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

This study tested three possible mechanisms that could explain the prolonged breath-holds (BH) previously observed in humans during submersion in 35 degrees 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 (PETCO2) was slower (P < 0.05) by 31% (compatible with increased CO2 storage capacity), but the breaking-point PETCO2 (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 (VCO2), 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 VCO2, R, and rate of rise in PETCO2 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.