TAGARAKIS, C. V. M., W. BLOCH, G, HARTMANN, W, HOLLMANN, and K, ADDICKS. Testosterone-propionate impairs the response of the cardiac capillary bed to exercise. Med. Sci. Sports Exerc., Vol. 32, No. 5, pp. 946–953, 2000.
Experimental application of anabolic-androgenic steroids and exercise training induce cardiac hypertrophy. This study quantifies for the first time, on microscopical level, the adaptation of the cardiac capillaries and myocytes to the concomitant application of testosterone-propionate and exercise training.
Female SPF-NMRI mice were studied over 3 and 6 wk. Experimental groups: (i) sedentary control (C); (ii) exercise (treadmill running, E); (iii) testosterone-propionate (TP); and (iv) testosterone-propionate+exercise (TPE). Morphometric parameters: 1) papillary muscles: capillary density, intercapillary distance, number of capillaries around a myocyte, and minimal myocyte diameter; and 2) left ventricular wall: capillary density and intercapillary distance.
Papillary muscle: A striking suppression of the exercise-induced improvement in capillary supply occurs in the testosterone-propionate+exercise groups over 3 and 6 wk. Exercise without drugs increases significantly (P < 0.05) the capillary density , shortens significantly (P < 0.05) the intercapillary distance, whereas it increases the number of capillaries around a myocyte. These alterations are not observed in the testosterone-propionate treated sedentary animals; e.g., capillary density after 6 wk (mean values ± standard deviation, capillaries·mm−2): C: 4272 ± 287, E: 5411 ± 758, TP: 4221 ± 364, and TPE: 3997 ± 397. Moreover , only in the testosterone-propionate+exercise groups occurs a mild myocyte hypertrophy after both time periods: there is a trend toward hypertrophy (P < 0.1) in comparison with the C groups and a significant hypertrophy (P < 0.05) in comparison with the E groups.
Testosterone-propionate profoundly inhibits the exercise-induced augmented capillarization, whereas (under training conditions) it leads to a mild myocyte hypertrophy. The microvascular impairment could trigger an imbalance between the myocardial oxygen supply and demand, especially during physical exercise.
Institute I of Anatomy, University of Cologne; Institute of Cardiology and Sports Medicine, German Sport University, Cologne; and Bayer Vital GmbH & Co. KG, Geschäftsbereich Pharma, Leverkusen, GERMANY
Submitted for publication April 1998.
Accepted for publication July 1999.
Address for correspondence: Christos V. M. Tagarakis, Institute I of Anatomy, University of Cologne, Joseph-Stelzmann-Str. 9, 50931 Cologne, Germany.