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A Brilliant Explanation of the Process of Cardiac Muscle Contraction

Cardiac Muscle Contraction
The rhythmic beating of the heart is a result of the collective contraction and relaxation of atrial and ventricular muscles. Bodytomy describes the mechanism of cardiac muscle contraction including the phases of cardiac action potential, excitation-contraction coupling, and the cross-bridge cycle.
Bodytomy Staff
Last Updated: Dec 21, 2017
About one-third of the volume of a cardiac muscle cell is occupied by mitochondria (powerhouse of the cell). This is why the heart muscles can contract and relax continuously, without getting tired.
Mitochondria cross section
Mitochondria
Myocardium, composed of bundles of cardiac muscle fibers, forms the middle layer of the heart wall. The coordinated contraction of these muscle fibers is responsible for the pumping action of the heart.

Similar to skeletal muscles, these muscles are striated, and contain myofibrils composed of thick and thin protein filaments, called myosin and actin respectively. These muscle cells are connected through intercalated discs and gap junctions, to form branched muscle fibers.

The sarcotubular system comprises sarcoplasmic reticulum and large transverse tubules (T-tubules), formed through the invagination of the sarcolemma (plasma membrane of the muscle cells).
Process of Cardiac Muscle Contraction
Heart muscle contraction is a myogenic contraction, and is triggered through an action potential that is initiated by the pacemaker cells of the sinoatrial (SA) node or atrioventricular (AV) node. Owing to the presence of intercalated discs and gap junctions, the action potential quickly spreads to other cardiac cells. Thus, the muscle cells get excited, and contract as a single unit called the functional syncytium.

The heart muscles form two such syncytia - the atrial syncytium and the ventricular syncytium. A systole is the period when the heart muscles contract, whereas diastole is the period when heart muscles relax. The perfectly regulated contraction of the atrial syncytia followed by the ventricular syncytia gives rise to the typical rhythmic beating of the heart.
Action Potential
Action potential refers to the change in membrane potential that occurs due to the movement of sodium (Na+), potassium (K+), and calcium (Ca2+) ions across the sarcolemma. The movement of these ions occurs through intermembrane pumps or channels, some of which open and close in a voltage-dependent manner.

Typically, the resting membrane potential of a cardiac cell is -85 to -95 mV, and is maintained by the outward movement of K+ ions through specialized potassium channels called leak channels. The different phases of a typical action potential in a heart muscle cell have been illustrated and described below.
Action potential for a ventricular myocyte
Fig. Action potential for a Ventricular Myocyte
❤ Phase 0: Rapid Depolarization
For the action potential to develop, rapid depolarization (loss of negative charge) of the membrane is required. This occurs through the rapid influx of Na+ ions through the voltage-sensitive sodium channels. As a result of this, the membrane potential increases from -85 to 0 mV, and then overshoots to reach a value of +20 to +30 mV.
❤ Phase 1: Partial Repolarization
The sodium channels close, and voltage-sensitive potassium channels open up, leading to an outward movement of K+ ions. This corrects the overshoot in membrane potential, and reduces the value to about +20 to -10 mV.
❤ Phase 2: Plateau
This long phase involves maintenance of membrane potential near +20 mV. It is characterized by a slow influx of Ca2+ ions through voltage-dependent calcium channels called L-type calcium channels. This influx of Ca2+ ions from the extracellular fluid is unique to cardiac muscle cells, and is not required for the contraction of skeletal muscles.

The outward movement of positive ions is achieved by the closure of potassium channels. This prevents repolarization of the membrane, and maintains the plateau phase. It is during this phase that these muscles actively contract in the excitation-contraction coupling, and the cross-bridge cycle.
❤ Phase 3: Repolarization
During this phase the membrane is repolarized, and the membrane potential again comes down to the resting potential. It is achieved through the closure of the slow calcium channels, and opening of the voltage-dependent and calcium-dependent potassium channels, as well as through sodium-calcium exchangers.
❤ Phase 4: Resting Potential
Once the resting potential is attained, the voltage-gated potassium channels close, and the leak channels (responsible for maintaining the resting potential) open. This is the phase where the muscles are inactive.
Refractory Period
The time interval between the stimulation of a muscle fiber, and the subsequent contraction, within which the muscle fiber cannot be stimulated again, is termed refractory period. During this period, the muscle does not respond to the electrical stimuli. These muscles exhibit a long refractory period, as compared to skeletal muscles, which ensures that enough time is available for the filling and emptying of the chambers of the heart. In addition, they cannot be tetanized owing to the long refractory period.
Excitation-contraction Coupling
The sequence of events, which accompany the changes in electrical activity and calcium influx, for the activation of contractile machinery of the muscle cell is termed excitation-contraction coupling. These events occur during the plateau phase.

1) The influx of Ca2+ ions through the sarcolemma and T-tubules, leads to a local increase in the concentration of Ca2+ ions inside the cell.

2) This stimulates the release of Ca2+ ions from the sarcoplasmic reticulum, which brings about an overall increase in the intracellular calcium concentration. This is known as calcium-induced calcium release.

3) The increased concentration of Ca2+ ions activates the contractile machinery that comprises actin and myosin filaments, and triggers the cross-bridge cycle.
The Cross-bridge Cycle
Cross-bridges or myosin heads refer to projections that arise from the myosin filaments, and extend towards the actin filaments. The cross-bridge cycle is the process through which the actin filaments slide across the myosin filaments, thereby reducing the total length of each sarcomere. The cross-bridge cycle in cardiac muscle cells is similar to those occurring in skeletal muscle cells, and is also known as the sliding filament mechanism.

The sarcomeres are dependent on calcium because of two complex proteins called troponin C and tropomyosin. Tropomyosin is a thin filament composed of two intertwined polypeptides, and is bound to the actin filaments in such a way that it blocks the myosin-binding sites on actin. The tropomyosin molecules are held in this position by a set of calcium-binding globular proteins called troponin C.
1) The increase in intracellular calcium level results in the binding of Ca2+ ions to troponin C molecules, leading to a conformational change in troponin C.

2) This causes the associated tropomyosin molecules to move, exposing the myosin-binding sites on actin. This causes the myosin heads to bind tightly to the actin filaments.

3) Adenosine triphosphate (ATP) molecule binds to the myosin head causing it to detach from the actin filament. This ATP molecule is hydrolyzed by myosin ATPase giving rise to adenosine diphosphate (ADP) and inorganic phosphate (Pi), thus energizing the myosin head.

4) The energized myosin head binds to the actin filaments, which triggers a release of the hydrolysis products. The release of ADP and Pi gives rise to a power stroke that causes the actin filament to slide.

5) Another ATP molecule now binds to the myosin head, initiating the cycle again. The collective action of several myosin heads brings about the contraction of the sarcomeres.
At the end of the plateau phase, the cytoplasmic Ca2+ ions are transported back into the sarcoplasmic reticulum, and are ejected out through the sodium-calcium exchangers. The reduction in cytoplasmic calcium concentration causes the dissociation of Ca2+ ions from troponin C, thus causing relaxation of the sarcomeres.
The atria and ventricles contract and relax alternately, owing to the incredible electrical conduction system of the heart. This ensures an efficient functioning of the cardiovascular system, as well as the timely transport of oxygen and nutrients required by every cell of the body.