Document Type : Original Article

Authors

1 Ph.D. Student of Deptment of Physical education and Sport Sciences, Science and Research Branch, Islamic Azad University, Tehran, Iran

2 Assistant professor of Deptment of Physical education and Sport Sciences, Science and Research Branch, Islamic Azad University, Tehran, Iran

3 Professor of Deptment of Physical education, University of Tehran, Tehran, Iran

4 Professor of Deptment of Physical education and Sport Science, Shahid Beheshti University, Tehran, Iran

Abstract

Introduction: One of the side effects of myocardial infarction is to increase slow-twitch to fast-twitch fibers phenotypic changes due to decreased mitochondrial density. Mitochondrial biogenesis with its ability to create new mitochondria and increase mitochondrial density can minimize these complications. One of the most effective genes in the mitochondrial biogenesis is the camK and PGC-1α. Therefore, this study aimed to investigate the effect of eight weeks of high-intensity interval training on the expression of camK and PGC-1α genes in the rats with myocardial infarction.
Methods: In this development research, 12 Wistar male rats with myocardial infarction were divided into experimental (30 minutes on a treadmill regularly and 4 minutes running with the severity of 90-85% VO2max and two minutes of active recovery with 50% -60% VO2max three days a week for eight weeks) and control(without exercise) groups. The expression of camK and PGC-1α genes was studied with Real-time PCR as an effective factor in downstream mitochondrial biogenesis.
Results: The results showed that the expression of camK and PGC-1α genes increased significantly (P =0.001).
Conclusion: Generally, eight weeks of high-intensity interval training by increasing the expression of camK and PGC-1α genes which are effective in the mitochondrial biogenesis process, can improve mitochondrial function in ST in rats with myocardial infarction and improve their quality of life.

