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The Journal of Physiological Sciences

, Volume 69, Issue 3, pp 523–530 | Cite as

Strength training attenuates post-infarct cardiac dysfunction and remodeling

  • Michael A. Garza
  • Emily A. Wason
  • Justin R. Cruger
  • Eunhee Chung
  • John Q. ZhangEmail author
Original Paper
  • 56 Downloads

Abstract

Post-myocardial infarction (MI) exercise has been employed to improve cardiac function. However, most studies have focused on endurance training (Et). Although Et has been reported to preserve cardiac function, evidence suggests that Et increases left ventricle (LV) interior dimensions as a result of albumin-induced plasma expansion. In contrast, strength training (St) induces concentric cardiac hypertrophy and improved cardiac function without causing ventricular dilation. Therefore, the purpose of this study was to investigate the effects of St on cardiac function and remodeling in rats with MI. MI was surgically induced in 7-week-old rats via ligation of the coronary artery. Survivors were assigned to two experimental groups, MI-Sed (No exercise; n = 9), MI-St (St; n = 10), with a Sham group (no MI, no St; n = 9). MI-St rats began training 1-week post-MI by climbing a ladder with weights for 10 weeks. Echocardiographic measurements were performed prior to, and following exercise training, while in vivo LV hemodynamic analysis was conducted at the end of the experimental period. Our data revealed that St induced shortening of the LV end-diastolic dimension in the MI-St group compared with the MI-Sed group (P < 0.05). The peak velocities of contraction (+ dP/dt max) and relaxation (− dP/dt max) were significantly greater in the MI-St group than the MI-Sed group (P < 0.05). These training effects contributed to the improved fractional shortening (%FS). Our results demonstrate that St may be beneficial for post-MI by attenuating LV dilation and concomitant cardiac dysfunction associated with MI.

Keywords

Myocardial infarction Cardiac function Strength training Rats 

Notes

Funding

This study was funded by the University of Texas at San Antonio Faculty Research Award (0614).

Compliance with ethical standards

Ethical approval

All applicable international, national, and/or institutional guidelines for the care and use of animals were followed.

