|Age and exercise training alter signaling through reactive oxygen species in the endothelium of skeletal muscle arterioles.|
|PMID: 23288555 Owner: NLM Status: MEDLINE|
|Exercise training ameliorates age-related impairments in endothelium-dependent vasodilation in skeletal muscle arterioles. Additionally, exercise training is associated with increased superoxide production. The purpose of this study was to determine the role of superoxide and superoxide-derived reactive oxygen species (ROS) signaling in mediating endothelium-dependent vasodilation of soleus muscle resistance arterioles from young and old, sedentary and exercise-trained rats. Young (3 mo) and old (22 mo) male rats were either exercise trained or remained sedentary for 10 wk. To determine the impact of ROS signaling on endothelium-dependent vasodilation, responses to acetylcholine were studied under control conditions and during the scavenging of superoxide and/or hydrogen peroxide. To determine the impact of NADPH oxidase-derived ROS, endothelium-dependent vasodilation was determined following NADPH oxidase inhibition. Reactivity to superoxide and hydrogen peroxide was also determined. Tempol, a scavenger of superoxide, and inhibitors of NADPH oxidase reduced endothelium-dependent vasodilation in all groups. Similarly, treatment with catalase and simultaneous treatment with tempol and catalase reduced endothelium-dependent vasodilation in all groups. Decomposition of peroxynitrite also reduced endothelium-dependent vasodilation. Aging had no effect on arteriolar protein content of SOD-1, catalase, or glutathione peroxidase-1; however, exercise training increased protein content of SOD-1 in young and old rats, catalase in young rats, and glutathione peroxidase-1 in old rats. These data indicate that ROS signaling is necessary for endothelium-dependent vasodilation in soleus muscle arterioles, and that exercise training-induced enhancement of endothelial function occurs, in part, through an increase in ROS signaling.|
|Amy L Sindler; Rafael Reyes; Bei Chen; Payal Ghosh; Alvaro N Gurovich; Lori S Kang; Arturo J Cardounel; Michael D Delp; Judy M Muller-Delp|
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|Type: Journal Article; Research Support, N.I.H., Extramural Date: 2013-01-03|
|Title: Journal of applied physiology (Bethesda, Md. : 1985) Volume: 114 ISSN: 1522-1601 ISO Abbreviation: J. Appl. Physiol. Publication Date: 2013 Mar|
|Created Date: 2013-03-04 Completed Date: 2014-01-13 Revised Date: 2014-03-07|
Medline Journal Info:
|Nlm Unique ID: 8502536 Medline TA: J Appl Physiol (1985) Country: United States|
|Languages: eng Pagination: 681-93 Citation Subset: IM|
|APA/MLA Format Download EndNote Download BibTex|
Arterioles / drug effects, metabolism, physiology
Catalase / metabolism
Cyclic N-Oxides / metabolism
Endothelium, Vascular / drug effects, metabolism*, physiology
Endothelium-Dependent Relaxing Factors / pharmacology
Glutathione Peroxidase / metabolism
Hydrogen Peroxide / metabolism
Muscle, Skeletal / blood supply*, drug effects, metabolism*, physiology
NADPH Oxidase / metabolism
Nitric Oxide / metabolism
Physical Conditioning, Animal / physiology*
Rats, Inbred F344
Reactive Oxygen Species / metabolism*
Signal Transduction / drug effects, physiology*
Superoxides / metabolism
Vasodilation / drug effects, physiology
|HL-077224/HL/NHLBI NIH HHS; R01 HL-090937/HL/NHLBI NIH HHS; R01 HL081734/HL/NHLBI NIH HHS|
|0/Cyclic N-Oxides; 0/Endothelium-Dependent Relaxing Factors; 0/Reactive Oxygen Species; 0/Spin Labels; 11062-77-4/Superoxides; 2226-96-2/tempol; 31C4KY9ESH/Nitric Oxide; BBX060AN9V/Hydrogen Peroxide; EC 1.11.1.-/glutathione peroxidase GPX1; EC 220.127.116.11/Catalase; EC 18.104.22.168/Glutathione Peroxidase; EC 22.214.171.124/NADPH Oxidase; N9YNS0M02X/Acetylcholine|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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