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Prior exercise training improves the outcome of acute myocardial infarction in the rat

Heart structure, function, and gene expression

Sarit Freimann, PhD^*,, Mickey Scheinowitz, PhD^,, Daniel Yekutieli, PhD, Micha S. Feinberg, MD^||, Michael Eldar, MD^|| and Gania Kessler-Icekson, PhD^*,*

^* Felsenstein Medical Research Center, Tel-Aviv University, Tel-Aviv, Israel
Neufeld Cardiac Research Institute, Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel
Department of Biomedical Engineering, Tel-Aviv University, Tel-Aviv, Israel
Department of Statistics and Operation Research, Tel-Aviv University, Tel-Aviv, Israel
^|| The Heart Institute, Sheba Medical Center, Tel-Aviv University, Tel-Aviv, Israel

Manuscript received July 15, 2004; revised manuscript received October 20, 2004, accepted November 11, 2004.

^* Reprint requests and correspondence: Dr. Gania Kessler-Icekson, Felsenstein Medical Research Center, Beilinson Campus, Rabin Medical Center, Petach Tikva 49100, Israel (Email: icekson{at}post.tau.ac.il).

OBJECTIVES: The aim of this research was to investigate the structural, functional, and molecular features of the remodeling heart in prior swim-trained infarcted rats.

BACKGROUND: Physical exercise training is a known protective factor against cardiovascular morbidity and mortality. The structural and molecular aspects underlying this protection in the remodeling heart have not been investigated.

METHODS: After seven weeks of swimming exercise training, rats underwent surgical ligation of the left coronary artery followed by a four-week sedentary period. Untrained control rats underwent the same surgical protocol. Left ventricular function was assessed by echocardiography four weeks after infarction, and hearts were sampled for histological and molecular analysis. Ribonucleic acid from the surviving left ventricle was analyzed by complementary deoxyribonucleic acid arrays followed by Northern blotting or quantitative reverse transcription polymerase chain reaction of selected messenger ribonucleic acids (mRNAs).

RESULTS: Scar area was 1.6-fold smaller (p = 0.0002), arteriolar density was 1.7-fold higher (p = 0.0002), and left ventricular shortening fraction was 1.9-fold higher (p = 0.003) in the exercise-trained compared with sedentary hearts. Eleven genes whose expression level varied by at least ±1.5-fold distinguished the prior exercised rats from their sedentary counterparts. Compared with sedentary, the exercised hearts displayed 9- and 2.4-times lower levels of atrial natriuretic peptide and aldolase mRNA (p = 0.03 and 0.04, respectively), and a 2.7- and 1.9-fold higher abundance of cytochrome c-oxidase and fatty acid binding protein, respectively (p < 0.03, each).

CONCLUSIONS: Swimming exercise training before acute myocardial infarction reduces scar size, increases arteriole density, and manifests adaptation of stress- and energy-metabolism-related genes that may contribute to the improved heart function observed during remodeling.

Abbreviations and Acronyms   ANP = atrial natriuretic peptide   COX = cytochrome c-oxidase   Ex = exercise   LV = left ventricle/ventricular   LVEDD = left ventricular end-diastolic diameter   LVESD = left ventricular end-systolic diameter   MI = myocardial infarction   mRNA = messenger ribonucleic acid   qRT-PCR = quantitative reverse transcription polymerase chain reaction   Sed = sedentary   SF = shortening fraction

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