Atrial fibrillation (AF) is the most common cardiac arrhythmia and is an important risk factor for stroke¹. The risk of AF development is strongly age dependent and thus the prevalence of AF is increasing as society ages. Despite this little is known regarding how intracellular Ca handling in the atria is altered by the ageing process and if age associated remodelling predisposes the aged heart to arrhythmias. We have investigated if the sources and sinks of Ca in atrial myocytes are altered during the ageing process. Young adult (18 months old) and old sheep (>8 years) were euthanased with 200 mg/kg^-1 intravenous pentobarbitone. Myocytes were isolated from the left atrium by enzymatic digestion. Atrial myocytes were stimulated at 0.5Hz under voltage clamp control using the perforated patch clamp technique. Changes in [Ca]_i were measured using Fluo-5F AM. All experiments were performed at 37^oC. Data are presented as mean ± SEM from n experiments and statistical analysis was carried out using a t-test. Ageing resulted in atrial myocyte hypertrophy as measured by capacitance (60.5±2.2 and 72.8±2.8pF, young versus old; n=76 to 81 p<0.001). This was primarily due to a 20% increase in myocyte width in the aged heart (15.0±0.2 to 18.1±0.5µM; n=230 to 347 p<0.001) although a modest increase in cell length was evident. The amplitude of the systolic Ca transient was decreased in the aged atria (1.5±0.1 to 1.2±0.1 expressed as F/F0, young versus aged; n=35-38 p<0.05) and was associated with a decrease in peak L-type Ca current (2.3±0.2 to 1.8±0.1pA.pF^-1; n=39-47 p<0.05). The rate of decay of the systolic Ca transient was slowed in the aged atria and this was due to a decrease in SERCA function. Ca removal by sarcolemmal pathways was unaltered by ageing. Whilst a decrease in SERCA function and a decrease in systolic Ca transient amplitude both point to a reduction in SR Ca content, integration of the caffeine evoked Na-Ca exchanger current showed that SR Ca content was increased in the aged atria (p<0.01). In summary, a decrease in the trigger for Ca induced Ca release (L-type Ca current) may underlie the reduction in Ca transient amplitude in the aged atria. It remains to be determined if this reduction is sufficient to fully account for the reduced Ca transient amplitude in the aged atria in the presence of increased SR Ca content. The mechanism and role of the age associated increase in SR Ca content remains unexplained and further work is required to determine if these changes are related to spatial characteristics of Ca release.