Citation

Muth CM, Radermacher P, Pittner A, Steinacker J, Schabana R, Hamich S, Paulat K, Calzia E. Int. J. Sports Med. 2003; 24(2): 104-107.

Affiliation

Division of Pathophysiology and Process Development in Anaesthesia, Department of Anaesthesiology, University Medical School Ulm, Parkstrasse 11, 89073 Ulm, Germany. claus-martin.muth@medizin.uni-ulm.de

Copyright

(Copyright © 2003, Georg Thieme Verlag)

DOI

10.1055/s-2003-38401

PMID

12669255

Abstract

Elite apnea divers have considerably extended the limits of dive depth and duration but the mechanisms allowing humans to tolerate the compression- and decompression-induced changes in alveolar gas partial pressures are still not fully understood. Therefore we measured arterial blood gas tensions and acid-base-status in two elite apnea divers during simulated wet dives lasting 3 : 55 and 5 : 05 minutes, respectively. Arterial pO2 followed the compression-(from 13.8/16.9 kPa before the dive to 30 kPa at the start of the bottom time) and decompression-induced (from 13.7/21.0 kPa to 3.3/4.9 kPa immediately after surfacing) variations of ambient pressure, while the arterial pCO2 remained within the physiologic range (3.0/3.9 kPa before diving vs. 5.7/5.9 kPa at the end of the bottom time), probably due to the CO2 storage capacity of the blood. These findings may help to explain why humans can sustain deep and long apnea dives without major increases in respiratory drive.

Language: en