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Journal of Experimental Biology, Vol 204, Issue 6 1191-1199, Copyright © 2001 by Company of Biologists
JOURNAL ARTICLES |
AJ Natali, DL Turner, SM Harrison and E White
School of Biomedical Sciences, University of Leeds, Leeds LS2 9JT, UK.
A model of voluntary exercise, in which rats are given free access to a running wheel over a 14-week period, led to left ventricular hypertrophy. To test whether the hypertrophic response to exercise was uniformly distributed across the ventricular wall, single ventricular myocytes were isolated from the sub-epicardium (EPI) and sub-endocardium (ENDO) of exercised rats and from sedentary rats for comparison. Cellular hypertrophy (approximately 20 % greater cell volume) was seen in ENDO cells from exercised animals, but no significant changes were observed in EPI cells when compared with sedentary controls. This regional effect of exercise may be a response to transmural changes in ventricular wall stress and/or strain. Cell contraction was measured as cell shortening in ENDO and EPI cells at stimulation frequencies between 1 and 9 Hz at 37 degrees C. Exercise training had no effect on cell shortening. Positive and negative contraction-frequency relationships (CFRs) were found in both EPI and ENDO cells between 1 and 5 Hz; at higher frequencies (5-9 Hz), all myocytes displayed a negative CFR. The CFR of a myocyte was, therefore, independent of regional origin and unaffected by exercise. These results suggest that, in vivo, the rat heart displays a negative CFR. We conclude that increased cell size may be a more important adaptive response to exercise than a modification of excitation-contraction coupling.
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