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Journal of Applied Physiology, Vol 79, Issue 3 1002-1007, Copyright © 1995 by American Physiological Society
ARTICLES |
G. R. Adams, P. W. Bodell and K. M. Baldwin
Department of Physiology and Biophysics, University of California, Irvine 92717, USA.
Several published reports have indicated that derangement of the phosphocreatine/creatine (Cr) energy-buffering system via Cr analogue feeding results in cardiomyopathy when cardiac performance is assessed in vitro. The present study was designed to examine indexes of cardiac performance in rats that have been chronically Cr depleted. Adult (180 +/- 4 g) rats were assigned to a normal diet (ND) (n = 8) or a Cr-depletion diet (CD) group (n = 10). After 61 +/- 1 days of ad libitum feeding, measurements of steady-state exercise O2 consumption were made. Hemodynamic indexes were then assessed during incremental running to peak sustained levels. Rats were then killed and the left ventricle was excised. In the CD group Cr was depleted 82% and V1 isomyosin decreased while V2 increased. O2 consumption during steady-state running was not different in CD rats. The respiratory exchange ratios of CD rats reflected a bias toward fat utilization during the latter stages of prolonged exercise. The exercise heart rates and peak systolic blood pressures of CD rats were slightly lower than those of ND rats. Both negative and positive rates of left ventricular pressure development were significantly reduced at all running speeds in the CD rats. CD rats were capable of exercise performance equal to that of ND animals. The hemodynamic and metabolic data suggest that the adaptations seen in the CD animals may be similar to those reported after endurance training. These results indicate that chronic Cr depletion does not impair either the circulatory or exercise capacity of rodents.
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