Pascale Kippelen

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, CO 2 output and O 2 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 CO 2 , higher breathing frequency, arterial partial pressure of O 2 , arteriovenous CO 2 and O 2 differences, and elevated CO 2 output and unchanged O 2 uptake despite a reduced pulmonary circulation. The increased was closely related to the rise in T c and circulating catecholamines ( R 2 ≥ 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.