Background: Skeletal muscle mass, which is regulated by a balance between muscle protein synthesis and degradation, is an important factor for movement to meet everyday needs, especially in pathological conditions and aging. The purpose of the present investigation was to compare the alterations of the gene expression involved in muscle protein synthesis and degradation signaling pathways induced by two exercise training protocols.
Methods: Eight weeks old Wistar rats have been assigned to the present experimental study, which was conducted from August 2018 to October 2018 at the animal laboratory of Tehran University. They were randomly divided into two resistance and endurance training groups and one control group, and run on a treadmill, 5 sessions per week for 8 weeks. 48 hours after the last exercise session, the rats in the two groups were anesthetized, and the dissected soleus muscles from euthanized animals were stored at -80° for RT-PCR and Western blot analysis later. Between-group differences were analyzed by the parametric and non-parametric tests for normally and non-normally distributed data respectively, at the significance level of α˂0.05.
Results: Compared with the control group, mTORC1 gene expression was increased significantly just in the endurance group (P=0.022), whereas both endurance and resistance exercise protocols caused a significant increase in Rps6kb1 (P˂0.001 and P=0.001 respectively). In protein degradation pathway, although, FOXO3a did not alter significantly (P=0.463), eIF4Ebp1 gene expression was inhibited by both endurance and resistance exercise training protocols (P˂0.001 and P=0.001 respectively). The alterations of Rps6kb1 and FOXO3a gene expression were confirmed by Western blot analysis.
Conclusion: The results showed that the exercise training protocols of the present study had approximately similar effects on alterations of gene expression involved in skeletal muscle protein synthesis and degradation pathways. Therefore, application of the protocols may be considered to prevent or reduce the muscle atrophy in pathological conditions such as motor neuron disease, aging, and/or muscle strength improvement in athletes.
