Summary
Characteristics of cerebrovascular, cardiorespiratory and autonomic responses to CO2 in breath-hold divers.
Hypercapnic cerebrovascular reactivity is decreased in obstructive sleep apnea perhaps as a result of repeated apneas.
To test the hypothesis that repeated apneas blunt cerebrovascular reactivity to hypercapnia, we studied breath hold divers and determined cerebrovascular reactivity by measuring changes in middle cerebral artery velocity (MCAV, cm/s) per mmHg change in end-tidal partial CO2 pressure (PETCO2) in response to two hyperoxic hypercapnia rebreathing maneuvers (modified Read protocol) in elite breath-hold divers (BHD, N=7) and non-divers (ND, N=7).
In addition, ventilation and central hemodynamics (beat-to-beat stroke volume measurement with Modelflow technique) were
determined.
Ventilatory responses to hypercapnia were blunted in BHD vs ND largely due to lower breathing frequency.
Cerebrovascular reactivity did not differ between groups (3.7±1.4 vs 3.4±1.3 %/mmHg PETCO2 in BHD and ND, respectively; p=0.90) and the same was found for cerebral vascular resistance and MCAV recovery to baseline after termination of the CO2
challenge.
Cardiovascular parameters were not changed significantly during rebreathing in either group, except for small increase in mean arterial pressure for both groups.
Our findings indicate that regulation of cerebral circulation in response to hypercapnia is intact in elite breath-hold divers, potentially as a protective mechanism against chronic intermittent cerebral hypoxia and/or hypercapnia that occurs during breath-hold diving.
These data also suggest that factors other than repeated apneas contribute to the blunting of cerebrovascular reactivity in conditions like sleep apnea.