Respiratory and cerebral circulatory control during exercise at .21 and 2.0 atmospheres inspired pO₂

¹ Laboratory of Pharmacology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania

Respiratory and cerebral hemodynamic responses to leg exercise during respiration of air at 1.0 atm. and O₂ at 2.0 atm. were studied in relation to changes in arterial and internal jugular venous blood oxygen composition, pH, pCO₂ 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 pCO₂ toward resting levels and caused venous pCO₂ 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 pCO₂ 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 O₂ at 2.0 atm., without gross elevation of cerebral venous pO₂. Observed changes in cerebral vascular resistance during exercise at .21 and 2.0 atm. inspired pO₂ appear related to concomitant alterations in arterial pCO₂, with no detectable relationship either to brain oxygen requirement of cerebral venous acid-base composition.