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1 Dipartimento di Scienze e Tecnologie Biomediche, Università degli Studi di Milano, I-20090 Segrate (MI), Italy
2
Department of Medicine, University of California, San Diego, La Jolla, CA 92093, USA
3
Department of Health and Human Performance, Auburn University, Auburn, AL 36849, USA
Nitric oxide (NO) has an inhibitory action on O2 uptake 
at the level of the mitochondrial respiratory chain. The aim of this study was to evaluate the effects of NO synthase (NOS) inhibition on muscle 
kinetics. Isolated canine gastrocnemius muscles in situ (n = 6) were studied during transitions from rest to 4-min of electrically stimulated contractions corresponding to 
60% of the muscle peak 
. Two conditions were compared: (i) Control (CTRL) and (ii) L-NAME, in which the NOS inhibitor L-NAME (20 mg kg–1) was administered. In both conditions the muscle was pump-perfused with constantly elevated blood flow 
, at a level measured during a preliminary contraction trial with spontaneous self-perfused
. A vasodilatory drug was also infused. Arterial and venous O2 concentrations were determined at rest and at 5–7 s intervals during the transition. 
was calculated by Fick's principle. Muscle biopsies were obtained at rest and during contractions. Muscle force was measured continuously. Phosphocreatine hydrolysis and the calculated substrate level phosphorylation were slightly (but not significantly) lower in L-NAME than in CTRL. Significantly (P < 0.05) less fatigue was found in L-NAME versus CTRL. The time delay (TDf) and the time constant (
f) of the ‘fundamental’ component of 
kinetics were not significantly different between CTRL (TDf 7.2 ± 1.2 s; and f 10.6 ± 1.3, ± S.E.M.) and L-NAME (TDf 9.3 ± 0.6; and f 10.4 ± 1.0). Contrary to our hypothesis, NOS inhibition did not accelerate muscle 
kinetics. The down-regulation of mitochondrial respiration by NO does not limit the kinetics of adjustment of oxidative metabolism at exercise onset.
(Received 6 May 2005;
accepted after revision 31 July 2005;
first published online 4 August 2005)
Corresponding author B. Grassi: Dipartimento di Scienze e Tecnologie Biomediche, Università degli Studi di Milano, LITA – Via Fratelli Cervi 93, I -20090 Segrate (MI), Italy. Email: bruno.grassi{at}unimi.it
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