Send to

Choose Destination
Iran J Basic Med Sci. 2018 Aug;21(8):818-823. doi: 10.22038/IJBMS.2018.29294.7076.

Exercise training has restorative potential on myocardial energy metabolism in rats with chronic heart failure.

Author information

Department of Physical Education, Shandong University, Weihai, Weihai 264209, Shandong Province, China.
Medical Imaging Faculty, Weifang Medical University, Weifang 261053, Shandong Province, China.
Division of physical education, General course Teaching Department, Weifang Medical University, Weifang 261053, Shandong Province, China.



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).


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.


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.


Basal metabolism; Blood pressure; Exercise; Fatty acid; Heart failure; Myocardial infarction

Supplemental Content

Full text links

Icon for PubMed Central
Loading ...
Support Center