In cardiac muscle, depolarization of the sarcolemma initiates Ca2+ release by activating sarcolemmal L-type Ca2+ channels, providing a small increase in cytoplasmic calcium concentration in the junctional space of the dyad. This initiates [Ca2+]-dependent activation of the sarcoplasmic reticulum (SR) Ca2+ release channels known as ryanodine receptors (RyRs). The subsequent release of calcium from the SR further increases the [Ca2+] in the junctional space and leads to regenerative RyR activation, in a process called calcium-induced calcium release (CICR)(1). In such a regenerative process, the larger SR Ca2+ flux should prevent subsequent control by the surface membrane as well as SR Ca2+ store depletion. However, the quantity of Ca2+ released from the SR has a graded dependence on the magnitude of the Ca2+ influx across the sarcolemma and the SR releases only ~50% of its total content (e.g. (2)). The discovery of Ca2+ sparks (3) provided a solution to this problem by showing that graded responses can result from the spatio-temporal summation of individual Ca2+ release sites which are spatially uncoupled to limit regenerative behaviour. However, local regeneration in CICR during Ca2+ sparks might still prevent reliable Ca2+ spark termination. Using computer modelling to recover the flux associated with a Ca2+ spark places limits on (for example) the number of RyRs involved in their generation as well as SR release time course. Our work shows that RyR closure appears to occur more slowly than the SR release flux, suggesting that local depletion of the SR store may be key to termination. In addition, by incorporating measured RyR gating (from planar lipid bilayer experiments) we find that the termination of SR release can be explained by a process we call induction decay(4). Induction decay provides robust termination of SR Ca2+ release because the falling RyR single channel current (as the local SR depletes) leads to a rapid increase in RyR closed time. This prevents RyRs reopening before an open RyR closes, thereby breaking the regenerative feedback during CICR. This is essentially the reversal of Ca2+ release inducing process within CICR (which prompted our naming it induction decay). Therefore after 30 years of work, the mechanisms that activate and terminate Ca2+ sparks (and the whole cell Ca2+ transient) are gradually becoming clearer, although fine details such as the role of RyR gating modulation remain to be clarified. In addition, the possible remodelling of the junction between the surface membrane and SR in disease may also contribute to the development of dyssynchrony in Ca2+ release (e.g. 5). Recent developments in ultra high resolution imaging (e.g. 6) may provide the much needed structural information to explain such effects with more anatomically accurate computer models.