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لیست داوران سال 1401

لیست داوران سال 1400

اثر تمرین هوازی و امگا 3 بر شاخص‌های آتروفی بافت قلب موش‌های سالمند تغذیه شده با رژیم غذایی پرچرب

نوع مقاله : مقاله پژوهشی Released under (CC BY-NC) license I Open Access I

نویسندگان

1 گروه تربیت بدنی و علوم ورزشی، واحد آیت الله آملی، دانشگاه آزاد اسلامی، آمل، ایران

2 دانشیار گروه فیزیولوژی ورزشی، واحد آیت الله آملی، دانشگاه آزاد اسلامی، آمل، ایران

3 گروه فیزیولوژی ورزشی، واحد آیت الله آملی، دانشگاه آزاد اسلامی، آمل، ایران

چکیده

هدف: عملکرد قلب با افزایش سن وچاقی کاهش می‌یابد. چاقی عامل خطر اصلی در پیشرفت بیماری‌های قلبی عروقی (CVDs) است. قلب پیر دچار تغییرات متعددی در سطوح مولکولی، سلولی و فیزیولوژیکی می‌شود که عملکرد انقباضی آن را کاهش می‌دهد. هدف از پژوهش حاضر بررسی اثر اثر تمرین هوازی و امگا 3 بر شاخص‌های آتروفی بافت قلب موش‌های سالمند تغذیه شده با رژیم غذایی پرچرب بود. روش‌شناسی: در این مطالعه تجربی، 40 سر موش صحرایی نر نژاد ویستار (میانگین وزن 24/18±82/148) در پنج گروه رژیم غذایی نرمال (ND)، رژیم غذایی پرچرب (HFD)، رژیم غذایی پرچرب-تمرین (HFDT)، رژیم غذایی پرچرب- امگا-3 (HFDω3)، تمرین-رژیم غذایی پرچرب-امگا-3 (HFDTω3) قرار گرفتند. گروه‌های مکمل، طی دوره مداخله روزانه 1 ‌گرم امگا-3 (به ازای هر کیلوگرم وزن بدن) را به صورت خوراکی دریافت کردند. برنامه تمرین هوازی شامل دویدن روی تردمیل با شدت 60-50 درصد اکسیژن مصرفی (VO2max)، پنج روز هفته به مدت هشت هفته اجرا شد. داده‌ها به روش تحلیل واریانس یک‌طرفه و آزمون تعقیبی توکی در سطح معنی‌داری p<0.05 تجزیه و تحلیل شد. یافته‌ها: بیان ژن FoxO3a، MAFbx و MuRF1 در گروه‌های HFDT (به‌ترتیب 039/0P=، 016/0p= و 043/0p=)، HFDω3 (به‌ترتیب 035/0p=، 044/0p= 030/0p=) و HFDTω3 (به‌ترتیب 0001/0p=، 0001/0p= و 0001/0p=) کاهش معنی‌داری داشت. همچنین کاهش معنی‌داری در بیان FoxO3a در گروه HFDTω3 نسبت به HFDT (040/0P=) و HFDω3 (045/0P=) مشاهده شد. بحث: تمرین هوازی و امگا-3 باعث محافظت در برابر آتروفی قلبی ناشی از HFD در موش‌های سالمند شد، با این وجود اثر هم‌زمان تمرین هوازی و امگا-3 بهتر بود.

کلیدواژه‌ها

موضوعات

عنوان مقاله [English]

The Effect of Aerobic Exercise and Omega-3 on Atrophy Indices in the Cardiomyocytes of Elderly HFD Rats

نویسندگان [English]

  • Ghasem Torabi Palat Kaleh 1
  • Ahmad Abdi 2
  • Asieh Abbassi Daloii 3

1 Department of Physical Education and Sports Science, Ayatollah Amoli Branch, Islamic Azad University, Amol, Iran.

2 Associate Professor, Department of Exercise Physiology, Ayatollah Amoli Branch, Islamic Azad University, Amol, Iran.

3 Department of Physical Education and Sport Science, Ayatollah Amoli Branch, Islamic Azad University, Amol, Iran

چکیده [English]

