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Disparate Regulation of Signaling Proteins after Exercise and Myocardial Infarction

GOSSELIN, HUGUES1; BÉLIVEAU, LOUISE3; BURELLE, YAN3; CLÉMENT, ROBERT1; LAJOIE, CLAUDE4; EL-HELOU, VIVIANE1,2; CALDERONE, ANGELINO1,2

Medicine & Science in Sports & Exercise: March 2006 - Volume 38 - Issue 3 - pp 455-462
doi: 10.1249/01.mss.0000205138.02440.79
BASIC SCIENCES: Original Investigations

Introduction: The signaling proteins extracellular signal-regulated kinase (ERK1/2) and protein kinase B (PKB) were implicated in the development of pathological cardiac hypertrophy. The present study examined whether the progression of physiological eccentric cardiac hypertrophy was associated with ERK1/2 and PKB recruitment.

Methods and Results: Following 1 and 3 wk of voluntary exercise, female Sprague-Dawley rats ran a total distance of 55 ± 10 and 195 ± 19 km, respectively. Left ventricular hypertrophy was detected in 3-wk-exercised rats, albeit prepro-ANP protein expression was unchanged. ERK1/2 was not recruited in the left ventricle (LV) of either 1-wk-exercised rats or the hypertrophied LV of 3-wk-exercised rats. In 1-wk-exercised rats, PKB Thr308 and Ser473 phosphorylation were significantly reduced, whereas a selective increase of PKB Ser473 phosphorylation was observed in the hypertrophied LV of 3-wk-exercised rats. In both 1- and 3-wk-exercised rats, an upward electrophoretic mobility band shift of p70 ribosomal S6 kinase (p70 S6K) was detected. In 1-wk post-myocardial-infarcted (MI) female Sprague-Dawley rats, scar formation was associated with increased left ventricular end-diastolic pressure. In the hypertrophied noninfarcted left ventricle (NILV), ERK1/2, p70 S6K, PKB Ser473, and Thr308 phosphorylation were increased.

Conclusions: These data support the premise that ERK1/2 and PKB were differentially regulated during the development of eccentric physiological and pathological cardiac hypertrophy. It remains to be determined whether the chronic activation of either ERK1/2 and/or PKB in the NILV of post-MI rats may contribute in part to maladaptive cardiac remodelling.

1Research Centre, Montreal Heart Institute, Montreal, Quebec, CANADA; 2Department of Physiology, University of Montreal, Montreal, Quebec, CANADA; 3Department of Kinesiology, University of Montreal, Montreal, Quebec, CANADA; and 4Department of Human Kinetics, Laurentian University, Sudbury, Ontario, CANADA

Address for correspondence: Angelino Calderone, PhD, Research Center, Montreal Heart Institute, 5000 Belanger Street East Montreal, Quebec, Canada, H1T 1C8; E-mail: angelo.calderone@umontreal.ca.

Submitted for publication June 2005.

Accepted for publication September 2005.

©2006The American College of Sports Medicine