Data on pulmonary gas exchange were collected in breathhold dives to 90 feet in a tank and in open-sea breathhold dives to depths of 217.5 and 225 feet. Thoracic blood volume displacements were measured at depths of 25, 50, 90, and 130 feet, by use of the impedance plethysmograph. The open-sea dives were carried out with an average speed of descent of 3.95 feet per second and an average rate of ascent of 3.50 feet per second. End-dive alveolar oxygen tensions did not fall below 36 millimeters of mercury, while alveolar carbon dioxide tension did not rise above 40 millimeters of mercury except in one case. These findings indicate that for diver Croft, who has unusual lung capacity, neither hypoxia nor hypercapnia determined the depth limits under those conditions. At depths of 90 and 130 feet blood was forced into the thorax, amounting to 1047 and 850 milliliters respectively.

Twenty-one subjects were exposed to 1.5% CO2 in 21% O2 for 42 days with pre- and postexposure periods on air for 9 days. Respiratory minute volume (Ve) and alveolar pCO2 were increased throughout the exposure to CO2. After transition to air Ve decreased, while pCO2 remained elevated for 9 days. CO2 retention with uncompensated respiratory acidosis lasted for 23 days. CO2 excretion was increased during the 9-day recovery period indicating release of CO2 from the CO2 stores. Oxygen consumption did not change significantly during the experiment. Respiratory acclimatization to CO2 involved a continuous increase in tidal volume while the respiratory rate declined slowly after an initial increase. Changes in respiratory pattern were associated with an increase in physiological and anatomical dead space. A significant increase in the arterial-alveolar pCO2 and alveolar-arterial pO2 gradient indicated the development of an alveolar dead space. The ventilatory response to 5% CO2 was markedly reduced at the end of CO2 exposure. chronic CO2 exposure; chronic hypercapnia; chronic respiratory acidosis Submitted on August 31, 1961

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