Aim: Heart performance declines with age and obesity. Aging and obesity a major risk factor toward the development of cardiovascular diseases (CVDs). The aging heart undergoes several changes at the molecular, cellular and physiological levels, which diminishes its contractile function. The aim of the present study was to investigate the effect of aerobic training and omega-3 on atrophy indices in the cardiomyocytes of elderly HFD rats. Methods: In this experimental study, 40 male Wistar rats (mean weight 148.82±18.24) were divided into 5 groups: Normal Diet (ND), High-Fat Diet (HFD), High-Fat Diet-Training (HFDT), High-Fat Diet-Omega3 (HFDω3) and High-Fat Diet-Training-Omega3 (HFDTω3). The supplement groups received 1 g of Omega3 (per kg of body weight) orally during the intervention period. Aerobic exercise program including running on treadmill with an intensity of 50-60% oxygen consumption (VO2max), was performed 5 days a week for eight weeks. Data were analyzed by one-way analysis of variance and Tukey post hoc test at the P<0.05. Results: Significant decrease were seen in FoxO3a, MAFbx, and MuRF1 gene expression levels in HFDT (p=0.039, p=0.016, and p=0.043, respectively), HFDω3 (p=0.035, p=0.044, p=0.030, respectively), and HFDTω3 (p=0.0001, p=0.0001 and p=0.0001 respectively). Also, a significant decrease in FoxO3a expression was observed in the HFDTω3 group compared to HFDT (P=0.040) and HFDω3 (P=0.045). Conclusion: Aerobic training and omega-3 protected against HFD-induced cardiac atrophy in elderly rats, however, the combined effect of aerobic exercise and omega-3 was better.

کلیدواژه‌ها [English]

