Introduction: Hyperthermic hyperventilation has been well documented in humans; however, the mechanisms and the physiological relevance of such a response remains unclear. Reductions in mean arterial pressure (MAP) often coincide with hyperthermia due to heat dissipation mechanisms. Given that reductions in MAP stimulate increases in ventilation this study tested the hypothesis that arterial baroreceptor loading would reverse heat-induced increases in ventilation and accompanying decreases in end-tidal carbon dioxide (PETCO2). Methods: Eleven individuals (26 ±5 y; 71 ±15 kg) underwent passive heat stress via a water perfused suit while lying supine with their lower legs resting off the end of the bed, their knees at an angle of ~80° and their feet supported. This was done to aid venous pooling and augment heat-related reductions in MAP. Intestinal temperature (HQ Inc.), mean skin temperature, MAP (Finometer Pro), central venous pressure (central venous catheter, n=4), minute ventilation, tidal volume, respiratory rate (Parvo-Medics) and PETCO2 (capnograph) were monitored continuously. After intestinal temperature was elevated (P<0.05) 1.8 ±0.5°C, causing a sustained rise in ventilation (by 4.9 ±2.7 L.min-1, P<0.01) and reductions in PETCO2 (by 5 ±2 mm Hg, P<0.01) plus MAP (by 9 ±7 mm Hg, P<0.01), phenylephrine was infused over 5 min to restore MAP to normothermic values. Results: Phenylephrine infusion increased MAP by 11 ±5 mm Hg (P<0.01), restoring it to normothermic values, but did not change (P>0.05) ventilation or PETCO2. Intestinal and skin temperatures did not change (P>0.05) with phenylephrine infusion. See Table. Conclusion: The absence of a reduction in ventilation upon returning arterial baroreceptor loading to pre-heat stress levels indicates that hyperthermic hyperventilation is not caused by arterial baroreceptor unloading coincident with the heat stress.