Elevation of core temperature leads to increases in ventilation in both resting subjects and those engaged in prolonged exercise. We compared the characteristics of the hyperthermic hyperventilation elicited during passive heating at rest and during prolonged moderate and light exercise. Twelve healthy men performed three trials: a rest trial in which subjects were passively heated using hot-water immersion (41°C) and a water-perfused suit and two exercise trials in which subjects exercised at 25% (light) or 50% (moderate) of peak oxygen uptake in the heat (37°C and 50% relative humidity) after first using water immersion (18°C) to reduce resting esophageal temperature (T(es)). This protocol enabled detection of a T(es) threshold for hyperventilation during the exercise. When minute ventilation (Ve) was expressed as a function of T(es), 9 of the 12 subjects showed T(es) thresholds for hyperventilation in all trials. The T(es) thresholds for increases in Ve during light and moderate exercise (37.1 ± 0.4 and 36.9 ± 0.4°C) were both significantly lower than during rest (38.3 ± 0.6°C), but the T(es) thresholds did not differ between the two exercise intensities. The sensitivity of Ve to increasing T(es) (slope of the T(es)-Ve relation) above the threshold was significantly lower during moderate exercise (8.7 ± 3.5 l · min(-1) · °C(-1)) than during rest (32.5 ± 24.2 l · min(-1) · °C(-1)), but the sensitivity did not differ between light (10.4 ± 13.0 l · min(-1) · °C(-1)) and moderate exercise. These results suggest the core temperature threshold for hyperthermic hyperventilation and the hyperventilatory response to increasing core temperature in passively heated subjects differs from that in exercising subjects, irrespective of whether the exercise is moderate or light.

We tested the hypothesis that short-term exercise-heat acclimation (EHA) attenuates hyperthermia-induced hyperventilation in humans exercising in a hot environment. Twenty-one male subjects were divided into the two groups: control (C, n = 11) and EHA (n = 10). Subjects in C performed exercise-heat tests [cycle exercise for ~75 min at 58% [Formula: see text] (37°C, 50% relative humidity)] before and after a 6-day interval with no training, while subjects in EHA performed the tests before and after exercise training in a hot environment (37°C). The training entailed four 20-min bouts of exercise at 50% [Formula: see text] separated by 10 min of rest daily for 6 days. In C, comparison of the variables recorded before and after the no-training period revealed no changes. In EHA, the training increased resting plasma volume, while it reduced esophageal temperature (T (es)), heart rate at rest and during exercise, and arterial blood pressure and oxygen uptake ([Formula: see text]) during exercise. The training lowered the T (es) threshold for increasing forearm vascular conductance (FVC), while it increased the slope relating FVC to T (es) and the peak FVC during exercise. It also lowered minute ventilation ([Formula: see text]) during exercise, but this effect disappeared after removing the influence of [Formula: see text] on [Formula: see text]. The training did not change the slope relating ventilatory variables to T (es). We conclude that short-term EHA lowers ventilation largely by reducing metabolism, but it does not affect the sensitivity of hyperthermia-induced hyperventilation during submaximal, moderate-intensity exercise in humans.

Nishiyasu T. Effect of initial core temperature on hyperthermic hyperventilation during prolonged submaximal exercise in the heat. Am J Physiol Regul Integr Comp Physiol 302: R94 -R102, 2012. First published September 28, 2011 doi:10.1152/ajpregu.00048.2011.-We investigated whether a core temperature threshold for hyperthermic hyperventilation is seen during prolonged submaximal exercise in the heat when core temperature before the exercise is reduced and whether the evoked hyperventilatory response is affected by altering the initial core temperature. Ten male subjects performed three exercise trials at 50% of peak oxygen uptake in the heat (37°C and 50% relative humidity) after altering their initial esophageal temperature (Tes). Initial Tes was manipulated by immersion for 25 min in water at 18°C (Precooling), 35°C (Control), or 40°C (Preheating). Tes after the water immersion was significantly higher in the Preheating trial (37.5 Ϯ 0.3°C) and lower in the Precooling trial (36.1 Ϯ 0.3°C) than in the Control trial (36.9 Ϯ 0.3°C). In the Precooling trial, minute ventilation (V E) showed little change until Tes reached 37.1 Ϯ 0.4°C. Above this core temperature threshold, V E increased linearly in proportion to increasing Tes. In the Control trial, V E increased as Tes increased from 37.0°C to 38.6°C after the onset of exercise. In the Preheating trial, V E increased from the initially elevated levels of Tes (from 37.6 to 38.6°C) and V E. The sensitivity of V E to increasing Tes above the threshold for hyperventilation (the slope of the Tes-V E relation) did not significantly vary across trials (Precooling trial ϭ 10.6 Ϯ 5.9, Control trial ϭ 8.7 Ϯ 5.1, and Preheating trial ϭ 9.2 Ϯ 6.9 L·min Ϫ1 ·°C Ϫ1 ). These results suggest that during prolonged submaximal exercise at a constant workload in humans, there is a clear core temperature threshold for hyperthermic hyperventilation and that the evoked hyperventilatory response is unaffected by altering initial core temperature.hyperpnea; hyperthermia; thermoregulation; precooling; preheating WHEN HUMANS ARE EXPOSED TO a hot environment, heat dissipation through cutaneous vasodilation and sweating increases in response to rising body core and skin temperatures. In addition to these thermoregulatory responses, Haldane found in 1905 that an increase in ventilation is also induced by a rise in body core temperature (13). Since that early report, many studies have confirmed the existence of hyperthermia-induced hyperventilation (5, 9 -11, 16, 26, 32, 38, 43) although its characteristic and significance remain unclear.When ventilation is expressed as a function of core temperature in passively-heated humans at rest, there is no significant change until core temperature reaches a temperature threshold for hyperventilation, ϳ37.8 -38.5°C. Above this threshold, ventilation increases linearly in proportion to increasing core temperature with minimal change in oxygen consumption (5, 10). As in resting subjects, metabolic factors contribute minimally to ventilation during prolo...

In humans, hyperthermia leads to activation of a set of thermoregulatory responses that includes cutaneous vasodilation and sweating. Hyperthermia also increases ventilation in humans, as is observed in panting dogs, but the physiological significance and characteristics of the hyperventilatory response in humans remain unclear. The relative contribution of respiratory heat loss to total heat loss in a hot environment in humans is small, and this hyperventilation causes a concomitant reduction in arterial CO2 pressure (hypocapnia), which can cause cerebral hypoperfusion. Consequently, hyperventilation in humans may not contribute to the maintenance of physiological homeostasis (i.e., thermoregulation). To gain some insight into the physiological significance of hyperthermia-induced hyperventilation in humans, in this review, we discuss 1) the mechanisms underlying hyperthermia-induced hyperventilation, 2) the factors modulating this response, and 3) the physiological consequences of the response.