We investigated whether heat-induced hyperventilation can be voluntarily prevented, and, if so, how this modulates respiratory mechanics and cerebral blood flow in resting heated humans. In two separate trials, 10 healthy men were passively heated using lower body hot-water immersion and a water-perfused garment covering their upper body (both 41°C) until esophageal temperature (T_es ) reached 39°C or volitional termination. In each trial, participants breathed normally (normal-breathing) or voluntarily controlled minute ventilation (V_E ) at a level equivalent to that observed after 5 min of heating (controlled-breathing). Respiratory gases, middle cerebral artery blood velocity (MCAV), work of breathing, and end-expiratory and inspiratory lung volumes were measured. During normal-breathing, V_E increased as T_es rose above 38.0 ± 0.3°C, whereas controlled-breathing diminished the increase in V_E (V_E at T_es = 38.6°C: 25.6 ± 5.9 and 11.9 ± 1.3 L min^-1 during normal- and controlled-breathing, respectively, P < 0.001). During normal-breathing, end-tidal CO₂ pressure and MCAV decreased with rising T_es , but controlled-breathing diminished these reductions (at T_es = 38.6°C, 24.7 ± 5.0 vs. 39.5 ± 2.8 mmHg; 44.9 ± 5.9 vs. 60.2 ± 6.3 cm sec^-1 , both P < 0.001). The work of breathing correlated positively with changes in V_E (P < 0.001) and was lower during controlled- than normal-breathing (16.1 ± 12.6 and 59.4 ± 49.5 J min^-1 , respectively, at heating termination, P = 0.013). End-expiratory and inspiratory lung volumes did not differ between trials (P = 0.25 and 0.71, respectively). These results suggest that during passive heating at rest, heat-induced hyperventilation increases the work of breathing without affecting end-expiratory lung volume, and that voluntary control of breathing can nearly abolish this hyperventilation, thereby diminishing hypocapnia, cerebral hypoperfusion, and increased work of breathing.

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