Effects of early exercise on cardiac function and lipid metabolism pathway in heart failure

FIGURE 1. Final treadmill exercise testing. AS, untrained aortic stenosis; AST, trained aortic stenosis; ShamT, trained Sham. Data are mean ± SD or relative frequency; anova and Goodman; *p < 0.05. **p < 0.001. (n = 14–16 each group).

FIGURE 2. (A–E) Representative photographs of immunohistochemistry staining (A) and quantitation of the expression level of the VEGF, vascular endothelial growth factor (B); VEGFR‐1, VEGF receptor type 1 (C) and 2 (D); and CD34, differentiation cluster 34 (E) in myocardium sections (indicated by black arrows). Scale bar, 50 μm. (F) Quantification of the protein expression of hypoxia‐inducible factor 1‐α. AS, untrained aortic stenosis; AS, untrained aortic stenosis; AST, trained aortic stenosis; ShamT, trained Sham. Data are mean ± SD; anova; *p < 0.05. **p < 0.001. (n = 6–8 each group).

FIGURE 3. (I) Quantification of the expression levels of proteins involved with cardiac fatty acids translocation and intracellular transport, and β‐oxidation. CD36, fatty acid (FA) translocase (A); FA‐binding protein, FABP3 (B); carnitine palmitoyltransferase 1, CPT1β (C); acetyl‐CoA dehydrogenase, ACADL (D); medium‐chain acyl‐CoA dehydrogenase, MCAD (E); 2,4‐dienoyl‐CoA reductase, DECR1 (F). (II) Quantification of the expression levels of metabolic sensors and transcriptional effectors. AMP‐activated protein kinase, AMPK (A); phosphorylated AMPK, pAMPK (B); sirtuin 1, SIRT1 (C); peroxisome proliferator activated receptor‐α, PPARα (D); receptor X retinoid, RXR (E); peroxisome proliferator‐activated receptor gamma coactivator 1α, PGC1α (F). AS, untrained aortic stenosis; AST, trained aortic stenosis; ShamT, trained Sham. Data are mean ± SD; Kruskal–Wallis and anova; *p < 0.05. **p < 0.001. (n = 6–8 each group).

FIGURE 4. AS, untrained aortic stenosis; AST, trained aortic stenosis; ATP, adenosine triphosphate; OHADH, beta‐hydroxyacyl‐CoA dehydrogenase; ShamT, trained Sham. Data are mean ± SD; anova; *p < 0.05. **p < 0.001. (n = 08 each group).

FIGURE 5. Global correlation map of angiogenesis, lipid energy metabolism, and cardiac function. Pairwise correlation of all parameters, resulting in a matrix of correlation coefficients where each variable is compared to all others. Red squares represent variables with a positive correlation with each other. The negative correlation is indicated in blue squares. ACADL, acyl‐CoA dehydrogenase; AKT, protein kinase B; AMPK, AMP‐activated protein kinase; CD34, differentiation cluster 34; CD36, fatty acid (FA) translocase; CK, creatine kinase; CPT1, carnitine palmitoyltransferase; CS, citrate synthase; DECR1, 2,4‐dienoyl‐CoA reductase; E'/A', ratio between E' to TDI of late diastolic velocity of mitral annulus; E/A, ratio between early (E) to late (A) diastolic mitral inflow; E/E', ratio between E and TDI of early diastolic velocity of mitral annulus (E'); EDT, E‐wave deceleration time; EFS, endocardial fractional shortening; FABP3, FA‐binding protein; HIF1α; hypoxia inducible factor 1‐α; IVRT, isovolumetric relaxation time; LA, left atrium; LVDD and LVSD, left ventricular (LV) diastolic and systolic diameters; MCAD, medium‐chain acyl‐CoA dehydrogenase; MFS, mesocardial fractional shortening;…

FIGURE 6. Overview of the effects of pressure overload (PO) and PO plus exercise on cardiac function, angiogenesis and lipid energy metabolism. ACADL, acyl‐CoA dehydrogenase; CD34, differentiation cluster 34; CD36, fatty acid (FA) translocase; CK, creatine kinase; CPT1, carnitine palmitoyltransferase; CS, citrate syinthase; DECR1, 2,4‐dienoyl‐CoA reductase; FABP3, FA‐binding protein; MCAD, medium‐chain acyl‐CoA dehydrogenase; OHADH, beta‐hydroxyacyl‐CoA dehydrogenase; PPARα, peroxisome proliferator activated receptor‐α; SIRT1, sirtuin 1; VEGF, vascular endothelial growth factor; VEGFR‐1 and VEGFR2, VEGF receptor type 1 and 2.