  • Exercise
  • Omega 3
  • Atrophy
  • Aging and High-Fat Diet
مراجع
  1. WHO—World Health Organization Noncommunicable Diseases. https://www.who.int/news-room/fact-sheets/detail/noncommunicable-diseases
  2. WHO—World Health Organization Obesity and Overweight. [(accessed on 26 May 2020)]. Available online: https://www.who.int/news-room/fact-sheets/detail/obesity-and-overweight
  3. Xu J, Ni B, Ma C, Rong S, Gao H, Zhang L, et al. Docosahexaenoic acid enhances hippocampal insulin sensitivity to promote cognitive function of aged rats on a high-fat diet. Journal of Advanced Research. 2023;45:31-42.
  4. Dai D-F, Chen T, Johnson SC, Szeto H, Rabinovitch PS. Cardiac aging: from molecular mechanisms to significance in human health and disease. Antioxidants & redox signaling. 2012;16(12):1492-526.
  5. López-Otín C, Blasco MA, Partridge L, Serrano M, Kroemer G. The hallmarks of aging. Cell. 2013;153(6):1194-217.
  6. Webb AE, Brunet A. FOXO transcription factors: key regulators of cellular quality control. Trends in biochemical sciences. 2014;39(4):159-69.
  7. Sandri M, Sandri C, Gilbert A, Skurk C, Calabria E, Picard A, et al. Foxo transcription factors induce the atrophy-related ubiquitin ligase atrogin-1 and cause skeletal muscle atrophy. Cell. 2004;117(3):399-412.
  8. Ronnebaum SM, Patterson C. The FoxO family in cardiac function and dysfunction. Annual review of physiology. 2010;72:81-94.
  9. Li H-H, Kedar V, Zhang C, McDonough H, Arya R, Wang D-Z, et al. Atrogin-1/muscle atrophy F-box inhibits calcineurin-dependent cardiac hypertrophy by participating in an SCF ubiquitin ligase complex. The Journal of clinical investigation. 2004;114(8):1058-71.
  10. Li H-H, Willis MS, Lockyer P, Miller N, McDonough H, Glass DJ, et al. Atrogin-1 inhibits Akt-dependent cardiac hypertrophy in mice via ubiquitin-dependent coactivation of Forkhead proteins. The Journal of clinical investigation. 2007;117(11):3211-23.
  11. Arya R, Kedar V, Hwang JR, McDonough H, Li H-H, Taylor J, et al. Muscle ring finger protein-1 inhibits PKCε activation and prevents cardiomyocyte hypertrophy. J Cell Biol. 2004;167(6):1147-59.
  12. Afshar H, Abdi A, Barari A, Azarbayjani M. The Effect of Aerobic Training on Expression of Indices of Myocardial Hypertrophy and Atrophy in Rats. Armaghane Danesh. 2021;26(1):45-58.
  13. Esmailee B, Abdi A, farzanegi p, Abbassi Daloii A. Protective Effect of Aerobic Training along with Resveratrol on the Expression of some Atrophic Biomarkers of Cardiomyocytes in Diabetic rats. Journal Of Neyshabur University Of Medical Sciences. 2019;7(3):27-37.
  14. Hood DA, Irrcher I, Ljubicic V, Joseph A-M. Coordination of metabolic plasticity in skeletal muscle. Journal of experimental biology. 2006;209(12):2265-75.
  15. Kazemi A, dehesh T. The Effect of 4 Weeks of High Intensity Training on Gene Expression of MST1 and MAFbx in EDL Muscle of Aged Mice. Sport Physiology & Management Investigations. 2019;11(3):47-58.
  16. sheibani s, daryanoosh f, salesi m, koushkie jahromi m, tanideh n. The effect of high-intensity training and detraining on FOXO3a/MuRF1 and MAFbx levels in soleus muscle of male rats. EBNESINA. 2018;20(1):31-9.
  17. Gingras AA, White PJ, Chouinard PY, Julien P, Davis TA, Dombrowski L, et al. Long‐chain omega‐3 fatty acids regulate bovine whole‐body protein metabolism by promoting muscle insulin signalling to the Akt–mTOR–S6K1 pathway and insulin sensitivity. The Journal of physiology. 2007;579(1):269-84.
  18. Pinkoski C, Chilibeck PD, Candow DG, Esliger D, Ewaschuk JB, Facci M, et al. The effects of conjugated linoleic acid supplementation during resistance training. Medicine & Science in Sports & Exercise. 2006;38(2):339-48.
  19. Da Boit M, Sibson R, Sivasubramaniam S, Meakin JR, Greig CA, Aspden RM, et al. Sex differences in the effect of fish-oil supplementation on the adaptive response to resistance exercise training in older people: a randomized controlled trial. The American journal of clinical nutrition. 2017;105(1):151-8.
  20. Mostafavian M, Abdi A, Mehrabani J, Barari A. Effect of Eight Weeks of Aerobic Progressive Training with Capsaicin on changes in PGC-1α and UPC-1 Expression in Visceral Adipose Tissue of Obese Rats With Diet. Complementary Medicine Journal. 2020;10(2):106-17.
  21. Ji N, Luan J, Hu F, Zhao Y, Lv B, Wang W, et al. Aerobic exercise‑stimulated Klotho upregulation extends life span by attenuating the excess production of reactive oxygen species in the brain and kidney. Experimental and therapeutic medicine. 2018;16(4):3511-7.
  22. de Andrade AM, Fernandes MdC, de Fraga LS, Porawski M, Giovenardi M, Guedes RP. Omega-3 fatty acids revert high-fat diet-induced neuroinflammation but not recognition memory impairment in rats. Metabolic Brain Disease. 2017;32(6):1871-81.
  23. Shortreed KE, Krause MP, Huang JH, Dhanani D, Moradi J, Ceddia RB, et al. Muscle-specific adaptations, impaired oxidative capacity and maintenance of contractile function characterize diet-induced obese mouse skeletal muscle. PloS one. 2009;4(10):e7293.
