Despite an increased aerobic exercise capacity and a greater maximal cardiac output, endurance athletes (ENDURANCE) also have a reduced hyperaemic perfusion of the heart (Heinonen et al., 2008). The mechanisms – and importantly the physiological implications – for this phenomenon are not known and we speculated that ENDURANCE may have a reduced diastolic heart muscle function related to the aerobic nature of their training, and that this would therefore be 1) exacerbated during conditions of low O2 availability and 2) absent in individuals with superior anaerobic buffering capacity. To test our hypothesis and its underlying mechanisms, we compared ‘aerobic’ ENDURANCE with ‘anaerobic’ sprint athletes (SPRINT) during exercise in normoxia and hypoxia (FiO2 = 12%), the latter being a strong stimulus for increased myocardial perfusion (Duncker et al., 2014). Additionally, the immediate re-oxygenation responses were studied. We measured heart rate (HR), blood pressure (BP) and used echocardiography to quantify conventional left ventricular (LV) function and systolic LV twist and diastolic LV untwisting rate, an essential component of normal in vivo LV relaxation (Wang et al., 2007; Opdahl et al., 2012). During exercise in both normoxia and hypoxia, BP, HR and cardiac index increased similarly between the three goups. However, ENDURANCE seemed to rely more on aerobic energy metabolism as reflected by greater O2 consumption and reduced lactate production in normoxia and hypoxia, whilst arterial desaturation was exacerbated in hypoxia as previously reported (Woorons et al., 2007). Conversely, SPRINT desaturated less and had a more specific metabolic response, showing a similar O2 consumption to ENDURANCE in normoxia, but (similar to UNTRAINED) a lower O2 consumption during hypoxia (Figure 1a). In agreement with our hypothesis, these general physiological responses were accompanied by the greatest LV untwisting rate in SPRINT and the lowest LV untwisting rate in ENDURANCE (Figure 1b). Immediately following hypoxia, SPRINT and UNTRAINED increased their LV untwisting rate while it was unchanged in ENDURANCE (Figure 1c). From these preliminary data, we conclude that endurance athletes appear to have a lower LV diastolic response during exercise in normoxia and hypoxia compared with sprint athletes. Moreover, endurance athletes do not augment their diastolic LV function following hypoxia. These data suggest that the type of exercise training may influence the cardiac response to hypoxia and re-oxygenation, which may have important implications for the cardiac responses to ischaemic events.