Bowen, T, Aakerøy, L, Eisenkolb, S et al. (10 more authors) (2017) Exercise Training Reverses Extrapulmonary Impairments in Smoke-exposed Mice. Medicine & Science in Sports & Exercise, 49 (5). pp. 879-887. ISSN 0195-9131
Abstract
Purpose: Cigarette smoking is the main risk factor for chronic obstructive pulmonary disease and emphysema. However, evidence on the extrapulmonary effects of smoke exposure that precede lung impairments remains unclear at present, as are data on nonpharmacological treatments such as exercise training. Methods: Three groups of mice, including control (n = 10), smoking (n = 10), and smoking with 6 wk of high-intensity interval treadmill running (n = 11), were exposed to 20 wk of fresh air or whole-body cigarette smoke. Exercise capacity (peak oxygen uptake) and lung destruction (histology) were subsequently measured, whereas the heart, peripheral endothelium (aorta), and respiratory (diaphragm) and limb (extensor digitorum longus and soleus) skeletal muscles were assessed for in vivo and in vitro function, in situ mitochondrial respiration, and molecular alterations. Results: Smoking reduced body weight by 26% (P < 0.05) without overt airway destruction (P > 0.05). Smoking impaired exercise capacity by 15% while inducing right ventricular dysfunction by ~20%, endothelial dysfunction by ~20%, and diaphragm muscle weakness by ~15% (all P < 0.05), but these were either attenuated or reversed by exercise training (P < 0.05). Compared with controls, smoking mice had normal limb muscle and mitochondrial function (cardiac and skeletal muscle fibers); however, diaphragm measures of oxidative stress and protein degradation were increased by 111% and 65%, respectively (P < 0.05), but these were attenuated by exercise training (P < 0.05). Conclusions: Prolonged cigarette smoking reduced exercise capacity concomitant with functional impairments to the heart, peripheral endothelium, and respiratory muscle that preceded the development of overt emphysema. However, high-intensity exercise training was able to reverse these smoke-induced extrapulmonary impairments.
Metadata
Item Type: | Article |
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Authors/Creators: |
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Copyright, Publisher and Additional Information: | © 2017 by the American College of Sports Medicine. This is an author produced version of a paper published in Medicine & Science in Sports & Exercise. Uploaded in accordance with the publisher's self-archiving policy. Unauthorized reproduction of this article is prohibited. |
Keywords: | Diaphragm; Skeletal muscle; Endothelium; High-intensity interval training; Mitochondrial function; COPD |
Dates: |
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Institution: | The University of Leeds |
Academic Units: | The University of Leeds > Faculty of Biological Sciences (Leeds) > School of Biomedical Sciences (Leeds) |
Depositing User: | Symplectic Publications |
Date Deposited: | 02 Nov 2017 14:57 |
Last Modified: | 01 May 2018 00:39 |
Status: | Published |
Publisher: | American College of Sports Medicine |
Identification Number: | 10.1249/MSS.0000000000001195 |
Open Archives Initiative ID (OAI ID): | oai:eprints.whiterose.ac.uk:123399 |