TY - JOUR
T1 - Effects of pyrogen administration on temperature regulation in exercising rats
AU - Tanaka, H.
AU - Kanosue, K.
AU - Yanase, M.
AU - Nakayama, T.
PY - 1990
Y1 - 1990
N2 - 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.
AB - 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.
KW - body temperature
KW - heat exposure
KW - interleukin 1
KW - tail vasomotor response
KW - thermoregulatory set point
KW - treadmill running
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U2 - 10.1152/ajpregu.1990.258.4.r842
DO - 10.1152/ajpregu.1990.258.4.r842
M3 - Article
C2 - 2331029
AN - SCOPUS:0025246295
SN - 0002-9513
VL - 258
SP - R842-R847
JO - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
JF - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
IS - 4 27-4
ER -