Ca itself or Ca-dependent signaling pathways play fundamental roles in various cellular processes from cell growth to death. The most representative example can be found in skeletal muscle cells where a well-timed and adequate supply of Ca is required for coordinated Ca-dependent skeletal muscle functions, such as the interactions of contractile proteins during contraction. Intracellular Ca movements between the cytosol and sarcoplasmic reticulum (SR) are strictly regulated to maintain the appropriate Ca supply in skeletal muscle cells. Added to intracellular Ca movements, the contribution of extracellular Ca entry to skeletal muscle functions and its significance have been continuously studied since the early 1990s. Here, studies on the roles of channel proteins that mediate extracellular Ca entry into skeletal muscle cells using skeletal myoblasts, myotubes, fibers, tissue, or skeletal muscle-originated cell lines are reviewed with special attention to the proposed functions of transient receptor potential canonical proteins (TRPCs) as store-operated Ca entry (SOCE) channels under normal conditions and the potential abnormal properties of TRPCs in muscle diseases such as Duchenne muscular dystrophy (DMD).