| Exercise Training Prevents TNF-α Induced Loss of Force in the Diaphragm of Mice. | |
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MedLine Citation:
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PMID: 23300968 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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RATIONALE: Inflammatory cytokines like tumor necrosis factor alpha (TNF-α) are elevated in congestive heart failure and are known to induce the production of reactive oxygen species as well as to deteriorate respiratory muscle function. OBJECTIVES: Given the antioxidative effects of exercise training, the aim of the present study was to investigate if exercise training is capable of preventing a TNF-α induced loss of diaphragmatic force in mice and, if so, to elucidate the potential underlying mechanisms. METHODS: Prior to intraperitoneal injection of TNF-α or saline, C57Bl6 mice were assigned to four weeks of exercise training or sedentary behavior. Diaphragmatic force and power generation were determined in vitro. Expression/activity of radical scavenger enzymes, enzymes producing reactive oxygen species and marker of oxidative stress were measured in the diaphragm. MAIN RESULTS: In sedentary animals, TNF-α reduced specific force development by 42% concomitant with a 2.6-fold increase in the amount of carbonylated α-actin and creatine kinase. Furthermore, TNF-α led to an increased NAD(P)H oxidase activity in both sedentary and exercised mice whereas xanthine oxidase activity and intramitochondrial ROS production was only enhanced in sedentary animals by TNF-α. Exercise training prevented the TNF-α induced force reduction and led to an enhanced mRNA expression and activity of glutathione peroxidase. Carbonylation of proteins, in particular of α-actin and creatine kinase, was diminished by exercise training. CONCLUSION: TNF-α reduces the force development in the diaphragm of mice. This effect is almost abolished by exercise training. This may be a result of reduced carbonylation of proteins due to the antioxidative properties of exercise training. |
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Authors:
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Norman Mangner; Axel Linke; Andreas Oberbach; Yvonne Kullnick; Stephan Gielen; Marcus Sandri; Robert Hoellriegel; Yasuharu Matsumoto; Gerhard Schuler; Volker Adams |
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Publication Detail:
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Type: Journal Article Date: 2013-01-02 |
Journal Detail:
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Title: PloS one Volume: 8 ISSN: 1932-6203 ISO Abbreviation: PLoS ONE Publication Date: 2013 |
Date Detail:
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Created Date: 2013-01-09 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101285081 Medline TA: PLoS One Country: United States |
Other Details:
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Languages: eng Pagination: e52274 Citation Subset: IM |
Affiliation:
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Heart Center Leipzig, University of Leipzig, Leipzig, Germany. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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