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      The Exercise Preconditioning Effect on Cardiac Tissue Injury following Induction of Myocardial Infarction in Male Rats

      1 , 2 , 3 , 4 ,
      BioMed Research International

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          Materials and Methods

          Twenty-four male rats were divided into 4 groups including MI, Sham, HIIT, and HIIT+MI ( N = 6). HIIT and HIIT+MI which underwent high-intensity interval training (HIIT) for 4 weeks (5 days a week). The training protocol included 10 intervals of 1-minute running, with 2 minutes rest between each interval. The training intensity was different every week according to the peak treadmill running speed (v peak) percentage of each rat. Isoproterenol injection was used to induce myocardial infarction (MI). Expressions of creatine kinase-MB (CK-MB), PGC-1 α troponin-I, mitochondrial transcription factor A (TFAM), vascular endothelial growth factor (VEGF), and microRNA 126 (miR-126) genes were measured. The variables were measured using biochemical and RT-PCR methods. The significance level ( P value≤0.05) was analyzed using ANOVA test.


          The results showed that 4 weeks of HIIT training led to a significant increase in PGC-1 α, TFAm, and VEGF levels in the MI, HIIT, and HIIT+MI groups compared to the sham group ( P = 0.001). HIIT exercises increased miR-126 in the different groups compared to the sham group; however, it was not significant.


          The results obtained showed that HIIT exercise exerts cardio-protective effects to reduce cardiac tissue injury and necrosis against MI. These effects increase mitochondrial biogenesis and angiogenesis by inducing the increased expression of VEGF, TFAM, PGC-1 α, and miR-126 genes in the heart tissue. Therefore, HIIT training, as a preconditioning program, was able to protect the cardiac tissue against MI.

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          Most cited references64

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          AMP-activated protein kinase (AMPK) action in skeletal muscle via direct phosphorylation of PGC-1alpha.

          Activation of AMP-activated kinase (AMPK) in skeletal muscle increases glucose uptake, fatty acid oxidation, and mitochondrial biogenesis by increasing gene expression in these pathways. However, the transcriptional components that are directly targeted by AMPK are still elusive. The peroxisome-proliferator-activated receptor gamma coactivator 1alpha (PGC-1alpha) has emerged as a master regulator of mitochondrial biogenesis; furthermore, it has been shown that PGC-1alpha gene expression is induced by exercise and by chemical activation of AMPK in skeletal muscle. Using primary muscle cells and mice deficient in PGC-1alpha, we found that the effects of AMPK on gene expression of glucose transporter 4, mitochondrial genes, and PGC-1alpha itself are almost entirely dependent on the function of PGC-1alpha protein. Furthermore, AMPK phosphorylates PGC-1alpha directly both in vitro and in cells. These direct phosphorylations of the PGC-1alpha protein at threonine-177 and serine-538 are required for the PGC-1alpha-dependent induction of the PGC-1alpha promoter. These data indicate that AMPK phosphorylation of PGC-1alpha initiates many of the important gene regulatory functions of AMPK in skeletal muscle.
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            AMP-activated/SNF1 protein kinases: conserved guardians of cellular energy.

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            The SNF1/AMP-activated protein kinase (AMPK) family maintains the balance between ATP production and consumption in all eukaryotic cells. The kinases are heterotrimers that comprise a catalytic subunit and regulatory subunits that sense cellular energy levels. When energy status is compromised, the system activates catabolic pathways and switches off protein, carbohydrate and lipid biosynthesis, as well as cell growth and proliferation. Surprisingly, recent results indicate that the AMPK system is also important in functions that go beyond the regulation of energy homeostasis, such as the maintenance of cell polarity in epithelial cells.
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              miR-126 regulates angiogenic signaling and vascular integrity.

              Precise regulation of the formation, maintenance, and remodeling of the vasculature is required for normal development, tissue response to injury, and tumor progression. How specific microRNAs intersect with and modulate angiogenic signaling cascades is unknown. Here, we identified microRNAs that were enriched in endothelial cells derived from mouse embryonic stem (ES) cells and in developing mouse embryos. We found that miR-126 regulated the response of endothelial cells to VEGF. Additionally, knockdown of miR-126 in zebrafish resulted in loss of vascular integrity and hemorrhage during embryonic development. miR-126 functioned in part by directly repressing negative regulators of the VEGF pathway, including the Sprouty-related protein SPRED1 and phosphoinositol-3 kinase regulatory subunit 2 (PIK3R2/p85-beta). Increased expression of Spred1 or inhibition of VEGF signaling in zebrafish resulted in defects similar to miR-126 knockdown. These findings illustrate that a single miRNA can regulate vascular integrity and angiogenesis, providing a new target for modulating vascular formation and function.

                Author and article information

                Biomed Res Int
                Biomed Res Int
                BioMed Research International
                13 July 2023
                : 2023
                : 3631458
                1Department of Physical Education and Sport Sciences, Fasa Branch, Islamic Azad University, Fasa, Iran
                2Department of Exercise Physiology, Faculty of Physical Education and Sports Science, Kharazmi University, Mirdamad Ave., Tehran, Iran
                3Department of Physiology, Fasa University of Medical Sciences, Fasa, Iran
                4Ionizing and Non-Ionizing Radiation Protection Research Center (INRPRC) Shiraz University of Medical Sciences, Shiraz, Iran
                Author notes

                Academic Editor: Hu Wang

                Author information
                Copyright © 2023 Fatemeh Heiat et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                : 11 March 2023
                : 25 May 2023
                : 21 June 2023
                Funded by: Fasa University of Medical Sciences
                Research Article


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