Journal of Applied Physiology
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J Appl Physiol 93: 116-126, 2002. First published March 8, 2002; doi:10.1152/japplphysiol.01095.2001
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Vol. 93, Issue 1, 116-126, July 2002

Role of lung inflammatory mediators as a cause of exercise-induced arterial hypoxemia in young athletes

Thomas J. Wetter1, Zhuzai Xiang2, David A. Sonetti1, Hans C. Haverkamp1, Anthony J. Rice1, Adnan A. Abbasi2, Keith C. Meyer2, and Jerome A. Dempsey1

1 John Rankin Laboratory of Pulmonary Medicine, Department of Preventive Medicine, and 2 Department of Medicine, Section of Pulmonary and Critical Care Medicine, Clinical Sciences Center, University of Wisconsin, Madison, Wisconsin 53705

We examined whether lung inflammatory mediators are increased during exercise and whether pharmacological blockade can prevent exercise-induced arterial hypoxemia (EIAH) in young athletes. Seventeen healthy athletes (9 men, 8 women; 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. Lung function, arterial blood gases, and inflammatory metabolites in plasma, urine, and induced sputum were assessed. 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-arterial oxygen difference widened to 28.1 ± 6.3 Torr (drug trial) and 29.3 ± 5.7 Torr (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 trials, and urinary leukotriene E4 and 11beta -prostaglandin F2alpha levels were unchanged after exercise. Postexercise sputum revealed no significant changes in markers of inflammation. These results demonstrate that EIAH in young athletes is not attenuated with acute administration of drugs targeting 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.

histamine; leukotrienes; prostaglandins; pulmonary gas exchange; respiratory resistance; arterial blood gases


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