Document Detail

Endurance training accelerates exhaustive exercise-induced mitochondrial DNA deletion and apoptosis of left ventricle myocardium in rats.
MedLine Citation:
PMID:  19730878     Owner:  NLM     Status:  MEDLINE    
Even though exhaustive exercise-induced oxidative stress increases the risk of tissue damage, regular endurance training is widely assumed to improve cardiac function and protects against heart disease. We tested the hypothesis that an endurance training program prevents exhaustive exercise-induced increases in cardiac dysfunction and apoptosis in left ventricle (LV). Thirty-two male Sprague-Dawley rats were randomly divided into four groups: sedentary control (C), trained (T), exhaustively exercised (E), and trained plus exhaustively exercised (TE). Rats in T and TE groups ran on a motorized treadmill for 12 weeks. Rats in groups E and TE performed an exhaustive running test on a treadmill. The main effects of training were indicated by increased running time to exhaustion (80 +/- 5 and 151 +/- 13 min for groups E and TE, respectively, P = 0.0001), myocardial hypertrophy (0.38% and 0.47% for untrained and trained rats, respectively, P = 0.0002), decreased LV ejection fraction (88% and 71% for untrained and trained rats, respectively, P < 0.0001), accelerated mitochondrial DNA 4834-bp large deletion (mtDNA4834 deletion), and up-regulated protein levels of heat shock protein-70, cytochrome C, cleaved capsase-3, and cleaved PARP in LV following a bout of exhaustive exercise. Contrary to our hypothesis, these results suggest that endurance training induced significant impairment of regional systolic and diastolic LV myocardial function and ejection fraction in rats. Our findings show that endurance training accelerates exhaustive exercise-induced mtDNA4834 deletion and apoptosis in the LV.
Chi-Chang Huang; Tien-Jen Lin; Chun-Chieh Chen; Wan-Teng Lin
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  European journal of applied physiology     Volume:  107     ISSN:  1439-6327     ISO Abbreviation:  Eur. J. Appl. Physiol.     Publication Date:  2009 Dec 
Date Detail:
Created Date:  2010-01-25     Completed Date:  2010-03-23     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100954790     Medline TA:  Eur J Appl Physiol     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  697-706     Citation Subset:  IM    
Agricultural Biotechnology Research Center, Academia Sinica, Taipei 11529, Taiwan, ROC.
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MeSH Terms
Body Weight / physiology
Caspase 3 / biosynthesis
Cytochromes c / biosynthesis
DNA, Mitochondrial / genetics*
HSP70 Heat-Shock Proteins / biosynthesis
Matrix Metalloproteinase 9 / biosynthesis
Physical Conditioning, Animal / physiology*
Physical Endurance / physiology*
Poly(ADP-ribose) Polymerases / biosynthesis
Rats, Sprague-Dawley
Sequence Deletion
Ventricular Dysfunction, Left / pathology,  physiopathology*
Reg. No./Substance:
0/DNA, Mitochondrial; 0/HSP70 Heat-Shock Proteins; 9007-43-6/Cytochromes c; EC Polymerases; EC 3.4.22.-/Caspase 3; EC Metalloproteinase 9

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

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