Maximal breath-holding time and immediate tissue CO₂ storage capacity during head-out immersion in humans

Abstract

This study tested three possible mechanisms that could explain the prolonged breath-holds (BH) previously observed in humans during submersion in 35°C (thermoneutral) water, including a reduced metabolism, a decreased CO₂ sensitivity, and an increased CO₂ storage capacity. During immersed BH (n = 13), maximal BH time was prolonged by 20.3% (P < 0.05), the rate of rise of end tidal partial pressure of carbon dioxide (P _ETCO₂) was slower (P < 0.05) by 31 % (compatible with increased CO₂ storage capacity), but the breaking-pointP _ETCO₂ (CO₂ sensitivity) and the rate of decrease of end tidal partial pressure of oxygen (metabolism) were unchanged. During air breathing (n = 5), immersion resulted in a significant decrease in tidal volume (11%), but did not affect O₂ uptake, CO₂ elimination$(\dot VCO_2 )$, or respiratory exchange ratio (R). During a 4-min CO₂-rebreathing (n = 9), the slope of the hypercapnic ventilatory response curve (CO₂ sensitivity index) was unchanged by immersion, but the significantly decreased$\dot VCO_2$,R, and rate of rise inPETCO₂ during immersed rebreathing indicated an increase in the acute CO₂ storage capacity (SC). The estimated SC (n = 9), based on an assumed cellular respiratory quotient of 0.8, were 0.52 (SEM 0.03) ml · kg⁻¹ · mmHg⁻¹ for control and 0.66 (SEM 0.04) ml · kg⁻¹ · mmHg⁻¹ for immersion. A proposed mechanism for the increased SC during immersed BH and during immersed rebreathing is that immersion accelerated CO₂ redistribution in the body by increasing perfusion to some low-perfused, low-metabolism, and high-capacity tissues, such as resting skeletal muscle. The increased SC during immersion, however, did not correlate with the prolonged BH duration (n = 9,P > 0.05). The mechanism of the latter remains unclear.