| Exercise training reverses age-related decrements in endothelium-dependent dilation in skeletal muscle feed arteries. | |
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MedLine Citation:
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PMID: 19299569 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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We tested two hypotheses, first that exercise training reverses age-related decrements in endothelium-dependent dilation in soleus muscle feed arteries and second that this improved endothelium-dependent dilation is the result of increased nitric oxide (NO) bioavailability due to increased content and phosphorylation of endothelial NO synthase (eNOS) and/or increased antioxidant enzyme content. Young (2 mo) and old (22 mo) male Fischer 344 rats were exercise trained (Ex) or remained sedentary (Sed) for 10-12 wk, yielding four groups of rats: 1) young Sed (4-5 mo), 2) young Ex (4-5 mo), 3) old Sed (24-25 mo), and 4) old Ex (24-25 mo). Soleus muscle feed arteries (SFA) were isolated and cannulated with two glass micropipettes for examination of endothelium-dependent (ACh) and endothelium-independent [sodium nitroprusside (SNP)] vasodilator function. To determine the mechanism(s) by which exercise affected dilator responses, ACh-induced dilation was assessed in the presence of N(omega)-nitro-l-arginine (l-NNA; to inhibit NO synthase), indomethacin (Indo; to inhibit cyclooxygenase), and l-NNA + Indo. Results indicated that ACh-induced dilation was blunted in old Sed SFA relative to young Sed SFA. Exercise training improved ACh-induced dilation in old SFA such that vasodilator responses in old Ex SFA were similar to young Sed and young Ex SFA. Addition of l-NNA, or l-NNA + Indo, abolished the exercise effect. Immunoblot analysis revealed that extracellular superoxide dismutase (SOD) protein content was increased by training in old SFA, whereas eNOS and SOD-1 protein content were not altered. Addition of exogenous SOD, or SOD + catalase, improved ACh-induced dilation in old Sed SFA such that vasodilator responses were similar to young Sed SFA. Addition of l-NNA abolished the effect of exogenous SOD in old Sed arteries. Collectively, these results indicate that exercise training reverses age-induced endothelial dysfunction in SFA by increasing NO bioavailability and that increases in vascular antioxidant capacity may play an integral role in the improvement in endothelial function. |
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Authors:
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Daniel W Trott; Filiz Gunduz; M Harold Laughlin; Christopher R Woodman |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2009-03-19 |
Journal Detail:
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Title: Journal of applied physiology (Bethesda, Md. : 1985) Volume: 106 ISSN: 8750-7587 ISO Abbreviation: J. Appl. Physiol. Publication Date: 2009 Jun |
Date Detail:
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Created Date: 2009-05-27 Completed Date: 2009-07-07 Revised Date: 2010-09-23 |
Medline Journal Info:
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Nlm Unique ID: 8502536 Medline TA: J Appl Physiol Country: United States |
Other Details:
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Languages: eng Pagination: 1925-34 Citation Subset: IM |
Affiliation:
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Department of Health and Kinesiology, Texas A&M University, College Station, TX 77843-4243, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acetylcholine
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pharmacology Aging / metabolism* Animals Arteries / drug effects, metabolism* Catalase / antagonists & inhibitors, pharmacology Endothelium, Vascular / drug effects, metabolism* Enzyme Inhibitors / pharmacology Indomethacin / pharmacology Male Muscle, Skeletal / blood supply* Nitric Oxide / metabolism* Nitric Oxide Synthase / antagonists & inhibitors, metabolism Nitroarginine / pharmacology Nitroprusside / pharmacology Physical Conditioning, Animal* Rats Rats, Inbred F344 Recovery of Function Superoxide Dismutase / antagonists & inhibitors, metabolism, pharmacology Vasodilation |
| Grant Support | |
ID/Acronym/Agency:
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AG-00988/AG/NIA NIH HHS; HL-36088/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Enzyme Inhibitors; 10102-43-9/Nitric Oxide; 15078-28-1/Nitroprusside; 2149-70-4/Nitroarginine; 51-84-3/Acetylcholine; 53-86-1/Indomethacin; EC 1.11.1.6/Catalase; EC 1.14.13.39/Nitric Oxide Synthase; EC 1.15.1.1/Superoxide Dismutase |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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