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Intrapulmonary shunting and pulmonary gas exchange during normoxic and hypoxic exercise in healthy humans

¹Department of Population Health Sciences, John Rankin Laboratory of Pulmonary Medicine; ²Department of Pediatrics; and ³Department of Biomedical Engineering, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin

Submitted 20 February 2007 ; accepted in final form 13 February 2008

Exercise-induced intrapulmonary arteriovenous shunting, as detected by saline contrast echocardiography, has been demonstrated in healthy humans. We have previously suggested that increases in both pulmonary pressures and blood flow associated with exercise are responsible for opening these intrapulmonary arteriovenous pathways. In the present study, we hypothesized that, although cardiac output and pulmonary pressures would be higher in hypoxia, the potent pulmonary vasoconstrictor effect of hypoxia would actually attenuate exercise-induced intrapulmonary shunting. Using saline contrast echocardiography, we examined nine healthy men during incremental (65 W + 30 W/2 min) cycle exercise to exhaustion in normoxia and hypoxia (fraction of inspired O₂ = 0.12). Contrast injections were made into a peripheral vein at rest and during exercise and recovery (3–5 min postexercise) with pulmonary gas exchange measured simultaneously. At rest, no subject demonstrated intrapulmonary shunting in normoxia [arterial PO₂ (Pa_O2) = 98 ± 10 Torr], whereas in hypoxia (Pa_O2 = 47 ± 5 Torr), intrapulmonary shunting developed in 3/9 subjects. During exercise, 90% (8/9) of the subjects shunted during normoxia, whereas all subjects shunted during hypoxia. Four of the nine subjects shunted at a lower workload in hypoxia. Furthermore, all subjects continued to shunt at 3 min, and five subjects shunted at 5 min postexercise in hypoxia. Hypoxia has acute effects by inducing intrapulmonary arteriovenous shunt pathways at rest and during exercise and has long-term effects by maintaining patency of these vessels during recovery. Whether oxygen tension specifically regulates these novel pathways or opens them indirectly via effects on the conventional pulmonary vasculature remains unclear.

alveolar-to-arterial oxygen tension difference; contrast echocardiography; pulmonary circulation; exercise-induced arterial hypoxemia

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