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Updated: Sep 19, 2025

MRI and PET in Mouse Models of Myocardial Infarction
Published on: December 19, 2013
Effect of exercise training on cardiac function and glucose metabolism in the ischemic border zone: insights from
Jun Zhang1,2,3, Chunrong Jin3, Xiao Han1,2
1Department of Nuclear Medicine, First Hospital of Shanxi Medical University, Taiyuan, Shanxi, China.
Aims:
This study aimed to evaluate the impact of early exercise following acute myocardial infarction (AMI) on cardiac function, myocardial remodeling, glucose metabolism, and its molecular changes using cardiac magnetic resonance (CMR) imaging and positron emission tomography (PET).
Methods And Results:
Thirteen rats (MI-exercise, MIE) underwent an 8-week treadmill exercise training initiated 1 week after AMI. Longitudinal assessments were conducted using 7T CMR and 18F-FDG PET/CT imaging at baseline, 4 weeks and 8 weeks following the commencement of exercise. Molecular and pathological analyses, including qPCR and Western blot, were conducted to evaluate mRNA and protein expression related to glucose metabolism. Exercise training led to significant improvements in stroke volume (SV), left ventricular ejection fraction (LVEF), and fraction wall thickening (WT%) from 4 weeks onward, as assessed by CMR, which strongly correlated with increased myocardial glucose uptake, as measured by 18F-FDG PET (P < 0.05). Histological analysis revealed a marked reduction in inflammatory cell infiltration and fibrosis percentage (MIE vs. MIC: 23.42 ± 5.4% vs. 40.63 ± 8.9%, P < 0.05), accompanied by an increase in myocardial cross-sectional area (MIE vs. MIC: 817.15 ± 36.54 μm2 vs. 379.28 ± 67.99 μm2, P = 0.002). RNA sequencing demonstrated upregulation of pathways associated with cellular metabolism. Additionally, the expression levels of GLUT4 and PFKFB3 mRNA and proteins were significantly elevated following exercise training.
Conclusions:
Early exercise post-AMI, as assessed by CMR and PET imaging, significantly improved cardiac function, reduced myocardial remodeling, and enhanced glucose metabolism. These benefits were mediated through the upregulation of GLUT4 and PFKFB3 expression, underscoring the potential of exercise as a therapeutic strategy in post-AMI management.
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