Abstract
In more than a thousand chronic obstructive lung disease (COLD) patients we have observed in six cases, that exercise-induced hypercapnia was accompanied by a concomitant improvement in arterial oxygen tension (PaO2) and a decrease in the alveolo-arterial O2. This behaviour was not due to technical errors. We explained the increase in PaO2 during exercise by three nonmutually exclusive mechanisms: 1) an increase in the respiratory quotient; 2) the exercise induced increase in alveolar ventilation, although inadequate to match the increase in CO2 production, would be redistributed to previously poorly ventilated regions of the lung, these regions therefore receiving enough oxygen to arterialize the blood flowing through the alveolar capillaries; 3) alternatively, perfusion would be redistributed in a more efficient way during exercise, so that even in the presence of hypoventilation, oxygenation would be improved.
