During the repolarization phase of an action potential, which ion movement is responsible for returning the membrane potential toward the resting level?

Explanation

## Repolarization Phase of Action Potential **Key Point:** Repolarization is the phase during which the membrane potential returns from the peak (+20 to +30 mV) back toward the resting potential (−70 mV). This is driven by **outward K⁺ current** through voltage-gated K⁺ channels. ### Timeline of Ion Movements in Action Potential ```mermaid flowchart TD A["Resting State: RMP = −70 mV"]:::outcome --> B["Stimulus: Threshold reached"]:::action B --> C["Depolarization Phase<br/>Na⁺ INFLUX<br/>Membrane depolarizes to +20 mV"]:::action C --> D{"Peak of Action Potential"}:::decision D --> E["Repolarization Phase<br/>K⁺ EFFLUX<br/>Membrane repolarizes toward −70 mV"]:::action E --> F["Hyperpolarization Phase<br/>K⁺ channels still open<br/>Brief undershoot to −90 mV"]:::action F --> G["Return to Resting State"]:::outcome ``` ### Mechanism of Repolarization | Phase | Ion | Channel Type | Direction | Effect | |-------|-----|--------------|-----------|--------| | **Depolarization** | Na⁺ | Voltage-gated (fast) | **IN** | Membrane becomes positive | | **Repolarization** | K⁺ | Voltage-gated (slow) | **OUT** | Membrane becomes negative again | **High-Yield:** K⁺ channels open **more slowly** than Na⁺ channels in response to depolarization. This delay is critical: - Na⁺ channels open first → depolarization - Na⁺ channels inactivate (become refractory) - K⁺ channels open (delayed response) → repolarization **Clinical Pearl:** **Potassium channel blockers** (e.g., amiodarone, sotalol) prolong the action potential duration by delaying K⁺ efflux and thus repolarization. This is the basis of Class III antiarrhythmic action. **Mnemonic:** **"Na⁺ IN, K⁺ OUT"** — Depolarization = Na⁺ influx; Repolarization = K⁺ efflux.