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This Article Full Text Full Text (PDF) All Versions of this Article: 91/3/581    most recent expphysiol.2005.032698v1 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 Baker, D. J. Articles by Hepple, R. T. Search for Related Content PubMed PubMed Citation Articles by Baker, D. J. Articles by Hepple, R. T. Related Collections Muscle

¹ Faculty of Kinesiology² Faculty of Medicine, University of Calgary, Alberta, Canada³ Faculty of Medicine, University of California San Diego, San Diego, CA, USA

The purpose of the present experiments was to test the hypotheses that: (i) nitric oxide synthase (NOS) inhibition reduces the O₂ cost of force development across a range of contractile demands; and (ii) this reduced O₂ cost of force development would be reflected in a sparing of intramuscular higher energy phosphates. Rat distal hindlimb muscles were pump perfused in situ and electrically stimulated (200 ms trains with pulses at 100 Hz, each pulse 0.05 ms duration) for 1 min each at 15, 30 and 60 tetani min^–1 and for 2 min at 90 tetani min^–1 in three groups: 0.01 mM adenosine; 1 mM D-NAME and 0.01 mM adenosine (D-NAME); and 1 mM L-NAME and 0.01 mM adenosine (L-NAME). The gastrocnemius–plantaris–soleus muscle group was freeze clamped post-contractions for metabolite analyses. Force was 19% higher and oxygen uptake was 20% lower with L-NAME versus adenosine, and there was a 35% reduction in /time-integrated tension versus adenosine and 24% versusD-NAME that was independent of contraction frequency. L-NAME treatment produced a 33% sparing of muscle phosphocreatine (PCr), and intramuscular lactate was no different between groups. In contrast, D-NAME reduced force by 30%, by 29% and the O₂ cost of force development by 15% compared with adenosine, but had no effect on the degree of intramuscular ATP and PCr depletion. These results show that NOS inhibition improved the metabolic efficiency of force development, either by improving the ATP yield for a given O₂ consumption or by reducing the ATP cost of force development. In addition, these effects were independent of contraction frequency.

(Received 5 November 2005; accepted after revision 3 February 2006; first published online 9 February 2006)
Corresponding author R. T. Hepple: Faculty of Kinesiology, University of Calgary, 2500 University Drive NW, Calgary, Alberta, T2N 1N4, Canada. Email: hepple{at}ucalgary.ca

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