This thesis examined the effect of heat stress, dehydration and exercise on global left ventricular (LV) function and LV twist, untwisting and strain (LV mechanics) in healthy individuals. The primary aim was to identify whether the different haemodynamics induced by heat stress, dehydration and exercise would be associated with alterations in systolic and diastolic LV mechanics as assessed by two-dimensional speckle tracking echocardiography. Study one showed that enhanced systolic and diastolic LV mechanics during progressively increasing heat stress at rest likely compensate in part for a lower venous return, resulting in a maintained stroke volume (SV). In contrast, heat stress during knee-extensor exercise did not significantly increase LV twist, suggesting that exercise attenuates the increase in LV mechanics seen during passive heat stress. Study two revealed that dehydration enhances systolic LV mechanics whilst diastolic mechanics remain unaltered at rest, despite pronounced reductions in preload. The maintenance of systolic and diastolic LV mechanics with dehydration during knee-extensor exercise further suggests that the large decline in SV with dehydration and hyperthermia is caused by peripheral cardiovascular factors and not impaired LV mechanics. During both, heat stress and dehydration, enhanced systolic mechanics were achieved solely by increases in basal rotation. In contrast, the third study demonstrated that when individuals are normothermic and euhydrated, systolic and diastolic basal and apical mechanics increase significantly during incremental exercise to approximately 50% peak power. The subsequent plateau suggests that LV mechanics reach their peak at sub-maximal exercise intensities. Together, the present findings emphasise the importance of acute adjustments in both, basal and apical LV mechanics, during periods of increased cardiovascular demand.