Exercise training improves cardiac function in infarcted rabbits: involvement of autophagic function and fatty acid utilization

Chen, Ching-Yi; Hsu, Hsiu-Ching; Lee, Bai-Chin; Lin, Hung‐Ju; Huang, Hui Chun; Ho, Yi‐Lwun; Chen, Ming-Fong

doi:10.1093/eurjhf/hfq028

Cited by 43 publications

(41 citation statements)

References 44 publications

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“…Cardioprotective interventions, such as caloric restriction [11,12] , exercise [13] , and chloramphenicol succinate [14] , have been reported to initiate autophagy. Ischemic preconditioning also induces autophagy to promote cardioprotective effects [15,16] .…”

Section: Introductionmentioning

confidence: 99%

Restoration of autophagic flux in myocardial tissues is required for cardioprotection of sevoflurane postconditioning in rats

et al. 2014

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Aim: Sevoflurane postconditioning (SpostC) has been shown to protect the heart from ischemia-reperfusion (I/R) injury. In this study, we examined whether SpostC affected autophagic flux in myocardial tissues that contributed to its cardioprotective effects in rats following acute I/R injury. Methods: SD rats underwent 30 min of left anterior descending coronary artery ligation followed by 120 min of reperfusion. The rats were subjected to inhalation of 2.4% (v/v) sevoflurane during the first 5 min of reperfusion, and chloroquine (10 mg/kg, ip) was injected 1 h before I/R. Myocardial infarct size was estimated using TTC staining. Autophagosomes in myocardial tissues were detected under TEM. Expression of LC3B-II, beclin-1, p62/SQSTM1, cathepsin B, caspase-3 and cleaved PARP was assessed using Western blot analysis. Plasma cardiac troponin I was measured using ELISA. Cardiomyocyte apoptosis was evaluated with TUNEL staining. Results: I/R procedure produced severe myocardium infarct and apoptosis accompanied by markedly increased number of autophagosomes, as well as increased levels of LC3B-II, beclin-1 and p62 in myocardial tissues. SpostC significantly reduced infarct size, attenuated myocardial apoptosis, restored intact autophagic flux and improved the lysosomal function in myocardial tissues. Administration of chloroquine that blocked autophagic flux abrogated the cardioprotective effects of SpostC. Conclusion: SpostC exerts its cardioprotective effects in rats following I/R injury via restoring autophagic flux in myocardial tissues.

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Section: Introductionmentioning

confidence: 99%

Restoration of autophagic flux in myocardial tissues is required for cardioprotection of sevoflurane postconditioning in rats

et al. 2014

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“…Iemitsu et al (26) demonstrated that regular exercise in aging rats prevented age-induced decreases in PPAR␣ expression and subsequent age-induced heart dysfunction. Similarly, exercise training improved cardiac function in rabbits with myocardial infarction-induced heart failure; this was associated with greater FA utilization (8). Therefore, changes in the amount or type of substrates for cardiac energy production might prevent or improve heart failure.…”

Section: Discussionmentioning

confidence: 93%

“…This may be attributed to the increase in cardiac mass that occurs with exercise and not changes in cardiac substrate usage (39). Other studies suggest that training improves FA utilization by the heart (8,49). Whether FAs or glucose are needed for both hypertrophy and improved cardiac function is not known.…”

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confidence: 99%

Rescue of heart lipoprotein lipase-knockout mice confirms a role for triglyceride in optimal heart metabolism and function

