| Autor: |
Grassi, Bruno, Hogan, Michael C, Kelley, Kevin M, Howlett, Richard A, Gladden, L Bruce |
| Jazyk: |
angličtina |
| Rok vydání: |
2005 |
| Předmět: |
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| Popis: |
Nitric oxide (NO) has an inhibitory action on O2 uptake (V˙O2) 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 V˙O2 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 V˙O2. 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 (Q˙), at a level measured during a preliminary contraction trial with spontaneous self-perfused Q˙. A vasodilatory drug was also infused. Arterial and venous O2 concentrations were determined at rest and at 5–7 s intervals during the transition. V˙O2 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 (τf) of the ‘fundamental’ component of V˙O2 kinetics were not significantly different between CTRL (TDf 7.2 ± 1.2 s; and τf 10.6 ± 1.3, ±s.e.m.) and l-NAME (TDf 9.3 ± 0.6; and τf 10.4 ± 1.0). Contrary to our hypothesis, NOS inhibition did not accelerate muscle V˙O2 kinetics. The down-regulation of mitochondrial respiration by NO does not limit the kinetics of adjustment of oxidative metabolism at exercise onset. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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