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This Article Full Text Full Text (PDF) All Versions of this Article: 582/2/723    most recent jphysiol.2007.128991v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Ivancev, V. Articles by Dujic, Z. Search for Related Content PubMed PubMed Citation Articles by Ivancev, V. Articles by Dujic, Z. Related Collections Cardiovascular

¹ Department of Physiology, University of Split School of Medicine, Split, Croatia
² Department of Anaesthesiology, Mayo Clinic College of Medicine, Rochester, MN, USA

Hypercapnic cerebrovascular reactivity is decreased in obstructive sleep apnoea and congestive heart disease perhaps as a result of repeated apnoeas. To test the hypothesis that repeated apnoeas 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^–1) per mmHg change in end-tidal partial pressure of CO₂ () in response to two hyperoxic hypercapnia rebreathing manoeuvres (modified Read protocol) in elite breath-hold divers (BHD, n = 7) and non-divers (ND, n = 7). In addition, ventilation and central (beat-to-beat stroke volume measurement with Modelflow technique) haemodynamics were determined. Ventilatory responses to hypercapnia were blunted in BHD versus ND largely due to lower breathing frequency. Cerebrovascular reactivity did not differ between groups (3.7 ± 1.4 versus 3.4 ± 1.3% mmHg^–1 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 a small increase in mean arterial pressure for both groups. Our findings indicate that the regulation of the cerebral circulation in response to hypercapnia is intact in elite breath-hold divers, potentially as a protective mechanism against the chronic intermittent cerebral hypoxia and/or hypercapnia that occurs during breath-hold diving. These data also suggest that factors other than repeated apnoeas contribute to the blunting of cerebrovascular reactivity in conditions like sleep apnoea.

(Received 24 January 2007; accepted after revision 4 April 2007; first published online 5 April 2007)
Corresponding author Z. Dujic: Department of Physiology, University of Split School of Medicine, Soltanska 2, 21000 Split, Croatia. Email: zdujic{at}bsb.mefst.hr