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

Abstract

Prolonged apnea in humans is reflected in progressive hypoxemia and hypercapnia. Here, we explore the cerebral metabolic responses under extreme hypoxia and hypercapnia 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 hypercapnia. Fourteen elite apnea-divers performed a maximal apnea (range: 3:36 to 7:26 min) under dry laboratory-conditions. In a subset study with the same divers, the impact of hypercapnia on cerebral metabolism was determined using varying levels of hypercapnic breathing, in the background of similar hypoxia. In both studies the CMRO₂ was calculated from the product of cerebral blood flow (ultrasound) and the radial artery-internal 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 similar backgrounds of hypoxia (arterial O₂ tension: ∼38.4 mmHg), severe hypercapnia (arterial CO₂ tension: ∼58.7 mmHg), but not mild-hypercapnia (arterial CO₂ tension: ∼46.3 mmHg), 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 hypercapnia can in part explain the reduction in CMRO₂ near apnea breakpoint. This hypercapnic-induced oxygen conservation may protect the brain against severe hypoxemia associated with prolonged apnea.

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