دوره 17، شماره 18 - ( 10-1398 )
جلد 17 شماره 18 صفحات 11-1 |
برگشت به فهرست نسخه ها
Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
Kazem A, Haghpanah A, Dakhili A. The effect of high-intensity exercise training on gene expression of tweak and Fn14 in EDL muscle of aged and adult mice. RSMT 2019; 17 (18) :1-11
URL: http://jsmt.khu.ac.ir/article-1-395-fa.html
URL: http://jsmt.khu.ac.ir/article-1-395-fa.html
کاظمی عبدالرضا، حق‌پناه علیرضا، دخیلی امیربهادر. تأثیر چهار هفته تمرین HIIT بر بیان ژن Tweak و Fn14عضلۀ EDL موشهای پیر و بالغ. پژوهش در طب ورزشی و فناوری. 1398; 17 (18) :1-11
چکیده: (3886 مشاهده)
آتروفی عضلانی از پیامدهای سالمندی است و فعالیت ورزشی ممکن است از آن جلوگیری کند. هدف پژوهش حاضر بررسی اثر تمرین تناوبی شدید بر بیان ژنهای Tweak و Fn14 عضلۀ EDL موشهای پیرنژاد C57bl/6 است. به این منظور، 28 سر موش C57bl/6 پیر (14=n) 24 تا 26 ماه و بالغ (14=n) چهار تا شش ماه در دو گروه تمرین (7=n) و کنترل (7=n) قرار گرفت. گروههای تمرین پس از یکهفته آشناسازی، در برنامۀ چهار هفته‌ای تمرین تناوبی شدید روی تردمیل با شدت 85 درصد سرعت بیشینه در هفتۀ اول تا 95 درصد سرعت بیشینه در هفتۀ آخر، در تناوبهای دو دقیقهای (شش وهله در هفتۀ اول تا ده وهله در هفتۀ آخر) یا یک دقیقه استراحت غیرفعال، مشارکت داده شدند. 48 ساعت پس از آخرین جلسۀ تمرینی، عضلۀ EDL استخراج شد و میزان بیان ژنهای Tweak و Fn14 اندازه‌گیری شد. نتایج نشان داد که پیری اثر معنیداری بر وزن عضلۀ EDL دارد (0/032=P)؛ همچنین، پیری موجب افزایش معنیدار بیان Tweak و Fn14 شده است (به ترتیب 0/001=P و 0/002=P)؛ تمرین ورزشی بیان این ژنها را در عضلۀ EDL هر دو نوع موش بالغ و پیر کاهش داد (0/001=P)؛ از سوی دیگر، با اینکه تمرین ورزشی وزن عضله را مقداری افزایش داد اما این مقدار به‌لحاظ آماری در هر دو گروه بالغ (0/117=P) و پیر (0/321=P) معنیدار نبود؛ بنابراین، افزایش سن با افزایش بیان ژنهای Tweak و Fn14 همراه است که ممکن است به تغییرات تودۀ عضلانی همراه با افزایش سن مربوط باشد و با توجه به کاهش بیان این ژنها بر اثر تمرینات شدید، این تمرینات ممکن است در دوران سالمندی به منظور حفظ تودۀ عضلانی مؤثر باشد.
