Mangner, N, Bowen, T, Werner, S et al. (7 more authors) (2016) Exercise Training Prevents Diaphragm Contractile Dysfunction in Heart Failure. Medicine & Science in Sports & Exercise, 48 (11). pp. 2118-2124. ISSN 0195-9131
Abstract
Purpose: Patient studies have demonstrated the efficacy of exercise training in attenuating respiratory muscle weakness in chronic heart failure (HF), yet direct assessment of muscle fiber contractile function together with data on the underlying intracellular mechanisms remains elusive. The present study, therefore, used a mouse model of HF to assess whether exercise training could prevent diaphragm contractile fiber dysfunction by potentially mediating the complex interplay between intracellular oxidative stress and proteolysis. Methods: Mice underwent sham operation (n = 10) or a ligation of the left coronary artery and were randomized to sedentary HF (n = 10) or HF with aerobic exercise training (HF + AET; n = 10). Ten weeks later, echocardiography and histological analyses confirmed HF. Results: In vitro diaphragm fiber bundles demonstrated contractile dysfunction in sedentary HF compared with sham mice that was prevented by AET, with maximal force 21.0 ± 0.7 versus 26.7 ± 1.4 and 25.4 ± 1.4 N·cm−2, respectively (P < 0.05). Xanthine oxidase enzyme activity and MuRF1 protein expression, markers of oxidative stress and protein degradation, were ~20% and ~70% higher in sedentary HF compared with sham mice (P < 0.05) but were not different when compared with the HF + AET group. Oxidative modifications to numerous contractile proteins (i.e., actin and creatine kinase) and markers of proteolysis (i.e., proteasome and calpain activity) were elevated in sedentary HF compared with HF + AET mice (P < 0.05); however, these indices were not significantly different between sedentary HF and sham mice. Antioxidative enzyme activities were also not different between groups. Conclusion: Our findings demonstrate that AET can protect against diaphragm contractile fiber dysfunction induced by HF, but it remains unclear whether alterations in oxidative stress and/or protein degradation are primarily responsible.
Metadata
Item Type: | Article |
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Authors/Creators: |
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Copyright, Publisher and Additional Information: | © 2016 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: | myocardial infarction; skeletal muscle; oxidative stress; mouse; CHF; atrophy |
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: | 07 Nov 2017 16:12 |
Last Modified: | 07 Nov 2017 16:15 |
Status: | Published |
Publisher: | American College of Sports Medicine |
Identification Number: | 10.1249/MSS.0000000000001016 |
Open Archives Initiative ID (OAI ID): | oai:eprints.whiterose.ac.uk:123400 |