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[Physiology](https://durgical.com/en/physiology/) · [Nerve and muscle](https://durgical.com/en/physiology/#s-nerve_muscle)

# Skeletal muscle excitation–contraction coupling

- Mechanism
- Exam priority: high

The electrical signal dives into the muscle fiber through tiny tubes and makes an internal store release calcium, which switches on contraction.

Updated 2026-11-01

Also called: E–C coupling, Triad

**See it in 3D:** [Biceps (long head)](https://durgical.com/en/anatomy/biceps-brachii-long-head/)

## Key points

- Triad = one T tubule flanked by two terminal cisternae of the sarcoplasmic reticulum (SR).
- Skeletal muscle: DHPR acts as a voltage sensor that pulls RyR1 open mechanically; extracellular Ca²⁺ entry is not required (unlike cardiac muscle).
- Ca²⁺ binds troponin C → tropomyosin moves → myosin heads can bind actin.
- Relaxation needs ATP: SERCA pumps Ca²⁺ back into the SR; calsequestrin stores it there.
- Malignant hyperthermia: a RyR1 variant leaks Ca²⁺ when exposed to volatile anesthetics or succinylcholine: rigidity, hypercapnia, rising temperature.

## What it is

Excitation–contraction coupling links the muscle action potential to the release of Ca²⁺ that lets actin and myosin interact. In skeletal muscle the action potential runs down the transverse (T) tubules; a voltage sensor there (the dihydropyridine receptor, DHPR) is mechanically linked to the ryanodine receptor (RyR1) of the sarcoplasmic reticulum. Ca²⁺ floods the cytosol, binds troponin C and uncovers the myosin-binding sites on actin.

## How it works, step by step

- The muscle action potential spreads over the sarcolemma from the end plate.
- It travels into the fiber along the T tubules, reaching every myofibril almost at once.
- DHPR (L-type Ca²⁺ channel structure) senses the depolarization and changes shape.
- Through a direct protein link it opens RyR1, the Ca²⁺ release channel of the terminal cisternae.
- Cytosolic Ca²⁺ rises about a hundred-fold, from ≈ 0.1 µM to ≈ 10 µM or more.
- Ca²⁺ binds troponin C; the troponin–tropomyosin complex shifts and exposes the binding sites on actin.
- Cross-bridge cycling produces force for as long as Ca²⁺ stays high.
- SERCA pumps (ATP-dependent) return Ca²⁺ to the SR; troponin releases Ca²⁺ and the fiber relaxes.

### Action potential

**Rest** −90 mV **Threshold** −60 mV **Peak** +30 mV **Duration** ≈ 2–4 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⁺
- Rest
- Threshold
- ARP: absolute refractory period
- RRP: relative refractory period

The brief skeletal spike that runs down the T tubules; compare its length with a twitch.

## Reference values

| Parameter | Value | Note |
| --- | --- | --- |
| Resting cytosolic Ca²⁺ | ≈ 0.1 µM (10⁻⁷ M) | |
| Cytosolic Ca²⁺ during contraction | ≈ 10 µM or higher | |
| Muscle action potential duration | ≈ 1–5 ms | far shorter than the twitch it triggers |

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

## Clinical notes

- Malignant hyperthermia: a pharmacogenetic RyR1 disorder; uncontrolled Ca²⁺ release raises ATP use, CO₂ and heat. Dantrolene acts by blocking RyR1.
- Rigor mortis: after death ATP runs out, SERCA stops and myosin cannot detach from actin, so muscles stiffen.
- Because skeletal muscle uses its own internal Ca²⁺ store, Ca²⁺ channel blockers used for blood pressure do not weaken skeletal muscle.

## Memory aid

T for Trigger: the T tubule triggers, the SR spills, troponin lets go of the brakes.

## Test yourself

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

## Why does skeletal muscle keep contracting in a Ca²⁺-free bath for a while, but cardiac muscle stops almost at once?

Skeletal DHPR opens RyR1 mechanically, so Ca²⁺ comes from the SR. Cardiac muscle needs Ca²⁺ entry through L-type channels to trigger RyR2 (Ca²⁺-induced Ca²⁺ release).

## Why does relaxation need ATP even though contraction is the active process?

SERCA uses ATP to pump Ca²⁺ back into the SR, and ATP binding is what detaches myosin from actin. Without ATP the fiber stays locked, as in rigor mortis.

## During anesthesia a patient develops jaw rigidity, rising end-tidal CO₂ and fever. What is the cellular mechanism?

Malignant hyperthermia: a RyR1 variant releases Ca²⁺ uncontrollably on exposure to the trigger. Constant cross-bridge cycling and Ca²⁺ pumping burn ATP and produce CO₂, lactate and heat.

## What is the role of the T tubules in a large-diameter muscle fiber?

They carry the action potential deep into the fiber so all myofibrils release Ca²⁺ together. Without them, inner myofibrils would activate late and contraction would be weak and uneven.

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

## See it in 3D

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

- [Biceps (long head)](https://durgical.com/en/anatomy/biceps-brachii-long-head/)

## Related topics

- [The neuromuscular junction](https://durgical.com/en/physiology/the-neuromuscular-junction/)
- [Sliding filaments and the cross-bridge cycle](https://durgical.com/en/physiology/sliding-filaments-and-the-cross-bridge-cycle/)
- [Skeletal, cardiac and smooth muscle compared](https://durgical.com/en/physiology/skeletal-cardiac-and-smooth-muscle-compared/)
- [Motor units, recruitment and summation](https://durgical.com/en/physiology/motor-units-recruitment-and-summation/)

## In Biochemistry

- [ATP (adenosine triphosphate)](https://durgical.com/en/biochemistry/molecules/atp/)

[← 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: [10.3 Muscle Fiber Contraction and Relaxation](https://openstax.org/books/anatomy-and-physiology-2e/pages/10-3-muscle-fiber-contraction-and-relaxation) (OpenStax (Rice University), 2022); [10.2 Skeletal Muscle](https://openstax.org/books/anatomy-and-physiology-2e/pages/10-2-skeletal-muscle) (OpenStax (Rice University), 2022); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 7). 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/skeletal-muscle-excitation-contraction-coupling/