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[Physiology](https://durgical.com/en/physiology/) · [Cardiovascular](https://durgical.com/en/physiology/#s-cardio)

# Cardiac excitation–contraction coupling

- Mechanism
- Exam priority: medium

How each beat's electrical signal becomes force: a small calcium influx triggers a much larger calcium release inside the cell.

Updated 2026-11-01

Also called: Calcium-induced calcium release

**See it in 3D:** [Left ventricle](https://durgical.com/en/anatomy/left-ventricle/)

## Key points

- The trigger is calcium entering through L-type channels during the plateau; with no extracellular calcium the heart stops contracting (unlike skeletal muscle).
- Ryanodine receptor 2 (RyR2) releases most of the beat's calcium: calcium-induced calcium release.
- Relaxation costs ATP too: SERCA2a pumps calcium back into the SR and the Na⁺/Ca²⁺ exchanger (3 Na⁺ for 1 Ca²⁺) removes it from the cell.
- Sympathetic β1 → cAMP → PKA phosphorylates L-type channels (more calcium), phospholamban (faster relaxation) and troponin I.
- Digoxin inhibits the Na⁺/K⁺-ATPase: intracellular Na⁺ rises, the exchanger removes less calcium and the SR loads more: more force.

## What it is

In heart muscle, the action potential opens membrane calcium channels, and that calcium makes the sarcoplasmic reticulum release far more. Free calcium switches on troponin and the muscle contracts; removing it relaxes the muscle. How much calcium is cycled per beat sets contractility.

## How it works, step by step

- The action potential runs along the sarcolemma and down the T tubules.
- In the plateau (phase 2), L-type calcium channels (dihydropyridine receptors) open and a small Ca²⁺ current enters.
- That Ca²⁺ opens RyR2 on the nearby sarcoplasmic reticulum and cytosolic calcium rises about tenfold.
- Ca²⁺ binds troponin C; tropomyosin shifts and uncovers the binding sites on actin.
- Myosin heads form cross-bridges and, using ATP, slide the filaments: systole.
- SERCA2a pumps Ca²⁺ back into the SR and the Na⁺/Ca²⁺ exchanger expels it; troponin lets go of calcium and diastole follows.
- The Na⁺/K⁺-ATPase keeps up the sodium gradient the exchanger needs to keep removing calcium.

### Action potential

**Rest** −90 mV **Threshold** −70 mV **Peak** +25 mV **Duration** ≈ 280 ms

Tap a phase (the pills above or its band) or a refractory period (ARP, RRP) at the base of the plot.

- Mainly Na⁺
- Mainly K⁺
- Mainly Ca²⁺
- Rest
- Threshold
- ARP: absolute refractory period
- RRP: relative refractory period

Illustrative model drawn by Durgical from typical values; each cell type has its own time scale and values are approximate, not for clinical decisions.

## Reference values (approximate)

| Parameter | Value | Note |
| --- | --- | --- |
| Cytosolic Ca²⁺ in diastole | ≈0.1 µmol/L | resting cell |
| Cytosolic Ca²⁺ at peak systole | ≈1 µmol/L | about tenfold higher |
| Extracellular ionized Ca²⁺ | ≈1.1–1.3 mmol/L | plasma |
| Share of the beat's calcium from the SR | ≈70–80% | human; the rest enters from outside |

Approximate values for a healthy adult at rest; each laboratory sets its own ranges.

## Regulation

- *+* **Sympathetic nerves and epinephrine (β1 → cAMP → PKA)**: More calcium per beat (inotropy) and faster reuptake (lusitropy).
- *+* **High heart rate (staircase or Bowditch effect)**: Intracellular calcium builds up and each beat gets stronger.
- *+* **Fiber stretch (preload)**: Troponin becomes more sensitive to calcium: the cellular basis of Frank–Starling.
- *−* **Acidosis and ischemia**: H⁺ competes with calcium at troponin and SERCA runs short of ATP: less force, slow relaxation.
- *−* **Beta blockers and calcium channel blockers**: Less trigger calcium: contractility falls.

