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Published ahead of print on May 7, 2009
Am. J. Respir. Cell Mol. Biol. 2009, doi:10.1165/rcmb.2009-0038OC
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Submitted on January 29, 2009
Accepted on May 6, 2009

Repeated Bouts of Moderate Intensity Aerobic Exercise Reduce Airway Reactivity in a Murine Asthma Model

Matt Hewitt1, Kim Estell1, Ian C. Davis2, and Lisa M Schwiebert3*

1 Physiology and Biophysics, University of Alabama at Birmingham, Birmingham, Alabama, United States, 2 Veterinary Biosciences, Ohio State University, Columbus, Ohio, United States, 3 Physiology and Biophysics, University of Alabama at Birmingham, MCLM 966, Birmingham, Alabama, 35294-0005, United States

* To whom correspondence should be addressed. E-mail: lschwieb{at}uab.edu.

We have reported that moderate intensity aerobic exercise training attenuates airway inflammation in mice sensitized/challenged with ovalbumin (OVA). The current study determined the effects of repeated bouts of aerobic exercise at a moderate intensity on airway hyperresponsiveness (AHR) in these mice. Mice were sensitized/challenged with OVA or saline and exercised at a moderate intensity 3X / wk for 4 wks. At protocol completion, mice were analyzed for changes in AHR via mechanical ventilation. Results show that exercise decreased total lung resistance 60% in OVA-treated mice as compared with controls; exercise also decreased airway smooth muscle (ASM) thickness. In contrast, exercise increased circulating epinephrine levels 3-fold in saline- and OVA-treated mice. Because epinephrine binds {beta}2-adrenergic receptors (AR), which facilitate bronchodilatation, the role of {beta}2-AR in exercise-mediated improvements in AHR was examined. Application of the {beta}2-AR antagonist butoxamine HCl blocked the effects of exercise on lung resistance in OVA-treated mice. In parallel, ASM cells were examined for changes in the protein expression of {beta}2-AR and G-protein receptor kinase-2 (GRK-2); GRK-2 promotes {beta}2-AR desensitization. Exercise had no effect {beta}2-AR expression in ASM cells of OVA-treated mice; however, exercise decreased GRK-2 expression by 50% as compared with controls. Exercise also decreased prostaglandin E2 (PGE2) production 5-fold but had no affect on E prostanoid-1 (EP1) receptor expression within the lungs of OVA-treated mice; both PGE2 and the EP1 receptor have been implicated in {beta}2-AR desensitization. Together, these data indicate that moderate intensity aerobic exercise training attenuates AHR via a mechanism that involves {beta}2-AR.
Key words: b2-adrenergic receptor • asthma • airway hyperresponsiveness • aerobic exercise






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