Prior resistance training exerts cardioprotection against cardiac remodelling after myocardial infarction.

IF 2.7 4区医学 Q3 ENDOCRINOLOGY & METABOLISM

Archives of Physiology and Biochemistry Pub Date : 2025-09-22 DOI:10.1080/13813455.2025.2548815

Flávio André Silva, Leslie Andrews Portes, Ednei Luiz Antonio, Luis Felipe Neves Dos Santos, Helenita Antonia Oliveira, Ighor Luiz Azevedo Teixeira, André Rodrigues Lourenço Dias, Paulo José Ferreira Tucci, Andrey Jorge Serra

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Abstract

Background: The cardioprotective properties of resistance training (RT) in infarcted rats have been poorly investigated. This study aimed to evaluate the effects of eight weeks of RT prior myocardial infarction (MI) in rats. Method: Groups: SSh: sedentary sham surgery; SMI: sedentary MI; TMI: trained MI. At the end of the eighth week, the animals underwent either MI or sham surgery and were analysed four weeks later. Results: The TMI presented MI sizes, scar areas, masses of the atria, right ventricle, heart, left atrial area, E wave, and E/A ratio, smaller than the SMI. The protein expression related to Ca²⁺ handling were not affected by the RE. The maximal load (ML) of the TMI was greater than that of the SMI group. The VO₂ peak and maximum speed (Vmax) were lower in the infarcted groups. Conclusion: Prior RT confers cardioprotection against cardiac remodelling by attenuating infarct size progression, myocardial hypertrophy, and diastolic dysfunction.

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先前的抗阻训练对心肌梗死后心脏重构具有保护作用。

背景：对梗死大鼠抗阻训练（RT）的心脏保护作用研究甚少。本研究旨在评价大鼠心肌梗死（MI）前8周RT治疗的效果。方法：各组：SSh：久坐假手术；SMI：久坐性MI；TMI：训练心肌梗死。在第八周结束时，动物进行心肌梗死或假手术，并在四周后进行分析。结果：TMI在心肌梗死大小、瘢痕面积、心房、右心室、心脏肿块、左房面积、E波、E/A比值等方面均小于SMI。与Ca2+处理相关的蛋白表达不受RE的影响。TMI的最大负荷（ML）大于SMI组。梗死组的VO2峰值和最大速度（Vmax）均较低。结论：先前的RT可通过减轻梗死面积进展、心肌肥厚和舒张功能障碍来保护心脏免受心脏重构。

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来源期刊

Archives of Physiology and Biochemistry ENDOCRINOLOGY & METABOLISM-PHYSIOLOGY

CiteScore

6.90

自引率

3.30%

发文量

期刊介绍： Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders. The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications. Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics: -Dysregulation of hormone receptors and signal transduction -Contribution of gene variants and gene regulatory processes -Impairment of intermediary metabolism at the cellular level -Secretion and metabolism of peptides and other factors that mediate cellular crosstalk -Therapeutic strategies for managing metabolic diseases Special issues dedicated to topics in the field will be published regularly.