Tissue oxygen and carbon dioxide stores and breath-hold diving in humans.

Alveolar gas exchange was studied in 11 submerged subjects during and after 75-s breath holds with or without a transient increase of ambient pressure to 3 ATA (20 msw). During surface breath holds (SBH), cardiac index fell to 73% of eupneic control but was partially restored at depth to 88% of control during breath-hold dives (BHD). O2 uptake fell to 84% of control during SBH and was restored to control level during BHD. The turnover of O2 stores was much slower during SBH than during the ensuing recovery. Carbon dioxide store dynamics were markedly slowed after BHD. We conclude that SBH and BHD are associated with large shifts in tissue O2 and CO2 stores and that much of these shifts can be explained by primary circulatory events. The changes in turnover rate for tissue O2 and CO2 stores could not be explained by the cardiac index changes alone but were compatible with peripheralization of venous blood volume and preferential peripheral vasoconstriction induced by apnea with elevated intrathoracic pressure during SBH. The transient compression during BHD reversed these central and peripheral circulatory changes by counteracting the increase in intrathoracic pressure.