Store-operated Ca²⁺ entry (SOCE) has been found to be a rapidly activated robust mechanism in skeletal muscle fibres. It is conducted across the junctional membranes by stromal interacting molecule 1 (STIM1) and Orai1, which are housed in the sarcoplasmic reticulum (SR) and tubular (t-) system, respectively. These molecules that conduct SOCE appear evenly distributed throughout the SR and t-system of skeletal muscle, allowing for rapid and local control in response to depletions of Ca²⁺ from SR. The significant depletion of SR Ca²⁺ required to reach the activation threshold for SOCE could only be achieved during prolonged bouts of excitation–contraction coupling (EC coupling) in a healthy skeletal muscle fibre, meaning that this mechanism is not responsible for refilling the SR with Ca²⁺ during periods of fibre quiescence. While Ca²⁺ in SR remains below the activation threshold for SOCE, a low-amplitude persistent Ca²⁺ influx is provided to the junctional cleft. This article reviews the properties of SOCE in skeletal muscle and the proposed molecular mechanism, assesses its potential physiological roles during EC coupling, namely refilling the SR with Ca²⁺ and simple balancing of Ca²⁺ within the cell, and also proposes the possibility of SOCE as a potential regulator of t-system and SR membrane protein function.