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.