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Nitric oxide synthase inhibition reduces O 2 cost of force development and spares high‐energy phosphates following contractions in pump‐perfused rat hindlimb muscles
Author(s) -
Baker David J.,
Krause Daniel J.,
Howlett Richard A.,
Hepple Russell T.
Publication year - 2006
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.2005.032698
Subject(s) - phosphocreatine , adenosine , chemistry , nitric oxide synthase , hindlimb , contraction (grammar) , atp synthase , medicine , nitric oxide , muscle contraction , soleus muscle , skeletal muscle , biophysics , endocrinology , anatomy , biochemistry , energy metabolism , enzyme , biology , organic chemistry
The purpose of the present experiments was to test the hypotheses that: (i) nitric oxide synthase (NOS) inhibition reduces the O 2 cost of force development across a range of contractile demands; and (ii) this reduced O 2 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 m m adenosine; 1 m m d ‐NAME and 0.01 m m adenosine ( d ‐NAME); and 1 m m l ‐NAME and 0.01 m m 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% versus d ‐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 O 2 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 O 2 consumption or by reducing the ATP cost of force development. In addition, these effects were independent of contraction frequency.