Document Detail

Nitric oxide in the regulation of vasomotor tone in human skeletal muscle.
MedLine Citation:
PMID:  10362675     Owner:  NLM     Status:  MEDLINE    
The role of nitric oxide (NO) as a regulator of vasomotor tone has been investigated in resting and exercising human skeletal muscle. At rest, NO synthase (NOS) inhibition by intra-arterial infusion of NG-monomethyl-L-arginine decreased femoral artery blood flow (FABF, ultrasound Doppler) from 0.39 +/- 0.08 to 0.18 +/- 0.03 l/min (P < 0. 01), i.e., by approximately 52%, and increased leg O2 extraction from 62.1 +/- 9.8 to 100.9 +/- 4.5 ml/l (P < 0.004); thus leg O2 uptake (VO2, 22 +/- 4 ml/min, approximately 0.75 ml. min-1. 100 g-1) was unaltered [not significant (P = NS)]. Mean arterial pressure (MAP) increased by 8 +/- 2 mmHg (P < 0.01). Heart rate (HR, 53 +/- 3 beats/min) was unaltered (P = NS). The NOS inhibition had, however, no effect on the initial rate of rise or the magnitude of FABF (4.8 +/- 0.4 l/min, approximately 163 ml. min-1. 100 g-1), MAP (117 +/- 3 mmHg), HR (98 +/- 5 beats/min), or leg VO2 (704 +/- 55 ml/min, approximately 24 ml. min-1. 100 g-1, P = NS) during submaximal, one-legged, dynamic knee-extensor exercise. Similarly, FABF (7.6 +/- 1.0 l/min, approximately 258 ml. min-1. 100 g-1), MAP (140 +/- 8 mmHg), and leg VO2 (1,173 +/- 139 ml/min, approximately 40 ml. min-1. 100 g-1) were unaffected at termination of peak effort (P = NS). Peak HR (137 +/- 3 beats/min) was, however, lowered by 10% (P < 0.01). During recovery, NOS inhibition reduced FABF by approximately 34% (P < 0.04), which was compensated for by an increase in the leg O2 extraction by approximately 41% (P < 0.04); thus leg VO2 was unaltered (P = NS). In conclusion, these findings indicate that NO is not essential for the initiation or maintenance of active hyperemia in human skeletal muscle but support a role for NO during rest, including recovery from exercise. Moreover, changes in blood flow during rest and recovery caused by NOS inhibition are accompanied by reciprocal changes in O2 extraction, and thus VO2 is maintained.
G Rådegran; B Saltin
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The American journal of physiology     Volume:  276     ISSN:  0002-9513     ISO Abbreviation:  Am. J. Physiol.     Publication Date:  1999 Jun 
Date Detail:
Created Date:  1999-07-22     Completed Date:  1999-07-22     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0370511     Medline TA:  Am J Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  H1951-60     Citation Subset:  IM    
Copenhagen Muscle Research Centre, Rigshospitalet, and University of Copenhagen, DK-2200 Copenhagen, Denmark.
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MeSH Terms
Acetylcholine / pharmacology
Arginine / pharmacology
Blood Pressure / drug effects
Drug Interactions
Enzyme Inhibitors / pharmacology
Exercise / physiology
Femoral Artery / drug effects,  physiology
Heart Rate / drug effects
Leg / physiology
Muscle, Skeletal / physiology*
Nitric Oxide / physiology*
Nitric Oxide Synthase / antagonists & inhibitors
Nitroprusside / pharmacology
Oxygen Consumption / drug effects
Regional Blood Flow / drug effects
Vasomotor System / physiology*
omega-N-Methylarginine / pharmacology
Reg. No./Substance:
0/Enzyme Inhibitors; 10102-43-9/Nitric Oxide; 15078-28-1/Nitroprusside; 17035-90-4/omega-N-Methylarginine; 51-84-3/Acetylcholine; 74-79-3/Arginine; EC Oxide Synthase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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