The effect of light and moderate exercise (400, 625, and 700 kpm/min) on the alveolar‐arterial O 2 tension difference (A—aD) in the sitting position was studied in healthy, young adults by comparing the mean alveolar and arterial gas tensions determined over a 3 min rest period and over the ensuing 5th and 6th min of exercise. Arterial gas tensions were obtained from continuous measurements of arterial pH, oxygen saturation, and temperature. Alveolar O 2 tension was calculated by the alveolar gas equation, substituting arterial for alveolar CO 2 . At all three levels of exercise the arterial P O2 increased significantly by about 5mm Hg. In the experiments at 625 kpm/min, in which the respiratory exchange ratio (R) was also determined, A–aD decreased from a mean value of 14.7 mm Hg at rest, to 11.0 mm Hg during exercise. In the experiments at 400 and 700 kpm/min, where no ventilatory measurements were made in order to avoid interference with free respiration, it was found that, for the range of possible R values, the A–aD remained unchanged or decreased during exercise. The arterial O 2 deficit, i. e. the difference in O 2 content between pulmonary end‐capillary blood and systemic arterial blood, was calculated to decrease from a mean value of 0.27 vol‐% O 2 at rest, to 0.18–0.22 vol‐% O 2 during exercise. Likewise, the calculated total venous admixture to the systemic blood flow decreased from a mean value of 4.7 per cent of cardiac output at rest, to 1.7–1.8 per cent of cardiac output during exercise. All the above changes are ascribed mainly to a reduction of the virtual shunt created by uneven distribution of alveolar ventilation to pulmonary capillary blood flow.
No takes yet. Share an insight, caveat, or question.
Hesser et al. (1965) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: