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Abstract 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 N G -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 ∼52%, and increased leg O 2 extraction from 62.1 ± 9.8 to 100.9 ± 4.5 ml/l ( P < 0.004); thus leg O 2 uptake (V˙ o 2 , 22 ± 4 ml/min, ∼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, ∼163 ml ⋅ min −1 ⋅ 100 g −1 ), MAP (117 ± 3 mmHg), HR (98 ± 5 beats/min), or legV˙ o 2 (704 ± 55 ml/min, ∼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, ∼258 ml ⋅ min −1 ⋅ 100 g −1 ), MAP (140 ± 8 mmHg), and leg V˙ o 2 (1,173 ± 139 ml/min, ∼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 ∼34% ( P < 0.04), which was compensated for by an increase in the leg O 2 extraction by ∼41% ( P < 0.04); thus legV˙ o 2 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 O 2 extraction, and thusV˙ o 2 is maintained. blood flow circulation exercise metabolism vasodilatation Footnotes Address for reprint requests and other correspondence: G. Rådegran, Copenhagen Muscle Research Centre, Rigshospitalet, Sect. 7652, Tagensvej 20, DK-2200 Copenhagen N, Denmark (E-mail: goran@rh.dk ). The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “ advertisement ” in accordance with 18 U.S.C. §1734 solely to indicate this fact. Copyright © 1999 the American Physiological Society
AJP - Heart and Circulatory Physiology – The American Physiological Society
Published: Jun 1, 1999
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