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Articles in PresS, published online ahead of print March 8, 2002
J Appl Physiol, 10.1152/jap.01095.2001
Submitted on November 1, 2001
Accepted on March 5, 2002
1 Department of Preventive Medicine, University of Wisconsin - Madison, Madison, WI, USA
2 Department of Medicine, Section of Pulmonary and Critical Care Medicine, Clinical Sciences Center, University of Wisconsin - Madison, Madison, WI, USA
* To whom correspondence should be addressed. E-mail: tjwetter{at}yahoo.com.
We examined whether lung inflammatory mediators are increased during exercise and whether pharmacologic blockade can prevent exercise-induced exercise hypoxemia (EIAH) in young athletes. Seventeen healthy athletes (9 males, 8 females; age 23 ± 3 yr) with varying degrees of EIAH completed maximal incremental treadmill exercise tests after administration of fexofenadine, zileuton, and nedocromil sodium or placebo in a randomized double-blind crossover study. Maximal flow volume loops, total respiratory resistance, and exhaled nitric oxide were obtained both pre- and post-exercise. Arterial blood gases were measured during exercise. Inflammatory metabolites in plasma, urine, and cell counts and mediator levels in induced sputum were measured before and after exercise. Drug administration did not improve EIAH or gas exchange during exercise. At maximal exercise, oxygen saturation fell to 91.4 ± 2.6% (drug trial) and 91.9 ± 2.1% (placebo trial) and alveolar to arterial oxygen difference (A-aDO2) widened to 28.1 ± 6.3 mmHg (drug trial) and 29.3 ± 5.7 mmHg (placebo trial). Oxygen consumption, ventilation and other exercise variables were similarly unaffected by drug treatment. Although plasma histamine increased with exercise, values did not differ between drug and placebo trials and urinary leukotriene E4 and 11ß-Prostaglandin F2
levels were unchanged after exercise. Post-exercise sputum did not reveal significant changes in markers of inflammation. These results demonstrate that EIAH in young athletes is not attenuated with acute administration of drugs that target histamine and bioactive lipids. We conclude that airway inflammation is of insufficient magnitude to cause impairments in gas exchange and does not appear to be linked to EIAH in healthy young athletes.
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