Iranian Journal of

---

Background: AMPK and P53 proteins regulate the TOR protein in the TORC1 complex, which regulates many physiological processes. The aim of this study was to evaluate the effect of AMPK and P53 proteins on the TOR pathway following endurance training in the left ventricle of the heart of diabetic rats by streptozotocin and nicotinamide.
Methods: In this experimental study, 12 head two-month-old Sprague-Dawley rats with a mean weight of 270±20 g were selected. After diabetic induction with streptozotocin and Nicotinamide, rats were randomly assigned to two groups, training and control (6 heads in group each). The training group performed endurance training on a treadmill for rodents for 6 weeks and 4 sessions per week for 42 minutes with an intensity of about 50 to 70% of the maximum speed. SPSS software version 23 and independent t-test were used to analyze the data.
Results: Six weeks of endurance training led to significant increase in the protein content of AMPK (P=0.009) and TOR (P=0.005) between training and control groups in the left ventricular tissue of the heart muscle. In contrast, a significant decrease in P53 protein content was observed between the training and control groups in the left ventricular tissue of the heart muscle (P=0.0001).
Conclusion: The results showed that endurance training can with increase the content of AMPK and TOR proteins and decrease the content of P53 protein to regulate processes such as metabolism, mitochondrial biogenesis, cardiac hypertrophy, inhibition of autophagy in the hearts of diabetic subjects.
 

---

Background: FOXO family proteins are important factors in autophagy pathway. Protein kinase-B is an important regulator for this family that can be regulated through exercise training. Therefore, the aim of this study is to investigate the effect of protein kinase-B (PKB) on FOXO autophagy family proteins (FOXO1 and FOXO3a) following high intensity interval training (HIIT) in the left ventricle of the heart of diabetic rats by streptozotocin (STZ) and nicotinamide.
Methods: In this experimental study, 12 two-month-old Sprague-Dawley rats with a mean weight of 270±20 g were selected. After type 2 diabetes induction with STZ and Nicotinamide, rats were randomly assigned to two groups, diabetic training (6 heads) and diabetic control (6 heads). The training group trained for 4 days a week in accordance with the training program for 8 weeks. SPSS software version 23 and independent t-test were used to analyze the data. Significance level is considered p≤0.05.
Results: HIIT training resulted in a significant increase in PKB protein content between training and control groups (P=0.0001). In contrast, a significant decrease in protein content of FOXO1 (P=0.003) and FOXO3a (P=0.006) was observed between the training and control groups.
Conclusion: It seems based on the results HIIT with increasing and regulating PKB leads to a decrease and inactivation of FOXO1 and FOXO3a proteins in the hearts of diabetic subjects. Inhibition of these proteins can prevent excessive cardiac autophagy in diabetic subjects.

---

Background: MAFbx and MuRF1 proteins are important factors in the ubiquitin pathway and are responsible for muscle atrophy. The purpose of this study was to investigate the effect of long-term high-intensity interval training (HIIT) on the intracellular content of MAFbx and MuRF1 proteins in the left ventricular of the heart of rats with type 2 diabetes.
Methods: In this experimental study, 18 rats 2-month-old male Sprague-Dawley rats with a mean weight of 270±20 g were selected. 12 rats became diabetic by intraperitoneal injection of Streptozotocin and nicotinamide solutions. These rats were randomly divided into 2 groups: diabetic training and diabetic control; A healthy control group was also considered. The training group practiced HIIT 4 days a week for 8 weeks. Data were analyzed using SPSS software version 23 and one-way ANOVA and Tukey post hoc tests.
Results: MAFbx protein content showed a significant decrease after 8 weeks of HIIT (P=0.0001); Tukey post hoc test showed that this change was significant between pairs groups of diabetic training and diabetic control and also between pairs groups of diabetic control and healthy control (P=0.0001). MuRF1 protein content showed a significant decrease (P=0.0001); This was a significant difference between the pairs groups of diabetic training and diabetic control, diabetic training and healthy control groups, as well as diabetic control and healthy control groups (P=0.0001).
Conclusion: HIIT seems to can inhibit the process of atrophy and autophagy of cardiomyocytes by reducing the content of MAFbx and MuRF1 proteins in the hearts of diabetic subjects.

---

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.

---

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.