Exercise training has restorative potential on myocardial energy metabolism in rats with chronic heart failure

Document Type: Original Article


1 Department of Physical Education, Shandong University, Weihai, Weihai 264209, Shandong Province, China

2 Medical Imaging Faculty, Weifang Medical University, Weifang 261053, Shandong Province, China

3 Division of physical education, General course Teaching Department, Weifang Medical University, Weifang 261053, Shandong Province, China


Objective(s): Exercise training is a well-known accelerator for the treatment of chronic heart failure (CHF). The current study aimed to investigate the restorative effects of aerobic interval training (AIT) intervention on myocardial energy metabolism in CHF rats.
Materials and Methods: Post-myocardial infarction (MI) heart failure animal model was established. The Sprague-Dawley rats were randomly divided into sham operation group (Sham group), CHF model group, and CHF exercise group (Exercise-CHF group).
Results: Our data showed that when compared to the Sham group, the left ventricular systolic pressure (LVSP), myocardial glycogen content, and expression levels of key components of AMP-activated protein kinase (AMPK) pathway were decreased significantly (P<0.05) in the CHF-model group, while the left ventricular end diastolic pressure (LVEDP), fatty acid (FA) concentration, lactic acid content, and AMPKα phosphorylation (p-AMPKα) were increased significantly (P<0.05) in the CHF-model group. Importantly, AIT reversed these alterations induced by post-MI.
Conclusion: Findings of this study demonstrated that AIT could improve the metabolic remodeling and enhance cardiac function, which may be associated with the activation of AMPK/ peroxisome proliferator activated receptor α (PPARα) and its downstream signaling pathway.


Main Subjects

1. Doshi D, Burkhoff D. Cardiovascular Simulation of Heart Failure Pathophysiology and Therapeutics. J Card Fail 2016; 22: 303-311.
2. Pietrangelo T, Di Filippo ES, Mancinelli R, Doria C, Rotini A, Fano-Illic G, et al. Low Intensity Exercise Training Improves Skeletal Muscle Regeneration Potential. Front Physiol 2015; 6: 399.
3. Miller LE, McGinnis GR, Peters BA, Ballmann CG, Nanayakkara G, Amin R, et al. Involvement of the delta-opioid receptor in exercise-induced cardioprotection. Exp Physiol 2015; 100: 410-421.
4. Andersen K, Jonsdottir S, Sigurethsson AF, Sigurethsson SB. [The effect of physical training in chronic heart failure]. Laeknabladid 2006; 92: 759-764.
5. Leosco D, Parisi V, Femminella GD, Formisano R, Petraglia L, Allocca E, et al. Effects of exercise training on cardiovascular adrenergic system. Front Physiol 2013; 4: 348.
6. Hu ST, Tang Y, Shen YF, Ao HH, Bai J, Wang YL, et al. Protective effect of oxymatrine on chronic rat heart failure. J Physiol Sci 2011; 61: 363-372.
7. Wisloff U, Brubakk AO. Aerobic endurance training reduces bubble formation and increases survival in rats exposed to hyperbaric pressure. J Physiol 2001; 537: 607-611.
8. Makkar RR, Smith RR, Cheng K, Malliaras K, Thomson LE, Berman D, et al. Intracoronary cardiosphere-derived cells for heart regeneration after myocardial infarction (CADUCEUS): a prospective, randomised phase 1 trial. Lancet 2012; 379: 895-904.
9. Sun Y, Weber KT. Infarct scar: a dynamic tissue. Cardiovasc Res 2000; 46: 250-256.
10. Jugdutt BI, Amy RW. Healing after myocardial infarction in the dog: changes in infarct hydroxyproline and topography. J Am Coll Cardiol 1986; 7: 91-102.
11. Jugdutt BI, Schwarz-Michorowski BL, Khan MI. Effect of long-term captopril therapy on left ventricular remodeling and function during healing of canine myocardial infarction. J Am Coll Cardiol 1992; 19: 713-721.
12. Rosca MG, Hoppel CL. Mitochondria in heart failure. Cardiovasc Res 2010; 88: 40-50.
13. Roede JR, Jones DP. Reactive species and mitochondrial dysfunction: mechanistic significance of 4-hydroxynonenal. Environ Mol Mutagen 2010; 51: 380-390.
14. Bulteau AL, Lundberg KC, Humphries KM, Sadek HA, Szweda PA, Friguet B, et al. Oxidative modification and inactivation of the proteasome during coronary occlusion/reperfusion. J Biol Chem 2001; 276: 30057-30063.
15. Farout L, Mary J, Vinh J, Szweda LI, Friguet B. Inactivation of the proteasome by 4-hydroxy-2-nonenal is site specific and dependant on 20S proteasome subtypes. Arch Biochem Biophys 2006; 453: 135-142.
16. Liu Q, Wang H, Singh A, Shou F. Expression and function of microRNA-497 in human osteosarcoma. Mol Med Rep 2016; 14: 439-445.
17. Hu X, Kong X, Wang C, Ma L, Zhao J, Wei J, et al. Proteasome-mediated degradation of FRIGIDA modulates flowering time in Arabidopsis during vernalization. Plant Cell 2014; 26: 4763-4781.
18. Ferreira JC, Rolim NP, Bartholomeu JB, Gobatto CA, Kokubun E, Brum PC. Maximal lactate steady state in running mice: effect of exercise training. Clin Exp Pharmacol Physiol 2007; 34: 760-765.
19. Ferreira JC, Moreira JB, Campos JC, Pereira MG, Mattos KC, Coelho MA, et al. Angiotensin receptor blockade improves the net balance of cardiac Ca(2+) handling-related proteins in sympathetic hyperactivity-induced heart failure. Life Sci 2011; 88: 578-585.
20. Ferreira JC, Bacurau AV, Evangelista FS, Coelho MA, Oliveira EM, Casarini DE, et al. The role of local and systemic renin angiotensin system activation in a genetic model of sympathetic hyperactivity-induced heart failure in mice. Am J Physiol Regul Integr Comp Physiol 2008; 294: R26-32.
21. Kido M, Du L, Sullivan CC, Li X, Deutsch R, Jamieson SW, et al. Hypoxia-inducible factor 1-alpha reduces infarction and attenuates progression of cardiac dysfunction after myocardial infarction in the mouse. J Am Coll Cardiol 2005; 46: 2116-2124.
22. Alp PR, Newsholme EA, Zammit VA. Activities of citrate synthase and NAD+-linked and NADP+-linked isocitrate dehydrogenase in muscle from vertebrates and invertebrates. Biochem J 1976; 154: 689-700.