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1 John Rankin Laboratory of Pulmonary Medicine, University of Wisconsin-Madison, Madison, WI, USA; Department of Pediatrics, University of Wisconsin-Madison, Madison, WI, USA; Department of Biomedical Engineering, University of Wisconsin, Madison, WI, USA
2 Department of Surgery, University of Wisconsin, Madison, WI, USA
3 Department of Medicine, University of California-Davis, Davis, CA, USA
4 VM: Anatomy, Physiology and Cell Biology, University of California, Davis, CA, USA
* To whom correspondence should be addressed. E-mail: meldridge{at}wisc.edu.
Strenuous exercise may be a significant contributing factor for development of high altitude pulmonary edema (HAPE), particularly at low or moderate altitudes. Thus, we investigated the effects of heavy cycle ergometer exercise (90% maximal effort) under hypoxic conditions in which the combined effects of a marked increase in pulmonary blood flow and non-uniform hypoxic pulmonary vasoconstriction could add significantly to augment the mechanical stress on the pulmonary microcirculation. We postulated that intense exercise at altitude would result in an augmented permeability edema. We recruited eight endurance athletes and examined their bronchoalveolar lavage fluid (BALF) for red blood cells (RBC), protein, inflammatory cells and mediators, and vascular endothelial growth factor (VEGF) at 2 and 26 hours following intense exercise under normoxic and hypoxic conditions. Following heavy exercise, under all conditions, the athletes developed a permeability edema with high BALF RBC and protein concentrations in the absence of inflammation. We found that exercise at altitude (3810 m) caused significantly greater leakage of RBC (9.2 ± 3.1 x 104 cells.ml-1) into the alveolar space than that seen with normoxic exercise (5.4 ± 1.2 x 104 cells. ml-1). At altitude, the 26-hour post exercise BALF revealed significantly higher RBC and protein concentrations suggesting an ongoing capillary leak. Interestingly, the BALF profiles following exercise at altitude are similar to that of early HAPE. These findings suggest that pulmonary capillary disruption occurs with intense exercise in healthy humans, and that hypoxia augments the mechanical stresses on the pulmonary microcirculation.
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