Optimising the acquisition and retention of heat acclimation.

Heat acclimation (HA) often starts in a moderately hot environment to prevent thermal overload and stops immediately prior to athletic activities. The aims of this study were (1) to establish whether acclimation to a moderately hot climate is sufficient to provide full acclimation for extreme heat and (2) to investigate the physiological responses to heat stress during the HA decay period. 15 male subjects exercised for 9 consecutive days at 26° C Wet Bulb Globe Temperature (WBGT) and 3 days at 32° C WBGT on a cycle ergometer for up to 2 h per day and repeated the exercise 3, 7 and 18 days later in 26° C WBGT. Rectal temperature (T (re)) and heart rate (HR) were measured during 60 min of steady state exercise (∼45% of maximum oxygen uptake). During days 1-9, end-exercise T (re) was reduced from 38.7±0.1 to a plateau of 38.2±0.1° C (p<0.05), HR was reduced from 156±10 to 131±11 bpm (p<0.05). No changes in HR and T (re) occurred during the 3 days in the very hot environment. However, T (re) during rest and exercise were significantly lower by 0.4-0.5° C after HA compared with day 9, suggesting that heat acclimation did not decay but resulted in further favourable adaptations.

Effects of hyperthermia on the metabolic responses to repeated high-intensity exercise.

In this study, we investigated the metabolic and performance responses to hyperthermia during high-intensity exercise. Seven males completed two 30-s cycle sprints (SpI and SpII) at an environmental temperature of 20.6 (0.3) degrees C [mean (SD)] with 4 min recovery between sprints. A hot or control treatment preceded the sprint exercise. For the hot trial, subjects were immersed up to the neck in hot water [43 degrees C for 16.0 (3.2) min] prior to entering an environmental chamber [44.2 (0.8) degrees C for 30.7 (7.1) min]. For the control trial, subjects were seated in an empty bath (15 min) and thereafter in a normal environment [20.2 (0.6) degrees C for 29.0 (1.9) min]. Subjects' core temperature prior to exercise was 38.1 (0.3) degrees C in the hot trial and 37.1 (0.3) degrees C in the control trial. Mean power output (MPO) was significantly higher in the hot condition for SpI [683 (130) W hot vs 646 (119) W control ( P<0.025)]. Peak power output (PPO) tended to be higher in the hot trial compared with the control trial for SpI [1057 (260) W hot vs 990 (245) W control ( P=0.03, NS)]. These differences in power output were a consequence of a faster pedal cadence in the hot trial ( P<0.025). There were no differences in sprint performance in SpII in the hot trial compared to the control trial; however, MPO was significantly reduced from SpI to SpII in the hot condition but not in the control condition ( P<0.025). Plasma ammonia was higher in the hot trial at 2 min post-SpI [169 (65) micromol l(-1 )hot vs 70 (26) micromol l(-1) control ( P<0.01)], immediately and at 2 min post-SpII [231 (76) micromol l(-1) hot vs 147 (72) micromol l(-1) control ( P<0.01)]. Blood lactate was higher in the hot trial compared with the control trial at 5 min post-SpII ( P<0.025). The results of this study suggest that an elevation in core body temperature by 1 degrees C can improve performance during an initial bout of high-intensity cycle exercise but has no further beneficial effect on subsequent power production following a 4-min recovery period.