BACKGROUND The function of the sinoatrial node (SAN), the pacemaker of the heart, is known to decline with age, resulting in increased incidence of sinoatrial node dysfunction in the elderly. OBJECTIVE The aim of the study is to investigate the ionic mechanisms underlying age-associated SND. It is possible that SND with age may be the result of different ionic and molecular mechanistic “pathways”, each of which may result in either up-regulation or down-regulation of ion channel functions. METHODS A mathematical model of the electrical action potential of rat sinoatrial node myocytes, as developed by (Tao et al. 2011), was modified to simulate the functional impacts of age-induced changes on membrane ion channels and intracellular Ca2+ handling on cardiac pacemaking potentials based on experimental data from two independent studies on ageing in Wistar Hannover rat SAN cells. The first data set was from (Tellez et al. 2011) (noted as Ageing Study-1), and the second from (Huang et al. 2016)and (Jones et al. 2004) and (Hatch. 2012)(noted as Ageing Study-2). In both studies, the roles and relative importance of individually remodelled ion channels were evaluated by inclusive and exclusive methods, in which remodelling of specific currents was considered in isolation. RESULTS Previously reported age-induced changes in sarcolemmal ion currents result in a marked increase in CL, leading to HR reduction and thus producing bradycardial effects in the SAN. With both Ageing Study-1 and 2’s remodelled parameters, there was a 16% and 11% reduction in HR, respectively, where these reductions were comparable to experimental results of 18% and 8% reductions in heart rate in elderly rat SANs as compared to adult rats. The individual method showed that the altered ICaL, either increased or decreased, has notable effects of the AP profiles, modulating the pacemaking rate of APs. The decreased ICaL associated with an decreased amplitude of AP and abbreviated APD50, both of which accelerated repolarisation process, causing an incomplete repolarisation as a consequence of reduced AP amplitude and abbreviated APD50, therefore slowing down the pacemaking rate. Similarly, the increased ICaL produced increased amplitude of AP and prolonged APD50, slowing done the time course of repolarisation and therefore slowing down the pacemaking rate that contributes to ageing bradycardia. CONCLUSION With age, the changes in the expression of ion channel and Ca2+ clock genes in the SAN accounted qualitatively for HR reduction. The various changes in age-related remodelling of ICaL appears to have the most influence on the slowing of APs in rat SAN, which is known as the “Bradycardia effect”, indicating that SAN dysfunction could be the result of various mechanisms that come into effect during the ageing process. KEYWORDS Aging; SA node; Ion channel remodelling; ICaL