All ETDs from UAB

Advisory Committee Chair

Lisa M Schwiebert

Advisory Committee Members

Edward Postlethwait

Marcas Bamman

Ian Davis

Mitchell Olman

J Edwin Blalock

Document Type

Dissertation

Date of Award

2008

Degree Name by School

Doctor of Philosophy (PhD) Heersink School of Medicine

Abstract

Asthma is identified by the clinical symptoms of wheezing, chest tightness, dyspnea and cough, and by the presence of airway hyperresponsiveness (AHR) to inhaled stimuli. We have reported previously that repeated bouts of moderate intensity aerobic exercise attenuate airway inflammatory responses in a mouse model of atopic asthma. Because the effects of exercise on physiological responses are dependent upon several variables, including total exercise duration, the hypothesis of the current work was that differing amounts of moderate intensity aerobic exercise exert dissimilar effects on AHR and airway inflammation. The aims to test this hypothesis included: 1) determine the effect of multiple bouts of moderate intensity aerobic exercise on AHR; and 2) determine the effect of a single bout of moderate intensity aerobic exercise on AHR and airway inflammation. These aims were completed in two independent studies. In the first study, we determined the effects of moderate intensity aerobic exercise at repeated bouts on AHR in mice sensitized and challenged with ovalbumin (OVA). Results show that repeated bouts of exercise attenuate AHR in OVA-treated mice as compared with controls; these effects were blocked in the presence of a β2-adrenergic receptor (AR) antagonist. Repeated bouts of exercise also decreased ASM thickness and PGE2 production significantly in OVA-treated mice. Together, these data indicate that repeated bouts of moderate intensity aerobic exercise attenuate AHR via a mechanism that involves β2-AR. iv In the second study, we delineated the effects of a single bout of moderate intensity aerobic exercise on AHR and airway inflammation in OVA-treated mice. Results show that, within the lungs of OVA-treated mice, exercise attenuated inflammatory mediator production, leukocyte infiltration, and NF – κB activation as compared with controls. In contrast, a single bout of exercise had no effect on AHR and airway remodeling in OVA-treated mice. These findings suggest that a single bout of aerobic exercise at a moderate intensity attenuates airway inflammation but not AHR or airway remodeling in OVA-treated mice. From these studies, we hypothesize that moderate intensity aerobic exercise attenuates AHR and airway inflammation sequentially within the asthmatic lung; future studies to test this hypothesis are discussed.

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