A rapid, transient, rise in cytoplasmic free calcium ion concentration ([Ca2+]i-transient) couples electrical excitation to contraction in muscle. Such [Ca2+]i-transients in muscle are actually subcellular spatio-temporal events that are determined dynamically by i) diffusional fluxes of Ca2+, ii) by the binding or unbinding of Ca2+ to ligands such as troponin c and calmodulin, and iii) by the various cellular processes, such as release of Ca2+ from sarcoplasmic reticulum, that produce fluxes of Ca2+ across the membranes bounding organelles or the cell. In heart muscle, a particularly large number of cellular processes contribute to the cytoplasmic [Ca2+]i-transient, compared with skeletal muscle. In addition, the actual change in cytoplasmic free [Ca2+]i is now known to be a small fraction of the total [Ca] transient (free plus bound) because most (98 to 99%) of the Ca2+ that enters the cytoplasm binds to ligands. In this article it is shown that under most physiological conditions the SR is the major determinant of the [Ca2+]i-transient in heart, that release of Ca2+ from the SR is induced by Ca2+ entering via L-type Ca(2+)-channels, and that the Na/Ca exchanger is the major route by which Ca2+ leaves the cell. The precise quantitative contribution of all these processes to the [Ca2+]i-transient still remains to be determined, however.