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This Article Full Text Full Text (PDF) All Versions of this Article: 90/6/889    most recent expphysiol.2005.031567v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Krause, D. J Articles by Hepple, R. T Search for Related Content PubMed PubMed Citation Articles by Krause, D. J Articles by Hepple, R. T Related Collections Muscle

¹ Faculty of Medicine² Faculty of Kinesiology, University of Calgary, Calgary, Alberta, Canada ³ Faculty of Medicine, University of California San Diego, CA, USA

Nitric oxide (NO) is a physiological mediator of skeletal muscle function. Specifically, NO affects cellular respiration and muscle contractility; however, the reduced blood flow and convective O₂ delivery that result from impaired vasodilatation when NO synthase (NOS) is inhibited in vivo have obscured past interpretations of the effects of NO. Therefore, we studied the effect of NOS inhibition in an in situ pump-perfused rat hindlimb to test the hypothesis that NOS inhibition would improve contractile and aerobic metabolic performance. Pump perfusion permitted matching of convective O₂ delivery (516 ± 16 µmol O₂ min^–1 (100 g)^–1; mean ± S.E.M.) between groups, allowing us to investigate the effects of NOS inhibition independent of this variable. Three groups were studied. The perfusate of one group was treated with both adenosine (0.01 mM) and the NOS inhibitor, N-nitro-L-arginine methyl ester (L-NAME; 1 mM). Adenosine is a vasodilator that can act through both NO-dependent and -independent pathways; the NO-independent vasodilatory action of adenosine allowed us to match the perfusion rate and convective O₂ delivery in this L-NAME group to those of the other groups. In the second group the perfusate was treated with adenosine only (Ado). In the third group the perfusate received no treatment and served as a control (Con). Oxygen consumption () was on average 26 and 14% lower during the contraction bout in L-NAME and Ado, respectively, versus Con. In Ado, lactate efflux was similar to Con and force was reduced in proportion to versus Con, whereas L-NAME was associated with a 32% lower lactate efflux and similar force to Con. Therefore, the lower :force development ratio in the L-NAME group demonstrates that the O₂ cost of force development is reduced by NOS inhibition independent of convective O₂ delivery.

(Received 26 July 2005; accepted after revision 23 August 2005; first published online 25 August 2005)
Corresponding author R. T. Hepple: Faculty of Kinesiology, University of Calgary, 2500 University Dr. NW, Calgary, Alberta, Canada T2N 1 N4. Email: hepple{at}ucalgary.ca

This article has been cited by other articles:

				D. J. Baker, D. J. Krause, R. A. Howlett, and R. T. Hepple Nitric oxide synthase inhibition reduces O2 cost of force development and spares high-energy phosphates following contractions in pump-perfused rat hindlimb muscles Exp Physiol, May 1, 2006; 91(3): 581 - 589. [Abstract] [Full Text] [PDF]