Sara Panahi
1, Hamid Agha-Alinejad
1*, Reza Gharakhanloo
1, Rana Fayazmilani
2, Mehdi Hedayati
3, Alireza Safarzadeh
4, Maryam Zarkesh
31 Department of Physical Education and Sport Science, School of Humanity, Tarbiat Modares University, Tehran, Iran
2 Department of Exercise Physiology, School of Physical Education and Exercise Science, Shahid Beheshti University, Tehran, Iran
3 Cellular and Molecular Endocrine Research Center, Obesity Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran
4 Department of Exercise Physiology, School of Physical Education and Exercise Science, Mazandaran University, Babolsar, Iran
Abstract
Background & Objectives: Muscular atrophy is one of the most common complications of diabetes. In such cases, protein degradation is increased and protein synthesis is decreased. MuRF1 is an E3 ubiquitin ligase which has been identified as a mediator of skeletal muscle wasting in various skeletal muscle atrophy models, and its expression is upregulated in atrophy. Exercise training has been suggested as one of the treatment strategies for muscular atrophy. The aim of this study is to investigate the effects of 4 weeks of resistance training on MuRF1 gene expression in muscular atrophy in streptozotocin-diabetic wistar rats.
Material and Methods: Thirty six male Wister rats (288 ± 22 g) were randomly divided into four groups: non-diabetic control, non-diabetic trained, diabetic control and diabetic trained. The exercise groups were subjected to a resistance training program using a ladder (3 days/wk, for 4 wk). MuRF1 mRNA level was measured in Flexor Hallucis Longus muscle using Real-Time PCR. The results were studied by statistical methods.
Results: MuRF1 gene expression was increased in rats with diabetes (p=0.001); resistance training diminished the skeletal muscle wasting in diabetic rats (p=0.002) by inhibiting MuRF1 gene expression.
Conclusion: This study indicates that short term resistance training can overcome diabetes-induced atrophy in rats. Whether this kind of training might be a good way for countering atrophy in other diseases with similar catabolic situation to diabetes remains to be elucidated.