title: Reduction in alpha-adrenergic receptor-mediated vascular tone contributes to improved arterial compliance with endurance training.
abstract: BACKGROUND
  Regular aerobic exercise improves large artery compliance in middle-aged and older humans. However, the underlying mechanisms are unknown. We tested the hypothesis that the improved central arterial compliance with endurance training is mediated by decreased alpha-adrenergic tone and/or increased endothelial function.
  
  
  METHODS
  Seven sedentary healthy adults (60+/-3 years) underwent systemic alpha-adrenergic blockade (phentolamine) and nitric oxide synthase (NOS) inhibition using N(G)-monomethyl-L-arginine in sequence before and after a 3-month moderate endurance training (walk/jog, 4-5 days/week). Phentolamine was given first to isolate the contribution of nitric oxide to arterial compliance by minimizing reflex suppression of sympathetic tone resulting from systemic NOS inhibition as well as to assess the alpha-adrenergic receptor-mediated modulation of arterial compliance.
  
  
  RESULTS
  Baseline arterial compliance (via simultaneous ultrasound and applanation tonometry on the carotid artery) increased 34+/-12% after exercise training (P<0.01). When alpha-adrenergic blockade was performed, arterial compliance increased 37+/-6% (P<0.01) before the exercise training but did not change significantly after the training. Decreases in arterial compliance from the alpha-adrenergic blockade to the subsequent additional NOS blockade were not different before and after exercise training.
  
  
  CONCLUSIONS
  Our results suggest that the reduction in alpha-adrenergic receptor-mediated vascular tone contributes to the improved central arterial compliance with endurance training.
authors.affiliation: Institute for Human Science and Biomedical Engineering, National Institute of Advanced Industrial Science and Technology, Ibaraki, Japan. jun.sugawara@mail.utexas.edu
authors.forename: Jun
authors.initials: J
authors.lastname: Sugawara
authors.forename: Hidehiko
authors.initials: H
authors.lastname: Komine
authors.forename: Koichiro
authors.initials: K
authors.lastname: Hayashi
authors.forename: Mutsuko
authors.initials: M
authors.lastname: Yoshizawa
authors.forename: Takeshi
authors.initials: T
authors.lastname: Otsuki
authors.forename: Nobutake
authors.initials: N
authors.lastname: Shimojo
authors.forename: Takashi
authors.initials: T
authors.lastname: Miyauchi
authors.forename: Takashi
authors.initials: T
authors.lastname: Yokoi
authors.forename: Seiji
authors.initials: S
authors.lastname: Maeda
authors.forename: Hirofumi
authors.initials: H
authors.lastname: Tanaka
mesh_terms: D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000368:Aged; D002339:Carotid Arteries / Q000187:drug effects / Q000502:physiology*; D003187:Compliance / Q000187:drug effects / Q000502:physiology; D015444:Exercise / Q000502:physiology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010807:Physical Endurance / Q000187:drug effects / Q000502:physiology*; D011942:Receptors, Adrenergic, alpha / Q000502:physiology*; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology*; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*
chemical_list: D000317:Adrenergic alpha-Antagonists; D011942:Receptors, Adrenergic, alpha