Exercise Training after Myocardial Infarction Attenuates Dysfunctional Ventricular Remodeling and Promotes Cardiac Recovery

Figures

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  Fig. 1.. Exercise training positively regulates calcium homeostasis, improves the balance between MMP-1 and TIMP-1, and enhances the expression of β-adrenergic receptors. MMP-1, matrix metallopeptidase 1; TIMP-1, tissue inhibitor of metalloproteinases 1; SR, sarcoplasmic reticulum; β-ARs, β-adrenergic receptors.

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  Fig. 2.. Exercise training regulates myocardial cells energy metabolism. Exercise training causes adaptations in energy metabolism of the heart including glucose absorption and utilization and glycolysis. Akt, serine/threonine kinase; FFA, plasma free fatty acid; AMPK, AMP Activated Protein Kinase PFK2, 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase; ATP, adenosine triphosphate; G6P, glucose-6-phosphate.

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  Fig. 3.. Exercise training inhibits oxidative stress and promotes angiogenesis. Exercise training increases the expression of β3-AR after myocardial infarction and relieves oxidative stress of cardiomyocytes by regulating eNOS-NO signaling pathway. Exercise training also regulates the VEGF and NO expression and reverses arterial dysfunction in the endothelial vessel wall. In addition, exercise training upregulates the expression of HIF-1α, resulting in angiogenesis stimulation through PI3K-Akt-eNOS and MAPK signaling pathway. Alternatively, exercise training also stimulates skeletal muscle to secrete FSTL1 and promotes myocardium angiogenesis. β3-AR, β-adrenergic receptors; NOS, endothelial nitric oxide synthase; NO, nitric oxide; HIF-1α, hypoxia-Inducible factor 1-alpha; MAPK, mitogen-activated protein kinase; PI3K, phosphoinositide-3-kinase; VEGF, vascular endothelial growth factor; Akt, serine/threonine kinase; FSTL1, follistain like-1; DIP2A, disco-interacting protein 2 homolog A.

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  Fig. 4.. Summary of protective mechanisms involved in ventricular remodeling observed due to exercise training following myocardial infarction. Exercise training alleviates ventricular remodeling and restores cardiac function by altering microRNAs expression selectively; adjusting Ca2+ homeostasis and collagen accumulation to improve myocardial contractility; regulating energy metabolism of myocardial cells; inhibiting oxidative stress of cardiomyocytes; enhancing VEGF dependent angiogenesis pathways, and/or regulating inflammatory response. VEGF, vascular endothelial growth factor.