Document Detail


Exercise training reverses age-related decrements in endothelium-dependent dilation in skeletal muscle feed arteries.
MedLine Citation:
PMID:  19299569     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Daniel W Trott; Filiz Gunduz; M Harold Laughlin; Christopher R Woodman
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2009-03-19
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  106     ISSN:  8750-7587     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2009 Jun 
Date Detail:
Created Date:  2009-05-27     Completed Date:  2009-07-07     Revised Date:  2013-09-26    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1925-34     Citation Subset:  IM    
Affiliation:
Department of Health and Kinesiology, Texas A&M University, College Station, TX 77843-4243, USA.
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MeSH Terms
Descriptor/Qualifier:
Acetylcholine / 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:
AG-00988/AG/NIA NIH HHS; HL-36088/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
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

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