DISTURBANCE OF THERMAL HOMEOSTASIS DURING POSTEXERCISE HYPERTHERMIA

The response of core temperature to exercise was investigated during r ecovery in order to avoid the antagonistic competition between exercis e and thermal reflexes for the same effector systems which control ski n blood flow. Five healthy, non-training males [mean (SD) age, 23.8 (2 .04) years] were habituated to 29 degrees C at relative 50% humidity f or more than 2 h and then exercised by treadmill running at about 75% maximum oxygen uptake for 18 min. They then remained at 29 degrees C f or up to 65 min of recovery. Oesophageal (T-es), rectal (T-re) and ski n temperatures (T-sk) were recorded at 5-s intervals throughout. The a brupt fall of temperature gradient from the forearm to finger was used to identify the T-es for skin vessel dilatation (T-dil) during exerci se. Mean (SE) T-es rose from a resting value of 36.67 (0.15)degrees C to 38.22 (0.24)degrees C, mean T-re rose from 37.09 (0.25)degrees C to 38.23 (0.15)degrees C, and T-dil occurred at 37.39 (0.32)degrees C. W ithin 10 min of recovery mean T-es fell to 37.31 (0.24)degrees C, wher e it remained a significant 0.64 degrees C above its pre-exercise (PrE x) level (P less than or equal to 0.018) but insignificantly different from T-dil for the remaining 55 min of recovery. Meanwhile, T-re fell gradually throughout recovery to 37.64 (0.18)degrees C. The T-sk at a ll non-acral sites except the thigh had recovered to PrEx levels by 20 -30 min post-exercise (PoEx). The rapid PoEx fall of T-es to the level of T-dil and the subsequent plateau above PrEx values suggests that h eat dissipation during recovery was primarily passive once T-es had fa llen to T-dil, even though T-es and T-re were significantly elevated. The relationship of these results to the set-point and load error conc epts of thermal control is discussed.