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Respiratory and cerebral hemodynamic responses to leg exercise during respiration of air at 1.0 atm. and O 2 at 2.0 atm. were studied in relation to changes in arterial and internal jugular venous blood oxygen composition, pH, pCO 2 and bicarbonate concentration. The hyperpnea of exercise at 1.0 atm. was accompanied by arterial and venous acidemia and hypocapnia. Oxygen administration during exercise at 2.0 atm. lowered ventilation, restored arterial pH and pCO 2 toward resting levels and caused venous pCO 2 to rise above the resting level; cerebral venous cH remained elevated in spite of reduction of blood fixed acid concentration. The ventilatory response to exercise showed positive correlations with work load, oxygen consumption, and with changes in arterial and internal jugular venous cH and fixed acid. The observed negative correlations of changes in respiratory minute volume with changes in arterial and internal jugular venous pCO 2 and bicarbonate concentration suggest that these factors are functions, rather than primary determinants, of ventilation in exercise. Cerebral hemodynamics and oxygen consumption were not significantly altered by exercise at 1.0 atm. The data suggest either a slight elevation of cerebral blood flow or reduction in the rate of cerebral oxygen consumption during exercise breathing O 2 at 2.0 atm., without gross elevation of cerebral venous pO 2 . Observed changes in cerebral vascular resistance during exercise at .21 and 2.0 atm. inspired pO 2 appear related to concomitant alterations in arterial pCO 2 , with no detectable relationship either to brain oxygen requirement of cerebral venous acid-base composition. Submitted on November 25, 1958
Lambertsen et al. (Sun,) studied this question.