Maintenance of cellular calcium homeostasis is critical to regulating mitochondrial ATP production and cardiac contraction. The ion channel known as the L-type calcium channel is the main route for calcium entry into cardiac myocytes. The channel associates with cytoskeletal proteins that assist with the communication of signals from the plasma membrane to intracellular organelles, including mitochondria. This article explores the roles of calcium and the cytoskeleton in regulation of mitochondrial function in response to alterations in L-type calcium channel activity. Direct activation of the L-type calcium channel results in an increase in intracellular calcium and increased mitochondrial calcium uptake. As a result, mitochondrial NADH production, oxygen consumption and reactive oxygen species production increase. In addition the L-type calcium channel is able to regulate mitochondrial membrane potential via cytoskeletal proteins when conformational changes in the channel occur during activation and inactivation. Since the L-type calcium channel is the initiator of contraction, a functional coupling between the channel and mitochondria via the cytoskeleton may represent a synchronised process by which mitochondrial function is regulated in addition to calcium influx to meet myocardial energy demand on a beat to beat basis.