Following contraction of the heart, efficient relaxation (diastole) is essential for refilling the ventricles with blood. This review describes how ventricular relaxation is controlled by Ca(2+) homeostasis in cardiac muscle cells and how alterations in Ca(2+) cycling affect diastolic function in the normal and failing heart. These discussions illustrate that the diastolic phase is not simply a period of rest but rather involves highly regulated and dynamic Ca(2+) fluxes.