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1 John Rankin Laboratory of Pulmonary Medicine, Population Health Sciences, University of Wisconsin, Madison, WI, USA; Department of Pediatrics, University of Wisconsin, Madison, WI, USA
2 John Rankin Laboratory of Pulmonary Medicine, Population Health Sciences, University of Wisconsin, Madison, WI, USA
3 Department of Pediatrics, University of Wisconsin, Madison, WI, USA
* To whom correspondence should be addressed. E-mail: meldridge{at}wisc.edu.
We hypothesized that increasing exercise intensity recruits dormant arteriovenous intrapulmonary shunts, which may contribute to the widened A-aDO2 seen with exercise. Twenty-three healthy volunteers (13 males and 10 females, aged 23-48 years) with normal lung function and a wide range of fitness (mean VO2max = 126% predicted; range = 78-200% predicted) were studied using agitated saline contrast echocardiography (4-chamber apical view). All twenty-three subjects had normal resting contrast echocardiograms without evidence of intracardiac or intrapulmonary shunting. However, with cycle ergometer exercise, 21/23 (91%) of the subjects showed a delayed (>3 cardiac cycles) appearance of contrast bubbles in the left heart. This pattern is consistent with passage of contrast bubbles through the pulmonary circulation. Since the contrast bubbles are known to be significantly larger than pulmonary capillaries, we propose that they are traveling through direct arteriovenous intrapulmonary shunts. In all cases, the intrapulmonary shunting developed at submaximal oxygen consumptions (%VO2max = 59 ± 20 (SD)) and once evident persisted at all subsequent work rates. Within 3 minutes of terminating the exercise, the contrast echocardiograms with bubble injection showed no evidence of intrapulmonary shunting. These dynamic shunts will contribute significantly to the widened A-aDO2 seen with exercise. They may also act as a protective parallel vascular network limiting the rise in regional pulmonary vascular pressure while preserving cardiac output during exercise.
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