To study the mechanism of rise in body temperature during exercise, endogenous pyrogen was administered to exercising rats. At rest and at a neutral ambient temperature (T(a)) of 24°C, intravenous injection of recombinant human interleukin 1 (IL-1, 40 μg/kg) produced a 0.5°C rise in rectal temperature (T(re)) from 37.4°C. At T(a) of 34°C, at which T(re) was 38.6°C, T(re) rise in response to IL-1 was only 0.2°C greater than when saline was used. In the first series of exercise experiments, rats ran on a treadmill after IL-1 or saline injection at two different work intensities (estimated at 40 and 60% of maximal oxygen uptake) at 24°C T(a). At either work intensity, the magnitude of T(re) rise after IL-1 injection was ~ 0.5°C higher than after saline injection. Threshold T(re) for tail vasodilation increased when IL-1 was injected. The difference in the threshold T(re) between the IL-1 and saline conditions was 0.5°C at either work intensity. Evaporative heat loss was also suppressed and metabolic heat production facilitated when IL-1 was injected. In a second series of experiments, IL-1 was injected after T(re) reached a steady state (38.5°C) during exercise. After IL-1 injection T(re) increased another 0.5°C, but after saline injection T(re) did not change. These results suggest that body temperature rise during exercise is not induced merely by an insufficient capability of dissipating heat and that the thermoregulatory set point is reset during exercise.
|ジャーナル||American Journal of Physiology - Regulatory Integrative and Comparative Physiology|
|出版ステータス||Published - 1990|
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