Effect of 12 weeks of HIIT and Q10 supplementation on soleus muscle mitochondrial biogenesis in high-fat diet-induced obese rats

Document Type : original article

Authors

1 Department of Sports Science, Tabriz Branch, Islamic Azad University, Tabriz, Iran

2 Department of Sport Sciences, Tabriz branch, Islamic Azad University, Tabriz, Iran

3 Department of Sports Science, Faculty of Social Sciences, Imam Khomeini International University, Qazvin, Iran

Abstract

Purpose: little is known about the concomitant effects of HIIT and Q10 supplementation in modification of the mitochondorial biogenesis and function in obesity conditions. The aim of this study was to investigate the concomitant effects of HIIT and Q10 supplementation on soleus muscle mitochondorial content as well as NRF2, SIRT-1 and Tfam levels in obese male rarts.
Methods: 48 rats randomized into six groups of lean, obese reference, obese control, obese+HIIT, obese+Q10 and obese concomitant (HIIT+Q10). Obesity was induced by high fat diet and HIIT) were done for 12 weeks (five sessions/week, with 10 intrval bouts for four min at 85-90% of v VO2 peak each session), while Q10 was consumed 500 mg/kg.bw daily. Data were measuered using western blot and Mitotrackervmethods and were analyzed by one-way ANOVA.
Results: Mitochondorial content (P = 0.049) as well as NRF2 (P = 0.002), SIRT-1 (P = 0.007) and Tfam (P = 0.040) levels were significantly lower in obese control than lean group. Mitochondorial content and SIRT-1 levels of three intervention groups of obese+HIIT (P = 0.001), obese+Q10 (P = 0.001) and obese concomitant (P = 0.001) were significantly higher than obese control group and even could precede lean group values (with exception for mitochondorial content in obese+Q10 group (P = 0.001)). Moreover, only in both groups of obese+HIIT ( P= 0.033), and obese concomitant (P = 0.038), NRF2 levels were significantly higher compared to obese control group. However, in none of the intervention groups the Tfam levels had significant differences compared to obese control group (P > 0.05 in all three cases).
Conclusions: Obesity likely suppresses soleus muscle mitochondorial biogenesis, or at least increases the removal rate of pre-existing mitochondria. However, HIIT as well as Q10 supplementation seems to partially capable to restore this down regulation, with a greater effects expected for HIIT. However, more investigations remain to be done due to lack of similar evidence and study limitations.

