Cerebral oxidative metabolism is decreased with extreme apnea in humans; impact of acidosis

Abstract

Prolonged apnea in humans is reflected in progressive hypoxemia and acidosis. Here, we explore the cerebral metabolic responses under extreme hypoxia and acidosis associated with prolonged apnea. We hypothesized that the cerebral metabolic rate for oxygen (CMRO2) will be reduced near the termination of apnea, attributed in part to the acidosis. Fourteen elite apnea-divers performed a maximal apnea (range: 3:36 to 7:26 minutes) under dry laboratory-conditions. In a subset study with the same divers, the impact of acidosis on cerebral metabolism in the background of hypoxia was determined using varying levels of hypercapnic breathing. In both studies the CMRO2 was calculated from the product of cerebral blood flow (ultrasound) and the radial artery-jugular venous oxygen content difference. Non-oxidative cerebral metabolism was calculated from the ratio of oxygen and carbohydrate (lactate and glucose) metabolism. The CMRO2 was reduced by ~29% (P<0.01, Cohen’s d = 1.18) near the termination of apnea when compared to baseline, but non-oxidative metabolism remained unaltered. In the subset study, in the background of hypoxia (arterial oxygen tension: ~38.4 mmHg), severe acidosis (arterial pH: ~7.30), but not mild-acidosis (arterial pH: 7.38), significantly depressed the CMRO2 (~17%, P=0.04, Cohen’s d = 0.87). Similarly to the apnea, there was no change in the non-oxidative metabolism. These data indicate that hypercapnicinduced acidosis can in part explain the reduction in CMRO2 near apnea breakpoint. This acidosis-induced oxygen conservation may protect the brain against severe hypoxemia associated with prolonged apnea.