تأثیر هشت هفته تمرین هم‏زمان بر سطوح پلاسمایی NRF2 در مردان جوان

نوع مقاله: مقاله پژوهشی

نویسندگان

1 استادیار فیزیولوژی ورزشی، گروه علوم ورزشی، دانشکده علوم انسانی، دانشگاه سمنان، سمنان، ایران.

2 استادیار فیزیولوژی ورزشی، گروه علوم ورزشی، دانشکده علوم انسانی، دانشگاه سمنان، سمنان، ایران

3 کارشناس ارشد فیزیولوژی ورزشی، گروه علوم ورزشی، دانشکده علوم انسانی، دانشگاه سمنان، سمنان، ایران

چکیده

فعالیت بدنی می تواند باعث افزایش قابل ملاحظه‏ای در میزان NRF2 شود و همین امر در سالمندی منجر به کاهش القاء آنزیم‏های فسفات سدیم فاز II و حساسیت بیشتر به آسیب اکسیداتیو می‏شود. هدف پژوهش حاضر، تأثیر هشت هفته تمرین هم‏زمان بر سطوح پلاسمایی NRF2 در مردان جوان بود. در این پژوهش 16 مرد جوان تمرین نکرده (میانگین سنی 60/3±06/25 سال، وزن 21/8±37/71 کیلوگرم، BMI 52/3±09/24 کیلوگرم بر متر مربع) به‌طور تصادفی در دو گروه هشت نفری (تمرین همزمان و کنترل) تقسیم شدند. برنامه تمرینی شامل هشت هفته (سه جلسه در هفته) تمرینات مقاومتی با 40 درصد یک تکرار بیشینه و تمرینات هوازی با شدت 60 درصد حداکثر ضربان قلب بود. برای اندازه‏گیری متغیرهای خونی، در شرایط ناشتا یک بار قبل و  یک بار  هم بعد از مداخله تمرینی نمونه‏گیری خونی انجام شد. نتایج نشان داد که هشت هفته تمرین هم‏زمان منجر به افزایش سطوح پلاسمایی NRF2 گردید (035/0P=) اما تفاوت معنی‏داری بعد از هشت هفته در گروه کنترل مشاهده نشد (05/0P). با توجه به نتایج احتمال می‏رود که افزایش سطوح NRF2 در اثر تمرین هم‏زمان، منجر به سرکوب کردن رادیکال‏های آزاد و افزایش ظرفیت ضداکسایشی بدن خواهد شد.

کلیدواژه‌ها

موضوعات


عنوان مقاله [English]

The effects of eight weeks of Concurrent Training on Plasma Levels of NRF2 in Young Men

نویسندگان [English]

  • Seyed Mohsen Avandi 1
  • Rouhollah Hagh Shenas 2
  • Solmaz Abbasi 3
1 Assistant Professor of Exercise Physiology, Department of Sport Sciences, Semnan University, Semnan, Iran.
2 Assistant Professor of Exercise Physiology, Department of Sport Sciences, Semnan University, Semnan, Iran.
3 M.Sc of Exercise Physiology, Department of Sport Sciences, Semnan University, Semnan, Iran
چکیده [English]

Physical activity can dramatically increase cellular Nrf2 level, and this factor over time is associated with aging, resulting in decreased induction of Phosphate II Phase II enzymes and increased sensitivity to oxidative damage. This study aim was to investigate the effects of eight weeks concurrent training on plasma NRF2 levels in young men. In this study, 16 young men (age: 25.06 ± 3.60 years, weight: 71.37 ± 8.21 Kg, BMI: 24.09 ± 3.52 kg.m2) were randomly divided into Concurrent training and control groups (n=8). The exercise program consisted of eight weeks (three sessions per week) of resistance training at 40% of 1RM and an aerobic exercise program with a maximum intensity of 60% of maximum heart rate. Fasting blood samples were taken prior to and after the intervention. It was found that eight weeks of concurrent training resulted in plasma NRF2 elevation (P = 0/035). However, no significant difference was observed after 8 weeks in the control group (P≤0.05). According to the results, an upregulation of NRF2 occurred during concurrent training, will lead to decrease ROS production and therefore the antioxidative capacity of the body would be elevated. 

