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Review
. 2019 Jan;24(1):18-30.
doi: 10.1177/1074248418788575. Epub 2018 Jul 24.

Exercise and Cardioprotection: A Natural Defense Against Lethal Myocardial Ischemia-Reperfusion Injury and Potential Guide to Cardiovascular Prophylaxis

Mohammed Andaleeb Chowdhury  1   2 , Haden K Sholl  1   2 , Megan S Sharrett  1 , Steven T Haller  1 , Christopher C Cooper  1 , Rajesh Gupta  1 , Lijun C Liu  1
Affiliations
Review

Exercise and Cardioprotection: A Natural Defense Against Lethal Myocardial Ischemia-Reperfusion Injury and Potential Guide to Cardiovascular Prophylaxis

Mohammed Andaleeb Chowdhury et al. J Cardiovasc Pharmacol Ther. 2019 Jan.

Abstract

Similar to ischemic preconditioning, high-intensity exercise has been shown to decrease infarct size following myocardial infarction. In this article, we review the literature on beneficial effects of exercise, exercise requirements for cardioprotection, common methods utilized in laboratories to study this phenomenon, and discuss possible mechanisms for exercise-mediated cardioprotection.

Keywords: exercise; ischemic preconditioning; ischemic reperfusion; remote ischemic preconditioning.

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Conflict of interest statement

Declaration of Conflicting Interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Figures

Figure 1.
Figure 1.. Proposed mechanisms of exercise cardioprotection.
1. Lactate from skeletal muscle and intracellular cardiomyocytes provide substrate for ATP generation during anaerobic glycolysis. 2. NRG-1 levels increase binding to erbB2/erbB4, activating the PI3K/Akt pathway that inhibits MPTP opening during cellular hypoxia. 3. Intracellular calcium load is decreased, leading to decreased activation of calpain. 4. Decreased levels of MAO-A and increased SOD activity through activation of Nrf2 activation. 5. Endothelial eNOS and intracellular NO levels rise, inhibiting caspase 3 activity. 6. Decreased circulating sCD40L and increased production of IL-10. 7. Increased levels of miRNAs such as miR-222 and MiR-17–3p lead to inhibition of transcriptional and translation responses deleterious to cardiomyocyte function. 8. Genetic modification leads to de novo synthesis of effector proteins during second window of protection.
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