Why doesn't the heart go into spasms?
Unlike skeletal muscle, where the period of inexcitability (refractory period) is significantly shorter than the contraction itself, cardiomyocytes function differently. In skeletal muscles, a short refractory period allows impulses to overlap, causing summation and prolonged spasm — tetanus.
In the myocardium, the absolute refractory period covers the entire contraction period. This means that until the muscle fiber fully contracts and begins to relax, it is fundamentally incapable of responding to a new electrical stimulus. It is precisely this protective mechanism that prevents spastic circulatory arrest and ensures normal pumping function.
Time relationships in the heart chambers
To understand cardiac function, it is important to compare the duration of the action potential (AP) and mechanical contraction in its different structures:
- Atria. The AP duration here is about 180 ms, whereas the mechanical response takes only 100–110 ms. Since the electrical process lasts longer than the muscular one, a new excitation can engulf the tissue exclusively after complete relaxation of the fibers.
- Ventricles. In the working ventricular myocardium, the AP duration is practically equal to the duration of systole and is 330 ms.
- Atypical cardiomyocytes. In the cells of the cardiac conduction system, the AP is the longest — 450 ms, with the absolute inexcitability period accounting for 400 ms.
Response to superfrequent stimuli
If abnormally frequent impulses begin to arrive from the sinus node, the heart goes through several stages of adaptation. Initially, a simple increase in heart rate occurs. However, upon reaching a critical stimulation frequency, tetanus still does not occur.
Instead, fibrillation develops — a dangerous condition in which synchrony is disrupted. Individual cardiomyocytes begin to contract separately and chaotically. Normally, each subsequent myocardial contraction can be triggered strictly after the previous cardiac cycle is fully completed.
Intracellular calcium dynamics
$Ca^{2+}$ ions play a key role in the contraction mechanisms and its strength. Upon excitation of a cardiomyocyte, calcium is directed from the T-systems to the contractile proteins (actin-myosin complex). The peculiarity of the myocardium is that far from all of this calcium is expended on the current contraction.
A significant portion of the ions is sequestered in the sarcoplasmic reticulum (endoplasmic reticulum). This "stored" volume will be expended only during the subsequent cycle. Thus, the ionic shifts of the previous cardiac cycle directly dictate the strength of the next one: the more $Ca^{2+}$ has accumulated in the cell, the more powerful the response will be.
Clinical significance: paired stimulation
The dependency described above is actively used in modern cardiology. Knowing the features of calcium dynamics and chronoinotropic dependence, physicians use the method of paired-pulse stimulation.
The essence of the method is that a special device (cardiosynchronizer) delivers additional stimulation precisely at the moment of the natural excitation's onset. This provokes a massive additional release of $Ca^{2+}$ from the T-systems. The result is a potentiated (multi-fold enhanced) contraction of the heart muscle, which is important for correcting a number of pathologies.
Briefly: answers to topical questions
What phases are distinguished in the action potential of a typical cardiomyocyte?
Five sequential phases are distinguished in the action potential of typical ventricular cardiomyocytes.
- Phase 0 — rapid depolarization (massive influx of sodium ions into the cell).
- Phase 1 — initial rapid repolarization (entry of chlorine into the cell and the start of potassium efflux).
- Phase 2 — slow repolarization or plateau (balance of inward calcium and sodium currents and outward potassium current).
- Phase 3 — final rapid repolarization (closure of calcium channels and predominance of outward potassium flow).
- Phase 4 — resting potential or diastolic potential (operation of the sodium-potassium pump to maintain ionic balance).
Which ion channels provide the development of the plateau phase in the myocardium?
The development of the plateau phase (the second phase of the action potential) is provided by the balanced operation of several types of ion channels. The inward current is provided by slow Na-Ca channels. They are incapable of rapid inactivation, so the influx of sodium and calcium ions inside the cardiomyocyte continues through them. The outward current is provided by potassium channels, through which potassium ions leave the cell. During the plateau phase, the total inward flow of sodium and calcium equals the outward flow of potassium, thanks to which the cell membrane potential is held at a constant level.
What are the main differences between skeletal muscle contraction and myocardium, apart from refractoryness?
The main differences between myocardial contraction and skeletal muscle contraction lie in obedience to the "all-or-none" law and the sources of calcium supply.
| Sign | Myocardium | Skeletal muscle |
|---|---|---|
| Conduction of excitation | Via nexus junctions to all cells (functional syncytium) | Isolated conduction, does not pass from fiber to fiber |
| Response to stimulation | Obeys the "all-or-none" law (maximal contraction) | Does not obey (strength depends on the number of recruited fibers) |
| Source of calcium | Enters from outside during the plateau and from the reticulum | Enters only from the sarcoplasmic reticulum |
Imagine that the refractory period in the heart is an "electrical shield". In the myocardium, this shield is so wide that it completely covers the contraction time, so new impulses bounce off without causing tetanus.
Class and exam questions
Why is the heart muscle incapable of contraction summation?
Due to the fact that the absolute refractory period in cardiomyocytes lasts longer than the contraction period itself. A new excitation is physically impossible before the onset of relaxation.
What will happen to the myocardium during a critical increase in impulse frequency?
Instead of tetanus, which is characteristic of skeletal muscles, fibrillation will occur in the myocardium — a chaotic and separate contraction of individual muscle fibers.
Why is paired-pulse stimulation used in cardiology?
This method allows for artificially inducing an additional release of calcium ions from the T-systems, which leads to a powerful, potentiated heart contraction.
What else to study on this topic
- Mechanisms of chronoinotropic dependence
- Structure and function of cardiomyocyte T-systems
- The role of the sarcoplasmic reticulum in calcium sequestration
- Pathophysiology of ventricular and atrial fibrillation
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