The Effect of High- and Low-Intensity Interval Training on Myostatin Gene Expression Levels in Muscles Fibers of Rats with Myocardial Infarction

Document Type : Research Paper

Authors

1 Department of Physical education University of Tehran, Kish international campus, Kish, Iran.

2 Department of Exercise Physiology, Kermanshah Branch, Islamic Azad University, Kermanshah, Iran

Abstract

Introduction: Myocardial infarction (MI) is an essential coronary artery disease, which affects mitochondrial function and causes muscle atrophy due to vessel blockage and disruption in blood transfusion and oxygen transfer. Interval exercises reduce muscle atrophy, but the appropriate exercise intensity is still unknown. This study aimed to evaluate the effect of interval training with two for six weeks on Myostatin gene expression levels in slow (ST) and fast (FT) twitch muscles in rats with MI. Method: Eighteen ten-week male Wistar rats with MI were randomly assigned into high- (HIIT) (90-85% VO2max) and low-intensity interval training (LIIT) (50-60% VO2max) with a control group (CG, without training). Myostatin gene expression of FT and ST was investigated as a stimulant of muscle atrophy. The training protocol was 30-minute intermittent jogging sessions on a treadmill. Each interval included 4 min of running (85-90% VO2max for HIIT and 55-60% for LIIT) and 2-minute active recovery (50-60% for HIIT and 45-50% for LIIT) three days a week for six weeks. Results: LIIT significantly decreased myostatin expression in both ST and FT while HIIT only decreased myostatin expression in ST compared to CG (P = 0.002, P = 0.016, and P=0.011, respectively). HIIT induced myostatin expression reduction was higher in FT compared to CG (P = 0.078). There was a significant difference in myostatin expression between CG (8.87) and the two training groups (HIIT [0.949] and LIIT [3.11]) in ST (P≤0.05), and between  CG and LIITs and HIIT (1.22) and LIIT (0/975) in FT (P<0.05). Conclusion: Six weeks of HIIT and LIIT reduced myostatin gene expression and decreased ST and FT atrophy in rats with MI. 

