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Original Research: ASTHMA |

Exercise-Induced Asthma May Be Associated With Diminished Sweat Secretion Rates in Humans

Chan Park, MD; Christopher Stafford, MD, FCCP; Warren Lockette, MD
Author and Funding Information

*From the Departments of Emergency Medicine (Dr. Park) and Clinical Investigation (Dr. Lockette), and the Division of Pulmonary and Critical Care Medicine (Dr. Stafford), Naval Medical Center, San Diego, CA.

Correspondence to: Warren Lockette, MD, Clinical Investigations Department, Naval Medical Center, San Diego, 34800 Bob Wilson Dr, Mail Code KCA, San Diego, CA 92134; e-mail: ridiculo@umich.edu


The comments expressed represent the personal opinions of the authors and they do not necessarily reflect the views of the Department of the Navy or the Department of Defense.

The authors have reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/misc/reprints.shtml).


Chest. 2008;134(3):552-558. doi:10.1378/chest.08-0366
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Background:  Muscarinic receptor agonists increase water secretion from the acinar cells of respiratory, sweat, salivary, and lacrimal glands. Mice lacking the gene for aqueous water channel aquaporin (Aqp) 5 exhibit methacholine-induced bronchiolar hyperreactivity when compared to normal mice. Individuals with asthma also have enhanced airway responsiveness to methacholine and diminished airway hydration. Because Aqp5 in humans is also expressed in respiratory, sweat, salivary, and lacrimal glands, we hypothesized that those individuals with exercise-induced asthma and excessive bronchiolar reactivity should also have decreased muscarinic receptor-dependent sweat, salivary, and tear gland secretions.

Methods:  Healthy, athletic subjects who are suspected of having exercise-induced bronchospasm were recruited, and FEV1 values were determined following provocative airway challenges with methacholine. Measurements of pilocarpine-induced sweat secretion were taken in 56 volunteers, and some additional subjects also had timed collections of saliva and tear production.

Results:  Subjects manifesting excessive airway reactivity demonstrated by exaggerated methacholine-induced reductions in FEV1 also had diminished values for pilocarpine-induced sweat secretion (n = 56; r = − 0.59; p < 0.0001). The rate of pilocarpine-stimulated sweat secretion in our subjects correlated highly with salivary flow rate (r = 0.69; p < 0.0001) and tearing rate (r = 0.86; p < 0.001).

Conclusion:  Hyperhidrosis, sialorrhea, and excessive tearing are traits that may indicate a phenotype that predicts resistance to hyperactive airway diseases such as exercise-induced asthma in humans.

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