Abstract

The partial pressure of end tidal carbon dioxide (PETCO 2), ventilatory sensitivity to CO 2, 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 CO 2, cerebral perfusion, and cerebrovascular reactivity to CO 2. 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 + CO 2). A rebreathing test was conducted at baseline, 10, 30, 60 min, and post HOWI and Dry + CO 2. PETCO 2, minute ventilation, expired gases, blood pressure, heart rate, and middle cerebral artery blood velocity were recorded continuously. PETCO 2 increased throughout HOWI (baseline: 42 ± 2 mmHg; maximum at 10 min: 44 ± 2 mmHg, P ≤ 0.013) and Dry + CO 2 (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 + CO 2 (maximum difference at 60 min: 13.2 ± 1.9 vs. 16.2 ± 2.7 L/min, P < 0.001). Ventilatory sensitivity to CO 2 and middle cerebral artery blood velocity were greater during HOWI versus Dry + CO 2 (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 CO 2 decreased throughout HOWI and Dry + CO 2 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 CO 2 or middle cerebral artery blood velocity despite an attenuated cerebrovascular reactivity to CO 2.

Highlights

  • Thermoneutral (~35°C) head out water immersion (HOWI) induces central hypervolemia, which causes several hemodynamic alterations, such as immediate increases in stroke volume, cardiac output, pulmonary blood flow, and cerebral blood flow (Arborelius et al 1972; Farhi et al 1977; Carter et al 2014), while heart rate is slightly reduced (Farhi et al 1977)

  • The novel findings of our investigation are despite a greater minute ventilation, ventilatory sensitivity to CO2 was lower during dry conditions when breathing a hypercapnic gas to match the hypercapnia that occurs during HOWI when compared to HOWI

  • Cerebral perfusion was lower during dry conditions while breathing a hypercapnic gas to match the hypercapnia that occurs during HOWI when compared to HOWI, while cerebrovascular reactivity to CO2 was not different between conditions

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Summary

Introduction

Thermoneutral (~35°C) head out water immersion (HOWI) induces central hypervolemia, which causes several hemodynamic alterations, such as immediate increases in stroke volume, cardiac output, pulmonary blood flow, and cerebral blood flow (Arborelius et al 1972; Farhi et al 1977; Carter et al 2014), while heart rate is slightly reduced (Farhi et al 1977). Blood pressure does not change (Bonde-Petersen et al 1992; Sramek et al 2000; Watenpaugh et al 2000) or is slightly attenuated (Craig and Dvorak 1966; Sackett et al 2017) during HOWI due to a reduction in total peripheral resistance. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society. The partial pressure of end tidal carbon dioxide (PETCO2) is increased during HOWI (Sackett et al 2017, 2018), which indicates carbon dioxide (CO2) retention (Lanphier and Bookspan 1999)

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