تأثیر حاد تمرین تناوبی با شدت بالا (HIIT) بر بیان ژن‌های FNDC5 و PGC-1α در رت‌های نر دیابتی

نوع مقاله : مقاله پژوهشی

نویسندگان

1 دکتری فیزیولوژی ورزشی، دانشکدۀ تربیت بدنی و علوم ورزشی، دانشگاه گیلان، رشت، ایران

2 . استاد گروه فیزیولوژی ورزشی، دانشکدة تربیت بدنی و علوم ورزشی، دانشگاه تهران، تهران، ایران

3 استاد گروه فیزیولوژی ورزشی، دانشکدة تربیت بدنی و علوم ورزشی، دانشگاه تهران، تهران، ایران

4 . دانشجوی دکتری فیزیولوژی ورزشی، دانشکدة تربیت بدنی و علوم ورزشی، دانشگاه تهران، تهران، ایران

5 دانشیار دانشگاه تربیت مدرس، تهران، ایران

چکیده

بیان PGC-1α  ناشی از فعالیت ورزشی به افزایش بیان FNDC5 در عضله منجر می‌شود، این پروتئین غشایی  هورمون تازه شناسایی‌شدۀ ایرزین را ترشح می‌کند که سبب افزایش انرژی مصرفی، بهبود حساسیت انسولینی و تحمل گلوکز می‌شود. هدف از پژوهش حاضر بررسی تأثیر حاد تمرین تناوبی با شدت بالا (HIIT) بر بیان ژن‌های FNDC5 و PGC-1α رت‌های نر دیابتی است. در این مطالعه 18 سر رت نر دیابتی (12 هفته سن و با وزن 240-220 گرم) به سه گروه تقسیم شدند: تمرین تناوبی با شدت بالا بلافاصله (HIIT0)(6سر)، تمرین تناوبی با شدت بالا 2 ساعت بعد (HIIT2) (6سر) و کنترل (C) (5سر). هر دو گروه HIIT با سرعت vo2max90-95% در 12 تناوب 1 دقیقه‌ای با فواصل استراحتی 1 دقیقه‌ای به فعالیت روی نوار گردان پرداختند. برای بررسی بیان نسبی mRNA ژن‌های FNDC5 و PGC-1α بافت عضلانی از روش Real time PCR استفاده شد. از آزمون ANOVA و تست تعقیبی توکی برای تحلیل داده‌ها استفاده و سطح معنا‌داری 05/0 درنظر گرفته شد. تحلیل داده‌ها نشان داد که بین گروه‌های تحقیق در بیان ژن‌های FNDC5 و PGC-1α تفاوت معنا‌داری وجود دارد (01/0P≤). نتایج آزمون توکی نشان داد، بیان ژن‌های FNDC5 و PGC-1α در هر دو گروه تمرین تناوبی با شدت بالا (HIIT0-HIIT2) نسبت به گروه کنترل افزایش معنا‌داری داشتند (01/0P≤). بنابراین، نتایج این تحقیق نشان داد که یک جلسه تمرین تناوبی با شدت بالا (HIIIT) با القای PGC-1α به تحریک بیان ژن  FNDC5 در رت‌های دیابتی منجر می‌شود.

کلیدواژه‌ها


عنوان مقاله [English]

The acute effects of high intensity interval training (HIIIT) on PGC-1α and FNDC5 genes expression in diabetic rats

نویسندگان [English]

  • mousa khalafi 1
  • Ali Asghar Ravasi 2
  • Rahman Soori 3
  • Mohammad Moradi 4
  • Massoud Soleimani 5
1 PhD of Exercise Physiology, Faculty of Physical Education and Sport Sciences, University of Guilan, Rasht, Iran
2 Professor, Department of Exercise Physiology, Faculty of Physical Education and Sport Sciences, University of Tehran, Tehran, Iran,
3 Professor, Department of Exercise Physiology, Faculty of Physical Education, University of Tehran, Tehran, Iran
4 PhD Student of Exercise Physiology, Faculty of Physical Education and Sport Sciences, University of Tehran, Tehran, Iran
5 Associate Professor, Tarbiat Modares University, Tehran, Iran
چکیده [English]

