Document Type : Research Paper I Open Access I Released under CC BY-NC 4.0 license
Associate Prof, Dept of Physical Education, Faculty of Letters and Humanities, Vali E Asr University, Rafsanjan, Iran.
MSc, Department of Exercise Physiology, Kerman Branch, Islamic Azad University, Kerman,I ran, Physiology Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran
Neuromuscular dysfunction along with reduced physical activity has significant consequences on muscle function. Therefore, the aim of the present study was to investigate the effect of resistance and combined training on the MST1 and MAFbx genes expression in Plantaris muscle and behavioral tests in male Wistar rats before decreased physical activity in the form of spinal cord ligation (SNL).twenty four 8-week-old male rats with the mean weight of 250± 20 grams were randomly devided into 3 groups: 1) Sham-Spinal Nerve Ligation (Sham-SNL), 2) Resistance Training-Spinal Nerve Ligation (SNL-S), 3) Combined training-Spinal Nerve Ligation (SNL-CO). In all three groups, three branches of the sciatic nerve of rats were tightly tied after the end of training protocol. The duration of the SNL protocol was 4 weeks. At the end of the protocol, Plantaris muscle was extracted. Real-Time PCR method was used to measure the mRNA expression of the genes. MST1 and MAFbx gene expression in the Sham-SNL group was non-significantly higher than the training groups (P <0.05). On the other hand, the results of one-way ANOVA and Tukey’s tests showed that there is a significant difference in thermal hyperalgesia and mechanical allodynia test between Sham-SNL group and training groups (P <0.05). Considering the significant change of behavioral tests in the sham group compared to the training groups, it can be claimed that resistance and combination training can be useful for improving neuropathic pain.
- Hodges, P., et al., Rapid atrophy of the lumbar multifidus follows experimental disc or nerve root injury. Spine, 2006. 31(25): p. 2926-2933.
- Burnett, M.G. and E.L. Zager, Pathophysiology of peripheral nerve injury: a brief review. Neurosurgical focus, 2004. 16(5): p. 1-7
- Verhees, K.J., et al., Glycogen synthase kinase-3β is required for the induction of skeletal muscle atrophy. American Journal of Physiology-Cell Physiology, 2011. 301(5): p. C995-C1007.
- Fanzani, A., et al., Molecular and cellular mechanisms of skeletal muscle atrophy: an update. Journal of cachexia, sarcopenia and muscle, 2012. 3(3): p. 163-179.
- Giger, J.M., et al., Rapid muscle atrophy response to unloading: pretranslational processes involving MHC and actin. Journal of Applied Physiology, 2009. 107(4): p. 1204-1212.
- Rodriguez, J., et al., Myostatin and the skeletal muscle atrophy and hypertrophy signaling pathways. Cellular and Molecular Life Sciences, 2014. 71(22): p. 4361-4371.
- Radak, Z., et al., Single bout of exercise eliminates the immobilization-induced oxidative stress in rat brain. Neurochemistry international, 2001. 39(1): p. 33-38.
- Adams, G.R., V.J. Caiozzo, and K.M. Baldwin, Skeletal muscle unweighting: spaceflight and ground-based models. Journal of applied physiology, 2003. 95(6): p. 2185-2201.
- Fitts, R.H., D.R. Riley, and J.J. Widrick, Physiology of a microgravity environment invited review: microgravity and skeletal muscle. Journal of applied physiology, 2000. 89(2): p. 823-839.
- Bodine, S.C., et al., Akt/mTOR pathway is a crucial regulator of skeletal muscle hypertrophy and can prevent muscle atrophy in vivo. Nature cell biology, 2001. 3(11): p. 1014-1019.
- Cohen, S., et al., During muscle atrophy, thick, but not thin, filament components are degraded by MuRF1-dependent ubiquitylation. Journal of Cell Biology, 2009. 185(6): p. 1083-1095.
- Clavel, S., et al., Atrophy-related ubiquitin ligases, atrogin-1 and MuRF1 are up-regulated in aged rat Tibialis Anterior muscle. Mechanisms of ageing and development, 2006. 127(10): p. 794-801.
- Gomes, M.D., et al., Atrogin-1, a muscle-specific F-box protein highly expressed during muscle atrophy. Proceedings of the National Academy of Sciences, 2001. 98(25): p. 14440-14445.
- Bodine, S.C., et al., Identification of ubiquitin ligases required for skeletal muscle atrophy. Science, 2001. 294(5547): p. 1704-1708.
- Graves, J.D., et al., Both phosphorylation and caspase-mediated cleavage contribute to regulation of the Ste20-like protein kinase Mst1 during CD95/Fas-induced apoptosis. Journal of Biological Chemistry, 2001. 276(18): p. 14909-14915.
