A skeletal-muscle action potential occurs at the cell membrane, but the contractile myofibrils fill the interior of a large muscle fiber. Excitation–contraction coupling is the mechanism that converts membrane depolarization into a rapid rise of Ca$^{2+}$ throughout that interior.

Two membrane systems make this possible.

• T-tubules are inward extensions of the muscle-cell plasma membrane that carry the action potential deep into the fiber.
• The sarcoplasmic reticulum (SR) is a specialized intracellular membrane compartment that stores Ca$^{2+}$ at high concentration relative to the cytosol.

Voltage sensing triggers SR calcium release

In skeletal muscle, depolarization of a T-tubule changes the conformation of voltage-sensitive Ca$^{2+}$-channel proteins of the T-tubule membrane, commonly called dihydropyridine receptors (DHPRs) or Ca$_V$1.1 channels.

These voltage sensors are mechanically coupled to ryanodine receptor (RyR1) Ca$^{2+}$-release channels in the adjacent SR membrane.

The sequence is

muscle action potential
        ↓
T-tubule depolarization
        ↓
DHPR/CaV1.1 voltage-sensor change
        ↓
RyR1 channels in SR open
        ↓
Ca2+ leaves SR
        ↓
cytosolic Ca2+ rises near myofibrils

The released Ca$^{2+}$ then activates the troponin–tropomyosin regulatory system and permits cross-bridge cycling.

The triad places voltage sensors beside calcium stores

A skeletal-muscle triad consists of one T-tubule flanked by two expanded regions of SR. This close geometry lets a membrane-voltage change control Ca$^{2+}$ release over very short molecular distances.

The coupling mechanism is muscle-type specific

In skeletal muscle, the central coupling step is the conformational linkage between T-tubule voltage sensors and SR RyR1 channels. Extracellular Ca$^{2+}$ entry through the voltage sensor is not the main trigger required for each normal skeletal-muscle contraction.

Other muscle types can couple membrane excitation to internal Ca$^{2+}$ release differently. Heart muscle, for example, relies strongly on Ca$^{2+}$ entry through plasma-membrane channels to trigger additional Ca$^{2+}$ release from intracellular stores.

Excitation–contraction coupling therefore explains how an electrical membrane event becomes an intracellular Ca$^{2+}$ signal that controls mechanical force generation.