We tested the hypothesis that the shift in the cutaneous vasodilator response to hyperthermia seen with elevated female reproductive hormones is a prostaglandin-dependent resetting of thermoregulation to higher internal temperatures, similar to that seen in the febrile response to bacterial infection. Using water-perfused suits to control body temperature, we conducted heat stress experiments in resting women under conditions of low and high progesterone and estrogen and repeated these experiments after an acute dose of ibuprofen (800 mg). In six women the hormones were exogenous (oral contraceptives); three women had regular menstrual cycles and were tested in the early follicular and midluteal phases. Resting oral temperature (T_or) was significantly elevated with high hormone status (P < 0.05); this was not affected by ibuprofen treatment (P > 0.2). The T_or threshold for cutaneous vasodilation was significantly increased by high hormone status (+0.27 ± 0.07°C, P < 0.02); the shift was not affected by ibuprofen treatment (with ibuprofen: +0.29 ± 0.08°C, P > 0.2 vs. control experiments). The T_or threshold for sweating was similarly increased by high hormone status (+0.22 ± 0.05°C, P < 0.05); this shift was not influenced by ibuprofen (with ibuprofen: +0.35 ± 0.05, P > 0.1 vs. control experiments). Thus the shift in thermoregulatory control of skin blood flow and sweating mediated by female reproductive steroids is not sensitive to ibuprofen; it therefore appears that this shift is independent of prostaglandins.

skin blood flow; estrogen; progesterone; heat stress; active vasodilation; sweating; human; temperature regulation

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