The Effect of Incremental Resistance Training on the Expression of Gamma Acetylcholine Receptor Subunit Genes and Semaphorin-a3 in the Gastrocnemius Muscle of Male Rats.
Subject Areas : Physical Activity and Health
Mozhgan Hassanzadeh
1
,
Mohammad Azarbayjani
2
*
,
Shahin Riyahi Malayeri
3
,
مقصود پیری
4
,
حسن متین همائی
5
1 - Department of Exercise Physiology,Central Tehran Branch, Islamic Azad Univer
2 - Department of Exercise Physiology,Central Tehran Branch, Islamic Azad University, Tehran, Iran.
3 - Associate Professor of Exercise Physiology, Department of Physical Education and Sport Sciences, East Tehran Branch, Islamic Azad University, Tehran, Iran
4 - Department of Exercise Physiology,Central Tehran Branch, Islamic Azad University, Tehran, Iran.
5 - Department of Exercise Physiology,Central Tehran Branch, Islamic Azad University, Tehran, Iran.
Keywords: Increasing Resistance Training, CHRNG, Semaphorine-a3, Neuro Muscular Junction,
Abstract :
Aim: Increasing the activity of the gamma acetylcholine receptor subunit and semaphorin a3 by affecting the transmission of nerve messages to the muscle causes a decrease in skeletal muscle function. The evidence shows that regular physical activities can lead to the development of muscle function by affecting the expression of these two genes. The purpose of this study was to investigate the effect of increasing resistance training on the expression of acetylcholine receptor gamma (CHRNG) and semaphorin-a3 (Sema3A) subunit genes in the gastrocnemius muscle of male rats. Method: In an experimental study, 12 six-week-old male rats, with an average weight of 195-220 grams, were randomly divided into 2 groups (6 in each group), resistance training (RT) and control (Control). The resistance training group performed incremental resistance training 5 days a week for 4 weeks. Twenty-four hours after the last training and recovery session, the subjects' sacrificial and biceps muscles were extracted to determine the expression of CHRNG and Sema3A genes by Real-time method. Results: The expression of CHRNG (P=0.044) and Semaphorine-a3 (P=0.040) genes decreased significantly in the resistance training group compared to the control group. Conclusion: The results of the present study showed that incremental resistance training can improve neuromuscular function by reducing the expression of CHRNG and Sema3A genes in the neuromuscular junction. Based on this, it is recommended to use increasing resistance exercises to improve muscle performance.
1. Harridge SD. Plasticity of human skeletal muscle: gene expression to in vivo function. Experimental physiology. 2007;92(5):783-97.
2. Koulmann N, Bigard A-X. Interaction between signalling pathways involved in skeletal muscle responses to endurance exercise. Pflügers Archiv. 2006;452(2):125-39.
3. Kraemer WJ, Spiering BA. Skeletal muscle physiology: plasticity and responses to exercise. Hormone Research in Paediatrics. 2006;66(Suppl. 1):2-16.
4. Dendrou CA, Fugger L, Friese MA. Immunopathology of multiple sclerosis. Nature Reviews Immunology. 2015;15(9):545-58.
5. Suzuki T, Do M-KQ, Sato Y, Ojima K, Hara M, Mizunoya W, et al. Comparative analysis of semaphorin 3A in soleus and EDL muscle satellite cells in vitro toward understanding its role in modulating myogenin expression. The international journal of biochemistry & cell biology. 2013;45(2):476-82.
6. Bussolino F, Valdembri D, Caccavari F, Serini G. Semaphoring vascular morphogenesis. Endothelium. 2006;13(2):81-91.
7. Pumplin DW, Reese T, Llinas R. Are the presynaptic membrane particles the calcium channels? Proceedings of the National Academy of Sciences. 1981;78(11):7210-3.
8. Hoffmann K, Müller JS, Stricker S, Megarbane A, Rajab A, Lindner TH, et al. Escobar syndrome is a prenatal myasthenia caused by disruption of the acetylcholine receptor fetal γ subunit. The American Journal of Human Genetics. 2006;79(2):303-12.
9. Aagaard P, Suetta C, Caserotti P, Magnusson SP, Kjær M. Role of the nervous system in sarcopenia and muscle atrophy with aging: strength training as a countermeasure. Scandinavian journal of medicine & science in sports. 2010;20(1):49-64.
10. Venkova K, Christov A, Kamaluddin Z, Kobalka P, Siddiqui S, Hensley K. Semaphorin 3A signaling through neuropilin-1 is an early trigger for distal axonopathy in the SOD1G93A mouse model of amyotrophic lateral sclerosis. Journal of Neuropathology & Experimental Neurology. 2014;73(7):702-13.
11. Svensson A, Libelius R, Tågerud S. Semaphorin 6C expression in innervated and denervated skeletal muscle. Journal of molecular histology. 2008;39(1):5-13.
12. De Winter F, Vo T, Stam FJ, Wisman LA, Bär PR, Niclou SP, et al. The expression of the chemorepellent Semaphorin 3A is selectively induced in terminal Schwann cells of a subset of neuromuscular synapses that display limited anatomical plasticity and enhanced vulnerability in motor neuron disease. Molecular and Cellular Neuroscience. 2006;32(1-2):102-17.
