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

 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 hypercapnic-induced 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.