allowing calcium entry from extracellular space. |
| 3. CICR | Calcium entry triggers further calcium release from the SR. |
| 4. Calcium-Troponin Binding | Calcium binds to troponin, initiating conformational changes that enable cross-bridge cycling. |
| 5. Cross-Bridge Cycling | Myosin heads bind to actin, performing power strokes that cause sarcomere shortening. |
| 6. Calcium Reuptake | Calcium is pumped back into the SR and out of the cell, leading to relaxation. |
Key Points to Memorize
- Depolarization: Rapid Na+ influx initiates an action potential.
- Plateau Phase: Calcium influx prolongs contraction, preventing tetany.
- Excitation-Contraction Coupling: Links electrical signals to mechanical contraction via calcium dynamics.
- Cross-Bridge Cycling: Myosin heads attach to actin, causing sarcomere shortening and muscle contraction.
- Relaxation: Calcium is reuptake by the SR and extruded from the cell, allowing muscle relaxation.
Side Notes
- Calcium Channels: L-type calcium channels are crucial for the plateau phase and CICR.
- SERCA: Key enzyme for calcium reuptake into the SR, essential for muscle relaxation.
- Ryanodine Receptors: Calcium release channels on the SR, activated by calcium influx from L-type channels.
Bibliography
- Bers, D. M. (2002). Cardiac excitation-contraction coupling. Nature, 415(6868), 198-205.
- Katz, A. M. (2006). Physiology of the Heart (4th ed.). Lippincott Williams & Wilkins.
- Opie, L. H., & Gersh, B. J. (2013). Drugs for the Heart (8th ed.). Elsevier Health Sciences.
- Ringer, P., & Nerbonne, J. M. (2004). Molecular physiology of cardiac repolarization. Physiological Reviews, 84(2), 431-488.
- Severs, N. J. (2000). The cardiac muscle cell. In The Heart, Arteries and Veins (pp. 303-334). McGraw-Hill.