References

  1. 1.
    Zintzaras E et al (2009) APOE gene polymorphisms and response to statin therapy. Pharmacogenom J 9(4):248–257CrossRefGoogle Scholar
  2. 2.
    Brown NJ, Vaughan DE (1998) Angiotensin-converting enzyme inhibitors. Circulation 97(14):1411–1420CrossRefGoogle Scholar
  3. 3.
    Dargie HJ, Byrne J (1995) Pathophysiological aspects of the renin–angiotensin–aldosterone system in acute myocardial infarction. J Cardiovasc Risk 2(5):389–395CrossRefGoogle Scholar
  4. 4.
    Wan W et al (2007) Effect of post-myocardial infarction exercise training on the renin–angiotensin–aldosterone system and cardiac function. Am J Med Sci 334(4):265–273CrossRefGoogle Scholar
  5. 5.
    Xu X et al (2010) Exercise training combined with angiotensin II receptor blockade reduces oxidative stress after myocardial infarction in rats. Exp Physiol 95(10):1008–1015CrossRefGoogle Scholar
  6. 6.
    Mann DL, Bristow MR (2005) Mechanisms and models in heart failure: the biomechanical model and beyond. Circulation 111(21):2837–2849CrossRefGoogle Scholar
  7. 7.
    Zimmerman BG, Sybertz EJ, Wong PC (1984) Interaction between sympathetic and renin–angiotensin system. J Hypertens 2(6):581–587CrossRefGoogle Scholar
  8. 8.
    Padfield PL, Morton JJ (1977) Effects of angiotensin II on arginine-vasopressin in physiological and pathological situations in man. J Endocrinol 74(2):251–259CrossRefGoogle Scholar
  9. 9.
    Matsuki K et al (2015) Transforming growth factor beta1 and aldosterone. Curr Opin Nephrol Hypertens 24(2):139–144CrossRefGoogle Scholar
  10. 10.
    Rengo G et al (2013) Molecular aspects of the cardioprotective effect of exercise in the elderly. Aging Clin Exp Res 25(5):487–497CrossRefGoogle Scholar
  11. 11.
    Xu X et al (2008) Exercise training combined with angiotensin II receptor blockade limits post-infarct ventricular remodelling in rats. Cardiovasc Res 78(3):523–532CrossRefGoogle Scholar
  12. 12.
    Xu X et al (2008) Effects of exercise training on cardiac function and myocardial remodeling in post myocardial infarction rats. J Mol Cell Cardiol 44(1):114–122CrossRefGoogle Scholar
  13. 13.
    Xie J et al (2011) The impairment of ILK related angiogenesis involved in cardiac maladaptation after infarction. PLoS ONE 6(9):e24115CrossRefGoogle Scholar
  14. 14.
    Yabluchanskiy A et al (2016) Myocardial infarction superimposed on aging: MMP-9 deletion promotes M2 macrophage polarization. J Gerontol A Biol Sci Med Sci 71(4):475–483CrossRefGoogle Scholar
  15. 15.
    Redfield MM et al (2003) Burden of systolic and diastolic ventricular dysfunction in the community: appreciating the scope of the heart failure epidemic. JAMA 289(2):194–202CrossRefGoogle Scholar
  16. 16.
    Kavanagh T et al (2002) Prediction of long-term prognosis in 12 169 men referred for cardiac rehabilitation. Circulation 106(6):666–671CrossRefGoogle Scholar
  17. 17.
    Lawler PR, Filion KB, Eisenberg MJ (2011) Efficacy of exercise-based cardiac rehabilitation post-myocardial infarction: a systematic review and meta-analysis of randomized controlled trials. Am Heart J 162(4):571–584 (e2) CrossRefGoogle Scholar
  18. 18.
    Dylewicz P et al (1999) The influence of short-term endurance training on the insulin blood level, binding, and degradation of 125I-insulin by erythrocyte receptors in patients after myocardial infarction. J Cardiopulm Rehabil 19(2):98–105CrossRefGoogle Scholar
  19. 19.
    Adachi H et al (1996) Does appropriate endurance exercise training improve cardiac function in patients with prior myocardial infarction? Eur Heart J 17(10):1511–1521CrossRefGoogle Scholar
  20. 20.
    Bhattacharya AA, Grune T, Curry S (2000) Crystallographic analysis reveals common modes of binding of medium and long-chain fatty acids to human serum albumin. J Mol Biol 303(5):721–732CrossRefGoogle Scholar
  21. 21.
    Fredrickson DS, Gordon RS Jr (1958) The metabolism of albumin-bound C14-labeled unesterified fatty acids in normal human subjects. J Clin Invest 37(11):1504–1515CrossRefGoogle Scholar
  22. 22.
    Convertino VA (1991) Blood volume: its adaptation to endurance training. Med Sci Sports Exerc 23(12):1338–1348CrossRefGoogle Scholar
  23. 23.
    Convertino VA et al (1980) Exercise training-induced hypervolemia: role of plasma albumin, renin, and vasopressin. J Appl Physiol 48(4):665–669CrossRefGoogle Scholar
  24. 24.
    Mihl C, Dassen WR, Kuipers H (2008) Cardiac remodelling: concentric versus eccentric hypertrophy in strength and endurance athletes. Neth Heart J 16(4):129–133CrossRefGoogle Scholar
  25. 25.
    Calderone A et al (1995) Pressure- and volume-induced left ventricular hypertrophies are associated with distinct myocyte phenotypes and differential induction of peptide growth factor mRNAs. Circulation 92(9):2385–2390CrossRefGoogle Scholar
  26. 26.
    Vinereanu D et al (2002) Left ventricular long-axis diastolic function is augmented in the hearts of endurance-trained compared with strength-trained athletes. Clin Sci (Lond) 103(3):249–257CrossRefGoogle Scholar
  27. 27.
