Repolarization is the phase of an action potential where a cell’s electrical charge drops back down to its resting level after firing. During an action potential, a nerve or muscle cell rapidly spikes from about -60 millivolts to a positive peak, then repolarization brings it back down. It’s the “falling phase” of the electrical signal, and it happens because potassium ions rush out of the cell through voltage-gated channels that open in response to the initial spike.
How Repolarization Works at the Ion Level
To understand repolarization, it helps to know what the cell looks like at rest. A typical neuron holds potassium at high concentrations inside the cell (around 140 mmol/L) and sodium at high concentrations outside (also around 140 mmol/L). This imbalance creates a negative resting voltage of roughly -60 to -80 millivolts inside the cell relative to outside.
When the cell fires, sodium channels snap open and sodium floods inward, driving the voltage sharply positive. That’s depolarization. But the same voltage change that opens sodium channels also triggers voltage-gated potassium channels to open, just a fraction of a millisecond later. These potassium channels are slower to respond, which is why depolarization happens first. Once they do open, potassium flows outward down its concentration gradient, carrying positive charge out of the cell. At the same time, the sodium channels rapidly inactivate, slamming shut and stopping the inward flow of positive charge. These two events together, potassium leaving and sodium channels closing, pull the membrane voltage back toward its negative resting state. That falling slope is repolarization.
The Undershoot: Why the Cell Overshoots on the Way Down
Repolarization doesn’t stop neatly at the resting voltage. The membrane potential typically dips slightly more negative than its resting level, a brief phase called afterhyperpolarization or “undershoot.” This happens because those slow-to-open potassium channels are also slow to close. Even after the membrane hits its resting voltage, potassium is still flowing out, temporarily making the inside of the cell more negative than usual. The undershoot fades as potassium channels finally close and the resting voltage is restored.
In neurons that fire repeatedly, a longer-lasting version of this effect can develop. Calcium that enters during the action potentials activates a separate set of potassium channels, producing a slow afterhyperpolarization that can suppress further firing for a period. This acts as a built-in brake, preventing a neuron from firing nonstop.
Refractory Periods: How Repolarization Controls Timing
Repolarization directly determines when a cell can fire again, through what are called refractory periods. During the first millisecond or so after the spike, the sodium channels are physically inactivated. They can’t reopen regardless of how strong a stimulus arrives. This is the absolute refractory period: it is impossible to trigger another action potential during this window.
As repolarization continues and the membrane voltage drops further, sodium channels gradually recover from inactivation and return to their “closed but ready” state. However, the potassium channels are still open, actively pulling the voltage down. This means a stronger-than-normal stimulus is needed to push the cell back to its firing threshold. This window is the relative refractory period. You can trigger an action potential here, but it takes more effort. Together, these refractory periods ensure that action potentials travel in one direction along a nerve fiber and set an upper limit on how rapidly a cell can fire.
Repolarization in Heart Cells vs. Nerve Cells
Repolarization in a nerve cell takes about 1 to 2 milliseconds. In a heart muscle cell, the process is fundamentally different and much slower, lasting hundreds of milliseconds. The key difference is calcium. After the initial sodium spike in a cardiac cell, calcium channels open and allow calcium to flow inward, holding the membrane voltage at a positive level for an extended period. This is the plateau phase, and it’s what allows the heart muscle to sustain a contraction long enough to pump blood effectively.
Repolarization of the cardiac cell finally begins when those calcium channels slowly inactivate and delayed potassium channels activate. The interplay between fading calcium inflow and growing potassium outflow produces the gradual downslope that returns the heart cell to its resting potential. This prolonged timeline is essential: if heart cells repolarized as quickly as neurons, the heart wouldn’t maintain coordinated contractions.
How Repolarization Appears on an ECG
If you’ve ever seen an electrocardiogram (ECG), repolarization is what the T wave represents. The T wave records the collective repolarization of the heart’s ventricles, the main pumping chambers. Its shape and duration are used clinically to spot problems with the heart’s electrical activity. At the peak of the T wave, only about 25% of ventricular sites have actually completed repolarization. The rest are still in the process, which is why the T wave has measurable width rather than appearing as a sharp spike.
When repolarization is delayed or uneven across the heart, the T wave changes shape or the QT interval (the time from the start of ventricular contraction to the end of repolarization) gets longer. This is the hallmark of Long QT Syndrome, a genetic condition caused by mutations in potassium or sodium channel genes. Reduced potassium current slows repolarization, stretching out the QT interval and creating a window where dangerous heart rhythms can develop. The most concerning of these is a specific type of arrhythmia that can cause fainting or sudden cardiac death.
Restoring the Gradients After Repolarization
Repolarization restores the electrical voltage across the membrane, but it doesn’t fully restore the chemical balance. Each action potential lets a small amount of sodium leak in and potassium leak out. Over many action potentials, these ions would gradually accumulate on the wrong side of the membrane if nothing corrected the drift.
That correction comes from the sodium-potassium pump, a protein embedded in the cell membrane that uses energy from ATP to push 3 sodium ions out for every 2 potassium ions it pulls back in. This pump runs continuously, not just after action potentials, and it maintains the concentration gradients that make repolarization (and all electrical signaling) possible in the first place. A single action potential moves only a tiny fraction of the cell’s total ions, so the pump doesn’t need to work in bursts. But without it running in the background, the gradients would eventually collapse and the cell would lose its ability to fire.