Automaticity and Conduction of Excitation
A vital physiological property of the heart is automaticity. The organ is capable of generating impulses and contracting independently of external nervous stimulation. This process is driven by slow diastolic depolarization (SDD) of the membrane in pacemaker cells of the sinoatrial node.
Unlike skeletal muscle, the heart does not obey the law of isolated fiber conduction. Cardiomyocytes are integrated into a single functional syncytium via specialized gap junctions known as nexus junctions (intercalated discs). These allow excitation to spread instantaneously from cell to cell.
The presence of nexus junctions means the myocardium follows the «All-or-None» law:
- With a subthreshold stimulus, the muscle does not respond ("none").
- With a threshold or suprathreshold stimulus, excitation encompasses all cells without exception, and the heart responds with the maximum possible contraction ("all").
Note: Skeletal muscle does not follow this law because each fiber has its own threshold, and the overall tension depends on the number of recruited fibers. Furthermore, a new contraction of the myocardium is possible only after the complete completion of the previous one, due to its prolonged refractory period.
Regulation of Contraction Strength
Each cardiac cycle features the unique phases of isometric contraction and isometric relaxation. The force and velocity of the contractile act are flexibly regulated by several intracardiac mechanisms.
The first mechanism is chronoinotropic dependence (Bowditch staircase phenomenon). As heart rate increases, the force of contraction, contraction velocity, and subsequent relaxation velocity all increase, even if the initial fiber length remains constant.
The second mechanism is based on Starling's law (Frank-Starling mechanism), which states that the stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (end-diastolic volume).
- Weak contraction occurs with insufficient blood filling or low load (e.g., during an early extrasystole), because actin and myosin filaments are in a suboptimal overlap position.
- Postextrasystolic potentiation demonstrates the opposite effect. If a compensatory pause follows a ventricular extrasystole, the heart fills excessively with blood. The myocardium stretches significantly, leading to an abnormally powerful subsequent contraction.
Hemodynamic Self-Regulation
The intrinsic rhythm integrates cardiac activity, automatically adapting it to the body's current metabolic demands. The primary task is maintaining an ideal balance of blood flow, where the stroke volumes of the systemic and pulmonary circulations are equal.
Coordination of the output of the right and left sides of the heart occurs solely through hemodynamic self-regulation, completely independent of the nervous system.
This principle was classically demonstrated in physiological experiments using isolated heart preparations. In these experiments, the left and right sides of an animal's heart were replaced by two separate donor hearts (one working for the systemic circuit, the other for the pulmonary circuit). Initially, these organs exhibited different automaticity rates, initial stroke volumes, and asynchronous systoles. However, over time, intrinsic self-regulation mechanisms caused the cardiac output (CO) passing through both organs to equalize and become identical.
Metabolism and Oxygen Supply
The energy balance of the myocardium is maintained through the oxidation of three main substrates: glucose, free fatty acids (FFAs), and lactic acid (lactate).
- At rest, the heart utilizes glucose, FFAs, and lactate in roughly equal proportions, with the contribution of lactate being minimal.
- During physical exertion, a key feature is the active uptake of lactate produced by skeletal muscles. The energy substrate utilization shifts dramatically:
- 2/3 of energy is derived from lactate oxidation (the primary source);
- 1/5 of energy from FFA oxidation;
- 1/7 of energy from glucose oxidation.
Myocardial blood supply exhibits strict phasic behavior: blood flows through coronary vessels only during diastole. During systole, the powerfully contracting myocardium compresses the intramural coronary arteries, halting oxygen delivery from hemoglobin. This challenge is overcome thanks to the intracellular protein myoglobin. During diastole, myoglobin binds and stores oxygen, releasing it during systole to ensure continuous oxidative metabolism in cardiomyocytes.