title: Does detraining restore influence of exercise training on microvascular responses in streptozotocin-induced diabetic rats?
abstract: Several findings demonstrated that exercise training has therapeutic and protective effects in type 1 diabetes and could correct micro and macro vascular dysfunction. Regarding all benefits of exercise training on vascular function, however, the mechanisms and persistence of these benefits are only partially understood.
  
  
  METHODS
  Male Wistar rats (220±10g, N=85) were made diabetic by streptozotocin (60mg/kg, subcutaneously). One week after diabetes induction, animals were submitted to exercise training for 10weeks on a treadmill and detrained for 5weeks. To characterize cutaneous microvascular responses by Laser Doppler flowmetery, animals were deeply anaesthetized by intra peritoneal injection of pentobarbital sodium and placed on a heating pad, a rectal thermometer was inserted, and body temperature was maintained at 37±0.5°C. A tracheotomy was performed to minimize respiratory difficulties. Results in diabetic rats after training: (1) l-arginine (l-ARG) and Acetylcholine (Ach)-induced cutaneous perfusion were increased. However, these effects were reversed by detraining and Nw-nitro-l-arginine (l-NNA); (2) sodium nitroprusside (SNP)-induced cutaneous perfusion did not significantly change; and (3) cutaneous microvascular responses to SNP were reduced after detraining. The results suggest that in diabetic rats, beneficial effect of regular exercise on cutaneous microvascular endothelium-dependent dilatation and l-ARG/Nitric oxide pathway activity was approximately reversed by 5weeks of detraining. Training did not affect endothelium-independent dilatation; however, detraining reduced it significantly.
authors.affiliation: Department of Physical Education and Sport Science, Bu-Ali Sina university, Hamedan, Iran. heidarian317@gmail.com
authors.forename: Ali
authors.initials: A
authors.lastname: Heidarianpour
mesh_terms: D000279:Administration, Cutaneous; D000818:Animals; D001120:Arginine / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000150:complications / Q000378:metabolism / Q000503:physiopathology*; D003925:Diabetic Angiopathies / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D004791:Enzyme Inhibitors / Q000008:administration & dosage; D007478:Iontophoresis; D017078:Laser-Doppler Flowmetry; D008297:Male; D008833:Microcirculation / Q000187:drug effects; D008845:Microinjections; D055806:Microvessels / Q000378:metabolism / Q000503:physiopathology*; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D005082:Physical Exertion; D051381:Rats; D017208:Rats, Wistar; D012867:Skin / Q000098:blood supply*; D013997:Time Factors; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000008:administration & dosage
chemical_list: D004791:Enzyme Inhibitors; D014665:Vasodilator Agents; D009569:Nitric Oxide; D001120:Arginine; D019001:Nitric Oxide Synthase