  24. Choi SJ, Files DC, Zhang T, Wang Z-M, Messi ML, Gregory H, et al. Intramyocellular lipid and impaired myofiber contraction in normal weight and obese older adults. Journals of Gerontology Series A: Biomedical Sciences and Medical Sciences. 2016;71(4):557-64.
  25. Eshima H, Tamura Y, Kakehi S, Kurebayashi N, Murayama T, Nakamura K, et al. Long‐term, but not short‐term high‐fat diet induces fiber composition changes and impaired contractile force in mouse fast‐twitch skeletal muscle. Physiological reports. 2017;5(7):e13250.
  26. Ma J, Hwang SJ, McMahon GM, Curhan GC, Mclean RR, Murabito JM, et al. Mid‐adulthood cardiometabolic risk factor profiles of sarcopenic obesity. Obesity. 2016;24(2):526-34.
  27. Abrigo J, Rivera JC, Aravena J, Cabrera D, Simon F, Ezquer F, et al. High fat diet-induced skeletal muscle wasting is decreased by mesenchymal stem cells administration: implications on oxidative stress, ubiquitin proteasome pathway activation, and myonuclear apoptosis. Oxidative medicine and cellular longevity. 2016;2016 :9047821.
  28. Roy B, Curtis ME, Fears LS, Nahashon SN, Fentress HM. Molecular mechanisms of obesity-induced osteoporosis and muscle atrophy. Frontiers in physiology. 2016;7:439.
  29. Ferretti R, Moura EG, Dos Santos VC, Caldeira EJ, Conte M, Matsumura CY, et al. High-fat diet suppresses the positive effect of creatine supplementation on skeletal muscle function by reducing protein expression of IGF-PI3K-AKT-mTOR pathway. PloS one. 2018;13(10):e0199728.
  30. Zanchi NE, de Siqueira Filho MA, Lira FS, Rosa JC, Yamashita AS, de Oliveira Carvalho CR, et al. Chronic resistance training decreases MuRF-1 and Atrogin-1 gene expression but does not modify Akt, GSK-3β and p70S6K levels in rats. European journal of applied physiology. 2009;106(3):415-23.
  31. Murton A, Constantin D, Greenhaff P. The involvement of the ubiquitin proteasome system in human skeletal muscle remodelling and atrophy. Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease. 2008;1782(12):730-43.
  32. Foletta VC, White LJ, Larsen AE, Léger B, Russell AP. The role and regulation of MAFbx/atrogin-1 and MuRF1 in skeletal muscle atrophy. Pflügers Archiv-European Journal of Physiology. 2011;461(3):325-35.
  33. Baskin KK, Rodriguez MR, Kansara S, Chen W, Carranza S, Frazier OH, et al. MAFbx/Atrogin-1 is required for atrophic remodeling of the unloaded heart. Journal of molecular and cellular cardiology. 2014;72:168-76.
  34. Liu S-H, Chiu C-Y, Wang L-P, Chiang M-T. Omega-3 fatty acids-enriched fish oil activates AMPK/PGC-1α signaling and prevents obesity-related skeletal muscle wasting. Marine drugs. 2019;17(6):380.
  35. Hsueh T-Y, Baum JI, Huang Y. Effect of eicosapentaenoic acid and docosahexaenoic acid on myogenesis and mitochondrial biosynthesis during murine skeletal muscle cell differentiation. Frontiers in nutrition. 2018;5:15.
  36. Saini A, Sharples AP, Al-Shanti N, Stewart CE. Omega-3 fatty acid EPA improves regenerative capacity of mouse skeletal muscle cells exposed to saturated fat and inflammation. Biogerontology. 2017;18:109-29.
  37. Soni NK, Ross AB, Scheers N, Savolainen OI, Nookaew I, Gabrielsson BG, et al. Eicosapentaenoic and docosahexaenoic acid-enriched high fat diet delays skeletal muscle degradation in mice. Nutrients. 2016;8(9):543.
  38. Lee SR, Khamoui AV, Jo E, Zourdos MC, Panton LB, Ormsbee MJ, et al. Effect of conjugated linoleic acids and omega‐3 fatty acids with or without resistance training on muscle mass in high‐fat diet‐fed middle‐aged mice. Experimental Physiology. 2017;102(11):1500-12.
  39. Oh S-L, Lee S-R, Kim J-S. Effects of conjugated linoleic acid/n-3 and resistance training on muscle quality and expression of atrophy-related ubiquitin ligases in middle-aged mice with high-fat diet-induced obesity. Journal of exercise nutrition & biochemistry. 2017(3):11.
  40. Frier BC, Wan Z, Williams DB, Stefanson AL, Wright DC. Epinephrine and AICAR-induced PGC-1α mRNA expression is intact in skeletal muscle from rats fed a high-fat diet. American Journal of Physiology-Cell Physiology. 2012;302(12):C1772-C9.
  41. Sandri M, Lin J, Handschin C, Yang W, Arany ZP, Lecker SH, et al. PGC-1α protects skeletal muscle from atrophy by suppressing FoxO3 action and atrophy-specific gene transcription. Proceedings of the National Academy of Sciences. 2006;103(44):16260-5.
  42. Wang Y, Zhou Y, Graves DT. FOXO transcription factors: their clinical significance and regulation. BioMed research international. 2014;2014.
  43. Chen W-K, Tsai Y-L, Shibu MA, Shen C-Y, Chang-Lee SN, Chen R-J, et al. Exercise training augments Sirt1-signaling and attenuates cardiac inflammation in D-galactose induced-aging rats. Aging (Albany NY). 2018;10(12):4166.
  44. Lennon-Edwards S, Schellhardt TA, Kuczmarski JM. Antioxidant defense is increased in aged hearts following omega-3 supplementation in the absence of changes in inflammation. Physiological Research. 2015;64(3):433.
سوخت و ساز و فعالیت ورزشی
دوره 12، شماره 1 - شماره پیاپی 1
فروردین 1401
صفحه 73-87
فایل ها
سابقه مقاله
  • تاریخ دریافت: 11 اسفند 1401
  • تاریخ بازنگری: 23 اسفند 1401
  • تاریخ پذیرش: 27 اسفند 1401
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