کلیدواژه‌ها [English]

  • Oxidative ُStress
  • Concurrent Training
  • NRF2

 

1.    Berzosa C, Cebrian I, Fuentes-Broto L, Gomez-Trullen E, Piedrafita E, Martinez-Ballarin E, et al. Acute exercise increases plasma total antioxidant status and antioxidant enzyme activities in untrained men. BioMed Research International. 2011;2011.

2.    Uttara B, Singh AV, Zamboni P, Mahajan R. Oxidative stress and neurodegenerative diseases: a review of upstream and downstream antioxidant therapeutic options. Current neuropharmacology. 2009;7(1):65-74.

3.    Zhou S, Sun W, Zhang Z, Zheng Y. The role of Nrf2-mediated pathway in cardiac remodeling and heart failure. Oxidative medicine and cellular longevity. 2014;2014.

4.    Muthusamy VR, Kannan S, Sadhaasivam K, Gounder SS, Davidson CJ, Boeheme C, et al. Acute exercise stress activates Nrf2/ARE signaling and promotes antioxidant mechanisms in the myocardium. Free Radical Biology and Medicine. 2012;52(2):366-76.

5.    Mukaigasa K, Nguyen LT, Li L, Nakajima H, Yamamoto M, Kobayashi M. Genetic evidence of an evolutionarily conserved role for Nrf2 in the protection against oxidative stress. Molecular and cellular biology. 2012;32(21):4455-61.

6.    Kaspar JW, Niture SK, Jaiswal AK. Nrf2: INrf2 (Keap1) signaling in oxidative stress. Free Radical Biology and Medicine. 2009;47(9):1304-9.

7.    Pall ML, Levine S. Nrf2, a master regulator of detoxification and also antioxidant, anti-inflammatory and other cytoprotective mechanisms, is raised by health promoting factors. Sheng Li Xue Bao. 2015;67(1):1-18.

8.    Yuan X, Xu C, Pan Z, Keum YS, Kim JH, Shen G, et al. Butylated hydroxyanisole regulates AREmediated gene expression via Nrf2 coupled with ERK and JNK signaling pathway in HepG2 cells. Molecular carcinogenesis. 2006;45(11):841-50.

9.    Done AJ, Gage MJ, Nieto NC, Traustadóttir T. Exercise-induced Nrf2-signaling is impaired inaging. Free Radical Biology and Medicine. 2016;96:130-8.

10.  Djordjevic DZ, Cubrilo DG, Puzovic VS, Vuletic MS, Zivkovic VI, Barudzic NS, et al. Changes in athlete’s redox state induced by habitual and unaccustomed exercise. Oxidative medicine and cellular longevity. 2012;2012.

11.  Sen C, Packer L, Hänninen O. Handbook of oxidants and antioxidants in exercise: Elsevier; 2000.

12.  Heunks LM, Dekhuijzen PR. Respiratory muscle function and free radicals: from cell to COPD. Thorax. 2000;55(8):704-16.

13.  Anderson-Bill ES, Winett RA, Wojcik JR, Williams DM. Aging and the social cognitive determinants of physical activity behavior and behavior change: evidence from the guide to health trial. Journal of aging research. 2011;2011.

14.  Ashe MC, Miller WC, Eng JJ, Noreau L. Older adults, chronic disease and leisure-time physical activity. Gerontology. 2009;55(1):64-72.

15.  Holmström KM, Baird L, Zhang Y, Hargreaves I, Chalasani A, Land JM, et al. Nrf2 impacts cellular bioenergetics by controlling substrate availability for mitochondrial respiration. Biology open. 2013;2(8):761-70.

16.  Dugan LL, Quick KL. Reactive oxygen species and aging: evolving questions. Science's SAGE KE. 2005;2005(26):pe20.

17.  Safdar A, Tarnopolsky MA. Dysfunctional Nrf2–Keap1 redox signaling in skeletal muscle of the sedentary old. Free Radical Biology and Medicine. 2010;49(10):1487-93.

