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Local nitric oxide synthase inhibition reduces skeletal muscle glucose uptake but not capillary blood flow during in situ muscle contraction in rats

Ross, Renee M., Wadley, Glenn D., Clark, Michael G., Rattigan, Stephen and McConell, Glenn K. 2007, Local nitric oxide synthase inhibition reduces skeletal muscle glucose uptake but not capillary blood flow during in situ muscle contraction in rats, Diabetes, vol. 56, no. 12, pp. 2885-2892, doi: 10.2337/db07-0745.

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Title Local nitric oxide synthase inhibition reduces skeletal muscle glucose uptake but not capillary blood flow during in situ muscle contraction in rats
Author(s) Ross, Renee M.
Wadley, Glenn D.ORCID iD for Wadley, Glenn D. orcid.org/0000-0002-6617-4359
Clark, Michael G.
Rattigan, Stephen
McConell, Glenn K.
Journal name Diabetes
Volume number 56
Issue number 12
Start page 2885
End page 2892
Publisher American Diabetes Association
Place of publication New York, N. Y.
Publication date 2007-12
ISSN 0012-1797
1939-327X
Summary OBJECTIVE: We have previously shown in humans that local infusion of a nitric oxide synthase (NOS) inhibitor into the femoral artery attenuates the increase in leg glucose uptake during exercise without influencing total leg blood flow. However, rodent studies examining the effect of NOS inhibition on contraction-stimulated skeletal muscle glucose uptake have yielded contradictory results. This study examined the effect of local infusion of an NOS inhibitor on skeletal muscle glucose uptake (2-deoxyglucose) and capillary blood flow (contrast-enhanced ultrasound) during in situ contractions in rats.

RESEARCH DESIGN AND METHODS: Male hooded Wistar rats were anesthetized and one hindleg electrically stimulated to contract (2 Hz, 0.1 ms) for 30 min while the other leg rested. After 10 min, the NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME) (arterial concentration of 5 µmol/l) or saline was infused into the epigastric artery of the contracting leg.

RESULTS: Local NOS inhibition had no effect on blood pressure, heart rate, or muscle contraction force. Contractions increased (P < 0.05) skeletal muscle NOS activity, and this was prevented by L-NAME infusion. NOS inhibition caused a modest significant (P < 0.05) attenuation of the increase in femoral blood flow during contractions, but importantly there was no effect on capillary recruitment. NOS inhibition attenuated (P < 0.05) the increase in contraction-stimulated skeletal muscle glucose uptake by ~35%, without affecting AMP-activated protein kinase (AMPK) activation.

CONCLUSIONS: NOS inhibition attenuated increases in skeletal muscle glucose uptake during contraction without influencing capillary recruitment, suggesting that NO is critical for part of the normal increase in skeletal muscle fiber glucose uptake during contraction.
Language eng
DOI 10.2337/db07-0745
Field of Research 060199 Biochemistry and Cell Biology not elsewhere classified
Socio Economic Objective 970106 Expanding Knowledge in the Biological Sciences
HERDC Research category C1.1 Refereed article in a scholarly journal
Copyright notice ©2007, American Diabetes Association
Persistent URL http://hdl.handle.net/10536/DRO/DU:30019459

Document type: Journal Article
Collections: Faculty of Health
School of Exercise and Nutrition Sciences
Institute for Physical Activity and Nutrition
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