Cardiopulmonary and arterial baroreceptor unloading during passive hyperthermia does not contribute to hyperthermia-induced hyperventilation

This study tested the hypothesis that baroreceptor unloading during passive hyperthermia contributes to increases in ventilation and decreases in end‐tidal partial pressure of carbon dioxide (urn:x-wiley:09580670:media:eph1695:eph1695-math-0001) during that exposure. Two protocols were performed, in which healthy subjects underwent passive hyperthermia (increasing intestinal temperature by ∼1.8°C) to cause a sustained increase in ventilation and reduction in urn:x-wiley:09580670:media:eph1695:eph1695-math-0002. Upon attaining hyperthermic hyperventilation, in protocol 1 (n = 10; three females) a bolus (19 ± 2 ml kg−1) of warm (∼38°C) isotonic saline was rapidly (5–10 min) infused intravenously to restore reductions in central venous pressure, whereas in protocol 2 (n = 11; five females) phenylephrine was infused intravenously (60–120 μg min−1) to return mean arterial pressure to normothermic levels. In protocol 1, hyperthermia increased ventilation (by 2.2 ± 1.7 l min−1, P < 0.01), while reducing urn:x-wiley:09580670:media:eph1695:eph1695-math-0003 (by 4 ± 3 mmHg, P = 0.04) and central venous pressure (by 5 ± 1 mmHg, P <0.01). Saline infusion increased central venous pressure by 5 ± 1 mmHg (P < 0.01), restoring it to normothermic values, but did not change ventilation or urn:x-wiley:09580670:media:eph1695:eph1695-math-0004 (P > 0.05). In protocol 2, hyperthermia increased ventilation (by 5.0 ± 2.7 l min−1, P <0.01) and reduced urn:x-wiley:09580670:media:eph1695:eph1695-math-0005 (by 5 ± 2 mmHg, P < 0.01) and mean arterial pressure (by 9 ± 7 mmHg, P <0.01). Phenylephrine infusion increased mean arterial pressure by 12 ± 3 mmHg (P < 0.01), restoring it to normothermic values, but did not change ventilation or urn:x-wiley:09580670:media:eph1695:eph1695-math-0006 (P > 0.05). The absence of a reduction in ventilation upon reloading the cardiopulmonary and arterial baroreceptors to pre‐hyperthermic levels indicates that baroreceptor unloading with hyperthermia is unlikely to contribute to hyperthermic hyperventilation in humans.