Age associates with increasing problems in cardiac function. Even healthy progressive ageing limits the heart’s ability to respond to stress and is associated with increasing susceptibility to arrhythmias and myocardial dysfunction. This may be caused by altered regulation of intracellular calcium ions ([Ca²⁺]_i). Exercise has been suggested as a way to reverse or limit the effects of ageing on the heart (Bronikowski et al. 2003). This investigation sought to examine the effects of healthy progressive ageing on the mouse ventricle, focusing on changes in proteins regulating [Ca²⁺]_i. Further investigations assessed whether acute or life-long exercise influenced changes in the response of the heart to ageing, beneficially or otherwise. Mice (C57/Bl6) at 3 months & 24 months of age were randomly assigned to sedentary or exercise training groups. Exercise training was performed by treadmill running at 14 m.min^-1 for 15 minutes three times per week for a total of ten weeks. A further group of mice aged 12 months undertook this training protocol for 12 months. Immunohistochemical analysis was performed using fluorescently-labelled monoclonal antibodies to the L-type, D-type and T-type calcium channels and sodium-calcium exchanger (NCX), in conjunction with laser-scanning confocal microscopy. Results are displayed below (Table 1). Ageing and exercise both induced hypertrophy. Ageing had no effect on the L-type and D-type calcium channel but significantly increased T-type calcium channel and NCX expression. Exercise in young mice significantly increased L-type channel and NCX expression, however, no change in D-type and T-type calcium channel isoforms were observed. Exercise in the elderly induced significant increases of all calcium channels and NCX compared with young and old sedentary controls. No differences were observed between acute and long-term responses to exercise in the elderly heart. Exercise produces differential effects in the old and young heart but does not reverse the effects of ageing.