Characteristics of hyperthermia-induced hyperventilation in humans

Abstract

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.

Keywords: Hyperpnea; heat loss; respiratory alkalosis.

Figure 1.

Description of Haldane's experiment. Temperatures are presented in degrees Fahrenheit [°C = 5/9 (°F−32)]. Note the statement describing the increase in ventilation in a hot environment. Reproduced with permission from Cambridge University Press.

Figure 2.

Modulators of human hyperthermia-induced hyperventilation characterized based on its threshold and sensitivity to increasing body core temperature. Note that exercise and heat acclimation reduce the threshold, and that exercise, hypocapnia, increased aerobic capacity and increased heat loss capacity reduce the sensitivity. By contrast, exercise intensity does not affect the threshold, and exercise intensity, hypohydration, heat acclimation and sex do not affect the sensitivity.

Figure 3.

Body core (esophageal: T_es and tympanic: T_ty) temperature-dependent change in minute ventilation (V_I) during passive heating at rest (41°C bath immersion). Note that V_I increased at T_es of 38.5°C and T_ty of 38.1°C. Reprinted from Cabanac & White, with kind permission from Springer Science+Business Media.

Figure 4.

Body core (esophageal) temperature-dependent changes in minute ventilation (A), tidal volume (B) and respiratory frequency (C) during passive heating at rest (Rest), prolonged light exercise (25% of peak oxygen uptake) and moderate exercise (50% of peak oxygen uptake) in 9 subjects. Symbols show 30-s averaged data, and the symbols during exercise show data collected after 5 min of exercise. Arrows indicate the averaged thresholds. Note that the threshold and the sensitivity for minute ventilation were lower during passive heating than exercise, irrespective of exercise intensity, and that tidal volume has a threshold during passive heating but not during exercise (adapted from Tsuji et al. ¹⁸).

Figure 5.

Body core (esophageal) temperature-dependent changes in estimated PaCO₂ (PaCO_2estimated; A), minute ventilation (B) and middle cerebral artery blood flow velocity (C) during prolonged moderate exercise (50% of peak oxygen uptake) in room air (open circles) and CO₂-enriched air (filled circles). The CO₂-enriched air was a mixture of room air and 100% CO₂. We manually added 100% CO₂ to the inhaled air to maintain PaCO_2estimated throughout the exercise. Changes in esophageal temperature (Δ) were measured from the start of inhalation of CO₂-enriched air. The numbers adjacent to the symbols in A and C indicate the numbers of subjects still exercising at the corresponding temperature; the numbers in A also apply to B. *P < 0.05, room air vs. CO₂-enriched air; ^†P < 0.05 vs. Δesophageal temperature = 0°C. Note that when hyperthermic hyperventilation-induced hypocapnia was restored to normocapnic level, minute ventilation was increased and the cerebral blood flow velocity was largely restored to normocapnic level. Adapted from Hayashi et al.

Figure 6.

Schematic representation of the effects of hyperthermia-induced hyperventilation on physiological responses in humans.