Compared with the induction of heat acclimation (HA), studies investigating the decay and re-induction of HA (RA) are relatively sparse and have yielded conflicting results. Therefore, 16 semi-nude men were acclimated to dry-heat by undertaking an exercise protocol in a hot chamber (dry-bulb temperature 46.1 +/- 0.1 degrees C; relative humidity 17.9 +/- 0.1%) on 10 consecutive days (HA1-10) in winter UK. Thereafter, the subjects were divided into two groups and re-exposed to the work-in-heat tests after 12 and 26 days until RA was attained (RA(12), n = 8; RA(26), n = 8). The exercise protocol consisted of 60 min of treadmill walking (1.53 m s(-1)) at an incline individually set to induce a rectal temperature (T (re)) of approximately 38.5 degrees C during HA1 (equating to 45 +/- 4% peak oxygen uptake), followed by 10 min of rest and 40 min of further treadmill exercise, the intensity of which was increased across HA to maintain T(re )at approximately 38.5 degrees C. T(re), mean skin temperature, heart rate and rate of total water loss measured at 60 min did not change after HA7, and HA was taken as the mean of the responses during HA8-10. For both groups, there was no decay in T(re) and for all measured variables RA was attained after 2 and 4 days in RA(12) and RA(26), respectively. It is concluded that once adaptation to heat has been attained, the time that individuals may spend in cooler conditions before returning to a hot environment could be as long as one month, without the need for extensive re-adaptation to heat.

We have studied 12 recreationally active men to measure their responses to exercise in the heat and relate these to measures of hypothalamic function explored with a buspirone [5-hydroxytryptamine 1A (5-HT(1A)) agonist, dopaminergic D(2) antagonist] neuroendocrine challenge, with and without pretreatment with pindolol (5-HT(1A) antagonist). Pindolol treatment allowed the serotonergic and non-serotonergic components of prolactin release to be distinguished. Subjects exercised at 73 (5)% maximal rate of oxygen uptake (VO(2max)) until volitional fatigue at 35 degrees C (relative humidity, 30%). On another two occasions they underwent a buspirone challenge [0.5 mg (kg body mass)(-1)], once with, and once without, pindolol [0.5 mg (kg body mass)(-1)] pretreatment and the circulating plasma concentrations of prolactin were measured for the next 2.5 h. Rectal temperature increased throughout exercise, whilst mean skin temperature remained constant. There was a wide inter-subject variation in prolactin response to the neuroendocrine challenges. The proportion of the prolactin response to buspirone attributable to a non-serotonergic component (most likely dopaminergic) correlated both with exercise duration (r=0.657, P=0.028), rectal temperature at fatigue (r=0.623, P=0.041) and the rate of temperature rise (r=-0.669, P=0.024). Our results suggest that high activity of the dopaminergic pathways in the hypothalamus is a predictor of exercise tolerance in the heat.

The potentially deleterious influence of body cooling on the thermoregulatory and metabolic responses to prolonged walking exercise has not been established. To address this problem, 10 men completed a 6-h intermittent (15 min rest, 45 min exercise) walking protocol in a thermoneutral (+15 degrees C) condition (Neutral) and a cold (+5 degrees C), wet, and windy condition (Cold). The first two exercise periods were conducted at a higher intensity (Higher, 6 km/h and 10% incline) than the subsequent four exercise periods (Lower, 5 km/h and 0% incline). Rectal temperature was lower and heart rate no different in Cold compared with Neutral, whereas the following were higher: oxygen consumption, respiratory exchange ratio, plasma norepinephrine and epinephrine, and blood lactate and glucose. There was no environmental influence on these variables during Higher. In conclusion, heat production during Lower was not sufficient to offset heat loss to the cold environment, and the resulting reduction in rectal temperature and metabolic perturbations may be detrimental if exercise is prolonged.

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.