The effect of high-intensity interval training on the content of autophagy proteins (BECLIN1 and AMBRA1) in the skeletal muscle of aged rats
Subject Areas : Role of Genes in Health
Hamid Khodaverdi
1
,
Neda Aghaei Bahmanbeglou
2
,
saeedeh Shadmehri
3
1 - Department of Physical Education and Sport Sciences, Aliabad Katoul Branch, Islamic Azad University, Aliabad Katoul, Iran
2 - Department of Physical Education and Sport Sciences, Aliabad Katoul Branch, Islamic Azad University, Aliabad Katoul, Iran.
3 - Department of Physical Education and Sport Sciences, Islamic Azad University, Yadegar-e-imam Khomeini (RAH) Shahr-e Ray Branch, Tehran, Iran.
Keywords: High-Intensity Interval Training, Autophagy, Aging, BECLIN1 Protein, AMBRA1 Protein,
Abstract :
Introduction: One of the complications associated with aging is the reduction of muscle volume, which is caused by defects in cellular pathways such as autophagy. Exercises can be a key factor in reversing or increasing this complication; Therefore, the aim of this research is the effect of high-intensity interval training (HIIT) on the content of autophagy proteins (BECLIN1 and AMBRA1) in the skeletal muscle of aged rats. Materials and Methods: The current research is of experimental-fundamental type, in which 12, 20-month-old male Sprague-Dawley rats with an average weight of 400±30 grams were randomly divided into 2 groups: 1) control (6 head) and 2) HIIT (6 head). The HIIT training program consisted of 8 weeks and 3 sessions per week with an intensity of 85-90% of VO2max. After 48 hours after the last training session, the EDL muscle tissue of the rats was removed. Data analysis Data were analysed through independent t-test in SPSS version 27 and GraphPad Prism version 2.2.10 software. The significance level was less than p≥0.05. Results: Eight weeks of HIIT training increased BECLIN1 protein intracellular content (P=0.0001) and decreased AMBRA1 protein intracellular content (P=0.0001) in EDL muscle of aged rats. Conclusion: Considering the conflicting results in the content of BECLIN1 and AMBRA1 proteins, it suggests that the adaptive responses of HIIT differ in the regulation of the autophagy pathway.
1. Partridge L, Deelen J, Slagboom PE. Facing up to the global challenges of ageing. Nature. 2018;561(7721):45-56.
2. Fang EF, Xie C, Schenkel JA, Wu C, Long Q, Cui H, et al. A research agenda for ageing in China in the 21st century: focusing on basic and translational research, long-term care, policy and social networks. Ageing research reviews. 2020;64:101174.
3. Liang J, Zeng Z, Zhang Y, Chen N. Regulatory role of exercise-induced autophagy for sarcopenia. Experimental Gerontology. 2020;130:110789.
4. Xie G, Jin H, Mikhail H, Pavel V, Yang G, Ji B, et al. Autophagy in sarcopenia: Possible mechanisms and novel therapies. Biomedicine & Pharmacotherapy. 2023;165:115147.
5. Li W, He P, Huang Y, Li Y-F, Lu J, Li M, et al. Selective autophagy of intracellular organelles: recent research advances. Theranostics. 2021;11(1):222.
6. Mao J, Lin E, He L, Yu J, Tan P, Zhou Y. Autophagy and viral infection. Autophagy regulation of innate immunity. 2019:55-78.
7. Levine B, Kroemer G. Biological functions of autophagy genes: a disease perspective. Cell. 2019;176(1):11-42.
8. Chen R-H, Chen Y-H, Huang T-Y. Ubiquitin-mediated regulation of autophagy. Journal of Biomedical Science. 2019;26:1-12.
9. Li J, Tian M, Hua T, Wang H, Yang M, Li W, et al. Combination of autophagy and NFE2L2/NRF2 activation as a treatment approach for neuropathic pain. Autophagy. 2021;17(12):4062-82.
10. Ma X, Lu C, Chen Y, Li S, Ma N, Tao X, et al. CCT2 is an aggrephagy receptor for clearance of solid protein aggregates. Cell. 2022;185(8):1325-45. e22.
11. Campanario S, Ramírez-Pardo I, Hong X, Isern J, Muñoz-Cánoves P. Assessing autophagy in muscle stem cells. Frontiers in Cell and Developmental Biology. 2021;8:620409.
12. Vega-Rubín-de-Celis S. The Role of Beclin 1-Dependent Autophagy in Cancer. Biology. 2020;9(1):4.
13. Sun Y, Yao X, Zhang QJ, Zhu M, Liu ZP, Ci B, et al. Beclin-1-Dependent Autophagy Protects the Heart During Sepsis. Circulation. 2018;138(20):2247-62.
