مقایسة اثر تمرین تناوبی شدید و مقاومتی فزاینده بر بیان ژن ATF3 عضلة قلبی موش‌های صحرایی دیابتی نر

نوع مقاله : علمی - پژوهشی

نویسندگان

1 دانشکده تربیت بدنی و علوم ورزشی، دانشگاه خوارزمی، تهران، ایران

2 دانشکده علوم و فناوری زیستی، دانشگاه شهید بهشتی، تهران، ایران

چکیده

هدف: با توجه به تناقضات موجود دربارة نقش عامل رونویسی فعال‌شدة 3 به‌عنوان یک شاخص غیرالتهابی فعالیت میوکاردی در ناهنجاری‌های متابولیکی مانند دیابت، پژوهش حاضر با هدف مقایسة اثر دو تمرین تناوبی شدید و مقاومتی فزاینده بر بیان ژن ATF3 عضلة قلبی موش‌های صحرایی دیابتی نر انجام گرفت.
روش‌ها: 60 سر موش صحرایی نر 6 هفته‌ای با میانگین وزنی 150 گرم به‌صورت تصادفی به پنج گروه دیابتی (D)، دیابت- تناوبی شدید (DIT)، تناوبی شدید (HIIT)، مقاومتی  (RT)و دیابت- مقاومتی  (DRT)تقسیم شدند. تمرین تناوبی شدید شامل 10 تکرار 1 دقیقه‌ای دویدن روی نوار گردان با 2 دقیقه استراحت و تمرین مقاومتی فزاینده شامل 4 صعود از نردبان مقاومتی همراه وزنه بود. برنامة تمرین، 3 روز در هفته، به مدت 6 هفته همزمان انجام گرفت. تجزیه‌وتحلیل داده‌ها با آزمون فیشر و M-ANOVA در سطح معناداری 01/0P≤ انجام گرفت.
نتایج: میزان افزایش معنادار بیان ATF3 در دیابت-تناوبی شدید نسبت به دیابت بیشتر بود (001/0P<). بین دو گروه افزایش معنادار (001/0P = ) بیشتر بود، پاسخ فزایندة بیان ژن ATF3 در گروه دیابت تناوبی شدید به‌طور معنادار بیشتر از پاسخ بیان ژن ATF3 گروه دیابت –تمرین مقاومتی بود (03/0P =).
نتیجه‌گیری: تمرین تناوبی شدید در مقایسه با تمرین مقاومتی فزاینده سازوکارهای سلولی مولکولی مختلف را به‌طور مؤثرتری فعال می‌کند و احتمالاً موجب کاهش چشمگیر تأثیرات منفی ناشی از بیماری دیابت بر دستگاه قلبی- عروقی می‌شود.

کلیدواژه‌ها

عنوان مقاله [English]

The Comparison of the effect of High Intensity Interval and Progressive Resistance Training on Activated Transcription Factor 3 myocardial gene expression in male Diabetic Rats

نویسندگان [English]

  • Shahabuddin Sefal Manesh 1
  • Neda Khaledi 1
  • Hamid Rajabi 1
  • Hossein Askari 2
1 Faculty of Physical Education and Sports Sciences, Kharazmi University, Tehran, Iran
2 Faculty of Life Sciences and Biotechnology, Shahid, Beheshti University, Tehran,, Iran,
چکیده [English]

Purpose: According to the controversy about the role of ATF3 as a non-inflammatory index of myocardia in metabolic abnormalities as diabetes, the purpose of this study was to compare the effect of high intensity interval versus progressive resistance training on ATF3 myocardial gene expression of male diabetic rats.
Methods: Sixty male six weeks rats with a weighing average of 150 g were randomly divided into five groups: diabetic (D), diabetes- high intensity interval training (DIT), high intensity interval training (HIIT), resistance (RT), and diabetes- resistance training (DRT). High intensity interval training included 10 repetitions of one minute running on a treadmill with two minutes of rest. Progressive resistance training included four climb of a resistance ladder with weights. The training program was performed three days a week for six weeks. Data analysis was performed using Fisher's and M-ANOVA tests at a significant level of P ≤ 0.01.
Results: Significant increase in expression of ATF3 in diabetes- high intensity interval training group was observed between diabetes and diabetes- high intensity interval training (P <0.001). Between two groups of diabetes and diabetes- resistance training (P = 0.001), there was a significant increase in expression in diabetes- resistance training. In comparison between DIT and DRT groups, progressive respond were observed in DIT versus DRT (P = 0.03).
Conclusion: high intensity interval training has been shown to be more effective in comparison with the progressive resistance training, because it activates more different molecular cell mechanisms, perhaps, significantly reduces the negative effects of diabetes mellitus on cardiovascular disease.
 

