Preconditioning Effect of High-Intensity Aerobic Training on Myocardial Ischemia-Reperfusion Injury and Beclin-1 Gene Expression in Rats

Abstract

Purpose: Ischemia-Reperfusion (IR) injury is one of the most common cardiac disorders leading to irreversible heart damage. Many underlying mechanisms seem to be involved, among which disruption of cellular autophagy balance. Since physical training has a beneficial effect on the improvement of autophagy balance, it may have a cardioprotective effect against IR injury. This study investigates the protective role of aerobic training from cardiac IR injury and the autophagy process as a possible mechanism.Methods: Thirty-two male Wistar rats (8 weeks old) were divided into control, sham, control plus IR, and training plus IR groups (8 rats each). The training group was exercised aerobically on a treadmill for 8 weeks (5 d/wk). After 8 weeks, the anesthetized rats underwent left thoracotomy (sham, control plus IR, and training plus IR groups) to access the left anterior descending coronary artery, which was occluded by a silk suture for 30 min and then released for 90 min of reperfusion (IR groups). Triphenyltetrazolium chloride staining was used to determine the infarct size. The gene expression of Beclin-1 was evaluated by real-time polymerase chain reaction. One-way ANOVA was used for statistical analysis with the significance level set at P≤0.05. Results:The cardiac infarct size was smaller in training plus IR (20.24±5.7%) group compared to that in the control plus IR (35.9±2.3%) group (P≤0.05). On the other hand, IR operation significantly increased the gene expression of Beclin-1, while exercise training prevented expression of the mentioned gene in training plus IR group (P≤0.05). Conclusion:Aerobic training can protect the heart against Ischemia-Reperfusion injury. It seems that improvement of autophagy balance during IR injury may be involved in exercise-induced cardioprotection against Ischemia-Reperfusion.

Effect of exercise training on cardiac mitochondrial respiration, biogenesis, dynamics, and mitophagy in ischemic heart disease

“…Moreover, two ( 2 ) studies reported an increased LC3II expression ( 27 , 31 ), while two other studies reported increased Beclin1 levels in IHD ( 27 , 32 ) as compared to normal controls. On the contrary, ET reversed these downregulated autophagosomal biomarkers in IHD ( 27 , 31 , 32 ).…”

“…As part of the essential mechanisms involved in the mitochondrial quality control, four studies ( 27 , 30 – 32 ) investigated the effect of IHD and ET on the mitophagy biomarkers ( Tables 2 , 4B ).…”

“…However, one study reported an increase in P62 levels in IHD in comparison to normal controls ( 31 ). With ET, increased PINK ( 31 ) and Parkin ( 30 , 32 ) levels were noted. The latter two studies, on the other hand, reported contrasting results on the effect of ET in P62, wherein both studies reported an increased and a decreased level of P62 in the exercise-trained IHD ( 30 , 32 ).…”