title: Vigorous exercise training improves reactivity of cerebral arterioles and reduces brain injury following transient focal ischemia.
abstract: OBJECTIVE
  Our objective was to examine whether vigorous exercise training (VExT) could influence nitric oxide synthase (NOS)-dependent vasodilation and transient focal ischemia-induced brain injury. Rats were divided into sedentary (SED) or VExT groups.
  
  
  METHODS
  Exercise was carried out 5 days/week for a period of 8-10 weeks. First, we measured responses of pial arterioles to an eNOS-dependent (ADP), an nNOS-dependent (NMDA) and a NOS-independent (nitroglycerin) agonist in SED and VExT rats. Second, we measured infarct volume in SED and VExT rats following middle cerebral artery occlusion (MCAO). Third, we measured superoxide levels in brain tissue of SED and VExT rats under basal and stimulated conditions.
  
  
  RESULTS
  We found that eNOS- and nNOS-dependent, but not NOS-independent vasodilation, was increased in VExT compared to SED rats, and this could be inhibited with L-NMMA in both groups. In addition, we found that VExT reduced infarct volume following MCAO when compared to SED rats. Further, superoxide levels were similar in brain tissue from SED and VExT rats under basal and stimulated conditions.
  
  
  CONCLUSIONS
  We suggest that VExT potentiates NOS-dependent vascular reactivity and reduces infarct volume following MCAO via a mechanism that appears to be independent of oxidative stress, but presumably related to an increase in the contribution of nitric oxide.
authors.affiliation: Department of Cellular Biology and Anatomy and the Center for Cardiovascular Diseases and Sciences, LSU Health Sciences Center-Shreveport, Shreveport, Louisiana, USA.
authors.forename: Denise M
authors.initials: DM
authors.lastname: Arrick
authors.forename: Shu
authors.initials: S
authors.lastname: Yang
authors.forename: Chun
authors.initials: C
authors.lastname: Li
authors.forename: Sergio
authors.initials: S
authors.lastname: Cananzi
authors.forename: William G
authors.initials: WG
authors.lastname: Mayhan
mesh_terms: D000818:Animals; D001160:Arterioles / Q000378:metabolism / Q000473:pathology; D001921:Brain / Q000098:blood supply* / Q000378:metabolism* / Q000473:pathology; D001930:Brain Injuries / Q000378:metabolism* / Q000473:pathology; D002545:Brain Ischemia / Q000378:metabolism* / Q000473:pathology; D002560:Cerebrovascular Circulation; D004791:Enzyme Inhibitors / Q000494:pharmacology; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D010805:Physical Conditioning, Animal; D051381:Rats; D017207:Rats, Sprague-Dawley; D013481:Superoxides / Q000378:metabolism; D019323:omega-N-Methylarginine / Q000494:pharmacology
chemical_list: D004791:Enzyme Inhibitors; D013481:Superoxides; D019323:omega-N-Methylarginine; D009569:Nitric Oxide; D052250:Nitric Oxide Synthase Type III; C496316:Nos3 protein, rat
keywords: ADP; NMDA; ischemia/reperfusion; middle cerebral artery occlusion; pial arterioles