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. Author manuscript; available in PMC: 2020 May 19.
Published in final edited form as: J Cardiovasc Pharmacol Ther. 2018 Jul 24;24(1):18–30. doi: 10.1177/1074248418788575

Figure 1. Proposed mechanisms of exercise cardioprotection.

Figure 1.

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.