Endurance training accelerates exhaustive exercise-induced mitochondrial DNA deletion and apoptosis of left ventricle myocardium in rats

Chi Chang Huang, Tien Jen Lin, Chun Chieh Chen, Wan Teng Lin

研究成果: 雜誌貢獻文章

33 引文 (Scopus)

摘要

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 (mtDNA 4834 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.
原文英語
頁(從 - 到)697-706
頁數10
期刊European Journal of Applied Physiology
107
發行號6
DOIs
出版狀態已發佈 - 十二月 2009

指紋

Mitochondrial DNA
Heart Ventricles
Myocardium
Apoptosis
HSP70 Heat-Shock Proteins
Cytochromes
Running
Hypertrophy
Sprague Dawley Rats
Heart Diseases
Oxidative Stress
Education
Control Groups
Proteins

ASJC Scopus subject areas

  • Public Health, Environmental and Occupational Health
  • Orthopedics and Sports Medicine
  • Physiology (medical)

引用此文

Endurance training accelerates exhaustive exercise-induced mitochondrial DNA deletion and apoptosis of left ventricle myocardium in rats. / Huang, Chi Chang; Lin, Tien Jen; Chen, Chun Chieh; Lin, Wan Teng.

於: European Journal of Applied Physiology, 卷 107, 編號 6, 12.2009, p. 697-706.

研究成果: 雜誌貢獻文章

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abstract = "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 (mtDNA 4834 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.",
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