Forced vital capacity and not central chemoreflex predicts maximal hyperoxic breath-hold duration in elite apneists.

The determining mechanisms of a maximal hyperoxic apnea duration in elite apneists have remained unexplored. We tested the hypothesis that maximal hyperoxic apnea duration in elite apneists is related to forced vital capacity (FVC) but not the central chemoreflex (for CO2). Eleven elite apneists performed a maximal dry static-apnea with prior hyperoxic (100% oxygen) pre-breathing, and a central chemoreflex test via a hyperoxic re-breathing technique (hyperoxic-hypercapnic ventilatory response: HCVR); expressed as the increase in ventilation (pneumotachometry) per increase in arterial CO2 tension (PaCO2; radial artery). FVC was assessed using standard spirometry. Maximal apnea duration ranged from 807 to 1262s (mean=1034s). Average HCVR was 2.0±1.2Lmin-1mmHg-1 PaCO2. The hyperoxic apnea duration was related to the FVC (r2=0.45, p<0.05), but not the HCVR (r2<0.01, p>0.05). These findings were interpreted to suggest that during a hyperoxic apnea, a larger initial lung volume prolongs the time before reaching intolerable discomfort associated with pending lung squeeze, while CO2 sensitivity has little impact.

Hypercapnia is essential to reduce the cerebral oxidative metabolism during extreme apnea in humans.

The cerebral metabolic rate of oxygen (CMRO2) is reduced during apnea that yields profound hypoxia and hypercapnia. In this study, to dissociate the impact of hypoxia and hypercapnia on the reduction in CMRO2, 11 breath-hold competitors completed three apneas under: (a) normal conditions (NM), yielding severe hypercapnia and hypoxemia, (b) with prior hyperventilation (HV), yielding severe hypoxemia only, and (c) with prior 100% oxygen breathing (HX), yielding the greatest level of hypercapnia, but in the absence of hypoxemia. The CMRO2 was calculated from the product of cerebral blood flow (ultrasound) and the radial artery-jugular venous oxygen content difference (cannulation). Secondary measures included net-cerebral glucose/lactate exchange and nonoxidative metabolism. Reductions in CMRO2 were largest in the HX condition (-44 ± 15%, p < 0.05), with the most severe hypercapnia (PaCO2 = 58 ± 5 mmHg) but maintained oxygen saturation. The CMRO2 was reduced by 24 ± 27% in NM ( p = 0.05), but unchanged in the HV apnea where hypercapnia was absent. A net-cerebral lactate release was observed at the end of apnea in the HV and NM condition, but not in the HX apnea (main effect p < 0.05). These novel data support hypercapnia/pH as a key mechanism mediating reductions in CMRO2 during apnea, and show that severe hypoxemia stimulates lactate release from the brain.

Surviving Without Oxygen: How Low Can the Human Brain Go?

Bailey, Damian M., Christopher K. Willie, Ryan L. Hoiland, Anthony R. Bain, David B. MacLeod, Maria A. Santoro, Daniel K. DeMasi, Andrea Andrijanic, Tanja Mijacika, Otto F. Barak, Zeljko Dujic, and Philip N. Ainslie. Surviving without oxygen: how low can the human brain go? High Alt Med Biol 18:73-79, 2017.-Hypoxic cerebral vasodilation is a highly conserved physiological response coupling cerebral O2 delivery (CDO2) to metabolic demand with increasingly important roles identified for the red blood cell (sensor) and nitric oxide (effector). In the current article, we reexamine previously published cerebral blood flow (CBF) and arterial blood gas data obtained in freedivers and mountaineers, extreme athletes in whom the lowest arterial partial pressures of O2 (19-23 mmHg) and greatest extremes of carbon dioxide (16-61 mmHg) were recorded during (acute) maximal static dry apnea or (chronic) exposure to terrestrial high altitude. Data highlight compensatory increases in CBF (+96% in freedivers to +209% in mountaineers relative to normoxic baseline controls) that were sufficient to sustain CDO2 (+24% in freedivers to +183% in mountaineers) even in the face of the most severe reductions in arterial O2 content (-61% in freedivers to -9% in mountaineers) reported in the literature, consistent with the conservation of mass principle. These unique findings highlight to what extent cerebral vasodilation likely contributes toward these athletes' extraordinary abilities to survive in such harsh environments characterized by physiological extremes of hypoxemia, alkalosis, and acidosis helping define the human brain's remarkable limits of tolerance.