تاثیر هشت هفته تمرین استقامتی بر محتوای پروتئین‌ مرتبط با داینامین 1 (DRP1) و آتروفی اپتیک 1 (OPA1) در بطن چپ موش‌های سفید بزرگ آزمایشگاهی سالمند

نوع مقاله : مقاله پژوهشی

نویسندگان

1 گروه تربیت بدنی و علوم ورزشی، واحد علی‌آباد کتول، دانشگاه آزاد اسلامی، علی‌آباد کتول، ایران

2 گروه آموزش تربیت بدنی، دانشگاه فرهنگیان، تهران، ایران

چکیده

مقدمه و هدف: پویایی میتوکندری توسط شکافت و همجوشی، نقش مهمی در شرایط فیزیولوژیکی و پاتولوژیکی در پیری ایفا می‌کند. اختلال دینامیک میتوکندری به بیماری‌های قلبی عروقی مرتبط با سن کمک می‌کند در حالی که ورزش درمانی برای جلوگیری از این فرآیند پیشنهاد شده است.
مواد و روش ها: پژوهش حاضر از نوع تجربی بود، که با 12 سر موش‌ سفید بزرگ آزمایشگاهی نر 20 ماهه از نژاد ویستار با میانگین وزنی 30 ± 400 گرم انجام شدند. موش‌های سفید بزرگ آزمایشگاهی به صورت تصادفی به دو گروه تمرین استقامتی و کنترل (هر گروه 6 سر) تقسیم شدند. گروه تمرین به مدت 8 هفته‌ و هر هفته 5 جلسه بر روی تردمیل دویدند. شدت تمرین استقامتی 55-75 درصد سرعت بود؛ که در هفته اول با سرعت 12 متر در دقیقه شروع شد و در هفته هشتم به سرعت 33 متر بر دقیقه رسید. پس از 48 ساعت از آخرین جلسه تمرین، موش‌های سفید بزرگ آزمایشگاهی بی‌هوش شدند و با روش وسترن بلات متغییرها اندازه‌گیری شدند. داده‌ها از طریق آزمون t-مستقل در نرم‌افزار SPSS نسخه 29 و گراف‌پد پریسم نسخه 3/2/10تحلیل شدند و سطح معناداری 05/0≥P در نظر گرفته شد.
نتایج: هشت هفته تمرین استقامتی سبب افزایش معنی‌دار محتوای DRP1 شد (001/0P=)؛ در حالی که برای محتوای پروتئین OPA1 در قلب موش‌های سفید بزرگ آزمایشگاهی پیر تغییر معنی‌داری مشاهده نشد (16/0P=).
نتیجه‌گیری: به نظر می‌رسد تمرین استقامتی با شدت و مدت مناسب می‌تواند کنترل کیفیت میتوکندری را در بافت قلب بیماران سالمند بهبود بخشد.

کلیدواژه‌ها

عنوان مقاله [English]

The effect of eight weeks of endurance training on the contents of dynamin-related protein 1 (DRP1) and optic atrophy 1 (OPA1) related to mitochondrial fission and fusion in the left ventricle of aged rats

نویسندگان [English]

  • Mahdi Marezloo 1
  • Neda Aghaei Bahmanbeglou 1
  • Hamed Alizadeh pahlavani 2
  • Habib Asgharpour 1
1 Department of Physical Education and Sport Sciences, Aliabad Katoul Branch, Islamic Azad University, Aliabad Katoul, Iran
2 Department of Physical Education, Farhangian University, Tehran, Iran
چکیده [English]

