Regulation of Brain Blood Flow and Oxygen Delivery in Elite Breath-Hold Divers

Abstract

The roles of involuntary breathing movements (IBMs) and cerebral oxygen delivery in the tolerance to extreme hypoxemia displayed by elite breath-hold divers are unknown. Cerebral blood flow (CBF), arterial blood gases (ABGs), and cardiorespiratory metrics were measured during maximum dry apneas in elite breath-hold divers (n = 17). To isolate the effects of apnea and IBM from the concurrent changes on ABG, end-tidal forcing ('clamp') was then used to replicate an identical temporal pattern of decreasing arterial PO 2 (PaO 2 ) and increasing arterial PCO 2 (PaCO 2 ) while breathing. End-apnea PaO 2 ranged from 23 to 37 mm Hg (30 ± 7 mm Hg). Elevation in mean arterial pressure was greater during apnea than during clamp reaching +54 ± 24% versus 34 ± 26%, respectively; however, CBF increased similarly between apnea and clamp (93.6 ± 28% and 83.4 ± 38%, respectively). This latter observation indicates that during the overall apnea period IBM per se do not augment CBF and that the brain remains sufficiently protected against hypertension. Termination of apnea was not determined by reduced cerebral oxygen delivery; despite 40% to 50% reductions in arterial oxygen content, oxygen delivery was maintained by commensurately increased CBF.

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

“…Because a prolonged breath‐hold yields both extreme levels of hypoxia and hypercapnia (Willie et al . ; Bain et al . a ), it stands to reason that, in contrast to hypoxia alone, the CMRO 2 may be reduced during apnoea.…”

Influence of lung volume on the interaction between cardiac output and cerebrovascular regulation during extreme apnoea

“…However, findings from Willie et al . () demonstrate the maintenance of CDO 2 at the end of a maximal apnoea at TLC. Cerebral oxygen delivery was, however, reduced below baseline during replication of the arterial blood gas profile of a maximal apnoea via rapid manipulations of end‐tidal gases during spontaneous breathing (Willie et al .…”

“…); there are also anecdotal reports of syncope at apnoea end, when hypoxaemia is most severe (Willie et al . ). These findings suggest that cerebral blood flow (CBF) and oxygen delivery (CDO 2 ) might be attenuated by cardiac restriction secondary to high lung volumes.…”

“…Cerebral oxygen delivery was, however, reduced below baseline during replication of the arterial blood gas profile of a maximal apnoea via rapid manipulations of end‐tidal gases during spontaneous breathing (Willie et al . ). During this simulated apnoea, despite comparable arterial partial pressure of oxygen () and carbon dioxide (), mean arterial pressure (MAP) was ∼50% lower than during apnoea, highlighting the importance of cerebral perfusion pressure.…”

“…; Willie et al . ); they also tolerate forceful diaphragmatic contractions termed ‘involuntary breathing movements’ (IBMs) for up to 50% of the apnoea duration (Dujic et al . ).…”