13. Deschenes MR, Roby MA, Eason MK, Harris MB. Remodeling of the neuromuscular junction precedes sarcopenia related alterations in myofibers. Experimental gerontology. 2010;45(5):389-93.
14. Gyorkos AM, McCullough MJ, Spitsbergen JM. Glial cell line-derived neurotrophic factor (GDNF) expression and NMJ plasticity in skeletal muscle following endurance exercise. Neuroscience. 2014;257:111-8.
15. Smith MB, Mulligan N. Peripheral neuropathies and exercise. Topics in Geriatric Rehabilitation. 2014;30(2):131-47.
16. Gyorkos AM, Spitsbergen JM. GDNF content and NMJ morphology are altered in recruited muscles following high‐speed and resistance wheel training. Physiological reports. 2014;2(2):e00235.
17. Little JP, Safdar A, Bishop D, Tarnopolsky MA, Gibala MJ. An acute bout of high-intensity interval training increases the nuclear abundance of PGC-1α and activates mitochondrial biogenesis in human skeletal muscle. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. 2011.
18. Deschenes M, Tenny K, Wilson M. Increased and decreased activity elicits specific morphological adaptations of the neuromuscular junction. Neuroscience. 2006;137(4):1277-83.
19. Wilson MH, Deschenes MR. The neuromuscular junction: anatomical features and adaptations to various forms of increased, or decreased neuromuscular activity. International journal of neuroscience. 2005;115(6):803-28.
20. Gharakhanlou R, Chadan S, Gardiner P. Increased activity in the form of endurance training increases calcitonin gene-related peptide content in lumbar motoneuron cell bodies and in sciatic nerve in the rat. Neuroscience. 1999;89(4):1229-39.
21. Uchitel O, Protti D, Sanchez V, Cherksey B, Sugimori M, Llinas R. P-type voltage-dependent calcium channel mediates presynaptic calcium influx and transmitter release in mammalian synapses. Proceedings of the National Academy of Sciences. 1992;89(8):3330-3.
22. Maffiuletti NA, Zory R, Miotti D, Pellegrino MA, Jubeau M, Bottinelli R. Neuromuscular adaptations to electrostimulation resistance training. American journal of physical medicine & rehabilitation. 2006;85(2):167-75.
23. Lee S, Farrar RP. Resistance training induces muscle-specific changes in muscle mass and function in rat. Journal of Exercise physiology online. 2003;6(2).
24. Gardiner PF. Neuromuscular aspects of physical activity: Human Kinetics; 2001.
25. Scott BR, Slattery KM, Sculley DV, Dascombe BJ. Hypoxia and resistance exercise: a comparison of localized and systemic methods. Sports medicine. 2014;44(8):1037-54.
26. Sakuma K, Watanabe K, Sano M, Uramoto I, Nakano H, Li Y-J, et al. A possible role for BDNF, NT-4 and TrkB in the spinal cord and muscle of rat subjected to mechanical overload, bupivacaine injection and axotomy. Brain research. 2001;907(1-2):1-19.
27. Gil JH, Kim CK. Effects of different doses of leucine ingestion following eight weeks of resistance exercise on protein synthesis and hypertrophy of skeletal muscle in rats. Journal of exercise nutrition & biochemistry. 2015;19(1):31.
28. Azarbaijani M, Nikbakht H, Rasae M. Sabeti Kh Effect of exhaustive incremental exercise session on salivary testosterone and cortisol in wrestlers. The Journal of Applied Sport Science Research. 2002;4:101-14.
29. Fahim MA. Endurance exercise modulates neuromuscular junction of C57BL/6NNia aging mice. Journal of applied physiology. 1997;83(1):59-66.
30. Ciobica A, Popescu R, Haulica I, Bild W. Aspects regarding the neurobiology of psycho-affective functions. Journal of Medical Biochemistry. 2012;31(2):83-7.
31. Su Y-H, Su Z, Zhang K, Yuan Q-K, Liu Q, Lv S, et al. The changes of p-Akt/MuRF1/FoxO1 proteins expressions in the conditions of training and immobilization in rats' gastrocnemius muscle. Sheng li xue bao:[Acta physiologica Sinica]. 2014;66(5):589-96.
32. ایلخانلار ق, حسن, نورشاهی, خداقلی, قراخانلو. اثر8 هفته تمرین مقاومتی فزاینده بر میزان پروتئین آگرین در عضلات اسکلتی موش های سالمندنر ویستار. پژوهشنامه فیزیولوژی ورزشی کاربردی. 2016;12(23):87-98.
33. حرمتی ق, امینایی, دخیلی, امیربهادر, شکاری ا. تاثیر یک دوره تمرین ورزشی با شدت بالا بر بیان ژن سمافورین 3A در عضله بازکننده طویل انگشتان پای موشهای پیر C57BL/6. مجله علمی دانشگاه علوم پزشکی ایلام. 2017;25(1):92-102.
34. Gerrett N, Ouzzahra Y, Redortier B, Voelcker T, Havenith G. Female thermal sensitivity to hot and cold during rest and exercise. Physiology & behavior. 2015;152:11-9.