The effect of water immersion and acute hypercapnia on ventilatory sensitivity and cerebrovascular reactivity

The partial pressure of end tidal carbon dioxide (PETCO₂), ventilatory sensitivity to CO₂, and cerebral perfusion are augmented during thermoneutral head out water immersion (HOWI). We tested the hypotheses that HOWI and acute hypercapnia augments minute ventilation, ventilatory sensitivity to CO₂, cerebral perfusion, and cerebrovascular reactivity to CO₂. Twelve subjects (age: 24 ± 3 years, BMI: 25.3 ± 2.9 kg/m², 6 women) participated in two experimental visits: a HOWI visit (HOWI) and a matched hypercapnia visit (Dry + CO₂). A rebreathing test was conducted at baseline, 10, 30, 60 min, and post HOWI and Dry + CO₂. PETCO₂, minute ventilation, expired gases, blood pressure, heart rate, and middle cerebral artery blood velocity were recorded continuously. PETCO₂ increased throughout HOWI (baseline: 42 ± 2 mmHg; maximum at 10 min: 44 ± 2 mmHg, P ≤ 0.013) and Dry + CO₂ (baseline: 42 ± 2 mmHg; maximum at 10 min: 44 ± 2 mmHg, P ≤ 0.013) and was matched between conditions (condition main effect: P = 0.494). Minute ventilation was lower during HOWI versus Dry + CO₂ (maximum difference at 60 min: 13.2 ± 1.9 vs. 16.2 ± 2.7 L/min, P < 0.001). Ventilatory sensitivity to CO₂ and middle cerebral artery blood velocity were greater during HOWI versus Dry + CO₂ (maximum difference at 10 min: 2.60 ± 1.09 vs. 2.20 ± 1.05 L/min/mmHg, P < 0.001, and 63 ± 18 vs. 53 ± 14 cm/sec, P < 0.001 respectively). Cerebrovascular reactivity to CO₂ decreased throughout HOWI and Dry + CO₂ and was not different between conditions (condition main effect: P = 0.777). These data indicate that acute hypercapnia, matched to what occurs during HOWI, augments minute ventilation but not ventilatory sensitivity to CO₂ or middle cerebral artery blood velocity despite an attenuated cerebrovascular reactivity to CO₂.