Interaction of exercise training with taurine attenuates infarct size and cardiac dysfunction via Akt-Foxo3a-Caspase-8 signaling pathway.

This research aimed to investigate the synergistic protective effect of exercise training and taurine on Akt-Foxo3a-Caspase-8 signaling related to infarct size and cardiac dysfunction. Therefore, 25 male Wistar rats with MI were divided into five groups: sham (Sh), control-MI(C-MI), exercise training-MI(Exe-MI), taurine supplementation-MI(Supp-MI), and exercise training + taurine-MI(Exe + Supp-MI). The taurine groups were given a 200 mg/kg/day dose of taurine by drinking water. Exercise training was conducted for 8 weeks (5 days/week), each session alternated 2 min with 25-30% VO2peak and 4 min with 55-60% VO2peak for 10 alternations. Then, the left ventricle tissue samples were taken from all groups. Exercise training and taurine activated Akt and decreased Foxo3a. Expression of the caspase-8 gene was increased in cardiac necrosis after MI, While, after 12 weeks of intervention decreased. Results exhibited that exercise training combined with taurine has a greater effect than either alone on activating the Akt-Foxo3a-caspase signaling pathway (P < 0.001). MI-induced myocardial injury leads to increase collagen deposition (P < 0.001) and infarct size and results in cardiac dysfunction via reduced stroke volume, ejection fraction, and fractional shortening (P < 0.001). Exercise training and taurine improved cardiac functional parameters (SV, EF, FS) and infarct size (P < 0.001) after 8 weeks of intervention in rats with MI. Also, the interaction of exercise training and taurine has a greater effect than alone on these variables. Interaction of exercise training with taurine supplementation induces a general amelioration of the cardiac histopathological profiles and improves cardiac remodeling via activating Akt-Foxo3a-Caspase-8 signaling with protective effects against MI.

Exercise attenuates myocardial fibrosis and increases angiogenesis-related molecules in the myocardium of aged rats.

OBJECTIVES: The present study aimed to investigate the effect of two different exercise training protocols on myocardial fibrosis and the expression of some growth factors in aged rats. METHOD: Twenty-four male Wistar rats were randomly assigned to high-intensity interval training (HIIT) group, continuous exercise training (CET) group, and the control group. After 6 weeks of experiment, mRNA levels of fibroblast growth factor-2 (FGF-2), vascular endothelial growth factor (VEGF), adropin proteins, and myocardial fibrosis were assessed. RESULTS: HIIT and CET induced a significant increase in the FGF-2 and adropin and a decrease in the myocardial fibrosis in compared with the control group. HIIT induced a significant increase in the VEGF if compared with the control group. There was no significant difference between CET and control group. CONCLUSION: Six weeks of HIIT and CET attenuated age-related myocardial fibrosis thereby an increase in angiogenesis-related molecules in cardiac and endothelial tissues.

Hippocampal Oxidative Stress Induced by Radiofrequency Electromagnetic Radiation and the Neuroprotective Effects of Aerobic Exercise in Rats: A Randomized Control Trial.

BACKGROUND: The present study determined whether 4 weeks of moderate aerobic exercise improves antioxidant capacity on the brain of rats against oxidative stress caused by radiofrequency electromagnetic radiation emitted from cell phones. METHODS: Responses of malondialdehyde, catalase, glutathione peroxidase, and superoxide dismutase, as well as the number of hippocampal dead cells, were examined. Male Wistar rats (10-12 wk old) were randomly assigned to 1 of 4 groups (N = 8): (1) moderate aerobic exercise (EXE) (2 × 15-30 min at 1215 m/min speed with 5 min of active recovery between sets), (2) exposure to 900/1800 MHz radiofrequency electromagnetic waves 3 hours per day (RAD), (3) EXE + RAD, and (4) exposure to an experimental phone without battery. RESULTS: Following the exposure, the number of the hippocampal dead cells was significantly higher in group RAD compared with groups EXE, EXE + RAD, and control group. Malondialdehyde concentration in group RAD was significantly higher than that of groups EXE, EXE + RAD, and control group. Also, the activity of catalase, glutathione peroxidase, and superoxide dismutase in groups EXE, EXE + RAD, and control group was significantly higher compared with those of the exposure group. CONCLUSION: This study demonstrated that moderate aerobic exercise enhances hippocampal antioxidant capacity against oxidative challenge in the form of radiofrequency electromagnetic waves.

