Abstract
Myocardial infarction (MI) has been shown to induce cardiac dysfunction and insulin resistance. This study was designed to examine the effects of MI‐related insulin resistance on vaso relaxation function and its underlying mechanisms, with specific focus on the role of exercise in reversing vasorelaxation response. Adult male Sprague‐Dawley rats were divided into three groups: Sham, MI, and MI+Exercise. MI+Exercise rats were subjected to 8 weeks of treadmill training (50 min/day, 5 days/week). Myocardial infarction caused significant impairments in endothelial structure and vasodilation (P < 0.05‐0.01), which was evidenced by decreased arterial vasorelaxation to ACh and insulin. Myocardial infarction attenuated myocardial contractile response to insulin, decreased PI3K/Akt/eNOS expression and its phosphorylation by insulin, and increased IL‐1β, IL‐6, and TNF‐α (P < 0.05‐0.01). Exercise improved insulin sensitivity, facilitated arterial vasorelaxation to ACh and insulin, and increased arterial PI3K/Akt/eNOS activation in post‐MI rats. Inhibition of PI3K with LY294002, and eNOS with L‐NAME significantly blocked exercise‐facilitated arterial vasorelaxation and PI3K/Akt/eNOS activation response to insulin. In conclusion, these results demonstrate that endothelial dysfunction in response to insulin plays an important role in the development of myocardial infarction‐related insulin resistance. The reversal of insulin resistance by exercise is most likely associated with normalizes inflammatory cytokines, and PI3K/Akt/eNOS‐dependent improvement in insulin sensitivity.
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