18.  Jones TW, Walshe IH, Hamilton DL, Howatson G, Russell M, Price OJ, et al. Signaling Responses After Varying Sequencing of Strength and Endurance Training in a Fed State. International journal of sports physiology and performance. 2016;11(7):868-75.

19.  Cadore E, Pinto R, Lhullier F, Correa C, Alberton C, Pinto S, et al. Physiological effects of concurrent training in elderly men. International journal ofsports medicine. 2010;31(10):689-97.

20.  Di Blasio A, Gemello E, Di Iorio A, Di Giacinto G, Celso T, Di Renzo D, et al. Order effects of concurrent endurance and resistance training on post-exercise response of non-trained women. Journal of sports science & medicine. 2012;11(3):393.

21.  Seals DR, Kaplon RE, Gioscia-Ryan RA, LaRocca TJ. You9re Only as Old as Your Arteries: Translational Strategies for Preserving Vascular Endothelial Function with Aging. Physiology. 2014;29(4):250-64.

22.  Radak Z, Chung HY, Goto S. Systemic adaptation to oxidative challenge induced by regular exercise. Free Radical Biology and Medicine. 2008;44(2):153-9.

23.  Müller-Höcker J. Cytochrome-c-oxidase deficient cardiomyocytes in the human heart--an age-related phenomenon. A histochemical ultracytochemical study. The American journal of pathology. 1989;134(5):1167.

24.  Holmström KM, Kostov RV, Dinkova-Kostova AT. The multifaceted role of Nrf2 in mitochondrial function. Current opinion in toxicology. 2016;1:80-91.

25.  Narasimhan M, Hong J, Atieno N, Muthusamy VR, Davidson CJ, Abu-Rmaileh N, et al. Nrf2 deficiency promotes apoptosis and impairs PAX7/MyoD expression in aging skeletal muscle cells. Free Radical Biology and Medicine. 2014;71:402-14.

26.  Radak Z, Atalay M, Jakus J, Boldogh I, Davies K, Goto S. Exercise improves import of 8-oxoguanine DNA glycosylase into the mitochondrial matrix of skeletal muscle and enhances the relative activity. Free Radical Biology and Medicine. 2009;46(2):238-43.

27.  Gomes F, Chuffa L, Scarano W, Pinheiro P, Favaro W, Domeniconi R. Nandrolone decanoate and resistance exercise training favor the occurrence of lesions and activate the inflammatory response in the ventral prostate. Andrology. 2016;4(3):473-80.

28.  Salanova M, Schiffl G, Gutsmann M, Felsenberg D, Furlan S, Volpe P, et al. Nitrosative stress in human skeletal muscle attenuated by exercise countermeasure after chronic disuse. Redox biology. 2013;1(1):514-26.

29.  Li T, He S, Liu S, Kong Z, Wang J, Zhang Y. Effects of different exercisedurations on Keap1-Nrf2-ARE pathway activation in mouse skeletal muscle. Free radical research. 2015;49(10):1269-74.

30.  Merry TL, Ristow M. Nuclear factor erythroidderived 2like 2 (NFE2L2, Nrf2) mediates exerciseinduced mitochondrial biogenesis and the antioxidant response in mice. The Journal of physiology. 2016;594(18):5195-207.

31.  Wang P, Li CG, Qi Z, Cui D, Ding S. Acute exercise stress promotes Ref1/Nrf2 signalling and increases mitochondrial antioxidant activity in skeletal muscle. Experimental physiology. 2016;101(3):410-20.

32.  Eynon N, Alves AJ, Sagiv M, Yamin C, Sagiv M, Meckel Y. Interaction between SNPs in the NRF2 gene and elite endurance performance. Physiological genomics. 2010;41(1):78-81.

33.  Crilly MJ, Tryon LD, Erlich AT, Hood DA. The role of Nrf2 in skeletal muscle contractile and mitochondrial function. Journal of Applied Physiology. 2016;121(3):730-40.

34.  Gounder SS, Kannan S, Devadoss D, Miller CJ, Whitehead KS, Odelberg SJ, et al. Impaired transcriptional activity of Nrf2 inage-related myocardial oxidative stress is reversible by moderate exercise training. PloS one. 2012;7(9):e45697.