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

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 (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.

Moderate exercise training provides left ventricular tolerance to acute pressure overload

“…A potential explanation for the homogeneous cellular phenotype observed in EX ϩ Band might result from the functional demand imposed by exercise training, favoring the autophagic response and/or death of the most dysfunctional and susceptible cells to injury. This idea, although speculative, is supported by reports showing that endurance exercise training is accompanied by terminal deoxynucleotidyl-dUTP nick end labelingpositive nuclei and activation of apoptotic mediators (Bax, cytochrome c, cleaved caspase-3, and cleaved PARP) in LV cardiomyocytes (18) as well as enhanced abundance of cardiac progenitor cells (21). In addition, cardiac autophagy has been recently associated with exercise training, with some data pointing to its involvement in exercise-induced cardioprotection (4,40).…”

Effect of Conjugated Linoleic Acid Intake on Endurance Exercise Performance and Anti-fatigue in Student Athletes

“…Increase of these isozymes in serum is considered generally supportive of myocardial injury 47 . Huang et al 48 reported that endurance training accelerates exhaustive exercise-induced apoptosis in left ventricles of rats, as a result of exhaustive running tests on a treadmill. In this study, the amount of LD 1 variation after exercise in the CLA group was significantly lower than that of the Pla group.…”

Effects of anaerobic exercise and detraining on the caspase-3 expression of rat ventricular cardiomyocyte

“…Stretching cardiomyocyte and increased left ventricular wall stress can trigger death receptor as characterized by the increased expression of Fas protein. 22 High-intensity anaerobic physical exercise causes an increase of end-diastolic pressure due to excessive load and can lead to wall stress, which further stimulate sarcomer replication, fiber elongation, and enlargement of cardiac chamber or eccentric hypertrophy. 13 Acute increase of wall stress may lead to replication of sarcomeres, concentric wall thickening and hypertrophy associated with significant increase of left ventricular mass.…”