Keywords

References

  1. Bishop D, Botella J, Genders A, Lee M, Saner N, Kuang J, et al. High-Intensity Exercise and Mitochondrial Biogenesis: Current Controversies and Future Research Directions. Physiology (Bethesda, Md). 2019;34(1):56-70.
  2. Islam H, Bonafiglia JT, Granata C, Gurd BJ. Exercise-Induced Mitochondrial Biogenesis: Molecular Regulation, Impact of Training, and Influence on Exercise Performance. The Routledge Handbook on Biochemistry of Exercise: Routledge; 2020. p. 143-61.
  3. de Brito Monteiro L, Davanzo GG, de Aguiar CF, Moraes-Vieira PM. Using flow cytometry for mitochondrial assays. MethodsX. 2020;7:100938.
  4. Granata C, Jamnick NA, Bishop DJ. Principles of exercise prescription, and how they influence exercise-induced changes of transcription factors and other regulators of mitochondrial biogenesis. Sports Medicine. 2018;48(7):1541-59.
  5. Langley MR, Yoon H, Kim HN, Choi C-I, Simon W, Kleppe L, et al. High fat diet consumption results in mitochondrial dysfunction, oxidative stress, and oligodendrocyte loss in the central nervous system. Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease. 2020;1866(3):165630.
  6. Granata C, Jamnick NA, Bishop DJ. Training-Induced Changes in Mitochondrial Content and Respiratory Function in Human Skeletal Muscle. Sports Medicine. 2018;48(8):1809-28.
  7. Bakhtiyari A, Gaeni A, Chobineh S, Kordi MR, Hedayati M. Effect of 12-weeks high-intensity interval training on SIRT1, PGC-1α and ERRα protein expression in aged rats. Journal of Applied Health Studies in Sport Physiology. 2018;5(2):95-102.
  8. Pengam M, Amérand A, Simon B, Guernec A, Inizan M, Moisan C. How do exercise training variables stimulate processes related to mitochondrial biogenesis in slow and fast trout muscle fibres? Experimental Physiology. 2021;106(4):938-57.
  9. Chis B, Chis A, Muresan A, Fodor D. Q10 Coenzyme Supplementation can Improve Oxidative Stress Response to Exercise in Metabolic Syndrome in Rats. International journal for vitamin and nutrition research. 2019;90(1-2):33-41.
  10. Andreani C, Bartolacci C, Guescini M, Battistelli M, Stocchi V, Orlando F, et al. Combination of Coenzyme Q10 Intake and Moderate Physical Activity Counteracts Mitochondrial Dysfunctions in a SAMP8 Mouse Model. Oxidative Medicine and Cellular Longevity. 2018;2018:8936251.
  11. Rodrigues B, Figueroa DM, Mostarda CT, Heeren MV, Irigoyen M-C, De Angelis KJCd. Maximal exercise test is a useful method for physical capacity and oxygen consumption determination in streptozotocin-diabetic rats. Cardiovascular Diabetology. 2007;6(1):38-47.
  12. Picard M, Gentil BJ, McManus MJ, White K, St Louis K, Gartside SE, et al. Acute exercise remodels mitochondrial membrane interactions in mouse skeletal muscle. J Appl Physiol (1985). 2013;115(10):1562-71.
  13. Heo JW, No MH, Cho J, Choi Y, Cho EJ, Park DH, et al. Moderate aerobic exercise training ameliorates impairment of mitochondrial function and dynamics in skeletal muscle of high‐fat diet‐induced obese mice. The FASEB Journal. 2021;35(2):e21340.
  14. Ebadi B, Damirchi A, Alamdari KA, Darbandi-Azar A, Naderi N. Cardiomyocyte mitochondrial dynamics in health and disease and the role of exercise training: A brief review. Research in Cardiovascular Medicine. 2018;7(3):107-15.
  15. Pileggi CA, Parmar G, Harper ME. The lifecycle of skeletal muscle mitochondria in obesity. Obesity Reviews. 2021;22(5):e13164.
  16. Boyd JC, Simpson CA, Jung ME, Gurd BJ. Reducing the Intensity and Volume of Interval Training Diminishes Cardiovascular Adaptation but Not Mitochondrial Biogenesis in Overweight/Obese Men. PLoS ONE. 2013;8(7):e68091.
  17. Jacobs RA, Flück D, Bonne TC, Bürgi S, Christensen PM, Toigo M, et al. Improvements in exercise performance with high-intensity interval training coincide with an increase in skeletal muscle mitochondrial content and function. Journal of Applied Physiology. 2013;115(6):785-93.
  18. Lee J, Zhang X. Physiological determinants of VO2max and the methods to evaluate it: A critical review. Science & Sports. 2021.
  19. Bishop DJ, Granata C, Eynon N. Can we optimise the exercise training prescription to maximise improvements in mitochondria function and content? Biochimica et Biophysica Acta (BBA)-General Subjects. 2014;1840(4):1266-75.
  20. O’Neill HM, Holloway GP, Steinberg GR. AMPK regulation of fatty acid metabolism and mitochondrial biogenesis: Implications for obesity. Molecular and Cellular Endocrinology. 2013;366(2):135-51.
  21. Clark SA, Chen Z-P, Murphy KT, Aughey RJ, McKenna MJ, Kemp BE, et al. Intensified exercise training does not alter AMPK signaling in human skeletal muscle. American Journal of Physiology-Endocrinology and Metabolism. 2004;286(5):E737-E43.
  22. Jacobs RA, Siebenmann C, Hug M, Toigo M, Meinild AK, Lundby C. Twenty-eight days at 3454-m altitude diminishes respiratory capacity but enhances efficiency in human skeletal muscle mitochondria. FASEB journal : official publication of the Federation of American Societies for Experimental Biology. 2012;26(12):5192-200.
  23. Vancura A, Nagar S, Kaur P, Bu P, Bhagwat M, Vancurova I. Reciprocal regulation of AMPK/SNF1 and protein acetylation. International journal of molecular sciences. 2018;19(11):3314.
  24. Dengler F. Activation of AMPK under hypoxia: many roads leading to Rome. International journal of molecular sciences. 2020;21(7):2428.
  25. Merry TL, Ristow M. Nuclear factor erythroid-derived 2-like 2 (NFE2L2, Nrf2) mediates exercise-induced mitochondrial biogenesis and the anti-oxidant response in mice. The Journal of Physiology. 2016;594(18):5195-207.
  26. Ahn B, Pharaoh G, Premkumar P, Huseman K, Ranjit R, Kinter M, et al. Nrf2 deficiency exacerbates age-related contractile dysfunction and loss of skeletal muscle mass. Redox biology. 2018;17:47.
  27. 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.
  28. Gurd BJ, Little JP, Perry CG. Does SIRT1 determine exercise-induced skeletal muscle mitochondrial biogenesis: differences between in vitro and in vivo experiments? Journal of Applied Physiology. 2012;112(5):926-8.
  29. Xu C, Wang L, Fozouni P, Evjen G, Chandra V, Jiang J, et al. SIRT1 is downregulated by autophagy in senescence and ageing. Nature Cell Biology. 2020;22(10):1170-9.
  30. Torma F, Gombos Z, Jokai M, Takeda M, Mimura T, Radak Z. High intensity interval training and molecular adaptive response of skeletal muscle. Sports Medicine and Health Science. 2019;1(1):24-32.
  31. Norrbom J, Wallman SE, Gustafsson T, Rundqvist H, Jansson E, Sundberg CJ. Training response of mitochondrial transcription factors in human skeletal muscle. Acta physiologica (Oxford, England). 2010;198(1):71-9.
  32. Pham T, MacRae CL, Broome SC, D'souza RF, Narang R, Wang HW, et al. MitoQ and CoQ10 supplementation mildly suppresses skeletal muscle mitochondrial hydrogen peroxide levels without impacting mitochondrial function in middle‑aged men. European Journal of Applied Physiology. 2020;120(7):1657-69.
  33. Konokhova Y, Spendiff S, Jagoe RT, Aare S, Kapchinsky S, MacMillan NJ, et al. Failed upregulation of TFAM protein and mitochondrial DNA in oxidatively deficient fibers of chronic obstructive pulmonary disease locomotor muscle. Skeletal muscle. 2016;6(1):1-16.

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History

  • Receive Date: 07 November 2020
  • Revise Date: 29 June 2021
  • Accept Date: 09 July 2021
  • First Publish Date: 04 April 2022
  • Publish Date: 21 April 2022

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