14. Xia Q, Huang X, Huang J, Zheng Y, March ME, Li J, Wei Y. The Role of Autophagy in Skeletal Muscle Diseases. Frontiers in Physiology. 2021;12.
15. Bell RAV, Al-Khalaf M, Megeney LA. The beneficial role of proteolysis in skeletal muscle growth and stress adaptation. Skeletal Muscle. 2016;6(1):16.
16. Gambarotto L, Metti S, Chrisam M, Cerqua C, Sabatelli P, Armani A, et al. Ambra1 deficiency impairs mitophagy in skeletal muscle. Journal of Cachexia, Sarcopenia and Muscle. 2022;13(4):2211-24.
17. Yang B, Liu Q, Bi Y. Autophagy and apoptosis are regulated by stress on Bcl2 by AMBRA1 in the endoplasmic reticulum and mitochondria. Theoretical Biology and Medical Modelling. 2019;16(1):18.
18. Briand J, Tremblay J, Thibault G. Can Popular High-Intensity Interval Training (HIIT) Models Lead to Impossible Training Sessions? Sports. 2022;10(1):10.
19. Bacon AP, Carter RE, Ogle EA, Joyner MJ. VO2max trainability and high intensity interval training in humans: a meta-analysis. PloS one. 2013;8(9):e73182.
20. Buchheit M, Laursen PB. High-intensity interval training, solutions to the programming puzzle: Part I: cardiopulmonary emphasis. Sports medicine. 2013;43(5):313-38.
21. Liu Q-Q, Xie W-Q, Luo Y-X, Li Y-D, Huang W-H, Wu Y-X, Li Y-S. High intensity interval training: A potential method for treating sarcopenia. Clinical Interventions in Aging. 2022:857-72.
22. Mejías-Peña Y, Estébanez B, Rodriguez-Miguelez P, Fernandez-Gonzalo R, Almar M, de Paz JA, et al. Impact of resistance training on the autophagy-inflammation-apoptosis crosstalk in elderly subjects. Aging (Albany NY). 2017;9(2):408.
23. Kim YA, Kim YS, Oh SL, Kim H-J, Song W. Autophagic response to exercise training in skeletal muscle with age. Journal of physiology and biochemistry. 2013;69:697-705.
24. Hurst C, Weston KL, Weston M. The effect of 12 weeks of combined upper-and lower-body high-intensity interval training on muscular and cardiorespiratory fitness in older adults. Aging clinical and experimental research. 2019;31:661-71.
25. Kang JS, Kim MJ, Kwon ES, Lee KP, Kim C, Kwon KS, Yang YR. Identification of novel genes associated with exercise and calorie restriction effects in skeletal muscle. Aging (Albany NY). 2023;15(11):4667-84.
26. Schwalm C, Jamart C, Benoit N, Naslain D, Prémont C, Prévet J, et al. Activation of autophagy in human skeletal muscle is dependent on exercise intensity and AMPK activation. The FASEB Journal. 2015;29(8):3515-26.
27. Balasubramanian P, Howell PR, Anderson RM. Aging and caloric restriction research: a biological perspective with translational potential. EBioMedicine. 2017;21:37-44.
28. Delshad S, Yaghoubi A, Rezaeian N. The effect of high intensity interval training on skeletal muscle autophagy biomarkers in male elderly rats. Daneshvar Medicine. 2021;28(6):37-48.
29. Brandt N, Gunnarsson TP, Bangsbo J, Pilegaard H. Exercise and exercise training‐induced increase in autophagy markers in human skeletal muscle. Physiological reports. 2018;6(7):e13651.
30. Ju J-s, Jeon S-i, Park J-y, Lee J-y, Lee S-c, Cho K-j, Jeong J-m. Autophagy plays a role in skeletal muscle mitochondrial biogenesis in an endurance exercise-trained condition. The Journal of Physiological Sciences. 2016;66:417-30.
31. Tran S, Fairlie WD, Lee EF. BECLIN1: Protein Structure, Function and Regulation. Cells. 2021;10(6):1522.
32. Menon MB, Dhamija S. Beclin 1 Phosphorylation – at the Center of Autophagy Regulation. Frontiers in Cell and Developmental Biology. 2018;6.
33. Xia P, Wang S, Du Y, Zhao Z, Shi L, Sun L, et al. WASH inhibits autophagy through suppression of Beclin 1 ubiquitination. The EMBO journal. 2013;32(20):2685-96.
