The store-operated Ca²⁺ channel (SOC) located on the plasma membrane (PM) mediates capacitative entry of extracellular Ca²⁺ following depletion of intracellular Ca²⁺ stores in the endoplasmic or sarcoplasmic reticulum (ER/SR). It plays important roles in a variety of cell signaling processes, including proliferation, apoptosis, gene regulation and motility. In skeletal muscle, the L-type Ca²⁺ channel on the surface membrane has slow kinetics of activation in response to voltage stimulation, and therefore does not support entry of extracellular Ca²⁺. Recent studies have provided functional evidence for the existence of SOC in muscle cells. Severe dysfunction of SOC is identified in muscle cells lacking either ryanodine receptors located on the SR membrane, or mitsugumin 29 - a membrane protein located in the triad junction of skeletal muscle. These results indicate that SOC activation requires an intact interaction between PM and SR, and is linked to conformational changes of ryanodine receptors. The cumulative entry of Ca²⁺ through SOC not only provides the mechanism for refilling of intracellular Ca²⁺ stores, but may also add to the Ca²⁺ needed for muscle contraction under conditions of intensive exercise and fatigue. The proper coupling of PM with ER/SR, in the triad junction in skeletal muscle or dyad junction in cardiac muscle, is essential not only for the membrane excitation-induced intracellular Ca²⁺ release but also for the store depletion-initiated capacitative Ca²⁺ entry.