Background and Objective: Mitochondrial dynamics through fission and fusion play an important role in physiological and pathological conditions in aging. Disruption of mitochondrial dynamics contributes to age-related cardiovascular diseases, while exercise therapy has been proposed to prevent this process.
Materials and Methods: The current research is of an experimental type, which was conducted with 12, 20-month-old Wistar male rats with an average weight of 400 ± 30 gr. Rats were randomly divided into two endurance training and control groups (each group had 6 rats). The training group ran on the treadmill for 8 weeks and 5 sessions per week. The intensity of the endurance training was 55-75% of speed; which started with a speed of 12 meters per minute in the first week and reached a speed of 33 meters per minute in the eighth week. After 48 hours from the last training session, the rats were anesthetized and the variables were measured by western blot method. Data were analyzed through independent t-test in SPSS software version 29 and Graphpad Prism version 10.2.3 and the significance level was considered P≤0.05.
Results: Eight weeks of endurance training caused a significant increase in DRP1 content (P=0.001); While it was not significant for OPA1 protein content in the heart of old rats (P=0.16).
Conclusion: It seems that endurance training with appropriate intensity and duration can improve mitochondrial quality control in the heart tissue of elderly patients.

کلیدواژه‌ها [English]

  • Endurance training
  • Mitochondrial fusion
  • Dynamin-related protein 1
  • Optic atrophy 1
  • Left ventricle

