Exercise Preconditioning Plays a Protective Role in Exhaustive Rats by Activating the PI3K-Akt Signaling Pathway.

Jingjing Li,Peng Xu,Yu Zheng,Yang Wang,Zheng Ping,Xuebin Cao

doi:10.1155/2020/3598932

Abstract

Objective To investigate whether exercise preconditioning (EP) protects the rat heart from exhaustive exercise- (EE-) induced injury by inducing the PI3K-Akt signaling pathway. Methods 84 male Sprague-Dawley rats were randomly divided into 6 groups (n = 14 rats per group): control group (Con), exhaustive exercise group (EE), exercise preconditioning group (EP), exercise preconditioning + exhaustive exercise group (EP + EE), LY294002 (PI3K inhibitor) + exercise preconditioning + exhaustive exercise group (LY + EP + EE), and LY294002 group (LY). The Con and LY did not exercise. The remaining groups were subjected to treadmill running. The structure of myocardial tissue and serum biomarkers of myocardial injury were observed. Hemodynamic parameters were recorded with a pressure-volume catheter. TUNEL assay was used to detect the apoptosis of cardiac myocytes, and the level of mitochondrial membrane permeability transforming pore (mPTP) in myocardium was evaluated using ELISA. Pathway and apoptosis-related proteins in myocardium were assessed using western blotting. Results Compared to the Con group, the EE group showed remarkable myocardial injury, such as cardiac dysfunction and myocardial apoptosis. Compared to the EE group, the injuries in the EP + EE group were improved. EP increased the PI3K-Akt signaling pathway and regulated Bcl-2 family to decrease the mPTP openness level. However, the cardioprotective effects of EP were attenuated when pretreated with the LY294002. Conclusions EP protected the heart from EE-induced injury, and it may improve the cardiac function and reduce the cardiomyocyte apoptosis by activating the PI3K-Akt signaling pathway.

Highlights

Acute overload exercise, such as exhaustive exercise, has adverse effects on the heart
We could see the exercise group (EE)-induced microstructure alterations were significantly suppressed by exercise preconditioning (EP), but the protective effect of EP was partly attenuated by LY294002 (Figure 1(a))
We provided the first detailed key mechanisms that EP inhibited which include the mitochondrial pathway to reduce the myocardial apoptosis by activating the PI3K-Akt signaling pathway of cardiac damage by using the established rat model. e present studies indicated that for people who often engage in highintensity exercise, EP allows the heart to elicit adaptive responses to EE

Summary

Introduction

Acute overload exercise, such as exhaustive exercise (exercise intensity or duration exceeding the body’s limit, EE), has adverse effects on the heart. It causes EE-induced myocardial injury, which is manifested as pathological changes of myocardium, abnormal markers of myocardial injury, cardiac function decreases, and even sudden death of sports occurs. Erefore, we want to study the effects and related mechanisms of EP on improving cardiac injury caused by EE. E phosphatidylinositol 3 kinaseprotein kinase B (PI3K-Akt) signaling pathway plays an important role in the exercise-induced cardiac protection mechanism [9,10,11]. Huang et al found that EP activated the PI3K-Akt signaling pathway to maintain cardiac morphology and function.

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Results

Conclusion