{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,1]],"date-time":"2025-10-01T15:26:23Z","timestamp":1759332383102},"reference-count":25,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Applied Physiology"],"published-print":{"date-parts":[[2000,2,1]]},"abstract":"<jats:p> Habitual exercise results in a rightward shift in left ventricular end diastolic (LVED) pressure-volume or internal dimension (P-D) relationships [left ventricular (LV) remodeling]. However, exercise-mediated LV hypertrophy (LVH) produces an increased LV relative wall thickness [ratio ( h\/ r) of wall thickness ( h) to internal radius ( r)] and hence a decrement in diastolic wall stress despite LV remodeling. In this study, the effect of chronic administration of an androgenic steroid on exercise-induced LV remodeling and h\/ r was examined in rats. Habitual exercise on voluntary running wheels resulted in LVH and a rightward shift in the LVED P-D relationships. However, LVH was sufficient to increase LVED h\/r. Androgenic steroid administration to exercised rats, without influencing the development of exercise-induced LVH, produced a further rightward shift in the LVED P-D relationship associated with an increased diameter intercept. As a consequence, LVED h\/r was reduced to control values. The steroid-mediated effects were not associated with alterations in either the quantity or quality of LV collagen. In conclusion, high-dose androgenic steroid administration alters exercise-induced LV remodeling and subsequently reduces the beneficial effect of physiological LVH on LV h\/ r. <\/jats:p>","DOI":"10.1152\/jappl.2000.88.2.409","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T16:34:12Z","timestamp":1513960452000},"page":"409-415","source":"Crossref","is-referenced-by-count":23,"title":["Effects of an androgenic steroid on exercise-induced  cardiac remodeling in rats"],"prefix":"10.1152","volume":"88","author":[{"given":"A. J.","family":"Woodiwiss","sequence":"first","affiliation":[{"name":"Laboratory of Cardiovascular Pathophysiology, Department of Physiology, University of the Witwatersrand, 2193 Johannesburg, South Africa"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"B.","family":"Trifunovic","sequence":"additional","affiliation":[{"name":"Laboratory of Cardiovascular Pathophysiology, Department of Physiology, University of the Witwatersrand, 2193 Johannesburg, South Africa"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M.","family":"Philippides","sequence":"additional","affiliation":[{"name":"Laboratory of Cardiovascular Pathophysiology, Department of Physiology, University of the Witwatersrand, 2193 Johannesburg, South Africa"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"G. 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