مراجع

  1. Al Ojaimi M, Salah A, El-Hattab AW. Mitochondrial fission and fusion: molecular mechanisms, biological functions, and related disorders. Membranes. 2022;12(9):893.
  2. Traa A, Keil A, AlOkda A, Jacob‐Tomas S, Tamez González AA, Zhu S, et al. Overexpression of mitochondrial fission or mitochondrial fusion genes enhances resilience and extends longevity. Aging Cell. 2024:e14262.
  3. Wei T, Wang Q, Chen T, Zhou Z, Li S, Li Z, et al. The possible association of mitochondrial fusion and fission in copper deficiency-induced oxidative damage and mitochondrial dysfunction of the heart. Journal of Trace Elements in Medicine and Biology. 2024:127483.
  4. He X, Wang L, Tsang HY, Liu X, Yang X, Pu S, et al. GTPBP8 modulates mitochondrial fission through a Drp1-dependent process. Journal of Cell Science. 2024;137(8).
  5. Chen C, Dong X, Zhang W, Chang X, Gao W. Dialogue between mitochondria and endoplasmic reticulum-potential therapeutic targets for age-related cardiovascular diseases. Frontiers in Pharmacology. 2024;15:1389202.
  6. Gilkerson R, Kaur H, Carrillo O, Ramos I. OMA1-Mediated Mitochondrial Dynamics Balance Organellar Homeostasis Upstream of Cellular Stress Responses. International Journal of Molecular Sciences. 2024;25(8):4566.
  7. Wu M, Huang Z, Akuetteh PDP, Huang Y, Pan J. Eriocitrin prevents Sepsis-induced acute kidney injury through anti-inflammation and anti-oxidation via modulating Nrf2/DRP1/OPA1 signaling pathway. Biochimica et Biophysica Acta (BBA)-General Subjects. 2024;1868(7):130628.
  8. Somasundaram I, Jain SM, Blot-Chabaud M, Pathak S, Banerjee A, Rawat S, et al. Mitochondrial dysfunction and its association with age-related disorders. Frontiers in Physiology. 2024;15:1384966.
  9. Sheng Y, Zhu X, Wei L, Zou Y, Qi X, Shi R, et al. Aberrant expression of thyroidal hormone receptor α exasperating mitochondrial dysfunction induced sarcopenia in aged mice. Aging (Albany NY). 2024;16(8):7141.
  10. Maneechote C, Chattipakorn SC, Chattipakorn N. Future perspectives on the roles of mitochondrial dynamics in the heart in obesity and aging. Life Sciences. 2024:122575.
  11. Gojevic T, Gelade K, Da Silva NT, Tulleneers B, Mullens W, Hansen D. Effects of low vs. moderate intense resistance exercise training combined with endurance exercise training in patients with heart failure: a randomized clinical trial. European Journal of Preventive Cardiology. 2024;31(4):e9-e12.
  12. Sahl RE, Patsi I, Hansen MT, Rømer T, Frandsen J, Rasmusen HK, et al. Prolonged endurance exercise increases macrophage content and mitochondrial respiration in adipose tissue in trained men. The Journal of Clinical Endocrinology & Metabolism. 2024;109(2):e799-e808.
  13. Arroum T, Hish GA, Burghardt KJ, Ghamloush M, Bazzi B, Mrech A, et al. Mitochondria Transplantation: Rescuing Innate Muscle Bioenergetic Impairment in a Model of Aging and Exercise Intolerance. The Journal of Strength & Conditioning Research. 2024;38(7):1189-99.
  14. Arroum T, Hish GA, Burghardt KJ, McCully JD, Hüttemann M, Malek MH. Mitochondrial Transplantation’s Role in Rodent Skeletal Muscle Bioenergetics: Recharging the Engine of Aging. Biomolecules. 2024;14(4):493.
  15. Jang J, Kim Y, Song T, Park S, Kim HJ, Koh Jh, et al. Free essential amino acid feeding improves endurance during resistance training via DRP1‐dependent mitochondrial remodelling. Journal of Cachexia, Sarcopenia and Muscle. 2024.
  16. Frenzel S, Bülow R, Dörr M, Felix SB, Friedrich N, Völzke H, et al. Left ventricular hypertrophy as a risk factor for accelerated brain aging: Results from the Study of Health in Pomerania. Human Brain Mapping. 2024;45(3):e26567.
  17. Sengupta P. The laboratory rat: relating its age with human's. International journal of preventive medicine. 2013;4(6):624.
  18. Garcia NF, Sponton AC, Delbin MA, Parente JM, Castro MM, Zanesco A, et al. Metabolic parameters and responsiveness of isolated iliac artery in LDLr(-/-) mice: role of aerobic exercise training. Am J Cardiovasc Dis. 2017;7(2):64-71.
  19. Ghane M, Riyahi Malayeri S, Hosseini M. High-intensity interval training and intake nano-selenium supplementation on the gene expression of hepatic SOD and CAT in dexamethasone-induced rats. Sport Sciences for Health. 2024;20(1):177-84.
  20. Wang Q, Cui C, Zhang N, Lin W, Chai S, Chow SK-H, et al. Effects of physical exercise on neuromuscular junction degeneration during ageing: A systematic review. Journal of Orthopaedic Translation. 2024;46:91-102.
  21. Moore TM, Zhou Z, Cohn W, Norheim F, Lin AJ, Kalajian N, et al. The impact of exercise on mitochondrial dynamics and the role of Drp1 in exercise performance and training adaptations in skeletal muscle. Molecular metabolism. 2019;21:51-67.
  22. Moreira OC, Estébanez B, Martínez-Florez S, Paz JAd, Cuevas MJ, González-Gallego J. Mitochondrial function and mitophagy in the elderly: effects of exercise. Oxidative medicine and cellular longevity. 2017;2017(1):2012798.
  23. Gusdon AM, Callio J, Distefano G, O'Doherty RM, Goodpaster BH, Coen PM, et al. Exercise increases mitochondrial complex I activity and DRP1 expression in the brains of aged mice. Experimental gerontology. 2017;90:1-13.
  24. Dulac M, Leduc‐Gaudet JP, Cefis M, Ayoub MB, Reynaud O, Shams A, et al. Regulation of muscle and mitochondrial health by the mitochondrial fission protein Drp1 in aged mice. The Journal of Physiology. 2021;599(17):4045-63.
  25. No M-H, Heo J-W, Yoo S-Z, Kim C-J, Park D-H, Kang J-H, et al. Effects of aging and exercise training on mitochondrial function and apoptosis in the rat heart. Pflügers Archiv-European Journal of Physiology. 2020;472:179-93.
  26. Zampieri S, Mammucari C, Romanello V, Barberi L, Pietrangelo L, Fusella A, et al. Physical exercise in aging human skeletal muscle increases mitochondrial calcium uniporter expression levels and affects mitochondria dynamics. Physiological reports. 2016;4(24):e13005.
  27. Tezze C, Romanello V, Desbats MA, Fadini GP, Albiero M, Favaro G, et al. Age-associated loss of OPA1 in muscle impacts muscle mass, metabolic homeostasis, systemic inflammation, and epithelial senescence. Cell metabolism. 2017;25(6):1374-89. e6.
دانشور پزشکی
دوره 32، شماره 4 - شماره پیاپی 173
مهر و آبان 1403
صفحه 11-22

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