## Cardiac versus skeletal muscle

| Feature | Cardiac | Skeletal |
| --- | --- | --- |
| Trigger for calcium release | Ca²⁺ entry through L-type channels (chemical) | Mechanical L-type channel–RyR1 link |
| Needs extracellular calcium | Yes | No |
| How force is graded | Amount of calcium per beat | Number of motor units and summation |
| Tetanus | Impossible (long refractory period) | Possible |

## Clinical notes

- In heart failure SERCA2a activity falls and calcium transients fail: weaker beats and slow relaxation.
- Digitalis toxicity, made worse by hypokalemia, overloads the cell with calcium and causes delayed afterdepolarizations and arrhythmias.
- Severe hypocalcemia can depress contraction and prolongs the QT.

## Memory aid

"Small spark, big fire": the calcium that enters is the spark; the SR supplies the fire.

## Test yourself

Think of the answer, then tap the question to see it.

## Why does an isolated heart stop contracting when calcium is removed from its bath, while skeletal muscle keeps contracting?

Because cardiac SR release needs the calcium that enters through L-type channels (calcium-induced calcium release); in skeletal muscle the L-type channel opens RyR1 by direct mechanical contact.

## How does digoxin increase the force of contraction?

It inhibits the Na⁺/K⁺-ATPase, intracellular Na⁺ rises, the Na⁺/Ca²⁺ exchanger removes less calcium, and the SR loads more calcium for the next beat.

## What does PKA phosphorylation of phospholamban do?

It lifts phospholamban's brake on SERCA2a: calcium is taken up faster, relaxation speeds up (lusitropy) and more calcium is stored for the next beat.

## Why does ischemia impair both contraction and relaxation?

ATP runs short for cross-bridges and for SERCA, and acidosis lowers troponin C's affinity for calcium: force falls and relaxation slows.

[Add to my cards (4)](https://durgical.app/estudiar/?add=/en/physiology/cardiac-excitation-contraction-coupling/)

## See it in 3D

The structures of Durgical's 3D anatomy where it happens.

- [Left ventricle](https://durgical.com/en/anatomy/left-ventricle/)

## Related topics

- [The ventricular action potential](https://durgical.com/en/physiology/the-ventricular-action-potential/)
- [The Frank–Starling mechanism](https://durgical.com/en/physiology/the-frank-starling-mechanism/)
- [Preload, afterload and contractility](https://durgical.com/en/physiology/preload-afterload-and-contractility/)
- [Heart failure physiology](https://durgical.com/en/physiology/heart-failure-physiology/)
- [The ECG in potassium and calcium disorders](https://durgical.com/en/physiology/the-ecg-in-potassium-and-calcium-disorders/)

## Related conditions

- [Heart failure](https://durgical.com/en/conditions/heart-failure/)

## In Biochemistry

- [Na⁺/K⁺-ATPase (sodium pump)](https://durgical.com/en/biochemistry/enzymes/na-k-atpase/)
- [G protein-coupled receptors and cAMP](https://durgical.com/en/biochemistry/topics/g-protein-coupled-receptors-and-camp/)
- [ATP (adenosine triphosphate)](https://durgical.com/en/biochemistry/molecules/atp/)

## In Pharmacology

- [Cardiac glycosides](https://durgical.com/en/pharmacology/classes/cardiac-glycosides/)
- [Digoxin](https://durgical.com/en/pharmacology/digoxin/)
- [Beta blockers](https://durgical.com/en/pharmacology/classes/beta-blockers/)

[← All of physiology](https://durgical.com/en/physiology/)

Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: [19.2 Cardiac Muscle and Electrical Activity](https://openstax.org/books/anatomy-and-physiology-2e/pages/19-2-cardiac-muscle-and-electrical-activity) (OpenStax (Rice University), 2022); [19.4 Cardiac Physiology](https://openstax.org/books/anatomy-and-physiology-2e/pages/19-4-cardiac-physiology) (OpenStax (Rice University), 2022); [Heart Failure (Congestive Heart Failure)](https://www.ncbi.nlm.nih.gov/books/NBK430873/) (StatPearls (NCBI Bookshelf), 2025); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 9). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).

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Representative model, for educational purposes only.

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License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/physiology/cardiac-excitation-contraction-coupling/