Astragalus polysaccharide attenuates overexercise-induce myocardial injury via activating AMPK signaling pathway to suppress inflammation and oxidative stress.

Xinling Tuo,Huiping Gong,Hezhi Xie,Zhijian Deng,Guochao Huang

doi:10.1590/0001-3765202120210314

Abstract

Excessive exercise leads to myocardial injury or even sudden exercise death. For the vast sports population, appropriate physiological state is a necessary condition for exercise. The present study aims to investigate the cardioprotective effects and potent mechanism of astragalus polysaccharide (APS) treatment against the exercise-induced myocardial injury via in vitro cell-based assay and in vivo model rat. Efficacies of APS incubation on the inflammatory response and oxidative stress induced by LPS were both explored in H9c2 cells by using CCK-8 and western blotting method, respectively. Normal SD rats were randomly divided into saline-treated overexercise rat group, and APS-treated overexercise rat groups with three doses. Then long-term swimming training load cycle (8 week) were performed on these rats. Finally, the changes on body weight, myocardial morphological and injury indicators, as well as the inflammation-related proteins in overexercise-induced model rats were all assessed. Three concentrations of APS all significantly increased cell viability, and decreased the apoptosis of cardiomyocytes in LPS-treated H9c2 cells. Moreover, chronic treatment of APS at all three doses also could obviously decreased myocardial injury-related indicators. Furthermore, the histopathologic examination exhibited that the APS successfully attenuated the changes of myocardial tissues, reduced the lipid accumulation and the protein levels of IL-1β, TNF-α and NF-κB. Furthermore, the APS could activate the AMPK signaling pathway, enhance the autophagy and suppress the production of ROS. On conclusions, APS exerted the protective efficacies on overexercise-induced myocardial injury by activating the AMPK signaling pathway to increase autophagy and suppress the inflammation response, oxidative stress, apoptosis of myocardial cells.

Highlights

In recent years, sudden deaths during sports have occurred from time to time
Exercise is a double-edged sword, excessive exercise will lead to myocardial injury or even sudden exercise death, too little exercise will bring other health problems
With the development of sports science, how to carry out physical exercise and scientific training is well documented, but the problem of excessive exercise or excessive fatigue cannot be treated from the perspective of exercise alone, and should be judged from a wider perspective, such as dietary nutrition, routines, body sensation, etc., from the perspective of recent times, in addition to learning and mastering more knowledge about myocardial injury from the perspective of sports medicine, which is more conducive to the judgment of their own feelings

Summary

Introduction

Sudden deaths during sports have occurred from time to time. Scientific research has found that exercise training can produce adaptive changes in the morphological structure and physiological function of the human heart (Fletcher et al 2013). The increase in cardiac output mainly relies on an increase in heart rate, while professional athletes increase the output per beat. In this case, compensatory cardiomegaly occurs during long-term aerobic exercise, and cardiac load increases during exercise (Fletcher et al 2013). Hypertrophic cardiomyopathy is the leading cause of sudden cardiac death in young athletes, and cardiac morphology can be altered through long-term strenuous exercise. Long training cycle, short recovery time and other factors, it often causes overtraining syndrome in the body and induces pathological conditions of multiple organ dysfunction (Ghorayeb 1995, Liu 2013). Studies have shown that overtraining can evoke exercise-induced cardiac overload, and the damage of local tissue structure of the myocardium, and trigger a cascade of pathological and functional alterations (da Rocha et al 2018, Ghorayeb 1995)

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Conclusion