Change in adipose tissue phenotype caused by exercise training is new theory that as result of muscle FNDC5 gene expression. The aim of the present study is to investigate the acute effects of high intensity interval training (HIIT( on PGC-1α and FNDC5 genes expression of diabetic rats. In this study, 18 diabetic wistar rats(12 week- age, 220-240 gr- weight) were assigned to three groups: high intensity interval training Immediately (HIIE0)(n=6), high intensity interval training 2hours later (HIIE2)(n=6) and control(C)(n=5). Both HIIT groups activated on the treadmill with 90-95% vo2max in the 12 interval-one minute period and 1 minute rest intervals. Real time PCR method was used for the relative expression of mRNA FNDC5 and PGC-1α. One-way ANOVA and Tukey Post hoc test has used to data analysis, the level of significance has been consider at 0/05. Data Analysis showed significant differences Research groups in expression of mRNA FNDC5 and PGC-1α (p≤0/01.) Tukey test showed, FNDC5 and PGC-1α gene expression In the 2 groups high intensity interval training(HIIT0-HIIT2) compared to the control group significantly increased (p≤0/01).

کلیدواژه‌ها [English]

  • high intensity interval training (HIIIT)
  • FNDC5 gene expression
  • PGC-1α gene expression
  • diabetic rats
1.   Gulcelik, N.E., A. Usman, and A. Gürlek, Role of adipocytokines in predicting the development of diabetes and its late complications. Endocrine, 2009. 36(3): p. 397-403.
2.   Eckardt, K., et al., Myokines in insulin resistance and type 2 diabetes. Diabetologia, 2014. 57(6): p. 1087-1099.
3.   Raschke, S. and J. Eckel, Adipo-myokines: two sides of the same coin—mediators of inflammation and mediators of exercise. Mediators of inflammation, 2013. 2013.
4.   Boström, P., et al., A PGC1-α-dependent myokine that drives brown-fat-like development of white fat and thermogenesis. Nature, 2012. 481(7382): p. 463-468.
5.   Handschin, C. and B.M. Spiegelman, The role of exercise and PGC1α in inflammation and chronic disease. Nature, 2008. 454(7203): p. 463-469.
6.   van Marken Lichtenbelt, W.D., et al., Cold-activated brown adipose tissue in healthy men. New England Journal of Medicine, 2009. 360(15): p. 1500-1508.
7.   Pekkala, S., et al., Are skeletal muscle FNDC5 gene expression and irisin release regulated by exercise and related to health? The Journal of physiology, 2013. 591(21): p. 5393-5400.
8.   Mahajan, R.D. and S.K. Patra, Irisin, a novel myokine responsible for exercise induced browning of white adipose tissue. Indian Journal of Clinical Biochemistry, 2013. 28(1): p. 102.
9.   Choi, Y.-K., et al., Serum irisin levels in new-onset type 2 diabetes. Diabetes research and clinical practice, 2013. 100(1): p. 96-101.
10. Moholdt, T.T., et al., Aerobic interval training versus continuous moderate exercise after coronary artery bypass surgery: a randomized study of cardiovascular effects and quality of life. American heart journal, 2009. 158(6): p. 1031-1037.
11. Laursen, P.B. and D.G. Jenkins, The scientific basis for high-intensity interval training. Sports medicine, 2002. 32(1): p. 53-73.
12. Gibala, M.J., et al., Physiological adaptations to low‐volume, high‐intensity interval training in health and disease. The Journal of physiology, 2012. 590(5): p. 1077-1084.
13. Burgomaster, K.A., et al., Similar metabolic adaptations during exercise after low volume sprint interval and traditional endurance training in humans. The Journal of physiology, 2008. 586(1): p. 151-160.
14. Gibala, M.J. and S.L. McGee, Metabolic adaptations to short-term high-intensity interval training: a little pain for a lot of gain? Exercise and sport sciences reviews, 2008. 36(2): p. 58-63.
15. Helgerud, J., et al., Aerobic high-intensity intervals improve V˙ O2max more than moderate training. Medicine & Science in Sports & Exercise, 2007. 39(4): p. 665-671.
16. Perry, C.G., et al., High-intensity aerobic interval training increases fat and carbohydrate metabolic capacities in human skeletal muscle. Applied Physiology, Nutrition, and Metabolism, 2008. 33(6): p. 1112-1123.
17. Boutcher, S.H., High-intensity intermittent exercise and fat loss. Journal of obesity, 2011. 2011.