نوع مطالعه: پژوهشي |
دریافت: 1398/11/15 | پذیرش: 1398/11/15 | انتشار: 1398/11/15
دریافت: 1398/11/15 | پذیرش: 1398/11/15 | انتشار: 1398/11/15
فهرست منابع
1. Li, Y.P., Chen, Y., John, J., Moylan, J., Jin, B., Mann, D.L., Reid, M.B. (2005). TNF-alpha acts via p38 MAPK to stimulate expression of the ubiquitin ligase atrogin1/MAFbx in skeletal muscle. FASEB Journal. 19(3):362-70. [DOI:10.1096/fj.04-2364com]
2. Verhees, K.J., Schols, A.M., Kelders, M.C., Op den Kamp, C.M., van der Velden, J.L., Langen, R.C. (2011). Glycogen synthase kinase-3β Iis required for the induction of skeletal muscle atrophy. American Journal of Physiology-Cell Physiology. 301(5):995-1007. [DOI:10.1152/ajpcell.00520.2010]
3. Fanzani, A., Conraads, V.M., Penna, F., Martinet, W. (2012). Molecular and cellular mechanisms of skeletal muscle atrophy: an update. Journal of Cachexia and Sarcopenia Muscle. 3(3):163-79. [DOI:10.1007/s13539-012-0074-6]
4. Klitgaard, H., Mantoni, M., Schiaffino, S., Ausoni, S., Gorza, L., Laurent-Winter, C., Schnohr, P., Saltin, B. (1990). Function, morphology and protein expression of aging skeletal muscle: A cross‐sectional study of elderly men with different Ttraining backgrounds. Acta Physiologica Scandinavia. 140(1):41-54. [DOI:10.1111/j.1748-1716.1990.tb08974.x]
5. Dreyer, H.C., Blanco, C.E., Sattler, F.R., Schroeder, E.T., Wiswell, R.A. (2006). Satellite cell numbers in young and older men 24 hours after eccentric exercise. Muscle and Nerve. 33(2):242-53. [DOI:10.1002/mus.20461]
6. Edwards, J.N., Blackmore, D.G., Gilbert, D.F., Murphy, R.M., Launikonis, B.S. (2011). Store‐operated calcium entry remains fully functional in aged mouse skeletal muscle despite a decline in STIM1 protein expression. Aging Cell. 10(4):675-85. [DOI:10.1111/j.1474-9726.2011.00706.x]
7. Zhao, X ., Weisleder, N., Thornton, A., Oppong, Y., Campbell, R., Ma, J., Brotto, M. (2008). Compromised store‐operated Ca2+ entry in aged skeletal muscle. Aging Cell. 7(4):561-8. [DOI:10.1111/j.1474-9726.2008.00408.x]
8. Paul, P.K., Gupta, S.K., Bhatnagar, S., Panguluri, S.K., Darnay, B.G., Choi, Y., Kumar, A. (2010). Targeted ablation of TRAF6 inhibits skeletal muscle wasting in mice. Journal of Cell Biology. 191(7):1395-411. [DOI:10.1083/jcb.201006098]
9. Burkly, L.C., Michaelson, J.S., Zheng, T.S. (2011). TWEAK/Fn14 pathway: an immunological switch for shaping tissue responses. Immunological Reviwes. 244(1):99-114. [DOI:10.1111/j.1600-065X.2011.01054.x]
10. Dogra, C., Changotra, H., Mohan, S., Kumar, A. (2006). Tumor necrosis factor-like weak inducer of apoptosis inhibits skeletal myogenesis through sustained activation of nuclear factor-κB and degradation of MyoD protein. The Journal of Biological Chemistry. 281(15):10327-36. [DOI:10.1074/jbc.M511131200]
11. Clarke, B.A., Drujan, D., Willis, M.S., Murphy, L.O., Corpina, R.A., Burova, E., Rakhilin, S.V., Stitt, T.N., Patterson, C., Latres, E., Glass, D.J. (2007). The E3 Ligase MuRF1 degrades myosin heavy chain protein in dexamethasone-treated skeletal muscle. Cell Metabolism. 6(5):376-85. [DOI:10.1016/j.cmet.2007.09.009]
12. Bhatnagar, S., Mittal, A., Gupta, S.K., Kumar, A. (2012). TWEAK causes myotube atrophy through coordinated activation of ubiquitin‐proteasome system, autophagy, and caspases. Journal of Cellular Physiology. 227(3):1042-51. [DOI:10.1002/jcp.22821]