کلیدواژه‌ها [English]

  • Active Transcription Factor 3
  • Heart Tissue
  • High intensity Interval Training
  • Diabetes

مراجع

  1. Demmer RT, Allison MA, Cai J, Kaplan RC, Desai AA, Hurwitz BE, et al. Association of Impaired Glucose Regulation and Insulin Resistance With Cardiac Structure and FunctionCLINICAL PERSPECTIVE. Circulation: Cardiovascular Imaging. 2016;9(10):e005032.
  2. Brownrigg JR, Hughes CO, Burleigh D, Karthikesalingam A, Patterson BO, Holt PJ, et al. Microvascular disease and risk of cardiovascular events among individuals with type 2 diabetes: a population-level cohort study. The Lancet Diabetes & Endocrinology. 2016;4(7):588-97.
  3. Bugger H, Abel ED. Molecular mechanisms of diabetic cardiomyopathy. Diabetologia. 2014;57(4):660-71.
  4. Hölscher ME, Bode C, Bugger H. Diabetic Cardiomyopathy: Does the Type of Diabetes Matter? International Journal of Molecular Sciences. 2016;17(12):2136.
  5. Ghigo A, Frati G, Sciarretta S. A novel protective role for activating transcription factor 3 in the cardiac response to metabolic stress. The Oxford University Press; 2017.
  6. Lin H, Li H-F, Chen H-H, Lai P-F, Juan S-H, Chen J-J, et al. ATF3 Protects Against Pressure Overload Heart Failure Via Autophagy Molecule Beclin-1 Pathway. Molecular pharmacology. 2014:mol. 113.090092.
  7. Zmuda EJ, Qi L, Zhu MX, Mirmira RG, Montminy MR, Hai T. The roles of ATF3, an adaptive-response gene, in high-fat-diet-induced diabetes and pancreatic β-cell dysfunction. Molecular Endocrinology. 2010;24(7):1423-33.
  8. Holloway TM, Bloemberg D, da Silva ML, Simpson JA, Quadrilatero J, Spriet LL. High intensity interval and endurance training have opposing effects on markers of heart failure and cardiac remodeling in hypertensive rats. PloS one. 2015;10(3):e0121138.
  9. Goodwin ML. Blood glucose regulation during prolonged, submaximal, continuous exercise: a guide for clinicians. Journal of diabetes science and technology. 2010;4(3):694-705.
  10. Suh S-H, Paik I-Y, Jacobs K. Regulation of blood glucose homeostasis during prolonged. Mol cells. 2007;23:272-9.
  11. Veeranki S, Givvimani S, Kundu S, Metreveli N, Pushpakumar S, Tyagi SC. Moderate intensity exercise prevents diabetic cardiomyopathy associated contractile dysfunction through restoration of mitochondrial function and connexin 43 levels in db/db mice. Journal of molecular and cellular cardiology. 2016;92:163-73.
  12. Chrysohoou C, Tsitsinakis G, Vogiatzis I, Cherouveim E, Antoniou C, Tsiantilas A, et al. High intensity, interval exercise improves quality of life of patients with chronic heart failure: a randomized controlled trial. QJM. 2014;107(1):25-32.
  13. Castaneda C, Layne JE, Munoz-Orians L, Gordon PL, Walsmith J, Foldvari M, et al. A randomized controlled trial of resistance exercise training to improve glycemic control in older adults with type 2 diabetes. Diabetes care. 2002;25(12):2335-41.
  14. Songstad NT KK-H, Hafstad AD, Basnet P, Ytrehus K, Acharya G. Effects of High Intensity Interval Training on Pregnant Rats, and the Placenta, Heart and Liver of Their Fetuses. PloS one. 2015;10(11).
  15. Ali Gaeini A, Khaledi N, Fayazmilani R, Ravasi A, Sedghroohi G, Arabkari V. Changes in ACTN3 gene expression and fiber type composition in flexor hallucis longus muscle after eight weeks progressive resistance training in Sprague-Dawley rats. Tehran University Medical Journal. 2013;71(1).
  16. Kalfon R, Koren L, Aviram S, Schwartz O, Hai T, Aronheim A. ATF3 expression in cardiomyocytes preserves homeostasis in the heart and controls peripheral glucose tolerance. Cardiovascular Research. 2016:cvw228.
  17. Feng J, Sun Q, Wu T, Lu J, Qu L, Sun Y, et al. Upregulation of ATF-3 is correlated with prognosis and proliferation of laryngeal cancer by regulating Cyclin D1 expression. International journal of clinical and experimental pathology. 2013;6(10):2064.
  18. Ghigo A, Frati G, Sciarretta S. A novel protective role for activating transcription factor 3 in the cardiac response to metabolic stress. Oxford University Press; 2016.
  19. Suganami T, Yuan X, Shimoda Y, Uchio-Yamada K, Nakagawa N, Shirakawa I, et al. Activating transcription factor 3 constitutes a negative feedback mechanism that attenuates saturated Fatty acid/toll-like receptor 4 signaling and macrophage activation in obese adipose tissue. Circulation research. 2009;105(1):25-32.
  20. Kalfon R, Koren L, Aviram S, Schwartz O, Hai T, Aronheim A. ATF3 expression in cardiomyocytes preserves homeostasis in the heart and controls peripheral glucose tolerance. Cardiovascular research. 2016;113(2):134-46.
  21. Simonsen ML, Alessio HM, White P, Newsom DL, Hagerman AE. Acute physical activity effects on cardiac gene expression. Experimental physiology. 2010;95(11):1071-80.

فایل ها

سابقه مقاله

  • تاریخ دریافت: 06 شهریور 1397
  • تاریخ بازنگری: 08 خرداد 1399
  • تاریخ پذیرش: 18 خرداد 1399
  • تاریخ اولین انتشار: 01 مهر 1400
  • تاریخ انتشار: 01 مهر 1400

هم رسانی

ارجاع به این مقاله

آمار