|Roles of nitric oxide synthase and cyclooxygenase in leg vasodilation and oxygen consumption during prolonged low-intensity exercise in untrained humans.|
|PMID: 20558755 Owner: NLM Status: MEDLINE|
|The vasodilator signals regulating muscle blood flow during exercise are unclear. We tested the hypothesis that in young adults leg muscle vasodilation during steady-state exercise would be reduced independently by sequential pharmacological inhibition of nitric oxide synthase (NOS) and cyclooxygenase (COX) with NG-nitro-L-arginine methyl ester (L-NAME) and ketorolac, respectively. We tested a second hypothesis that NOS and COX inhibition would increase leg oxygen consumption (VO2) based on the reported inhibition of mitochondrial respiration by nitric oxide. In 13 young adults, we measured heart rate (ECG), blood pressure (femoral venous and arterial catheters), blood gases, and venous oxygen saturation (indwelling femoral venous oximeter) during prolonged (25 min) steady-state dynamic knee extension exercise (60 kick/min, 19 W). Leg blood flow (LBF) was determined by Doppler ultrasound of the femoral artery. Whole body VO2 was measured, and leg VO2 was calculated from blood gases and LBF. Resting intra-arterial infusions of acetylcholine (ACh) and nitroprusside (NTP) tested inhibitor efficacy. Leg vascular conductance (LVC) to ACh was reduced up to 53±4% by L-NAME+ketorolac infusion, and the LVC responses to NTP were unaltered. Exercise increased LVC from 4±1 to 33.1±2 ml.min(-1).mmHg(-1) and tended to decrease after L-NAME infusion (31±2 ml.min(-1).mmHg(-1), P=0.09). With subsequent administration of ketorolac LVC decreased to 29.6±2 ml.min(-1).mmHg(-1) (P=0.02; n=9). While exercise continued, LVC returned to control values (33±2 ml.min(-1).mmHg(-1)) within 3 min, suggesting involvement of additional vasodilator mechanisms. In four additional subjects, LVC tended to decrease with L-NAME infusion alone (P=0.08) but did not demonstrate the transient recovery. Whole body and leg VO2 increased with exercise but were not altered by L-NAME or L-NAME+ketorolac. These data indicate a modest role for NOS- and COX-mediated vasodilation in the leg of exercising humans during prolonged steady-state exercise, which can be restored acutely. Furthermore, NOS and COX do not appear to influence muscle VO2 in untrained healthy young adults.|
|William G Schrage; Brad W Wilkins; Christopher P Johnson; John H Eisenach; Jacqueline K Limberg; Niki M Dietz; Timothy B Curry; Michael J Joyner|
Related Documents :
|2600015 - Work capacity during 30 days of bed rest with isotonic and isokinetic exercise training.
1585815 - Characteristics of the carotid baroreflex in man during normal and flow-restricted exer...
21567805 - Introducing human population biology through an easy laboratory exercise on mitochondri...
20113455 - Predonation hydration and applied muscle tension combine to reduce presyncopal reaction...
3343055 - Inhibition by estrogens of conidium-to-yeast conversion in the fungus paracoccidioides ...
20132695 - The hip and knee book: developing an active management booklet for hip and knee osteoar...
|Type: Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2010-06-17|
|Title: Journal of applied physiology (Bethesda, Md. : 1985) Volume: 109 ISSN: 1522-1601 ISO Abbreviation: J. Appl. Physiol. Publication Date: 2010 Sep|
|Created Date: 2010-09-10 Completed Date: 2011-01-12 Revised Date: 2014-03-19|
Medline Journal Info:
|Nlm Unique ID: 8502536 Medline TA: J Appl Physiol (1985) Country: United States|
|Languages: eng Pagination: 768-77 Citation Subset: IM|
|APA/MLA Format Download EndNote Download BibTex|
administration & dosage
Catecholamines / blood
Cyclooxygenase Inhibitors / administration & dosage
Enzyme Inhibitors / administration & dosage
Ketorolac / administration & dosage
Muscle, Skeletal / blood supply*, drug effects, enzymology*
NG-Nitroarginine Methyl Ester / administration & dosage
Nitric Oxide Synthase / antagonists & inhibitors, metabolism*
Nitroprusside / administration & dosage
Oxygen / blood
Oxygen Consumption* / drug effects
Prostaglandin-Endoperoxide Synthases / metabolism*
Regional Blood Flow
Vasodilation* / drug effects
Vasodilator Agents / administration & dosage
|HL-091397/HL/NHLBI NIH HHS; HL-46493/HL/NHLBI NIH HHS; HL-78019/HL/NHLBI NIH HHS; L30 HL074824/HL/NHLBI NIH HHS; RR-017520/RR/NCRR NIH HHS; RR-024150/RR/NCRR NIH HHS|
|0/Catecholamines; 0/Cyclooxygenase Inhibitors; 0/Enzyme Inhibitors; 0/Vasodilator Agents; 169D1260KM/Nitroprusside; EC 188.8.131.52/Nitric Oxide Synthase; EC 184.108.40.206/Prostaglandin-Endoperoxide Synthases; N9YNS0M02X/Acetylcholine; S88TT14065/Oxygen; V55S2QJN2X/NG-Nitroarginine Methyl Ester; YZI5105V0L/Ketorolac|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Comparison of DXA and water measurements of body fat following gastric bypass surgery and a physiolo...
Next Document: Circulating platelet-neutrophil complexes are important for subsequent neutrophil activation and mig...