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Casup2+/supis an integral component of the functional and developmental regulation of the mitochondria. In skeletal muscle, Casup2+/supis reported to modulate the rate of ATP resynthesis, regulate the expression of peroxisome proliferator-activated receptor-gamma coactivator 1 (PGC1α) following exercise, and drive the generation of reactive oxygen species (ROS). Due to the latter, mitochondrial Casup2+/supoverload is recognized as a pathophysiological event but the former events represent important physiological functions in need of tight regulation. Recently, we described the relationship between [Casup2+/sup]submito/suband resting [Casup2+/sup]subcyto/suband other mitochondrial Casup2+/sup-handling properties of skeletal muscle. An important next step is to understand the triggers for Casup2+/supredistribution between intracellular compartments, which determine the mitochondrial Casup2+/supload. These triggers in both physiological and pathophysiological scenarios can be traced to the coupled activity of the ryanodine receptor 1 (RyR1) and store-operated Casup2+/supentry (SOCE) in the resting muscle. In this piece, we will discuss some issues regarding Casup2+/supmeasurements relevant to mitochondrial Casup2+/sup-handling, the steady-state relationship between cytoplasmic and mitochondrial Casup2+/sup, and the potential implications for Casup2+/suphandling by muscle mitochondria and cellular function.