    Bernardo BC et al (2012) Therapeutic inhibition of the miR-34 family attenuates pathological cardiac remodeling and improves heart function. Proc Natl Acad Sci USA 109(43):17615–17620CrossRefGoogle Scholar
  28. 28.
    Carmeliet P (2000) Mechanisms of angiogenesis and arteriogenesis. Nat Med 6(4):389–395CrossRefGoogle Scholar
  29. 29.
    Corsten MF et al (2010) Circulating MicroRNA-208b and MicroRNA-499 reflect myocardial damage in cardiovascular disease. Circ Cardiovasc Genet 3(6):499–506CrossRefGoogle Scholar
  30. 30.
    Fernandes T, Soci UP, Oliveira EM (2011) Eccentric and concentric cardiac hypertrophy induced by exercise training: microRNAs and molecular determinants. Braz J Med Biol Res 44(9):836–847CrossRefGoogle Scholar
  31. 31.
    Frey N et al (2004) Hypertrophy of the heart: a new therapeutic target? Circulation 109(13):1580–1589CrossRefGoogle Scholar
  32. 32.
    Pfeffer MA et al (1979) Myocardial infarct size and ventricular function in rats. Circ Res 44(4):503–512CrossRefGoogle Scholar
  33. 33.
    Lee S et al (2004) Viral expression of insulin-like growth factor-I enhances muscle hypertrophy in resistance-trained rats. J Appl Physiol 96(3):1097–1104CrossRefGoogle Scholar
  34. 34.
    Sahn DJ et al (1978) Recommendations regarding quantitation in M-mode echocardiography: results of a survey of echocardiographic measurements. Circulation 58(6):1072–1083CrossRefGoogle Scholar
  35. 35.
    Mulder P et al (2002) Long-term survival and hemodynamics after endothelin-a receptor antagonism and angiotensin-converting enzyme inhibition in rats with chronic heart failure: monotherapy versus combination therapy. Circulation 106(9):1159–1164CrossRefGoogle Scholar
  36. 36.
    Firth BG, Dunnmon PM (1990) Left ventricular dilatation and failure post-myocardial infarction: pathophysiology and possible pharmacologic interventions. Cardiovasc Drugs Ther 4(5):1363–1374CrossRefGoogle Scholar
  37. 37.
    Tournoy KG et al (2008) Transesophageal endoscopic ultrasound with fine needle aspiration in the preoperative staging of malignant pleural mesothelioma. Clin Cancer Res 14(19):6259–6263CrossRefGoogle Scholar
  38. 38.
    Pfeffer MA, Braunwald E (1990) Ventricular remodeling after myocardial infarction. Experimental observations and clinical implications. Circulation 81(4):1161–1172CrossRefGoogle Scholar
  39. 39.
    Kostuk WJ et al (1973) Left ventricular size after acute myocardial infarction. Serial changes and their prognostic significance. Circulation 47(6):1174–1179CrossRefGoogle Scholar
  40. 40.
    Barauna VG et al (2008) AT1 receptor participates in the cardiac hypertrophy induced by resistance training in rats. Am J Physiol Regul Integr Comp Physiol 295(2):R381–R387CrossRefGoogle Scholar
  41. 41.
    Kilgore JL et al (2002) Serum chemistry and hematological adaptations to 6 weeks of moderate to intense resistance training. J Strength Cond Res 16(4):509–515Google Scholar
  42. 42.
    Schmid JP et al (2008) Combined endurance/resistance training early on, after a first myocardial infarction, does not induce negative left ventricular remodelling. Eur J Cardiovasc Prev Rehabil 15(3):341–346CrossRefGoogle Scholar
  43. 43.
    Kasikcioglu E et al (2004) Left ventricular remodeling and aortic distensibility in elite power athletes. Heart Vessels 19(4):183–188CrossRefGoogle Scholar
  44. 44.
    Leosco D et al (2008) Exercise promotes angiogenesis and improves beta-adrenergic receptor signalling in the post-ischaemic failing rat heart. Cardiovasc Res 78(2):385–394CrossRefGoogle Scholar
  45. 45.
    Hashimoto T et al (2004) Expression of MHC-beta and MCT1 in cardiac muscle after exercise training in myocardial-infarcted rats. J Appl Physiol 97(3):843–851CrossRefGoogle Scholar
  46. 46.
    Delwing-de Lima D et al (2018) Effects of two aerobic exercise training protocols on parameters of oxidative stress in the blood and liver of obese rats. J Physiol Sci 68(5):699–706CrossRefGoogle Scholar
  47. 47.
    Xu X et al (2010) Effects of exercise and l-arginine on ventricular remodeling and oxidative stress. Med Sci Sports Exerc 42(2):346–354CrossRefGoogle Scholar
  48. 48.
    Wan W et al (2014) Exercise training induced myosin heavy chain isoform alteration in the infarcted heart. Appl Physiol Nutr Metab 39(2):226–232CrossRefGoogle Scholar
  49. 49.
    Xu X et al (2017) Post-myocardial infarction exercise training beneficially regulates thyroid hormone receptor isoforms. J Physiol Sci 68(6):743–748CrossRefGoogle Scholar
  50. 50.
    Kwon I et al (2018) Long-term resistance exercise-induced muscular hypertrophy is associated with autophagy modulation in rats. J Physiol Sci 68(3):269–280CrossRefGoogle Scholar

Copyright information

© The Physiological Society of Japan and Springer Japan KK, part of Springer Nature 2019

Authors and Affiliations

  1. 1.Laboratory of Cardiovascular Research, Department of Health, Kinesiology, and NutritionUniversity of Texas at San AntonioSan AntonioUSA
  2. 2.Laboratory of Cardiovascular Research, Department of Health, Kinesiology, and NutritionUniversity of Texas at San AntonioSan AntonioUSA

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