Effect of initial core temperature on hyperthermic hyperventilation during prolonged submaximal exercise in the heat

Abstract

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...

Voluntary suppression of hyperthermia-induced hyperventilation mitigates the reduction in cerebral blood flow velocity during exercise in the heat

“…Because oxygen uptake and blood lactate concentrations remain relatively constant during such exercise and are similar under hot and thermoneutral conditions (18,32), these results suggest that it is not metabolic factors, but the elevation in body temperature that mediates the increase in V E . During prolonged exercise, the elevation in core temperature, but not skin temperature (18,46), leads to an increase in V E beyond what would be expected from metabolic demand.…”

Ventilatory response to increasing body temperature: Characteristics and effect on central fatigue

“…On the other hand, White and Cabanac 7) reported that during incremental exercise, there is a core temperature threshold for hyperventilation around a tympanic temperature of 37.0-37.7 °C or a Tes of 37.5-37.9 °C, while Beaudin et al 8) and Sancheti and White 9) reported the Tes threshold for hyperventilation during incremental exercise to be around 37.1-38.2 °C. In addition, after pre-cooling subjects in cold water (18°C) to decrease body temperature enough to cause a 1°C drop in Tes, Tsuji et al 6,10) found that there is a Tes threshold for hyperventilation around 37°C during prolonged steadystate light and moderate intensity exercise (25% and 50% of peak oxygen uptake [V ・ O2peak], respectively). Above this threshold, V ・ E and respiratory frequency increased in proportion to the increase in Tes 3,5,6,10) (Fig.…”

“…In addition, after pre-cooling subjects in cold water (18°C) to decrease body temperature enough to cause a 1°C drop in Tes, Tsuji et al 6,10) found that there is a Tes threshold for hyperventilation around 37°C during prolonged steadystate light and moderate intensity exercise (25% and 50% of peak oxygen uptake [V ・ O2peak], respectively). Above this threshold, V ・ E and respiratory frequency increased in proportion to the increase in Tes 3,5,6,10) (Fig. 2), though no increases in tidal volume were seen.…”

“…Hyperventilation induced by increases in body temperature leads to excessive elimination of CO2 and a decrease of arterial PCO2 (PaCO2) both at rest and during prolonged exercise 3,5,6,10,11,[16][17][18] (Fig. 1C).…”

“…Taking the rating of perceived exertion (RPE) as an index of central command, it appears that the signal from central command is enhanced by a rise in body temperature 3,10,18,[48][49][50] , and that the increase in the signaling is induced by central fatigue caused by hyperthermia (see below). Furthermore, the activities of group III and IV muscle afferents are apparently increased by hyperthermia 51,52) .…”