Effects of exercise training on cardiac function, gene expression, and apoptosis in rats

1  Department of Cardiovascular Research and 2  Department of Pathology, Genentech Incorporated, South San Francisco, California 94080 This study determined the effects of exercise training on cardiac function, gene expression, and apoptosis. Rats exposed to a regimen of treadmill exercise for 13 wk...

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Veröffentlicht in:American journal of physiology. Heart and circulatory physiology 2000-12, Vol.279 (6), p.H2994-H3002
Hauptverfasser: Jin, Hongkui, Yang, Renhui, Li, Wei, Lu, Hsienwie, Ryan, Anne M, Ogasawara, Annie K, Van Peborgh, John, Paoni, Nicholas F
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Sprache:eng
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Zusammenfassung:1  Department of Cardiovascular Research and 2  Department of Pathology, Genentech Incorporated, South San Francisco, California 94080 This study determined the effects of exercise training on cardiac function, gene expression, and apoptosis. Rats exposed to a regimen of treadmill exercise for 13 wk had a significant increase in cardiac index and stroke volume index and a concomitant decrease in systemic vascular resistance compared with both age-matched and body weight-matched sedentary controls in the conscious state at rest. In exercise-trained animals, there was no change in the expression of several marker genes known to be associated with pathological cardiac adaptation, including atrial natriuretic factor, -myosin heavy chain, -skeletal and smooth muscle actins, and collagens I and III. Exercise training, however, produced a significant induction of -myosin heavy chain, which was not observed in rats with myocardial infarction. No histological features of cardiac apoptosis were observed in the treadmill-trained rats. In contrast, apoptotic myocytes were detected in animals with myocardial infarction. In summary, exercise training improves cardiac function without evidence of cardiac apoptosis and produces a pattern of cardiac gene expression distinct from pathological cardiac adaptation. treadmill; hemodynamics; physiological loads; pathological loads; myocardial infarction
ISSN:0363-6135
1522-1539
DOI:10.1152/ajpheart.2000.279.6.h2994