title: Time-course of endothelial adaptation following acute and regular exercise.
abstract: BACKGROUND
  Regular exercise training has emerged as a powerful tool to improve endothelium-dependent vasorelaxation. However, little is known about the magnitude of change and the permanence of exercise-induced adaptations in endothelial function.
  
  
  METHODS
  Rats were randomized to either 6 weeks of regular exercise or one bout of exercise. Rats were then sacrificed 0, 6, 12, 24, 48, 96 or 192 h post-exercise, and vascular responsiveness to acetylcholine was determined.
  
  
  METHODS
  Endothelium-dependent dilation was assessed by exposure to accumulating doses of acetylcholine in ring segments of the abdominal aorta from female Sprague-Dawley rats that either exercised regularly for 6 weeks or performed a single bout of exercise.
  
  
  RESULTS
  A single exercise session improved endothelium-dependent vasodilatation for about 48 h. Six weeks of regular exercise induced a significantly larger improvement that lasted for about 192 h. Sensitivity to acetylcholine was twofold higher in chronically trained animals than in those exposed to a single bout of exercise. The decay after a single bout of exercise was about eightfold faster than that after 6 weeks of training.
  
  
  CONCLUSIONS
  The present data extend our concept of exercise-induced adaptation of endothelium-dependent vasodilatation in two regards: (1) a single bout of exercise improves endothelium-dependent dilation for about 2 days, with peak effect after 12-24 h; (2) regular exercise further improves adaptation and increases the sensitivity to acetylcholine approximately fourfold, which slowly returns to sedentary levels within a week of detraining.
authors.affiliation: Department of Circulation and Medical Imaging, Norwegian University of Science and Technology, Trondheim, Norway.
authors.forename: Per Magnus
authors.initials: PM
authors.lastname: Haram
authors.forename: Volker
authors.initials: V
authors.lastname: Adams
authors.forename: Ole Johan
authors.initials: OJ
authors.lastname: Kemi
authors.forename: Alf O
authors.initials: AO
authors.lastname: Brubakk
authors.forename: Rainer
authors.initials: R
authors.lastname: Hambrecht
authors.forename: Oyvind
authors.initials: O
authors.lastname: Ellingsen
authors.forename: Ulrik
authors.initials: U
authors.lastname: Wisløff
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000222:Adaptation, Physiological / Q000502:physiology*; D000818:Animals; D001012:Aorta, Abdominal / Q000187:drug effects / Q000502:physiology*; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D005500:Follow-Up Studies; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism; D010101:Oxygen Consumption / Q000502:physiology; D010805:Physical Conditioning, Animal / Q000379:methods*; D005082:Physical Exertion / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D004791:Enzyme Inhibitors; D014665:Vasodilator Agents; D009569:Nitric Oxide; D000109:Acetylcholine; D019331:NG-Nitroarginine Methyl Ester