Contraction and relaxation of the heart result from cyclical changes of intracellular Ca2+ concentration ([Ca2+ ]i ). The entry of Ca2+ into the cell via the L-type Ca2+ current leads to the release of more from the sarcoplasmic reticulum (SR). Compared to other regulatory mechanisms such as phosphorylation, Ca2+ signalling is very rapid. However, since Ca2+ cannot be destroyed, Ca2+ signalling can only be controlled by pumping across membranes. In the steady state, on each beat, the amount of Ca2+ released from the SR must equal that taken back and influx and efflux across the sarcolemma must be equal. Any imbalance in these fluxes will result in a change of SR Ca2+ content and this provides a mechanism for regulation of SR Ca2+ content. These flux balance considerations also explain why simply potentiating Ca2+ release from the SR has no maintained effect on the amplitude of the Ca2+ transient. A low diastolic [Ca2+ ]i is essential for cardiac relaxation, but the factors that control diastolic [Ca2+ ]i are poorly understood. Recent work suggests that flux balance is also important here. In particular, decreasing SR function decreases the amplitude of the systolic Ca2+ transient and the resulting decrease of Ca2+ efflux results in an increase of diastolic [Ca2+ ]i to maintain total efflux.