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1 Acceleration Section, Aerospace Medical Laboratory, Wright Patterson Air Force Base, Dayton, Ohio
Inertial effects on pulmonary gas exchange were measured during forward acceleration at 6 and 8 g. During the 3-min-acceleration plateau, O2 uptake decreased a mean of 16 ml/min at 6 g and 71 ml/min at 8 g. CO2 excretion increased 62 ml/min at 6 g and only 30 ml/min at 8 g. The respiratory exchange ratio increased from 0.83 to 1.17 at 6 g and 1.24 at 8 g. There was a marked increase in the minute volume of ventilation. During the recovery periods, an additional 470 ml O2 was consumed; 360 ml CO2 was excreted above control values for 6 g; 650 ml O2 was consumed; and 580 ml CO2 was excreted for 8 g. The increased metabolic work at the g levels studied was small, representing approximately 150 ml/min O2. The respiratory exchange ratio was well above 1.00, and a large O2 debt accumulated. Exercise at 8 g resulted in a marked increase in O2 uptake, which eliminated the possibility that the observed effects were caused by impaired alveolar ventilation or diffusing capacity. Cardiac output has been reported essentially unchanged or slightly increased during forward acceleration and, therefore, the response cannot be explained by a decrease in pulmonary blood flow. The evidence suggests that the diminution in O2 exchange and impairment in CO2 excretion represents a combination of alteration in the pulmonary ventilation to blood flow ratios and peripheral arterial shunting.
Note:
(With the Technical Assistance of Justin L. Taylor)
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