Exertional heat illness continues to be a military problem during training and operations. Whereas the hospitalization rate of heat illness is declining, heat stroke has markedly increased.

The changes occurring in the esophageal temperature (Tes) thresholds for initiation of heat loss responses as affected by the circadian period and menstrual cycle were studied. Four women exercised at 60% peak Vo2 in 35 degrees C (ambient water vapor pressure 1.73 kPa) for 30 min at 0400 and 1600 during the follicular (F) and luteal (L) phase. Tes, arm sweating rate (msw), and forearm blood flow (FBF) were measured frequently. At rest, Tes averaged 0.3 degrees C higher during L than F at both 0400 and 1600 and approximately 0.4 degrees C higher at 1600 than at 0400 during both phases. During exercise transients, the slopes of the FBF:Tes and the msw:Tes relationships were not different among treatments. The thresholds for initiation of sweating and cutaneous vasodilation were higher at 1600 than 0400 during both phases. Thresholds during F at 0400 averaged 36.44 degrees C for msw and 36.80 degrees C for vasodilation. The thresholds during L at 1600 averaged 37.46 and 37.53 degrees C for sweating and vasodilation, respectively. Our data indicate that the thermoregulatory effector activity during exercise is a function of numerous inputs, and one of these may be hormonal or hormonal-like in action. Controlling time of day and menstrual cycle phase are as important as controlling for aerobic power, age, and fitness in studying female thermoregulatory responses during exercise.

No abstract

This experiment was performed to determine if plasma glucose homeostasis is maintained in normal human volunteers during light exercise (40% maximal oxygen consumption [VO2 Max]) when changes in insulin and glucagon are prevented. Hormonal control was achieved by the infusion of somatostatin, insulin, and glucagon. Glucose kinetics and oxidation rates were determined with stable isotopic tracers of glucose, and by indirect calorimetry. Two different rates of replacement of insulin and glucagon were used; in one group, insulin was clamped at 19.8±2.6 AU/ml (high-insulin group), and in the other group insulin was clamped at 9.2±1.3 jzU/ml (low-insulin group). Glucagon was maintained at 261±16.2 and 124±6.4 pg/ml, respectively, in the high-insulin and low-insulin groups.Without hormonal control, plasma glucose homeostasis was maintained during exercise because the increase in glucose uptake was balanced by a corresponding increase in glucose production. When changes in insulin and glucagon were prevented, plasma glucose concentration fell, particularly in the high-insulin group. Glucose uptake increased to a greater extent than when hormones were not controlled, and glucose production did not increase sufficiently to compensate. The increase in glucose uptake in the hormonal control groups was associated with an increased rate of glucose oxidation. When euglycemia was maintained by glucose infusion in the hormonal control subjects, the modest increase in glucose production that otherwise occurred was prevented.