Pulmonary ventilation and gas exchange during prolonged exercise in humans: Influence of dehydration, hyperthermia...

What is the central question of the study? Ventilation increases during prolonged intense exercise, but the impact of dehydration and hyperthermia, with associated blunting of pulmonary circulation, and independent influences of dehydration, hyperthermia and sympathoadrenal discharge on ventilatory and pulmonary gas exchange responses remain unclear. What is the main finding and its importance? Dehydration and hyperthermia led to hyperventilation and compensatory adjustments in pulmonary CO₂ and O₂ exchange, such that CO₂ output increased and O₂ uptake remained unchanged despite the blunted circulation. Isolated hyperthermia and adrenaline infusion, but not isolated dehydration, increased ventilation to levels similar to combined dehydration and hyperthermia. Hyperthermia is the main stimulus increasing ventilation during prolonged intense exercise, partly via sympathoadrenal activation.

The mechanisms driving hyperthermic hyperventilation during exercise are unclear. In a series of retrospective analyses, we evaluated the impact of combined versus isolated dehydration and hyperthermia and the effects of sympathoadrenal discharge on ventilation and pulmonary gas exchange during prolonged intense exercise. In the first study, endurance-trained males performed two submaximal cycling exercise trials in the heat. On day 1, participants cycled until volitional exhaustion (135 ± 11 min) while experiencing progressive dehydration and hyperthermia. On day 2, participants maintained euhydration and core temperature (T_c ) during a time-matched exercise (control). At rest and during the first 20 min of exercise, pulmonary ventilation ( $$ ), arterial blood gases, CO₂ output and O₂ uptake were similar in both trials. At 135 ± 11 min, however, $$ was elevated with dehydration and hyperthermia, and this was accompanied by lower arterial partial pressure of CO₂ , higher breathing frequency, arterial partial pressure of O₂ , arteriovenous CO₂ and O₂ differences, and elevated CO₂ output and unchanged O₂ uptake despite a reduced pulmonary circulation. The increased $$ was closely related to the rise in T_c and circulating catecholamines (R²  ≥ 0.818, P ≤ 0.034). In three additional studies in different participants, hyperthermia independently increased $$ to an extent similar to combined dehydration and hyperthermia, whereas prevention of hyperthermia in dehydrated individuals restored $$ to control levels. Furthermore, adrenaline infusion during exercise elevated both T_c and $$ . These findings indicate that: (1) adjustments in pulmonary gas exchange limit homeostatic disturbances in the face of a blunted pulmonary circulation; (2) hyperthermia is the main stimulus increasing ventilation during prolonged intense exercise; and (3) sympathoadrenal activation might partly mediate the hyperthermic hyperventilation.