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Exercise training has restorative potential on myocardial energy metabolism in rats with chronic heart failure
OBJECTIVE(S): Exercise training is a well-known accelerator for the treatment of chronic heart failure (CHF). The current study aimed to investigate the restorative effects of aerobic interval training (AIT) intervention on myocardial energy metabolism in CHF rats. MATERIALS AND METHODS: Post-myocar...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Mashhad University of Medical Sciences
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6118078/ https://www.ncbi.nlm.nih.gov/pubmed/30186569 http://dx.doi.org/10.22038/IJBMS.2018.29294.7076 |
Sumario: | OBJECTIVE(S): Exercise training is a well-known accelerator for the treatment of chronic heart failure (CHF). The current study aimed to investigate the restorative effects of aerobic interval training (AIT) intervention on myocardial energy metabolism in CHF rats. MATERIALS AND METHODS: Post-myocardial infarction (MI) heart failure animal model was established. The Sprague-Dawley rats were randomly divided into sham operation group (Sham group), CHF model group, and CHF exercise group (Exercise-CHF group). RESULTS: Our data showed that when compared to the Sham group, the left ventricular systolic pressure (LVSP), myocardial glycogen content, and expression levels of key components of AMP-activated protein kinase (AMPK) pathway were decreased significantly (P<0.05) in the CHF-model group, while the left ventricular end diastolic pressure (LVEDP), fatty acid (FA) concentration, lactic acid content, and AMPKα phosphorylation (p-AMPKα) were increased significantly (P<0.05) in the CHF-model group. Importantly, AIT reversed these alterations induced by post-MI. CONCLUSION: Findings of this study demonstrated that AIT could improve the metabolic remodeling and enhance cardiac function, which may be associated with the activation of AMPK/ peroxisome proliferator activated receptor α (PPARα) and its downstream signaling pathway. |
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