Mitochondria produce around 92% of the ATP used in the typical animal cell by oxidative phosphorylation using energy from their electrochemical proton gradient. Intramitochondrial free Ca(2+) concentration ([Ca(2+)](m)) has been found to be an important component of control of the rate of this ATP production. In addition, [Ca(2+)](m) also controls the opening of a large pore in the inner mitochondrial membrane, the permeability transition pore (PTP), which plays a role in mitochondrial control of programmed cell death or apoptosis. Therefore, [Ca(2+)](m) can control whether the cell has sufficient ATP to fulfill its functions and survive or is condemned to death. Ca(2+) is also one of the most important second messengers within the cytosol, signaling changes in cellular response through Ca(2+) pulses or transients. Mitochondria can also sequester Ca(2+) from these transients so as to modify the shape of Ca(2+) signaling transients or control their location within the cell. All of this is controlled by the action of four or five mitochondrial Ca(2+) transport mechanisms and the PTP. The characteristics of these mechanisms of Ca(2+) transport and a discussion of how they might function are described in this paper.