Endurance training accelerates exhaustive exercise-induced mitochondrial DNA deletion and apoptosis of left ventricle myocardium in rats
Endurance training accelerates exhaustive exercise-induced mitochondrial DNA deletion and apoptosis of left ventricle myocardium in rats
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DOI：
10.1007/s00421-009-1177-4
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发表时间：
2009-12-01
影响因子：
3
通讯作者：
Lin, Wan-Teng
中科院分区：
文献类型：
--
作者：
Huang, Chi-Chang;Lin, Tien-Jen;Lin, Wan-Teng
尽管力竭运动引起的氧化应激会增加组织损伤的风险，但人们普遍认为定期的耐力训练可以改善心脏功能，预防心脏病。我们测试了耐力训练计划可以防止力竭运动引起的心功能不全和左心室（LV）细胞凋亡增加的假设。将32只雄性SD大鼠随机分为4组：安静对照组（C组）、训练组（T组）、力竭运动组（E组）和训练加力竭运动组（TE组）。T组和TE组大鼠在电动跑台上跑12周。E组和TE组大鼠在跑台上进行力竭性跑步试验。训练的主要效果表现为跑至力竭的时间增加（E组和TE组分别为80 +/- A 5和151 +/- A 13 min，P = 0.0001），心肌肥厚（未经训练和训练的大鼠分别为0.38%和0.47%，P = 0.0002），左室射血分数降低（未经训练和训练的大鼠分别为88%和71%，P < 0.0001），加速线粒体DNA 4834-bp大缺失（mtDNA（4834）缺失），以及热休克蛋白-70，细胞色素C，切割的半胱氨酸蛋白酶-3，并在一次剧烈运动后在LV中分裂PARP。与我们的假设相反，这些结果表明，耐力训练诱导大鼠左室局部收缩和舒张心肌功能和射血分数的显着损害。我们的研究结果表明，耐力训练加速了力竭运动诱导的线粒体DNA（4834）缺失和细胞凋亡。
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 +/- A 5 and 151 +/- A 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 mtDNA(4834) deletion and apoptosis in the LV.