Figure 1.
Effects of exercise training on the myocardial hypertrophy induced by sympathetic hyperactivity.
Panel A, Body weight was evaluated at the end of study. Panel B, Absolute left ventricular (LV) mass of each experimental group. Panel C, LV mass was indexed by body weight of each animal. Panel D, Representative light micrographs of myocardial section stained with haematoxylin–eosin. Arrows indicate the cardiomyocyte nucleus on longitudinal orientation. The graph shows the results for nuclear volume of each experimental group. Panel E, Expression of hypertrophic mRNA markers for each experimental group determined by quantitative real-time RT-PCR. Same letters above bars into graphs indicate values not different in ANOVA. Different letters above bars into graphs indicate significant difference between means.
Figure 2.
Exercise training inhibits myocardial dysfunction induced by sympathetic hyperactivity.
Data were obtained at muscle lengths corresponding to 100% of Lmax. Panel A, Peak developed tension (DT). Panel B, Maximal positive time derivative of developed tension (+dT/dt). Panel C, Maximal negative time derivative of developed tension (−dT/dt). Same letters above bars into graphs indicate values not different in ANOVA. Different letters above bars into graphs indicate significant difference between means.
Figure 3.
Collagen content, capillary density and apoptosis are preserved in exercised rats on sympathetic hyperactivity.
Panel A–C, Representative polarized light micrographs of tissue stained with picrosirius red (magnification 40×). Panel D–E, Representative electron micrographs for capillaries visualization (magnification 1650×). Panel G–I, TUNEL assay for cardiomyocytes in apoptosis (magnification: 20×) as estimated from cells marked in red (magnification 20×). Quantitative analysis for collagen content, capillary density and positive apoptotic cells are shown in panel J, K and L, respectively. Same letters above bars into graphs indicate values not different in ANOVA. Different letters above bars into graphs indicate significant difference between means.
Figure 4.
Exercise modulates key components of the kallikrein-kinin pathway in the myocardial on sympathetic hyperactivity.
A significantly up-regulation of gene (Panel A) and protein (Panel B) expression was detected in the trained rats submitted to isoproterenol injection. The kinin B1 receptor gene was up-regulated in myocardial of sedentary isoproterenol-treated rats, whereas the exercised isoproterenol-treated rats the kinin B1 receptor gene was normalized (Panel C). Moreover, exercise also increased kinin B1 receptor in transcriptional level (Panel D). Same letters above bars into graphs indicate values not different in ANOVA. Different letters above bars into graphs indicate significant difference between means.
Figure 5.
Exercise modulates key components of the angiogenesis and apoptosis pathway in the myocardial on sympathetic hyperactivity.
It is remarkable that exercise increased mRNA of VEGF (Panel A), VEGF receptor 2 (Panel B) and eNOS (Panel C) in the isoproterenol-treated rats. The protein levels of VEGF (Panel D) and its receptor (Panel E) were also increased by exercise. Although total Akt protein has not been changed (Panel F), activated form of Akt was significantly up-regulated in the exercise animals (Panel G). Moreover, a beneficial effect of exercise was observed for proteins that modulate apoptosis (Panel: H and I). Same letters above bars into graphs indicate values not different in ANOVA. Different letters above bars into graphs indicate significant difference between means.