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In recent years it has become clear that Western societies face a rapidly increasing ageing population. With ageing comes a significant reduction in functional capacity, cardiovascular function, increased cardiovascular disease risk and thus increasing health care costs. Exercise interventions in the elderly may prove to be a valuable tool in coping with an ageing population. It was, therefore, the purpose of this thesis to investigate; a) the effects of healthy ageing upon cardiac structure and function in adult males and females, b) the effects of a progressive aerobic exercise training programme upon cardiac structure and function in post-menopausal females as well as c) the effects of competitive exercise training on cardiac structure and function in post-menopausal female athletes and controls. The exact nature of left ventricular (LV) remodelling with age is the source of some controversy. Within a cross-sectional design cardiac structure and function was assessed in 124 women and 74 men (18-76 years). Left ventricular mass was maintained across the adult age-span in females (r= 0.02, P > 0.05) but was significantly and negatively associated with age in males (r= - 0.36, P < 0.05). The maintenance of LV mass in females despite an age-related decrease in LV volume suggested that remodelling of the LV with age was concentric in nature in females, with a relative wall thickening. In males, however, the large decrease in LV mass along with a smaller decrease in LV volume suggested a form of "eccentric atrophy" of the LV. Other data suggested an increase in male RV volume with age (c. 25%), no depression in LV and RV systolic function with age in either males or females and an expected age-related decrease in LV and RV diastolic filling (E:A ratio). Twenty post-menopausal females completed a progressive 12-month aerobic exercise training programme. Despite a significant and progressive increase in maximal aerobic capacity (pre, 23.7 ± 3.1 ml.kg'l.min"; post, 32.2 ± 4.1 ml.kg'I.min-I) there were few alterations in cardiac structure and function. It seems, therefore, that healthy sedentary females do indeed lose the ability to induce LV hypertrophy (LV mass pre, 155 ± 41 g; post, 136 ± 30 g) with training. There was some evidence of an increase in LV volume with training (and a much smaller trend toward an increase in SV). Other data showed no change with progressive exercise including LV systolic and diastolic function as well as volume data, systolic and diastolic function in the RV. Finally, nine post-menopausal female athletes were compared to an age- and lean body mass-matched control group. In agreement with the intervention study LV mass was not different in the athletes and controls (sedentary, 146 ± 31; active, 143 ± 25 g). To support and extend the training study LV volume (18%) and SV (25%), as well as RV volume (15%), were significantly greater in the athletes than the controls. The athletes also demonstrated an enhanced LV E:A ratio (sedentary 1.12; active, 1.53) although the increase in RV E:A was non significant. Both LV and RV systolic function were not different between groups. In conclusion, there is some evidence that healthy ageing of cardiac structure and function is different in males and females. Further, whilst functional capacity increases with exercise training in post-menopausal women there seems to be a lack of a LV hypertrophic response.