Aerobic Training-induced Upregulation of YAP1 and Prevention of Cardiac Pathological Hypertrophy in Male Rats.

BACKGROUND: Pathological hypertrophy is one of the negative consequences of cardiac sympathetic hyperactivity. Recent studies have shown that YAP1 plays a critical role in cardiomyocytes hypertrophy. Considering the preventive role of exercise training in cardiovascular diseases, the present study was conducted to examine the effect of aerobic exercise training on YAP1 gene expression and its upstream components. METHODS: Eighteen male Wistar rats were randomly divided into aerobic training and control groups. Aerobic training was performed one hour/day, five days per week, for eight weeks, on a treadmill at 65-75% VO2 max. Pathological hypertrophy was induced by injecting 3 mg/kg-1 of isoproterenol for seven days. The left ventricle was separated, and YAP1, 3-mercaptopyruvate sulfurtransferase (MST), large tumor suppressor (LATS), and mitogen-activated protein 4 kinase (MAP4K) gene expressions were assessed and YAP1 protein levels were also assessed by western blotting. Cell apoptosis was detected by TUNEL assays. The between-group differences were evaluated using the T-test and P value <0.05 was considered statistically significant. RESULTS: There were no significant between-group differences in MST gene expression (P = 0.061); meanwhile, in the training group, LATS and Map4K expressions were suppressed, followed by a significant increase in YAP1 expression (P < 0.001). Compared to the control group, the left ventricular weight increased significantly in the training group while the cardiomyocyte apoptosis decreased. CONCLUSIONS: The results showed that, by reducing LATS, aerobic training-induced YAP1 upregulation can help prevent the propagation of cardiomyocyte apoptosis due to pathological conditions.

Taurine with combined aerobic and resistance exercise training alleviates myocardium apoptosis in STZ-induced diabetes rats via Akt signaling pathway.

AIM: The aim of this study was considering the effects of taurine supplementation with combined aerobic and resistance training (CARE) on myocardial apoptosis and Protein Kinase B (akt) level changes in diabetic rat. MAIN METHODS: Forty male Wistar rats were randomly divided in to 5 groups of 8 animals in each: 1) control, 2) Diabetes Mellitus (DM), 3) DM with taurine supplementation (DM/T), 4) DM with CARE (DM/CARE), and 5) DM with combination of taurine and CARE (DM/T/CARE). DM was induced by injection of streptozotocin (STZ) and nicotine amid (NA) for 2, 3, 4 and 5 groups. Supplement groups received taurine in gavage, 100 mg/kg of body weight, 6 day per weeks, 8 weeks. CARE was performed at maximal speed and 1RM (40-60% of maximum for both). KEY FINDINGS: The results of this study showed that DM significantly increased blood glucose and caspase 3, caspase 9 expressions and apoptosis cells in heart tissue and reduced Akt expression (p < 0.001). However, taurine and CARE interventions significantly decreased apoptosis markers (caspase 3 and caspase 9) and significantly increased Akt in heart of diabetic rats compare to DM groups (p < 0.05). The highest improvement observed in DM/T/CARE group (p < 0.05). SIGNIFICANCE: Based on these results, it seems that the use of taurine with combined aerobic and exercise training minimize the cardiac damage caused by diabetes (especially apoptosis) trough increasing protein kinase Akt expression. This could improve cardiac remodeling after diabetes. However, more research is needed, especially on the human samples.