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Articles in PresS, published online ahead of print November 7, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00761.2002
Submitted on August 30, 2002
Accepted on October 28, 2002
1 Department of Kinesiology, University of Wisconsin, Madison, WI, USA
2 Department of Pharmacy, University of Wisconsin, Madison, WI, USA
3 Center for Neuroscience, University of Wisconsin, Madison, WI, USA; Department of Molecular and Environmental Toxicololgy Center, University of Wisconsin, Madison, WI, USA
4 Center for Neuroscience, University of Wisconsin, Madison, WI, USA; Department of Molecular and Environmental Toxicololgy Center, University of Wisconsin, Madison, WI, USA; Department of Molecular and Environmental Toxicololgy Center, University of Wisconsin, Madison, WI, USA
* To whom correspondence should be addressed. E-mail: gmdiffee{at}facstaff.wisc.edu.
Previous studies have shown that endurance exercise training increases myocardial contractility. We have previously described training-induced alterations in myocardial contractile function at the cellular level, including an increase in Ca2+ sensitivity of tension. To determine the molecular mechanism(s) of these changes, oligonucleotide microarrays were used to analyze the gene expression profile in ventricles from endurance trained rats. We used an 11-week treadmill training protocol that we have previously shown results in increased contractility in cardiac myocytes. Following the training, the hearts were removed and RNA was isolated from ventricles of 9 trained and 9 control rats. Using the Affymetrix Rat Genome U34A Array, we detected altered expression of 27 genes. Several genes previously found to have increased expression in hypertrophied myocardium, such as atrial natriuretic factor and 
-skeletal actin, were decreased with training in this study. From the standpoint of altered contractile performance, the most significant finding was an increase in expression of atrial myosin light chain 1 (aMLC1) in the trained ventricular tissue. We confirmed the microarray results for aMLC1 using RT-PCR and also confirmed a training-induced increase in aMLC1 protein using 2D gel electrophoresis. aMLC1 content has previously been shown to be increased in human cardiac hypertrophy and has been associated with increased Ca2+ sensitivity of tension and increased power output. These results suggest that increased expression of aMLC1 in response to training may be responsible, at least in part, for previously observed training-induced enhancement of contractile function.
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