Does arterial PCO2 interfere with hypoxia in muscular metabolism in man?

To answer the question whether PCO2 affects the muscular metabolism, PO2, PCO2, pH, lactic acid concentration and hemoglobin were measured in the efferent muscular venous blood from common flexor digitorum, during forearm rhythmic exercise corresponding to VO2max. Exercise was carried out either in hypocapnic hypoxia i.e. in permanent high altitude residents and translocated lowlanders, or in hypercapnic hypoxia i.e. in chronic obstructive lung disease (COLD) patients. The results show that, during exercise: i) PO2 in muscular venous blood remains around 20 Torr in normoxia and hypocapnic hypoxia and even higher (25 torr) in COLD patients, despite low arterial PaO2, and ii) arterial and/or local PCO2 play a role in the control of the muscular blood flow. But we cannot conclude that a change in PaCO2 affects muscular metabolism itself, because lactic acid in the muscular venous blood, that we used to check this effect, is likely dependent on mechanisms other than anaerobic glycolysis, such as a change in lactic acid efflux from the myocytes. The increase in muscular venous PCO2 may enhance the myocyte permeability to lactic acid during exercise.