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Background: High oxidative stress in pregnant women leads to pathogenesis or progression of disease in newborns. The aim of this study was to investigate the Effect of Endurance Training in Maternal Metabolic Syndrome with Metformin on Oxidant and antioxidant Capacity in their Neonates.
Methods: To implementation of this experimental research, 16 female Wistar rats weighing 100 ± 20 gr randomly were divided into 4 groups including metabolic syndrome + control; metabolic syndrome + metformin; metabolic syndrome + endurance training; metabolic syndrome + metformin + endurance training. The metabolic syndrome model was performed using dietary change and confirmed by the Lee index. Metformin 500 mg was also given at a dose of 100 mg/kg, as well as by daily water intake to the rats. endurance training performed at 5 days a week for 15-40 min with speed of 10-25m/min on treadmill for 8 weeks. Pregnancy was confirmed in rats after vaginal plaque was observed After the pregnancy and delivery period of the rats, newborn babies (4 newborns from each mother as the main sample) were prepared one week after birth for explanation.
Results: The results showed that metformin had no significant effect on superoxide dismutase (SOD) and malondialdehyde (MDA) in comparison with control group, but endurance training and endurance training with metformin resulted in increased SOD and MDA reduction in neonatal heart tissue (p=0.000).
Conclusion: According to the results, it seems that the endurance training of mothers with metabolic syndrome has a protective effect on oxidative and antioxidant systems in their offspring.

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Background: The mTORC1 pathway is one of the important pathways for protein synthesis in the heart, which can lead to physiological or pathological hypertrophy. Diabetes can lead to defects in this pathway. The aim of this study was to examine the effect of 4 weeks’ aerobic training on the content of mTORC1 signaling pathway proteins in heart tissue of type 1 diabetes rats.

Methods: In this experimental study, 16 Sprague-Dawley male rats (mean weight of 300 ± 20 gr) were selected and after induction of diabetes by STZ was randomly assigned into two groups: diabetic training and diabetic control. The experimental group performed HIIT training for 4 weeks’ accordance with the training program (each session 42 minutes, 10-20 m/m) for 4 weeks, while the control group did not have any training program. Dependent t-test and independent T-test were used to analyze the data
 

Results: Significant increase was observed in the content of AKT1 (p<0.015), mTOR (p<0.001), P70S6K1 (p<0.006), 4EBP1 (p<0.05) proteins in the aerobic training group compared to control group.
Conclusion: Aerobic training for 4 weeks enabled to activate the pathway AKT1/mTOR/P70S6K1 and AKT1/mTOR/4E-BP1 in mTORC1 pathway; therefore, due to cardiac complications in type 1 diabetic patients, aerobic training can lead to protein synthesis and physiological cardiac hypertrophy through mTORC1 pathway.
 

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Background: Unc-51 Like Autophagy Activating Kinase-1 (ULK1) and FAK Family Kinase-Interacting Protein of 200 kDa (FIP200) play an essential role in controlling autophagy and muscle volume. The aim of this research is to investigate the effect of endurance training on the intracellular content of ULK1 and FIP200 proteins in the left ventricular of rats with type 1 diabetes.
Methods: In this experimental study, 18 rats 2-month-old male Sprague-Dawley rats with a mean weight of 300±20g were selected. 12 rats became diabetic by intraperitoneal injection of Streptozotocin solutions. These rats were randomly divided into 2 groups: diabetic training and diabetic control (6 heads per group); A healthy control group (6 heads)was also considered. The training group practiced endurance training 4 days a week for 6 weeks. Data were analyzed using SPSS software version 23 and one-way ANOVA and Tukey post hoc tests.
Results: The content of ULK1 (increase) and FIP200 (decrease) after endurance training showed a significant change among the research groups in the left ventricular (P=0.0001). Tukey's post hoc test showed that this change is significant between the pair of diabetic training groups to diabetic control, diabetic training to healthy groups, and also diabetic control to healthy groups (P≤0.05).
Conclusion: Endurance training showed that it can have a dual nature to control autophagy in diabetic subjects by increasing ULK1 and decreasing FIP200. There is a need for more investigations in the field of exercise physiology on the proteins responsible for autophagy, especially in type 1 diabetes subjects.

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Background: Diabetes can cause serious cardiovascular complications by disrupting the autophagy pathway. Therefore, this study aimed to investigate the effect of high-intensity interval training (HIIT) on the intracellular levels of autophagy proteins in the left ventricular tissue of rats with type 1 diabetes.
Methods: In this experimental study, 18 2-month-old male Sprague-Dawley rats with an average weight of 300±20 grams were selected. Twelve rats had type 1 diabetes after intraperitoneal injection of STZ (with a dose of 50 mg/kg of body weight) solution. Rats were randomly divided into two groups: diabetic training and diabetic control (each group, six heads). A healthy control group (six heads) was also considered. The training group underwent HIIT four days a week for six weeks. GraphPad Prism version 9.5 software and one-way ANOVA, and Tukey's post hoc tests were used to analyze the data. The significance level was considered P≤ 0.05.
Results: ULK1 and FIP200 levels showed a significant increase in the left ventricle after 6 weeks of HIIT training compared to the healthy control group and the diabetic control group (P= 0.0001).
Conclusion: Considering the increase in ULK1 and FIP200 proteins, it can be concluded that HIIT training can activate the autophagy pathway; Therefore, in prescribing this type of exercise for diabetic subjects, the intensity and duration of the exercise should be considered.