Khan

Yan

et al. 2013

American Journal of Physiology-Endocrinology and Metabolism

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IJ.Rescue of heart lipoprotein lipase-knockout mice confirms a role for triglyceride in optimal heart metabolism and function. Am J Physiol Endocrinol Metab 305: E1339 -E1347, 2013. First published October 1, 2013; doi:10.1152/ajpendo.00349.2013.-Hearts utilize fatty acids as a primary source of energy. The sources of those lipids include free fatty acids and lipoprotein triglycerides. Deletion of the primary triglyceride-hydrolyzing enzyme lipoprotein lipase (LPL) leads to cardiac dysfunction. Whether heart LPL-knockout (hLPL0) mice are compromised due a deficiency in energetic substrates is unknown. To test whether alternative sources of energy will prevent cardiac dysfunction in hLPL0 mice, two different models were used to supply nonlipid energy. 1) hLPL0 mice were crossed with mice transgenically expressing GLUT1 in cardiomyocytes to increase glucose uptake into the heart; this cross-corrected cardiac dysfunction, reduced cardiac hypertrophy, and increased myocardial ATP. 2) Mice were randomly assigned to a sedentary or training group (swimming) at 3 mo of age, which leads to increased skeletal muscle production of lactate. hLPL0 mice had greater expression of the lactate transporter monocarboxylate transporter-1 (MCT-1) and increased cardiac lactate uptake. Compared with hearts from sedentary hLPL0 mice, hearts from trained hLPL0 mice had adaptive hypertrophy and improved cardiac function. We conclude that defective energy intake and not the reduced uptake of fat-soluble vitamins or cholesterol is responsible for cardiac dysfunction in hLPL0 mice. In addition, our studies suggest that adaptations in cardiac metabolism contribute to the beneficial effects of exercise on the myocardium of patients with heart failure. triglyceride; heart failure; glucose; lactate; energetics; glucose transporters IN THE HEALTHY ADULT HUMAN HEART, most of the energy required for normal cellular processes is derived from the uptake and oxidation of fatty acids (FAs), with the remainder being contributed by glucose, lactate, and amino acids (36). FAs are delivered to the heart either as free fatty acids (FFAs) conjugated to albumin or via lipoprotein lipase (LPL)-mediated hydrolysis of lipoproteins, with subsequent uptake by FAT/CD36, other FA transporters, and nonreceptor mediated pathways (5).Cardiomyocyte deletion of LPL (hLPL0) leading to reduced triglyceride (TG) lipolysis increased cardiac glucose uptake and reduced expression of several peroxisomal proliferatoractivated receptor (PPAR) regulated genes (1). hLPL0 hearts developed reduced ejection fraction (2) and were unable to compensate when subjected to increased afterload due to aortic coarctation or hypertension (56). These data suggest that TG is an important source of lipid for cardiac energy.In heart failure, traditional cardiac substrate usage of FAs is perturbed, and as a result the heart shifts away from FA oxidation to glucose utilization. These changes in heart energy use have been studied experimentally in isolated hearts using buffers containing FFAs (35). W...

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“…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). However, the role of apoptosis and autophagy in the exercised heart is still under debate, and further data are needed to clarify this issue.…”

Section: Discussionmentioning

confidence: 95%

Moderate exercise training provides left ventricular tolerance to acute pressure overload

Moreira-Gonçalves

Henriques‐Coelho²,

Fonseca

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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The present study evaluated the impact of moderate exercise training on the cardiac tolerance to acute pressure overload. Male Wistar rats were randomly submitted to exercise training or sedentary lifestyle for 14 wk. At the end of this period, the animals were anaesthetized, mechanically ventilated, and submitted to hemodynamic evaluation with biventricular tip pressure manometers. Acute pressure overload was induced by banding the descending aorta to induce a 60% increase of peak systolic left ventricular pressure during 120 min. This resulted in the following experimental groups: 1) sedentary without banding (SED + Sham), 2) sedentary with banding (SED + Band), and 3) exercise trained with banding (EX + Band). In response to aortic banding, SED + Band animals could not sustain the 60% increase of peak systolic pressure for 120 min, even with additional narrowing of the banding. This was accompanied by a reduction of dP/d tmax and dP/d tmin and a prolongation of the time constant tau, indicating impaired systolic and diastolic function. This impairment was not observed in EX + Band ( P < 0.05 vs. SED + Band). Additionally, compared with SED + Band, EX + Band presented less myocardial damage, exhibited attenuated protein expression of active caspase-3 and NF-κB ( P < 0.016), and showed less protein carbonylation and nitration ( P < 0.05). These findings support our hypothesis that exercise training has a protective role in the modulation of the early cardiac response to pressure overload.

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Exercise training improves cardiac function in infarcted rabbits: involvement of autophagic function and fatty acid utilization

Cited by 43 publications

References 44 publications

Restoration of autophagic flux in myocardial tissues is required for cardioprotection of sevoflurane postconditioning in rats

Restoration of autophagic flux in myocardial tissues is required for cardioprotection of sevoflurane postconditioning in rats

Rescue of heart lipoprotein lipase-knockout mice confirms a role for triglyceride in optimal heart metabolism and function

Moderate exercise training provides left ventricular tolerance to acute pressure overload

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