- Wei, B., et al., MST1, a key player, in enhancing fast skeletal muscle atrophy. BMC biology, 2013. 11(1): p. 1-13.
- Sandri, M., et al., Foxo transcription factors induce the atrophy-related ubiquitin ligase atrogin-1 and cause skeletal muscle atrophy. Cell, 2004. 117(3): p. 399-412
- Reed, S., et al., Inhibition of IkappaB kinase alpha (IKKα) or IKKbeta (IKKβ) plus forkhead box O (Foxo) abolishes skeletal muscle atrophy. Biochemical and biophysical research communications, 2011. 405(3): p. 491-496
- Treede R-D, Jensen TS, Campbell J, Cruccu G, Dostrovsky J, Griffin J, et al. Neuropathic pain redefinition and a grading system for clinical and research purposes. Neurology. 2008;70(18):1630-5.
- Zaza C, Baine N. Cancer pain and psychosocial factors: a critical review of the literature. Journal of pain and symptom management. 2002;24(5):526-42.
- Gong W, Johanek LM, Sluka KA. Spinal Cord Stimulation Reduces Mechanical Hyperalgesia and Restores Physical Activity Levels in Animals with Noninflammatory Muscle Pain in a Frequency-Dependent Manner. Anesthesia and analgesia. 2014.
- Evans WJ. Skeletal muscle loss: cachexia, sarcopenia, and inactivity. The American journal of clinical nutrition. 2010;91(4):1123S-7S.
- Daemen M, Kurvers H, Bullens P, Slaaf D, Freling G, Kitslaar P, et al. Motor denervation induces altered muscle fibre type densities and atrophy in a rat model of neuropathic pain. Neuroscience letters. 1998;247(2):204-8.
- Jakobsen J, Brimijoin S, Sidenius P. Axonal transport in neuropathy. Muscle & nerve. 1983;6(2):164-6.
- Wei B, Dui W, Liu D, Xing Y, Yuan Z, Ji G. MST1, a key player, in enhancing fast skeletal muscle atrophy. BMC Biol 2013;11:12. doi:10.1186/1741-7007-11-12
- Lee, S. and R.P. Farrar, Resistance training induces muscle-specific changes in muscle mass and function in rat. Journal of Exercise physiology online, 2003. 6(2).
- Chae, C.-H. and H.-T. Kim, Forced, moderate-intensity treadmill exercise suppresses apoptosis by increasing the level of NGF and stimulating phosphatidylinositol 3-kinase signaling in the hippocampus of induced aging rats. Neurochemistry international, 2009. 55(4): p. 208-213.
- Høydal MA, Wisløff U, Kemi OJ, Ellingsen Ø. Running speed and maximal oxygen uptake in rats and mice: practical implications for exercise training. European Journal of Cardiovascular Prevention & Rehabilitation. 2007;14(6):753-60
- Kim, S.H. and J.M. Chung, An experimental model for peripheral neuropathy produced by segmental spinal nerve ligation in the rat. Pain, 1992. 50(3): p. 355-363
- Hole, K. and A. Tjølsen, Tail Flick Test, in Encyclopedia of Pain. 2007, Springer. p. 2392-2395
- Pfaffl MWJNar. A new mathematical model for relative quantification in real-time RT–PCR. 2001;29(9):e45-e
- Kazemi, A. and T. Dahesh, The Effect of 4 Weeks of High Intensity Training on Gene Expression of MST1 and MAFbx in EDL Muscle of Aged Mice. 2019
- KAZEMI, A., M. RAHMATI, and S. MONTAZER, THE EFFECT OF DECREASED ACTIVITY IN THE FORM OF SPINAL CORD LIGATION ON CDK5 EXPRESSION IN SCIATIC NERVE AND BEHAVIORAL TEST OF WISTAR MALE RATS WITH NEUROPATHIC PAIN. 2016.
- KAZEMI, A., M. RAHMATI, and A. ZIASISTANI, EFFECTS OF 6 WEEKS DECREASED ACTIVITY IN THE FORM OF NEUROPATHIC PAIN ON SUNDAY DRIVER GENE EXPRESSION IN THE RAT SCIATIC NERVE FIBERS. 2016.
