The Exercise Preconditioning Effect on Cardiac Tissue Injury following Induction of Myocardial Infarction in Male Rats.

Materials and Methods: Twenty-four male rats were divided into 4 groups including MI, Sham, HIIT, and HIIT+MI (N = 6). HIIT and HIIT+MI which underwent high-intensity interval training (HIIT) for 4 weeks (5 days a week). The training protocol included 10 intervals of 1-minute running, with 2 minutes rest between each interval. The training intensity was different every week according to the peak treadmill running speed (v peak) percentage of each rat. Isoproterenol injection was used to induce myocardial infarction (MI). Expressions of creatine kinase-MB (CK-MB), PGC-1α troponin-I, mitochondrial transcription factor A (TFAM), vascular endothelial growth factor (VEGF), and microRNA 126 (miR-126) genes were measured. The variables were measured using biochemical and RT-PCR methods. The significance level (P value≤0.05) was analyzed using ANOVA test. Results: The results showed that 4 weeks of HIIT training led to a significant increase in PGC-1α, TFAm, and VEGF levels in the MI, HIIT, and HIIT+MI groups compared to the sham group (P = 0.001). HIIT exercises increased miR-126 in the different groups compared to the sham group; however, it was not significant. Conclusion: The results obtained showed that HIIT exercise exerts cardio-protective effects to reduce cardiac tissue injury and necrosis against MI. These effects increase mitochondrial biogenesis and angiogenesis by inducing the increased expression of VEGF, TFAM, PGC-1α, and miR-126 genes in the heart tissue. Therefore, HIIT training, as a preconditioning program, was able to protect the cardiac tissue against MI.

Changes in mitochondrial biogenesis and fatty liver indicators in rat following continuous and high intensity interval training.

BACKGROUND: Oxidative stress and mitochondrial dysfunction can be tracked down in most liver diseases like non-alcoholic fatty liver disease (NAFLD). The most recommended preventative method is lifestyle modification, especially exercise. The aim of this study was the investigation of changes in the indexes of mitochondrial biogenesis and fatty liver indicators in rat following continuous and high intensity interval training. METHODS: Thirty healthy male rats were divided into three control (C=10), Continuous swimming training (CT=10) and High intensity interval swimming training groups (HIIT=10). The training groups performed their specific exercises 5 days a week for 8 weeks. 24 h after the last training session in order to prepare the serum, a blood sample was taken from the left ventricle of the rats. In addition, liver tissue was extracted and the SIRT3, PGC-1α, GSH:GSSG, MDA, LDL, HDL, LDL:HDL, TG, TC, AST, ALT and FBS variables were measured by ELISA and analysis of blood biochemistry. RESULTS: Continuous training (CT) increased the levels of PGC-1α, SIRT3 and significantly reduced LDL, LDL:HDL, TG and FBS (P<0.05) levels. High-intensity interval training (HIIT) caused a significant increase in SIRT3 and a significant decrease in FBS (P<0.05) levels. CONCLUSIONS: Adaptations resulting from further aerobic exercise can increase mitochondrial biogenesis factors such as PGC-1α and SIRT3 in hepatocytes, improve this process in hepatocytes, and ultimately improve the fatty liver markers. Therefore, CT may be more effective than HIIT in preventing fatty liver disease.

Acute and chronic exposure of chick embryo to ethanol alters brain neurosteroid levels

Neurosteroids are modulators of neuronal function that may play important role in brain maturation. The aim of the present investigation was to study the effect of prenatal exposure to acute and chronic ethanol on brain progesterone, estradiol, and testosterone concentration on 10th and 15th days following egg incubation. Eggs were exposed to ethanol at 10 % in chronic treatment and 70 % in acute treatment. Progesterone, estradiol, and testosterone were assayed by radioimmunoassay method. It was shown that brain progesterone level was significantly decreased (P < 0.05) in chronic ethanol group on embryonic day 10, but it was significantly decreased (P < 0.05) in acute and chronic groups on embryonic day 15. Brain estradiol level was significantly increased (P < 0.05) in chronic ethanol group on embryonic day 10, and it was decreased (P < 0.05) in acute and chronic groups of ethanol on embryonic day 15. Brain testosterone was significantly increased (P < 0.05) in acute and chronic ethanol-exposed groups on embryonic days 10 and 15. Our observations suggest that ethanol may modulate neurosteroid synthesis in the brain (AU)

Acute and chronic exposure of chick embryo to ethanol alters brain neurosteroid levels.

Neurosteroids are modulators of neuronal function that may play important role in brain maturation. The aim of the present investigation was to study the effect of prenatal exposure to acute and chronic ethanol on brain progesterone, estradiol, and testosterone concentration on 10th and 15th days following egg incubation. Eggs were exposed to ethanol at 10 % in chronic treatment and 70 % in acute treatment. Progesterone, estradiol, and testosterone were assayed by radioimmunoassay method. It was shown that brain progesterone level was significantly decreased (P < 0.05) in chronic ethanol group on embryonic day 10, but it was significantly decreased (P < 0.05) in acute and chronic groups on embryonic day 15. Brain estradiol level was significantly increased (P < 0.05) in chronic ethanol group on embryonic day 10, and it was decreased (P < 0.05) in acute and chronic groups of ethanol on embryonic day 15. Brain testosterone was significantly increased (P < 0.05) in acute and chronic ethanol-exposed groups on embryonic days 10 and 15. Our observations suggest that ethanol may modulate neurosteroid synthesis in the brain.