Introduction: cardiovascular diseases and disorders extensively spread throughout the worldwide and are expanding. Ischemic heart failure is the most common cardiovascular-related diseases. The major cause of myocardial ischemia is coronary artery disease. Blood flow reperfusion to ischemic tissues is essential to preserve and save it. However, reperfusion acts like a double-edged sword, and despite having beneficial effects on ischemic tissue preservation from death, it can cause more damage to the tissue. These damages all together called cardiac ischemia-reperfusion injuries (IRI). Of all the pathological events involved in the IR damage, increased production of ROS and increased levels of cytosolic calcium (calcium overload) plays a key role in the induction of the injury. Several studies have shown that physical activity can be protective and preventive against cardiac IR-induced damages. This review study investigates the proposed mechanisms involved in the role of exercise training as a protective strategy against ischemia-reperfusion injury as well as the importance of each other.
Methodology: With the key words of Ischemia-Reperfusion Injury, Exercise Training and Cardioprotection in the databases of Pubmed, Google Scholar and Science Direct were to search for articles in this field and among all articles available (118 cases), articles that studied cellular signaling pathways in this field were selected and studied (26 cases).
Results: The proposed cellular mechanisms of exercise-induced cardioprotection against ischemia-reperfusion injury includes: changes in coronary collateral circulation, increased cardiac glycolytic flux, altered nitric oxide signaling, elevated heat shock proteins (HSPS), increased myocardial COX-2 activity, elevated endoplasmic reticulim stress proteins, improved sarcolemmal and mitochondrial ATP-sensitive potassium channels performance, and increased cytosolic and mitochondrial antioxidant capacity. Studies have shown that among all the mechanisms, exercise-induced alterations in mitochondrial proteins and phenotype (especially increased gene expression of mitochondrial SOD2) IR injury plays a major role in cardioprotection against IR-injury.
Discussion: The major mechanism of exercise-induced cardioprotection against IR injury is alterations in mitochondrial proteins and phenotype. It seems that mitochondria plays a critical role in the induction of ischemia-reperfusion injury as well as prevention of these injuries with exercise training.