The Effect of Moderate-Intensity Interval Training (MIIT) on the Intracellular Content of Proteins Related to the Mitophagy Pathway in the Soleus Muscle of Male Wistar Rats

Sharif Bigdeli, Mohammad; Aghaei Bahmanbeglou, Neda; Rezaee Shirazi, Reza; Ahmadi, Mozhgan

doi:10.22059/jsb.2024.368627.1618

Document Type : Research Paper I Open Access I Released under CC BY-NC 4.0 license

Authors

¹ 1. Department of Physical Education and Sport Sciences, Aliabad Katoul Branch, Islamic Azad University, Aliabad Katoul, Iran.

² Corresponding Author, Department of Physical Education and Sport Sciences, Aliabad Katoul Branch, Islamic Azad University, Aliabad Katoul, Iran.

³ Department of Physical Education and Sport Sciences, Aliabad Katoul Branch, Islamic Azad University, Aliabad Katoul, Iran.

⁴ Department of Physical Education and Sport Science, Yadegar-e-Imam Khomeini (RAH) Shahre-Rey Branch, Islamic Azad University, Tehran, Iran.

10.22059/jsb.2024.368627.1618

Abstract

Introduction: Mitophagy is a multifunctional pathway that can lead to mitochondrial defects and greater efficiency in skeletal muscles. Exercise is an important factor in the regulation of mitophagy according to conditions, such as intensity, duration, and type. Therefore, the current study aimed to investigate the effect of moderate-intensity interval training (MIIT) on the intracellular content of proteins related to the mitophagy (FUNDC1 and NIX) pathway in the soleus muscle of male Wistar rats.

Methods: In this experimental study, 16 three-month-old Wistar rats with an average weight of 280±30 were randomly divided into two groups:1. Control group, 2. MIIT (8 rats per group). Rats in the MIIT group consisted of running on a treadmill for 8 weeks, 5 sessions per week, and each session consisted of 10 MIIT bouts of 3 minutes, separated by 2-minute rest periods. The average speed in the first week was 19 m/min, and in the last week, it reached 25 m/min. The content of the variables was measured using the western blotting laboratory method in the soleus muscle tissue. Data were analyzed using an independent t-test with GraphPad Prism software version 9.5. A significance level of p≥0.05 was considered.

Results: The content of FUNDC1 and NIX proteins were significantly lower in the MIIT group than in the control group (P<0.0001).

Conclusion: Considering the reduction in these factors, MIIT training can regulate the mitophagy process in skeletal muscles and help maintain mitochondrial health through related pathways. Therefore, further research is required.

Keywords

Main Subjects

Exercise Physiology

References

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Journal of Sport Biosciences

The Effect of Moderate-Intensity Interval Training (MIIT) on the Intracellular Content of Proteins Related to the Mitophagy Pathway in the Soleus Muscle of Male Wistar Rats

References

References

[1] Wu H, Chen Q. Hypoxia activation of mitophagy and its role in disease pathogenesis. Antioxidants & redox signaling. 2015;22(12):1032-46.https://doi.org/10.1089/ars.2014.6204

[2] Pickles S, Vigié P, Youle RJ. Mitophagy and quality control mechanisms in mitochondrial maintenance. Current Biology. 2018;28(4):170-85.https://doi.org/10.1089/ars.2014.6204

[3] Zhang Y, Oliveira AN, Hood DA. The intersection of exercise and aging on mitochondrial protein quality control. Experimental Gerontology. 2020;131:110824.https://doi.org/10.1016/j.exger.2019.110824

[4] Li J, Zhang Z, Bo H, Zhang Y. Exercise couples mitochondrial function with skeletal muscle fiber type via ROS-mediated epigenetic modification. Free Radical Biology and Medicine. 2024;213:409-25.https://doi.org/10.1016/j.freeradbiomed.2024.01.036

[5] Zhang W. The mitophagy receptor FUN14 domain-containing 1 (FUNDC1): a promising biomarker and potential therapeutic target of human diseases. Genes & diseases. 2021;8(5):640-54.https://doi.org/10.1016/j.gendis.2020.08.011

[6] Lv M, Wang C, Li F, Peng J, Wen B, Gong Q, et al. Structural insights into the recognition of phosphorylated FUNDC1 by LC3B in mitophagy. Protein & cell. 2017;8(1):25-38.https://doi.org/10.1007/s13238-016-0328-8

[7] Wang S, Long H, Hou L, Feng B, Ma Z, Wu Y, et al. The mitophagy pathway and its implications in human diseases. Signal Transduction and Targeted Therapy. 2023;8(1):1-28.https://doi.org/10.1038/s41392-023-01503-7

[8] Marinković M, Šprung M, Novak I. Dimerization of mitophagy receptor BNIP3L/NIX is essential for recruitment of autophagic machinery. Autophagy. 2021;17(5):1232-43.https://doi.org/10.1080/15548627.2020.1755120

[9] Rogov VV, Suzuki H, Marinković M, Lang V, Kato R, Kawasaki M, et al. Phosphorylation of the mitochondrial autophagy receptor Nix enhances its interaction with LC3 proteins. Scientific reports. 2017;7(1):1-12.https://doi.org/10.1038/s41598-017-01258-6

[10] Esteban-Martínez L, Boya P. BNIP3L/NIX-dependent mitophagy regulates cell differentiation via metabolic reprogramming. Autophagy. 2018;14(5):915-7.https://doi.org/10.1080/15548627.2017.1332567

[11] Alizadeh Pahlavani H, Laher I, Knechtle B, Zouhal H. Exercise and mitochondrial mechanisms in patients with sarcopenia. Frontiers in Physiology. 2022;13:1040381.https://doi.org/10.3389/fphys.2022.1040381