- Kazemi, A., The effect of the mechanical unloading of lower limb on MST1 and Atrogin1 gene expression in Plantaris and soleus muscles of Wistar rats. Journal of Knowledge & Health, 2018. 13(3): p. 34-4136-
- Moradi, Y., F. Zehsaz, and M.A. Nourazar, Concurrent exercise training and Murf-l and Atrogin-1 gene expression in the vastus lateralis muscle of male Wistar rats. Apunts Sports Medicine, 2020. 55(205): p. 21-27
- Tam, B., et al., Autophagic adaptation is associated with exercise‐induced fibre‐type shifting in skeletal muscle. Acta physiologica, 2015. 214(2): p. 221-236.
- Gonçalves, N.G., et al., Fructose ingestion impairs expression of genes involved in skeletal muscle’s adaptive response to aerobic exercise. Genes & nutrition, 2017. 12(1): p. 1-12.
- Stefanetti, R.J., et al., Regulation of ubiquitin proteasome pathway molecular markers in response to endurance and resistance exercise and training. Pflügers Archiv-European Journal of Physiology, 2015. 467(7): p. 1523-1537.
- Rezaeipour, S., et al., An Investigation of the Effect of Upper Limb Resistance Training after Lower Limb Immobilization on FoxO3a, MuRF1 and MAFbx Gene Expressions of Soleus Muscle in Trained Rats. 2020.
- Panahi, S., et al., The effect of 4 weeks resistance training on murf1 gene expression and muscle atrophy in diabetic wistar rats. Medical J Tabriz Uni Med Sci Health Serv, 2016. 38(2): p. 6-13.
- sheibani, s., et al., The effect of high-intensity training and detraining on FOXO3a/MuRF1 and MAFbx levels in soleus muscle of male rats. EBNESINA, 2018. 20(1): p. 31-39.
- Moradi, Y., F. Zehsaz, and M.A. Nourazar, Concurrent exercise training and Murf-l and Atrogin-1 gene expression in the vastus lateralis muscle of male Wistar rats. Apunts Sports Medicine, 2020. 55(205): p. 21-27.
- Sacheck, J.M., et al., IGF-I stimulates muscle growth by suppressing protein breakdown and expression of atrophy-related ubiquitin ligases, atrogin-1 and MuRF1. American Journal of Physiology-Endocrinology and Metabolism, 2004. 287(4): p. E591-E601
- Xu, M., et al., FoxO1: a novel insight into its molecular mechanisms in the regulation of skeletal muscle differentiation and fiber type specification. Oncotarget, 2017. 8(6): p. 10662.
- Adams, V., et al., Modulation of Murf-1 and MAFbx expression in the myocardium by physical exercise training. European Journal of Cardiovascular Prevention & Rehabilitation, 2008. 15(3): p. 293-299.
- Al-Nassan, S., et al., Chronic exercise training down-regulates TNF-α and atrogin-1/MAFbx in mouse gastrocnemius muscle atrophy induced by hindlimb unloading. Acta Histochemica et Cytochemica, 2012. 45(6): p. 343-349.
- Zhao, H.-X., et al., Exercise training suppresses Mst1 activation and attenuates myocardial dysfunction in mice with type 1 diabetes. Canadian Journal of Physiology and Pharmacology, 2020(ja)
- Borgenvik, M., W. Apró, and E. Blomstrand, Intake of branched-chain amino acids influences the levels of MAFbx mRNA and MuRF-1 total protein in resting and exercising human muscle. American Journal of Physiology-Endocrinology and Metabolism, 2012. 302(5): p. E510-E521.
- Malcangio M, Ramer MS, Boucher TJ, McMahon SB. Intrathecally injected neurotrophins and the release of substance P from the rat isolated spinal cord. Eur J Neurosci 2000; 12(1): 139-44.
- Malcangio M, Garrett NE, Cruwys S, Tomlinson DR. Nerve growth factor-and neurotrophin-3-induced changes in nociceptive threshold and the release of substance P from the rat isolated spinal cord. J Neurosci 1997; 17(21): 8459-67.
- Boucher TJ, Okuse K, Bennett DL, Munson JB, Wood JN, McMahon SB. Potent analgesic effects of GDNF in neuropathic pain states. Science 2000; 290(5489): 124-7.
- Deng Y-S, Zhong J-H, Zhou X-F. Effects of endogenous neurotrophins on sympathetic sprouting in the dorsal root ganglia and allodynia following spinal nerve injury. Exp Neurol 2000; 164(2): 344-50.
- Zhou XF, Deng YS, Xian C, Zhong JH. Neurotrophins from dorsal root ganglia trigger allodynia after spinal nerve injury in rats. Eur J Neurosci 2000; 12(1): 100-5.
- White DM. Neurotrophin-3 antisense oligonucleotide attenuates nerve injury-induced Aβ-fibre sprouting. Brain Res 2000; 885(1): 79-86.