13. Peterson, J.M., Bakkar, N., Guttridge, D.C. (2011). NF-kB signaling in skeletal muscle health and disease. Current Topics in Developmental Biology. 96:85-119. [DOI:10.1016/B978-0-12-385940-2.00004-8]
14. Mittal, A., Bhatnagar, S., Kumar, A., Lach-Trifilieff, E., Wauters, S., Li, H., Makonchuk, D.Y., Glass, D.J., Kumar, A. (2010). The TWEAK-Fn14 system is a critical regulator of denervation-induced skeletal muscle atrophy in mice. Journal of Cellular Biology. 188(6):833-49. [DOI:10.1083/jcb.200909117]
15. Meng, S.J., Yu, L.J. (2010). Oxidative stress, molecular inflammation and sarcopenia. International Journal of Molecullar Science. 11(4):1509-26. [DOI:10.3390/ijms11041509]
16. Sheffield-Moore, M., Yeckel, C.W., Volpi, E., Wolf, S.E., Morio, B., Chinkes, D.L., Paddon-Jones, D., Wolfe, R.R. (2004). Postexercise protein metabolism in older and younger men following moderate-intensity aerobic exercise. American Journal of Physiology-Endocrinology Metabolism. 287(3):513-22. [DOI:10.1152/ajpendo.00334.2003]
17. Raue, U., Slivka, D., Jemiolo, B., Hollon, C., Trappe, S. (2006). Myogenic gene expression at rest and after a bout of resistance exercise in young (18-30 yr) and old (80-89 yr) women. Journal of Applied Physiology. 101(1):53-9. [DOI:10.1152/japplphysiol.01616.2005]
18. Cunha, T.F., Bacurau, A.V., Moreira, J.B., Paixão, N.A., Campos, J.C., Ferreira, J.C., Leal, M.L., Negrão, C.E., Moriscot, A.S., Wisløff, U., Brum, P.C. (2012). Exercise training prevents oxidative stress and ubiquitin-proteasome system overactivity and reverse skeletal muscle atrophy in heart failure. PLoS One. 7(8):1-11. [DOI:10.1371/journal.pone.0041701]
19. Gielen, S., Sandri, M., Kozarez, I., Kratzsch, J., Teupser, D., Thiery, J., Erbs, S., Mangner, N., Lenk, K., Hambrecht, R., Schuler, G., Adams, V. (2012). Exercise training attenuates MuRF-1 expression in the skeletal muscle of patients with chronic heart failure independent of age the randomized leipzig exercise intervention in chronic heart failure and aging catabolism study. Circulation. 125(22):2716-27. [DOI:10.1161/CIRCULATIONAHA.111.047381]
20. Shefer, G., Rauner, G., Yablonka-Reuveni, Z., Benayahu, D. (2010). Reduced satellite cell numbers and myogenic capacity in aging can be alleviated by endurance exercise. PLoS One. 5(10):1-11. [DOI:10.1371/journal.pone.0013307]
21. Gibala, M.J., Little, J.P., van Essen, M., Wilkin, G.P., Burgomaster, K.A., Safdar, A., Raha, S., Tarnopolsky, M.A. (2006). Short‐term sprint interval versus traditional endurance training: similar initial adaptations in human skeletal muscle and exercise performance. The Journal of Physiology. 575(Pt 3):901-11. [DOI:10.1113/jphysiol.2006.112094]
22. Snijders, T., Verdijk, L.B., van Loon, L.J. (2009).The impact of sarcopenia and exercise training on skeletal muscle satellite cells. Ageing Research Reviews. 8(4):328-38. [DOI:10.1016/j.arr.2009.05.003]
23. Ferreira, J.C., Bacurau, A.V., Bueno, C.R., Cunha, T.C., Tanaka, L.Y., Jardim, M.A., Ramires, P.R., Brum, P.C. (2010). Aerobic exercise training improves Ca2+ handling and redox status of skeletal muscle in mice. Exprimental Biology Medicin (Maywood). 235(4):497-505. [DOI:10.1258/ebm.2009.009165]
24. Thomas, C., Bishop, D., Moore-Morris, T, Mercier, J. (2007). Effects of high-intensity training on Mct1, Mct4, and Nbc expressions in rat skeletal muscles: influence of chronic metabolic alkalosis. American Journal of Physiology-Endocrinology Metabolism. 293(4):E916-22. [DOI:10.1152/ajpendo.00164.2007]