Keywords


  1. Shahsavari S, Nazari F, Karimyar Jahromi M, Sadeghi M. Epidemiologic study of hospitalized cardiovascular patients in Jahrom hospitals in 2012-2013. J Cardiovasc Nurs. 2013; 2 (2):14-21.
  2. Zoll J, Monassier L, Garnier A, N'Guessan B, Mettauer B, Veksler V, Piquard F, Ventura-Clapier R, Geny B. ACE inhibition prevents myocardial infarction-induced skeletal muscle mitochondrial dysfunction. J Appl Physiol. 2006; 101: 385–91.
  3. Tao L, Bei Y, Lin S, 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. Cell Physiol Biochem. 2015;37(1):162-75.  
  4. Araki S.Izumiya Hanatani SH. Rokutanda T. Usuku H. Akasaki Y. Takeo T. Nakagata N.  Walsh K. and  Ogawa H. Akt1–Mediated Skeletal Muscle Growth Attenuates Cardiac Dysfunction and Remodeling After Experimental Myocardial Infarction. Circ Heart Fail.2012; 5(1): 116–25.
  5. Martinez PF, Okoshi K, Zornoff LA, Carvalho RF, Oliveira Junior SA, Lima AR, Campos DH, Damatto RL, Padovani CR, Nogueira CR, Dal Pai-Silva M,Okoshi MP. Chronic heart failure-induced skeletal muscle atrophy, necrosis, and changes in myogenic regulatory factors. Med Sci Monit.2010; 16(12):BR374-83.
  6. Bacurau AV, Jannig PR, de Moraes WM, Cunha TF, Medeiros A, Barberi L, Coelho MA, Bacurau RF, Ugrinowitsch C, Musarò A, Brum PC. Akt/mTOR pathway contributes to skeletal muscle anti-atrophic effect of aerobic exercise training in heart failure mice. Int J Cardiol. 2016; 214:137-47.
  7. Castillero Akashi H. Najjar M. George I. Cardiac myostatin upregulation occurs immediately after myocardial ischemia and is involved in skeletal muscle activation of atrophy. Biochem Biophys Res Commun.2015;457(1):106-11. 
  8. Joulia-Ekaza DCabello G. The myostatin gene: physiology and pharmacological relevance. Curr Opin Pharmacol.2007; 7(3):310-5.
  9. Laursen PB, Jenkins DG. The scientific basis for high- intensity interval training: optimizing training programmes and maximizing performance in highly trained endurance athletes. Sports Med .2002; 32: 53-73.
  10. Óscar Fabregat-Andrés, Alberto Tierrez, Manuel Mata, Jordi Estornell-Erill, Francisco Ridocci-Soriano, and María Monsalve. Induction of PGC-1α Expression Can Be Detected in Blood Samples of Patients with ST-Segment Elevation Acute Myocardial Infarction. 2011; 6(11): e26913.
  11. Rimbaud SGarnier AVentura-Clapier R.Mitochondrial biogenesis in cardiac pathophysiology. Pharmacol Rep.2009; 61(1):131-8.
  12. Khodaie K, Badri N, Moghadam MR. the Effect of Short-Term High Intensity Interval Training (HIIT) On Some Cardiovascular Indices. Anaerobic Power Output, Jump and Sprint Performances in Active Female Students. 2012; 4(8):25-34.
  13. Roth SM, Martel GF, Ferrell RE, Metter EJ, Hurley BF, Rogers MA. Myostatin gene expression is reduced in humans with heavy-resistance strength training: A brief communication. Exp Biol Med. 2003; 228(6):706-9.
  14. Willoughby DS. Effects of heavy resistance training on myostatin mRNA and protein expression. Med Sci Sports Exerc. 2004;36(4):574–82
  15. Saremi A, Gharakhanloo R, Sharghi S, Gharaati MR, Larijani B, Omidfar K. Effects of oral creatine and resistance training on serum myostatin and GASP-1. Mol Cell Endocrinol. 2010; 317(1-2):25-30.
  16. Diel P, Schiffer T, Geisler S, Hertrampf T, Mosler S, Schulz S, et al. Analysis of the effects of androgens and training on myostatin propeptide and follistatin concentrations in blood and skeletal muscle using highly sensitive Immuno PCR. Mol Cell Endocrinol. 2010; 330(1-2):1–9.
  17. Dargie HJ. Effect of carvedilol on outcome after myocardial infarction in patients with left ventricular dysfunction: the CAPRICORN randomised trial. Lancet. 2001: 5; 357(9266):1385-90.
  18. Wisloff U Helgerud JKemi OJEllingsen O. Intensity-controlled treadmill running in rats: VO2 max and cardiac hypertrophy. Am J Physiol Heart Circ Physiol. 2000; 280(3):H1301-10.
  19. Bodine SC, Stitt TN, Gonzalez M, Kline WO, Stover GL, et al. Akt/mTOR pathway is a crucial regulator of skeletal muscle hypertrophy and can prevent muscle atrophy in vivo. Nat Cell Biol. 2001;3: 1014-9.
  20. Fry AC. The role of the resistance exercise intensity on muscle fibre adaptations. Sports Med. 2004; 34: 663-79.
  21. Goldspink G. Gene expression in muscle in response to exercise. J Muscle Res Cell Motil. 2003; 24:121-6.
  22. Glass DJ. Signaling pathways that mediate skeletal muscle hypertrophy and atrophy. Nat Cell Biol. 2003;587-90.

 

Volume 10, Issue 4
October 2022
Pages 295-299
  • Receive Date: 08 November 2022
  • Revise Date: 08 December 2022
  • Accept Date: 17 December 2022
  • First Publish Date: 17 December 2022