Received November 5, 2005
Revised December 5, 2005
Accepted after revision February 3, 2006

¹ University of Calgary
² University of California San Diego

^* To whom correspondence should be addressed. E-mail: hepple{at}ucalgary.ca.

	Abstract

The purpose of the current experiments was to test the hypotheses that (i) 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, at 100 pps, each 0.05 ms duration) for 1 min each at 15, 30, and 60 tetani min^-1 and 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 & 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 VO₂ was 20% lower with L-NAME versus Adenosine, and there was a 35% reduction in VO₂/time-integrated tension versus Adenosine and 24% versus D-NAME that was independent of contraction frequency. L-NAME treatment produced a 31% sparing of muscle high energy phosphates (HEP; PCr + ATP), and intramuscular lactate was no different between groups. On the other hand, D-NAME reduced force by 30%, VO₂ by 29% and the O₂ cost of force development by 15% compared with Adenosine, but had no effect on the degree of intramuscular HEP depletion. These results show that NOS inhibition improved the metabolic efficiency of force development, by either improving the ATP yield for a given O₂ consumption or reducing the ATP cost of force development. In addition, these effects were independent of contraction frequency.

Key Words: Metabolism, Muscle contraction, Nitric oxide

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