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

Abstract

Hyperthermia during prolonged exercise leads to hyperventilation, which can reduce arterial CO2 pressure (PaCO2 ) and, in turn, cerebral blood flow (CBF) and thermoregulatory response. We investigated 1) whether humans can voluntarily suppress hyperthermic hyperventilation during prolonged exercise and 2) the effects of voluntary breathing control on PaCO2 , CBF, sweating, and skin blood flow. Twelve male subjects performed two exercise trials at 50% of peak oxygen uptake in the heat (37°C, 50% relative humidity) for up to 60 min. Throughout the exercise, subjects breathed normally (normal-breathing trial) or they tried to control their minute ventilation (respiratory frequency was timed with a metronome, and target tidal volumes were displayed on a monitor) to the level reached after 5 min of exercise (controlled-breathing trial). Plotting ventilatory and cerebrovascular responses against esophageal temperature (Tes) showed that minute ventilation increased linearly with rising Tes during normal breathing, whereas controlled breathing attenuated the increased ventilation (increase in minute ventilation from the onset of controlled breathing: 7.4 vs. 1.6 l/min at +1.1°C Tes; P < 0.001). Normal breathing led to decreases in estimated PaCO2 and middle cerebral artery blood flow velocity (MCAV) with rising Tes, but controlled breathing attenuated those reductions (estimated PaCO2 -3.4 vs. -0.8 mmHg; MCAV -10.4 vs. -3.9 cm/s at +1.1°C Tes; P = 0.002 and 0.011, respectively). Controlled breathing had no significant effect on chest sweating or forearm vascular conductance (P = 0.67 and 0.91, respectively). Our results indicate that humans can voluntarily suppress hyperthermic hyperventilation during prolonged exercise, and this suppression mitigates changes in PaCO2 and CBF.

Keywords: cerebral blood flow; hyperpnea; hyperthermia; voluntary control of breathing.

Fig. 1.

Time-dependent changes in esophageal temperature (A), heart rate (B), mean arterial pressure (MAP; C) and middle cerebral artery blood velocity (MCAV; D) during normal-breathing and controlled-breathing trials. †P < 0.05 vs. the 10-min level in the normal-breathing trial. ‡P < 0.05 vs. the 10-min level in the controlled-breathing trial.

Fig. 2.

Representative data showing time-dependent changes in minute ventilation during the normal-breathing and controlled-breathing trials. Symbols show 30-s averaged data.

Fig. 3.

Time-dependent changes in minute ventilation (A), tidal volume (B), respiratory frequency (C), and ratings of perceived exertion (D) during the normal-breathing and controlled-breathing trials. *P < 0.05, normal-breathing vs. controlled-breathing. †P < 0.05 vs. the 10-min level in the normal-breathing trial; ‡P < 0.05 vs. the 10-min level in the controlled-breathing trial.

Fig. 4.

Time-dependent changes in V̇_E/V̇_O2 (A), V̇_E/V̇_CO2 (B), estimated arterial CO₂ pressure (Pa_CO2estimated; C) and V̇_O2 (D) during normal- and controlled breathing trials. *P < 0.05, normal-breathing vs. controlled-breathing; †P < 0.05 vs. the 10-min level in the normal-breathing trial.

Fig. 5.

Time-dependent changes in forearm vascular conductance (A) and chest sweat rate (B) during normal breathing and controlled breathing trials. †P < 0.05 vs. the 10-min level in the normal-breathing trial. ‡P < 0.05 vs. the 10-min level in the controlled-breathing trial.

Fig. 6.

Esophageal temperature-dependent changes in minute ventilation (A), Pa_{CO2,estimated} (B), MCAV (C), and CVC (D) during normal-breathing and controlled-breathing trials. *P < 0.05, normal-breathing vs. controlled-breathing. †P < 0.05 vs. 0.1°C in the normal-breathing trial. Change in each parameter (Δ) shows data collected after the start of the controlled breathing (after 8 min of exercise). The numbers adjacent to the symbols indicate the number of subjects remaining at the corresponding temperature.