title: Testosterone-propionate impairs the response of the cardiac capillary bed to exercise.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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 x 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Institute I of Anatomy, University of Cologne, Germany.
authors.forename: C V
authors.initials: CV
authors.lastname: Tagarakis
authors.forename: W
authors.initials: W
authors.lastname: Bloch
authors.forename: G
authors.initials: G
authors.lastname: Hartmann
authors.forename: W
authors.initials: W
authors.lastname: Hollmann
authors.forename: K
authors.initials: K
authors.lastname: Addicks
mesh_terms: D000818:Animals; D002196:Capillaries / Q000187:drug effects / Q000502:physiology; D006332:Cardiomegaly / Q000209:etiology; D005260:Female; D006352:Heart Ventricles / Q000187:drug effects; D051379:Mice; D008854:Microscopy, Electron; D018485:Muscle Fibers, Skeletal / Q000648:ultrastructure; D009206:Myocardium / Q000166:cytology / Q000648:ultrastructure; D018919:Neovascularization, Physiologic; D010210:Papillary Muscles / Q000187:drug effects / Q000502:physiology*; D010805:Physical Conditioning, Animal; D012420:Running / Q000502:physiology; D013739:Testosterone / Q000494:pharmacology*; D016276:Ventricular Function
chemical_list: D013739:Testosterone