Athletic endurance competitions in hot environments have become more relevant in professional sports. The inception for this thesis was to understand why a group of elite endurance triathletes repeatedly failed to perform in hot environments. The subsequent aims were to explore the physiological basis of elite endurance performance in the heat, with a focus on cerebrovascular responses because they seemed relevant and yet remained relatively less well explored. Four sequential studies addressed the thesis: 1) observe and measure athletes` physiology and race behaviour, 2) measure physiological responses from short-duration, maximal-intensity exercise in controlled temperate (TEMP) vs hot (HOT) environments, 3) measure physiological responses from a simulated race performance in those controlled environments, and 4) develop and assess a heat-conditioning intervention to improve performance and reduce physiological limitations. Study One observed elite triathletes competing over 2010-11 in four races (two temperate, two hot environments). Run pace in the first kilometre was considerably slower and deteriorated more in hot environments. Cardiovascular responses were similar before, during and immediately after racing; indicating that athletes competed at the physiological limit of their cardiovascular systems. Based on the field observations, Study Two investigated maximal exercise performances over 10 s and 5 min in TEMP and HOT environments because this duration is sufficient for performance to be predominantly aerobic but short enough to limit core (incl. brain) temperature and gastro-intestinal (GI) system influence. Cycling in HOT produced 11% more power over 10 s but 3.4% less power over 5 min, and was associated with increased actual and perceptual thermal strain and lower prefrontal cortex oxygen saturation. Given the thermal strain and restricted physiological function observed within 5 min in Study Two, Study Three investigated elite athletes` performance and physiological profile of a triathlon race simulation (60-min SIM) in TEMP and HOT environments. Power profile was stochastic over 2-min periods throughout, but controlled externally for the first 40 min (FIXED). In HOT, power output was ~20% lower for the final 20-min self-selected paced efforts and all athletes experienced greater physiological strain during FIXED. To maintain homeostasis athletes may have reduced their power output during the self-selected section in response to prefrontal cortex oxygen desaturation, deteriorated affective state, leg muscle oxygen desaturation and blood flow redistribution that negatively influenced anticipatory pacing. Having now quantified the negative performance and physiological impact of HOT on an under-prepared athlete group, Study Four was a controlled, short-term heat acclimation to determine its physiological and ergogenic effectiveness in TEMP and HOT environments for elite athletes. Overall, heat acclimation had small and unclear influences on performance, cerebrovascular, cardiovascular, and psycho-physical responses to exercise in either TEMP or HOT conditions relative to those after control conditioning. The heat acclimation protocol may have been ineffective, or alternatively participants` training status may have constrained further adaptation. The thesis demonstrated that elite and highly-trained athletes competing in HOT environments produced more power for singular sprints but less power for 5-min efforts, 60-min race simulations and run pace in triathlon races; contributing to poor performance or volitional exhaustion. Physiological factors that influenced performance in HOT included greater thermal, cardiovascular, cerebrovascular and affective strain, which generally were not improved by a 10-d heat-acclimation regime.
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