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.