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

Abstract

We investigated the role of lung volume-induced changes in cardiac output (Q̇) on cerebrovascular regulation during prolonged apnoea. Fifteen elite apnoea divers (1F; 185 ± 7 cm, 82 ± 12 kg, 29 ± 7 years) attended the laboratory on two separate occasions and completed maximal breath-holds at total lung capacity (TLC) and functional residual capacity (FRC) to elicit disparate cardiovascular responses. Mean arterial pressure (MAP), internal jugular venous pressure (IJVP) and arterial blood gases were measured via cannulation, global cerebral blood flow (gCBF) was quantified by ultrasound and cardiac output via photoplethysmography. At FRC, stroke volume (SV) and cardiac output (Q̇) did not change from baseline (P>0.05). In contrast, during the TLC trial SV and Q̇ were decreased until 80% and 40% of apnoea, respectively (P<0.05). During the TLC trial, gCBF was significantly lower at 20%, but subsequently increased so that cerebral oxygen delivery was comparable to the FRC trial. IJVP was significantly higher throughout the TLC trial in comparison to FRC. MAP rose progressively in both trials but to a greater extent at TLC resulting in a comparable cerebral perfusion pressure between trials by apnoea end. In summary, although lung volume has a profound effect on Q̇ during prolonged breath-holding, these changes do not translate to the cerebrovasculature due to the greater sensitivity of CBF to arterial blood gases and MAP; regulatory mechanisms that facilitate the maintenance of cerebral oxygen delivery.

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