Keywords

  1. Nordlie MAWold LEKloner RA. Genetic contributors toward increased
    risk for ischemic heart disease. Journal of molecular and cellular cardiology. 2005.39(4):667–679.
  2. Zoll J. Monassier L. Garnier A. N’Guessan B. Mettauer. Veksler V. ois Piquard F. Ventura-Clapier R and Geny B. ACE inhibition prevents myocardial infarction-induced skeletal muscle mitochondrial dysfunction.J Appl Physio. 2006.101(2):385-91.
  3. Dominy JE and Puigserver P. Mitochondrial Biogenesis through Activation of Nuclear Signaling Proteins. Cold Spring Harb Perspect Biol. 2013.1:5(7):1-18.
  4. Lemieux HHoppel CL. Mitochondria in the human heart. J Bioenerg Biomembr. 2009.41(2):99-106.
  5. Sandri M. Lin J. Handschin CH. Yang W. Arany Z P. Lecker S H. Goldberg A L and Spiegelman BM. PGC-1α protects skeletal muscle from atrophy by suppressing FoxO3 action and atrophy-specific gene transcription. 2006.103(44):16260-5.
  6. Fernandez-Marcos P J and Auwerx J. Regulation of PGC-1α, a nodal regulator of mitochondrial biogenesis. Am J Clin Nutr. 2011.93(4):884S–90.
  7. Rimbaud SGarnier AVentura-Clapier R. Mitochondrial biogenesis in cardiac pathophysiology. Pharmacol Rep. 2009. 61(1):131-8.
  8. Hardie DG. AMP-activated/SNF1 protein kinases: conserved guardians of cellular energy. Nat. Rev. Mol. Cell Biol. 2007. 8(10):774-85.
  9. Meirhaeghe A, Crowley V, Lenaghan C, Lelliott C, Green K, Stewart A, Hart K, Schinner S, Sethi JK, Yeo G, et al. Characterization of the human, mouse and rat PGC1β(peroxisome-proliferator-activated receptor-γ co-activator 1β) gene in vitro and in vivo. Biochem J. 2003. 1:373(1):155-65.
  10. Kumphune S, Surinkaew S, Chattipakorn S C, Chattipakorn N. 2015. Inhibition of p38 MAPK activation protects cardiac mitochondria from ischemia/reperfusion injury. Pharm Biol.2015. 53(12):1831-41.
  11. Aline V.N. Bacurau, Paulo R. Jannig,  Wilson M.A.M. de Moraes,  Telma F. Cunha,  Alessandra Medeiros,  Laura Barberi,  Marcele A. Coelho,  Reury F.P. Bacurau,  Carlos Ugrinowitsch,  Antonio Musarò c,,  Patricia C Brum. Akt/mTOR pathway contributes to skeletal muscle anti-atrophic effect of aerobic exercise training in heart failure mice Aline. International Journal of Cardiology.2016; 214: 137–147.
  12. Tao L. Bei Y. Zhang H. Zhou Y. Jiang J. Chen P. Shen S. Xiao J. Li X. Exercise Training Protects Against Acute Myocardial Infarction via Improving Myocardial Energy
    Metabolism and Mitochondrial Biogenesis.  Cellular Physiology and Biochemistry. 2015.37(1):162-175.   
  13. Steiner JLMurphy EAMcClellan JLCarmichael MDDavis JM. J Appl Physiol. Exercise training increases mitochondrial biogenesis in the brain. 2011.111(4):1066-71.
  14. Morten A,  Hoydal MA,  Wisloff U,  Kemi OJ,  Ellingsen O. Running speed and maximal oxygen uptake in rats and mice: practical implications for exercise training. Eur J Cardiovasc Prev Rehabil. 2007.14(6):753-60.
  15. Wisloff U,  Helgerud J,  Kemi OJ,  Ellingsen O. Intensity-controlled treadmill running in rats: VO2 max and cardiac hypertrophy. Am J Physiol Heart Circ Physiol. 2000.280(3):1301-10.
  16. Little JP, Safdar A, Bishop D, Tarnopolsky MA, Gibala MJ. An acute bout of high-intensity interval training increases the nuclear abundance of PGC-1α and activates mitochondrial biogenesis in human skeletal muscle. Am J Physiol Regul Integr Comp Physiol. 2011.300(6):1303-10.
  17. 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. Appl Physiol Nutr Metab.
    2013.38(3):326-33.
  18. Azizi gGhochan Nezhad Z. Effect of high intensity interval tarining(HIIT) on PGC-1α Serum Level and Lipid Profile of Overweight Women(PhD thesis).Tehran. pardis daneshgahi.2013.(in persian).
  19. Sharafi Dehrhm F, Soori R, Rastegar Mogaddam Mansouri M, Abbasian S. The Effect of High Intensity Interval Training on Muscular Biomarkers of Mitochondrial Biogenesis in Male Rats. JBabol Univ Med Sci. 2017.19(6):57-63.(in persian).
  20. Kange C, O'Moore KM, Dickman JR, Ji LL. Exercise activation of muscle peroxisome proliferator-activated receptor-γ coactivator-1α signaling is redox sensitive. Free Radic Biol Med. 2009.15:47(10):1394-400.
  21. Chen Z-P, McConell GK, Michell BJ, Snow RJ, Canny BJ, Kemp BE. AMPK signaling in contracting human skeletal muscle: acetyl-CoA carboxylase and NO synthase phosphorylation. Am J Physiol Endocrinol Metab. 2000.279(5):1202-6.
  22. Gibala MJ, McGee SL, Garnham AP, Howlett KF, Snow RJ, Hargreaves M. Brief intense interval exercise activates AMPK and p38 MAPK signaling and increases the expression of PGC-1α in human skeletal muscle. J Appl Physiol. 2009.106(3):929-34.
  23. François R. Jornayvaz F R and Shulman G I. Regulation of mitochondrial biogenesis. Essays Biochem. 2010. 47:69-84.
  24. Mooren F, Völker K. Molecular and Cellular Exercise Physiology. Human Kinetics. 2004.451-457.