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Action Potential of a Typical Cardiomyocyte

For medical students2 min readUpdated 2026-10-10

The action potential of a typical cardiomyocyte is the sequential change in cell membrane potential that triggers muscle fiber contraction in the heart. Its hallmark feature is a prolonged plateau phase that ensures extended cellular inexcitability, protecting the myocardium from tetanic contractions.

Resting potentialNormally ranges from -90 to -100 mV

AP durationAbout 330 ms for working ventricular cells

RefractorinessAbsolute inexcitability lasts for 270 ms

Plateau ionCalcium current delays repolarization

Main Phases of the Electrical Cycle

The electrical activity of a typical ventricular cardiomyocyte differs significantly from nerve cells and consists of five sequential stages:

Phase 4 (Resting Membrane Potential). The cell is polarized, with a stable membrane potential of -90 to -100 mV. This level is maintained by high membrane permeability to K⁺ ions, whose intracellular concentration is much higher than extracellularly.
Phase 0 (Depolarization). A rapid change in charge occurs. The potential rises steeply from negative values, crossing zero (the overshoot reaches +20 mV).
Phase 1 (Early Rapid Repolarization). Immediately following the spike, a brief and minor drop in voltage is observed.
Phase 2 (Plateau — Slow Repolarization). The most specific part of the cycle. The potential is maintained near zero for a prolonged period. This phase prolongs the excitation process, matching the duration of the mechanical contraction of the cell.
Phase 3 (Rapid Final Repolarization). The membrane potential drops steeply, returning to the resting level (-100 mV).

Ionic Currents

Each stage of membrane potential change is driven by the movement of specific ions through specialized channels:

During depolarization, fast sodium channels open in an avalanche-like manner. Na⁺ ions rush massively into the cell down their concentration gradient.
At the onset of repolarization, the inward sodium current inactivates, while outward K⁺ current is activated.
During the plateau, a dynamic equilibrium is established. The outward potassium current is balanced by a strong inward Ca²⁺ current entering through slow L-type channels (along with a small residual sodium current). Calcium influx at this stage is critical for subsequent excitation-contraction coupling — the physical contraction of the myocyte.
During final repolarization, calcium and sodium channels close completely, and a massive outward K⁺ current rapidly restores the initial negative charge inside the cell.

Excitability Changes and Cardiac Protection

The ability of a cardiomyocyte to respond to new stimuli is strictly tied to the phases of the action potential. The prolonged electrical response guarantees a long refractory period.

Absolute Refractory Period (ARP). Covers the phases of depolarization, early repolarization, plateau, and the beginning of final repolarization. In the ventricles, this period lasts 270 ms. Excitability drops to zero: no stimulus, no matter how strong, can trigger a new impulse. The primary physiological significance of the ARP is protecting the myocardium from summation of contractions and tetanus. This ensures the heart has time to relax (enter diastole) and fill with blood.
Relative Refractory Period. Occurs at the end of rapid repolarization. Excitability gradually recovers to 100%. Triggering a new action potential at this moment is possible, but only with a suprathreshold (very strong) stimulus.
Supranormal Excitability. A brief time window immediately following the return to the resting potential, when the cell responds even to subthreshold stimuli. The risk of extrasystoles increases during this moment.

Mechanism of Excitation Propagation

The generation of an action potential in one area of the myocardium inevitably leads to its propagation. The outer surface of the excited area becomes negatively charged, while adjacent, resting membrane areas retain a positive charge.

Local electrical currents arise between these regions. Their strength initially rises and then falls, causing depolarization of adjacent areas. The repolarization process works similarly: areas that have restored their original charge become positive on the outside, while still-excited regions remain negative. The potential difference generated on the organ's surface forms an electromagnetic field that can be recorded on the body surface.

Frequently asked questions

How does the action potential of a typical cardiomyocyte differ from sinoatrial node cells (pacemakers)?

The action potential of a typical ventricular cardiomyocyte features a stable resting membrane potential and a plateau phase, whereas pacemaker cells lack a stable resting potential and exhibit slow diastolic depolarization (SDD) between action potentials.

Characteristic	Typical Ventricular Cardiomyocyte	Sinoatrial Node Cells
Resting Potential / Max Diastolic Potential	Phase 4 — resting potential approx. –90 to –100 mV	No stable resting potential; SDD starts from max diastolic potential around –60 mV
Phases	5 phases: 0 — depolarization, 1 — early rapid repolarization, 2 — slow repolarization (plateau), 3 — final rapid repolarization, 4 — resting potential	SDD; Phase 0 — depolarization; Phase 3 — repolarization
Depolarization	Driven by rapid, massive Na+ influx into the cell	Primarily calcium-dependent via slow L-type channels; Na+ influx is also involved
Plateau	Phase 2 — slow repolarization (plateau); Ca2+ influx delays repolarization and prolongs excitation	Phase 0 and Phase 3 are described in node cell APs
Automaticity	Described by classic AP phases and resting potential	SDD provides automaticity — the ability to self-excite

What role does the sodium-potassium pump play in maintaining the cardiomyocyte resting potential?

The sodium-potassium pump (Na⁺/K⁺-ATPase) maintains and restores the ionic gradients responsible for preserving the resting membrane potential.

The Na⁺/K⁺-ATPase uses ATP energy to transport ions against their concentration gradients.
Na⁺ ions are actively pumped out of the cell, while K⁺ ions are pumped inside.
At rest, K⁺ concentration is higher intracellularly and Na⁺ extracellularly; membrane permeability to K⁺ and K⁺ efflux contribute to the potassium equilibrium potential and resting potential.
Following an action potential, Na⁺/K⁺-ATPase activity restores the ionic balance and gradients.

Why is cardiac muscle incapable of tetanic contraction?

Due to the plateau phase, the absolute refractory period of cardiomyocytes is very prolonged (about 270 ms in the ventricles). The cell remains unexcitable for almost the entire duration of its mechanical contraction, making wave summation impossible.

Which ion maintains the action potential plateau?

The plateau phase is maintained by an inward current of calcium ions (Ca²⁺) through slow L-type channels, balancing the outward potassium current.

What happens during supranormal excitability?

Immediately following the restoration of the resting membrane potential, cell excitability transiently exceeds 100%. During this phase, even a weak (subthreshold) stimulus can trigger premature myocardial contraction.

Go deeper

Characteristics of pacemaker action potentials in the sinoatrial node
Slow diastolic depolarization (SDD) and the nature of automaticity
Differences between sodium depolarization in working myocytes and calcium depolarization in nodal cells
Role of chloride ions (Cl⁻) and Na⁺/K⁺-ATPase in pacemaker cells
Time parameters of refractoriness in the cardiac conduction system