[12] Wang Y, Li J, Zhang Z, Wang R, Bo H, Zhang Y. Exercise Improves the Coordination of the Mitochondrial Unfolded Protein Response and Mitophagy in Aging Skeletal Muscle. Life. 2023;13(4):1006.https://doi.org/10.3390/life13041006

[15] He C, Bassik MC, Moresi V, Sun K, Wei Y, Zou Z, et al. Exercise-induced BCL2-regulated autophagy is required for muscle glucose homeostasis. Nature. 2012;481(7382):511-5.https://doi.org/10.1038/nature10758

[16] Lo Verso F, Carnio S, Vainshtein A, Sandri M. Autophagy is not required to sustain exercise and PRKAA1/AMPK activity but is important to prevent mitochondrial damage during physical activity. Autophagy. 2014;10(11):1883-94.https://doi.org/10.4161/auto.32154

[17] 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.https://doi.org/10.14814/phy2.13651

[18] Vainshtein A, Desjardins E, Armani A, Sandri M, Hood DA. PGC-1α modulates denervation-induced mitophagy in skeletal muscle. Skeletal muscle. 2015;5(1):1-17.https://doi.org/10.1186/s13395-015-0033-y

[19] Chen CCW, Erlich AT, Hood DA. Role of Parkin and endurance training on mitochondrial turnover in skeletal muscle. Skeletal muscle. 2018;8:1-14.https://doi.org/10.1186/s13395-018-0157-y

[20] Ma L, Li K, Wei W, Zhou J, Li Z, Zhang T, et al. Exercise protects aged mice against coronary endothelial senescence via FUNDC1-dependent mitophagy. Redox Biology. 2023;62:102693.https://doi.org/10.1016/j.redox.2023.102693

[21] Bai X, Zhang Z, Li X, Yang Y, Ding S. FUNDC1: An Emerging Mitochondrial and MAMs Protein for Mitochondrial Quality Control in Heart Diseases. International Journal of Molecular Sciences. 2023;24(11):9151.https://doi.org/10.3390/ijms24119151

[22] Hoshino D, Yoshida Y, Kitaoka Y, Hatta H, Bonen A. High-intensity interval training increases intrinsic rates of mitochondrial fatty acid oxidation in rat red and white skeletal muscle. Applied physiology, nutrition, and metabolism. 2013;38(3):326-33.https://doi.org/10.1139/apnm-2012-0257

[23] Guan Y, Drake JC, Yan Z. Exercise-Induced Mitophagy in Skeletal Muscle and Heart. Exerc Sport Sci Rev. 2019;47(3):151-6.https://doi.org/10.1249/jes.0000000000000192

[24] 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.https://doi.org/10.1007/s12576-016-0440-9

[25] Yu L, Shi X-Y, Liu Z-M, Wang Z, Li L, Gao J-X, et al. Effects of exercises with different durations and intensities on mitochondrial autophagy and FUNDC1 expression in rat skeletal muscles. Sheng li xue bao:[Acta Physiologica Sinica]. 2020;72(5):631-42.PMID: 33106833

[26] Erlich AT, Hood DA. Mitophagy regulation in skeletal muscle: Effect of endurance exercise and age. Journal of Science in Sport and Exercise. 2019;1:228-36.https://doi.org/10.1007/s42978-019-00041-5

[27] Chatzinikita E, Maridaki M, Palikaras K, Koutsilieris M, Philippou A. The Role of Mitophagy in Skeletal Muscle Damage and Regeneration. Cells. 2023;12(5):716.https://doi.org/10.3390/cells12050716

[28] Zhao Y, Zhu Q, Song W, Gao B. Exercise training and dietary restriction affect PINK1/Parkin and Bnip3/Nix-mediated cardiac mitophagy in mice. General physiology and biophysics. 2018;37(6):657-66.PMID: 30431438

[29] Packer M. Autophagy-dependent and -independent modulation of oxidative and organellar stress in the diabetic heart by glucose-lowering drugs. Cardiovascular Diabetology. 2020;19(1):62.https://doi.org/10.1186/s12933-020-01041-4

[30] Li A, Gao M, Liu B, Qin Y, Chen L, Liu H, et al. Mitochondrial autophagy: Molecular mechanisms and implications for cardiovascular disease. Cell death & disease. 2022;13(5):444.https://doi.org/10.1038/s41419-022-04906-6

[31] Lei L, Yang S, Lu X, Zhang Y, Li T. Research Progress on the Mechanism of Mitochondrial Autophagy in Cerebral Stroke. Frontiers in Aging Neuroscience. 2021;13.https://doi.org/10.3389/fnagi.2021.698601

[32] Wang X-L, Feng S-T, Wang Y-T, Yuan Y-H, Li Z-P, Chen N-H, et al. Mitophagy, a Form of Selective Autophagy, Plays an Essential Role in Mitochondrial Dynamics of Parkinson’s Disease. Cellular and Molecular Neurobiology. 2022;42(5):1321-39.https://doi.org/10.1007/s10571-021-01039-w

[33] Roca-Agujetas V, de Dios C, Lestón L, Marí M, Morales A, Colell A. Recent Insights into the Mitochondrial Role in Autophagy and Its Regulation by Oxidative Stress. Oxidative Medicine and Cellular Longevity. 2019;2019:3809308.https://doi.org/10.1155/2019/3809308

Volume 16, Issue 1 - Serial Number 99
March 2024
Pages 49-60

References

Volume 16, Issue 1 - Serial Number 99March 2024Pages 49-60

Volume 16, Issue 1 - Serial Number 99
March 2024
Pages 49-60