Effect of different exercise training intensities on age-related cardiac damage in male mice

Figures

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  Figure 1. MET improves myocardial function in aging mice. (A) Representative M-mode echocardiogram. (B) LV ejection fraction (EF), LV fraction shortening (FS), LV internal dimension end-systolic (LVIDs), LV internal dimension end-diastolic (LVIDd), and heart rate were evaluated via echocardiography. n = 8 mice from each group, *P < 0.05.

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  Figure 2. Metabolic data and cardiac tissue damage in the different groups after exercise training. (A) Quantitative analysis of body weight (0 week and 24 weeks), heart/body weight, LDH, and CK-MB levels in the different groups. n = 8 per group. *P < 0.05. (B) Representative photomicrographs of myocardium stained with WGA (green fluorescence) and DAPI (blue fluorescence). (C) Graph showing the cardiomyocyte CSA. (D) H and E staining showing structure damage in cardiac tissue. Magnification 40×. The arrows indicate positively stained cells. n = 3 per group. *P < 0.05.

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  Figure 3. MET prevents cardiac remodeling and reduces myocardial fibrosis in aging mice. (A) The expression of cardiac remodeling-associated biomarkers, including ANP and BNP. (B) Quantification of the relative protein expression levels. (C) Sirius Red staining for collagen deposition in the cardiac tissue; (D) Quantification of positive staining. (E) Cardiac collagen III, α-SMA, and TGF-β levels as assessed by western blotting. (F) Quantification of relative protein expression levels. Magnification 40×. The arrows indicate positively stained cells. n = 6–8 per group. *P < 0.05.

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  Figure 4. MET decreases oxidative stress in aging mice. (A) Cardiac MDA and GSH levels were quantified using commercial assay kits. n = 8 per group. *P < 0.05. (B) Cardiac NRF2, HO-1, SOD, and NOX4 levels assessed by western blotting. (C) Quantification of relative protein expression levels. (D) Representative immunohistochemistry for NRF2, HO-1, SOD, and NOX4 in cardiac tissues. (E) Quantification of positive expression. Magnification 40×. The arrows indicate positively stained cells. n = 6–8 per group. *P < 0.05.

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  Figure 5. MET decrease the levels of natural aging markers in aging mice. (A) Cardiac P16, P21, and P53 mRNA levels assessed by real-time PCR. (B) Cardiac P16, P21, and P53 protein levels assessed by western blotting. (C) Quantification of relative protein expression levels. n = 6–8 per group. *P < 0.05.

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  Figure 6. MET decreases apoptosis in aging mice. (A) TUNEL-stained (green fluorescence) and DAPI-stained (blue fluorescence) photomicrographs. Magnification 40×. (B) Quantification of apoptotic cardiomyocytes. (C) Cardiac BAX, Bcl-2, Bak, and Bcl-XL levels assessed by western blotting. (D) Quantification of relative protein expression levels. n = 6–8 per group. *P < 0.05.

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  Figure 7. Schematic diagram showing how MET protects against cardiac damage in aging mice. MET regimen prevented cardiac dysfunction and reduced cardiac damage by reducing myocardial remodeling, myocardial fibrosis, apoptosis, aging related factor level and oxidative stress in the aging heart.