25. Vinciguerra, M., Musaro, A., Rosenthal, N. (2010). Regulation of muscle atrophy in aging and disease. Advances in Experimental Medicine and Biology. 694:211-33. [DOI:10.1007/978-1-4419-7002-2_15]
26. Li, H., Malhotra, S., Kumar, A. (2008). Nuclear factor-kappa B signaling in skeletal muscle atrophy. Journal of Molecular Medicine (Berl). 86(10):1113-26. [DOI:10.1007/s00109-008-0373-8]
27. Chicheportiche, Y., Bourdon, P.R., Xu, H., Hsu, Y.M., Scott, H., Hession, C., Garcia, I., Browning, J.L. (1997). TWEAK, a new secreted ligand in the tumor necrosis factor family that weakly induces apoptosis. The Journal of Biological Chemistry. 272(51):32401-10. [DOI:10.1074/jbc.272.51.32401]
28. Kumar, A., Bhatnagar, S., Paul, P.K. (2012).TWEAK and TRAF6 regulate skeletal muscle atrophy. Current Opinion in Clinical Nutrition and Metabolic Care.15(3):233-9. [DOI:10.1097/MCO.0b013e328351c3fc]
29. Tajrishi, M.M., Sato, S., Shin, J., Zheng, T.S., Burkly, L.C., Kumar, A. (2014). The TWEAK-Fn14 dyad is involved in age-associated pathological changes in skeletal muscle. Biochemical and Biophysical Research Communication. 446(4):1219-24. [DOI:10.1016/j.bbrc.2014.03.084]
30. Shi, J., Jiang, B., Qiu, Y., Guan, J., Jain, M., Cao, X., Bauer, M., Su, L., Burkly, L.C., Leone, T.C., Kelly, D.P., Liao, R. (2013). PGC1alpha plays a critical role in TWEAK-induced cardiac dysfunction. PLoS One. 8(1):e54054. [DOI:10.1371/journal.pone.0054054]
31. Gomes, A.V., Waddell, D.S., Siu, R., Stein, M., Dewey, S., Furlow, J.D., Bodine, S.C. (2012). Upregulation of proteasome activity in muscle RING finger 1-null mice following denervation. FASEB Journal. 26(3):2886-99. [DOI:10.1096/fj.12-204495]
32. Arbat-Plana, A., Cobianchi, S., Herrando-Grabulosa, M., Navarro, X., Udina, E. (2017). Endogenous modulation of TrkB signaling by treadmill exercise after peripheral nerve injury. Neuroscience. 340:188-200. [DOI:10.1016/j.neuroscience.2016.10.057]
33. English, A.W., Wilhelm, J.C., Sabatier, M.J. (2011). Enhancing recovery from peripheral nerve injury using treadmill training. Annals of Anatomy.193(4):354-61. [DOI:10.1016/j.aanat.2011.02.013]
34. Gleeson, M., Bishop, N.C., Stensel, D.J., Lindley, M.R., Mastana, S.S. Nimmo, M.A. (2011). The anti-inflammatory effects of exercise: mechanisms and implications for the prevention and treatment of disease. Nature Reviews Immunology. 11(9):607-15. [DOI:10.1038/nri3041]
35. Moreira, J.B., Bechara, L.R., Bozi, L.H., Jannig, P.R., Monteiro, A.W., Dourado, P.M., Wisløff, U., Brum, P.C. (2013). High- versus moderate-intensity aerobic exercise training effects on skeletal muscle of infarcted rats. Journal of Applied Physiology. 114(8):1029-41. [DOI:10.1152/japplphysiol.00760.2012]
36. Little, J.P., Safdar, A., Bishop, D., Tarnopolsky, M.A., Gibala, M.J. (2011). 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. 300(6):R1303-10. [DOI:10.1152/ajpregu.00538.2010]
37. Gurd, B.J., Perry, C.G., Heigenhauser, G.J., Spriet, L.L., Bonen, A. (2010). High-intensity interval training increases SIRT1 activity in human skeletal muscle. Applied Physiology, Nutrition and Metabolism. 35(3):350-7. [DOI:10.1139/H10-030]
| بازنشر اطلاعات | |
 |
این مقاله تحت شرایط Creative Commons Attribution-NonCommercial 4.0 International License قابل بازنشر است. |