18. Gibala, M.J., et al., Brief intense interval exercise activates AMPK and p38 MAPK signaling and increases the expression of PGC-1α in human skeletal muscle. Journal of applied physiology, 2009. 106(3): p. 929-934.
19. Khalafi, M., et al., The impact of moderate-intensity continuous or high-intensity interval training on adipogenesis and browning of subcutaneous adipose tissue in obese male rats. Nutrients, 2020. 12(4): p. 925.
20. Khalafi, M., H. Mohebbi, and P. Karimi, High-intensity interval training increases mitochondria biogenesis in adipose tissue and improves insulin resistance in high fat diet-induced obese rat. International Journal of Applied Exercise Physiology, 2019. 8(1): p. 43-50.
21. Soyal, S., et al., PGC-1α: a potent transcriptional cofactor involved in the pathogenesis of type 2 diabetes. Diabetologia, 2006. 49(7): p. 1477-1488.
22. Liang, H. and W.F. Ward, PGC-1α: a key regulator of energy metabolism. Advances in physiology education, 2006.
23. Calcutt, N.A., Modeling diabetic sensory neuropathy in rats, in Pain Research. 2004, Springer. p. 55-65.
24. Høydal, M.A., et al., Running speed and maximal oxygen uptake in rats and mice: practical implications for exercise training. European Journal of Cardiovascular Prevention & Rehabilitation, 2007. 14(6): p. 753-760.
25. Huh, J.Y., et al., FNDC5 and irisin in humans: I. Predictors of circulating concentrations in serum and plasma and II. mRNA expression and circulating concentrations in response to weight loss and exercise. Metabolism, 2012. 61(12): p. 1725-1738.
26. Shaban, N., K. Kenno, and K. Milne, The effects of a 2 week modified high intensity interval training program on the homeostatic model of insulin resistance (HOMA-IR) in adults with type 2 diabetes. The Journal of sports medicine and physical fitness, 2014. 54(2): p. 203-209.
27. Wenz, T., et al., Increased muscle PGC-1α expression protects from sarcopenia and metabolic disease during aging. Proceedings of the National Academy of Sciences, 2009. 106(48): p. 20405-20410.
28. Wende, A.R., et al., A role for the transcriptional coactivator PGC-1α in muscle refueling. Journal of Biological Chemistry, 2007. 282(50): p. 36642-36651.
29. Lin, J., et al., Defects in Adaptive Energy Metabolism with CNS-Linked Hyperactivity in PGC-1α Null Mice. Cell, 2004. 119(1): p. 121-135.
30. Little, J.P., et al., 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. 300(6): p. R1303-R1310.
31. Raschke, S. and J. Eckel, Adipo-Myokines: Two Sides of the Same Coin—Mediators of Inflammation and Mediators of Exercise. Mediators of Inflammation, 2013. 2013: p. 320724.
32. Tjønna, A.E., et al., Aerobic Interval Training Versus Continuous Moderate Exercise as a Treatment for the Metabolic Syndrome. Circulation, 2008. 118(4): p. 346-354.
33. Pekkala, S., et al., Are skeletal muscle FNDC5 gene expression and irisin release regulated by exercise and related to health? J Physiol, 2013. 591(21): p. 5393-400.
34. Huh, J.Y., et al., FNDC5 and irisin in humans: I. Predictors of circulating concentrations in serum and plasma and II. mRNA expression and circulating concentrations in response to weight loss and exercise. Metabolism, 2012. 61(12): p. 1725-38.
35. Chen, Z.-P., et al., AMPK signaling in contracting human skeletal muscle: acetyl-CoA carboxylase and NO synthase phosphorylation. American Journal of Physiology-Endocrinology and Metabolism, 2000. 279(5): p. E1202-E1206.
36. Jäger, S., et al., AMP-activated protein kinase (AMPK) action in skeletal muscle via direct phosphorylation of PGC-1α. Proceedings of the National Academy of Sciences, 2007. 104(29): p. 12017-12022.
37. Knutti, D., D. Kressler, and A. Kralli, Regulation of the transcriptional coactivator PGC-1 via MAPK-sensitive interaction with a repressor. Proceedings of the National Academy of Sciences, 2001. 98(17): p. 9713-9718.
38. Huh, J.Y., et al., Exercise-induced irisin secretion is independent of age or fitness level and increased irisin may directly modulate muscle metabolism through AMPK activation. The Journal of Clinical Endocrinology & Metabolism, 2014. 99(11): p. E2154-E2161.
39. Tsuchiya, Y., et al., High-intensity exercise causes greater irisin response compared with low-intensity exercise under similar energy consumption. The Tohoku journal of experimental medicine, 2014. 233(2): p. 135-140.