For almost half a century it has been thought that the initiation of each heartbeat is driven by surface membrane voltage-gated ion channels (M clocks) within sinoatrial nodal cells. It has also been assumed that pacemaker cell automaticity is initiated at the maximum diastolic potential (MDP). Recent experimental evidence based on confocal cell imaging and supported by numerical modelling, however, shows that initiation of cardiac impulse is a more complex phenomenon and involves yet another clock that resides under the sarcolemma. This clock is the sarcoplasmic reticulum (SR): it generates spontaneous, but precisely timed, rhythmic, submembrane, local Ca²⁺ releases (LCR) that appear not at the MDP but during the late, diastolic depolarization (DD). The Ca²⁺ clock and M clock dynamically interact, defining a novel paradigm of robust cardiac pacemaker function and regulation. Rhythmic LCRs during the late DD activate inward Na⁺/Ca²⁺ exchanger currents and ignite action potentials, which in turn induceCa²⁺ transients and SR depletions, resetting the Ca²⁺ clock. Both basal and reserve protein kinaseA-dependent phosphorylation of Ca²⁺ cycling proteins control the speed and amplitude of SR Ca²⁺ cycling to regulate the beating rate by strongly coupled Ca²⁺ and M clocks.