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)
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 mVThreshold −60 mVPeak +30 mVDuration ≈ 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
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.
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.
See it in 3D
The structures of Durgical's 3D anatomy where it happens.
Related topics
- The neuromuscular junction
- Sliding filaments and the cross-bridge cycle
- Skeletal, cardiac and smooth muscle compared
- Motor units, recruitment and summation
In Biochemistry
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 (OpenStax (Rice University), 2022); 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.