Document Detail


Exercise Training Prevents TNF-α Induced Loss of Force in the Diaphragm of Mice.
MedLine Citation:
PMID:  23300968     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
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.
Authors:
Norman Mangner; Axel Linke; Andreas Oberbach; Yvonne Kullnick; Stephan Gielen; Marcus Sandri; Robert Hoellriegel; Yasuharu Matsumoto; Gerhard Schuler; Volker Adams
Related Documents :
8894548 - Elemental composition of muscle at rest and potassium levels in muscle, plasma and swea...
23511698 - Emg evaluation of hip adduction exercises for soccer players: implications for exercise...
23295038 - Worsening in oxygen saturation and exercise capacity predict adverse outcome in patient...
24673178 - T helper cell cytokine profiles after endurance exercise.
833958 - The treatment of the uninhibited bladder with dicyclomine.
11055958 - Oxygen-dependent growth of the sulfate-reducing bacterium desulfovibrio oxyclinae in co...
Publication Detail:
Type:  Journal Article     Date:  2013-01-02
Journal Detail:
Title:  PloS one     Volume:  8     ISSN:  1932-6203     ISO Abbreviation:  PLoS ONE     Publication Date:  2013  
Date Detail:
Created Date:  2013-01-09     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101285081     Medline TA:  PLoS One     Country:  United States    
Other Details:
Languages:  eng     Pagination:  e52274     Citation Subset:  IM    
Affiliation:
Heart Center Leipzig, University of Leipzig, Leipzig, Germany.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Gleevec, an Abl family inhibitor, produces a profound change in cell shape and migration.
Next Document:  High altitude bird migration at temperate latitudes: a synoptic perspective on wind assistance.