Background & Aims: There are many metabolic diseases that are associated with insulin deficiency, increased blood glucose, and disturbances in carbohydrate, fat, and protein metabolism. Several studies have pointed to the role of exercise in fat metabolism. Regular physical activity leads to the improvement of fat and glucose metabolism by increasing insulin sensitivity and reducing triglycerides. It is often accepted that long-term sports training can increase the body's response to insulin and increase insulin sensitivity by increasing glucose transporters into muscle cells and insulin receptor substrates. It is useful in preventing obesity and its subsequent complications, i.e. type 2 diabetes. Glucose is a potential fuel for tissues such as muscle, liver, and adipose tissue. The sugars in the daily diet, if congenital, can be found in large amounts in different parts of the body such as the liver, and skeletal muscles, and in a very small amount in the heart, blood cells, and parts of the uterus and in astrocytes. Brain cells are stored as glycogen. Liver glycogen is a storage source that can be made from blood glucose, and if needed, it can be converted back into glucose and released into the blood; In addition to the liver, muscles can also store glycogen, to the extent that muscle glycogen can be easily broken down for the muscle's energy needs. On the other hand, one of the conditions that can upset the energy balance in the cell and impose certain needs on the cell is the increase in energy expenditure due to physical stress, including physical activity and exercise. A large number of target proteins bind to specific enzymes and cellular structures and scaffolding proteins collect enzyme intermediates. Insulin increases the accumulation of glycogen by phosphorylating these enzymes and as a result, activates glycogen synthase and deactivates glycogen Desynthase. Although the activation of protein phosphatase 1 (PP1) by insulin has an important role in increasing the storage of glucose as glycogen, although the inactivation of upstream kinases such as Phosphorylase kinase is part of the mediator of the regulation of glycogen metabolism, the activation of protein phosphatase 1 to Insulin plays an essential role in increasing the storage of glucose as glycogen. The activity of protein phosphatase 1 is regulated by inhibitory proteins. The direct regulation of glycogen-targeted protein phosphatase 1 by inhibitors has not been widely investigated. The results of the studies showed that protein phosphatase 1 is a gene involved in glycogen metabolism, and during exercise, the amount of protein phosphatase 1 gene decreases with insulin reduction, and glycogen synthesis decreases, and increases after exercise and at rest. As mentioned, most studies have investigated the effect of endurance and resistance training on insulin resistance and fat profile. Therefore, the study of an alternative type of physical activity with similar metabolic adaptations and without significant time commitment is needed. One of the appropriate exercise protocols is interval training with moderate intensity, which is associated with more variety and less fatigue and has attracted many enthusiasts. Compared to continuous sports activity with medium to low intensity, intermittent training causes adaptation of metabolism in skeletal muscle, which favors the process of fat oxidation (fat burning). In the studies, it was shown that with the reduction of insulin, the expression of genes involved in glycogen synthase, such as protein phosphatase 1, is reduced, but there was no study investigating the effect of this type of exercise on the level of protein phosphatase 1 gene expression, so the main question of this The study was whether a moderate intensity exercise session has a significant effect on protein phosphatase 1 marker gene expression in the liver tissue of male Wistar rats.
Methods: In this experimental study, 16 8-week-old male Wistar rats with an average weight of 237±33 grams were divided into groups of 4 rats into 2 control groups (8 rats) and an experimental group (8 rats). In order to get familiar with the conditions of the laboratory and the treadmill, the animals ran on the treadmill for 2 weeks, 5 days per week and for 10 to 15 minutes each day at a speed of 5 to 15 m/min. Due to the lack of access to direct tools, the maximum oxygen consumption of the animals was assessed indirectly with the Faz-Ade test on the treadmill. The moderate-intensity exercise program for 8 weeks included swimming (swimming and staying afloat). The interval training protocol with moderate intensity was implemented in such a way that in the first week, 5 minutes of warming up, 5 minutes of cooling down, and 20 minutes of the main body of the exercise, including running with an intensity of 65% of the maximum oxygen consumption at a speed of 20 meters per minute, and weekly The training was increased so that in the sixth week, the training time reached 37 minutes and remained constant until the end of the eighth. Also, the training speed was unchanged from the first week to the eighth week and was equal to 20 m/min. After the training period, the rats were anesthetized and blood sampling and tissue separation were done, and the data obtained from the PCR-Real time device were measured and analyzed.
Results: The results of this test showed that there is a significant difference between the two research groups in protein phosphatase 1 gene expression. The comparison between groups showed that there is a significant difference in the expression of protein phosphatase 1 gene of Wistar rats between the moderate intensity exercise group compared to the control group (P ≥ 0.001) so that it is 0.011 units compared to decreased the control group.
Conclusion: In general, it can be concluded that aerobic training with moderate intensity for 8 weeks can improve the function of glycogen metabolism and insulin pathway because, in this process, the level of genes involved in glycogen metabolism such as the PP1 gene was adjusted. Exercises produce favorable changes in the metabolic system of the liver. These effects were seen in moderate-intensity aerobic exercise. Aerobic training with moderate intensity for 8 weeks can decrease protein phosphatase-1 gene expression. Among the limitations of the present study, we can point out the lack of control of the number of calories consumed by rats and the lack of control of physical activity outside of the animal research program. Despite this, the research background on the effect of the current study's training protocols on protein phosphatase 1 in liver tissue is very limited and needs more investigation.