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Departments of 1 Medicine, 2 Pharmacology, 3 Radiology, 4 Molecular Physiology and Biophysics, and 5 Mouse Metabolic Physiology Center, Vanderbilt University School of Medicine, Nashville, Tennessee 37232
Isotopic techniques were
used to test the hypothesis that exercise and nitric oxide synthase
(NOS) inhibition have distinct effects on tissue-specific fatty acid
and glucose uptakes in a conscious, chronically catheterized mouse
model. Uptakes were measured using the radioactive tracers
125I-labeled
-methyl-p-iodophenylpentadecanoic acid (BMIPP) and deoxy-[2-3H]glucose (DG) during treadmill exercise with
and without inhibition of NOS. [125I]BMIPP uptake at rest
differed substantially among tissues with the highest levels in heart.
With exercise, [125I]BMIPP uptake increased in both heart
and skeletal muscles. In sedentary mice, NOS inhibition induced by
nitro-L-arginine methyl ester (L-NAME) feeding
increased heart and soleus [125I]BMIPP uptake. In
contrast, exercise, but not L-NAME feeding, resulted in
increased heart and skeletal muscle [2-3H]DG uptake.
Significant interactions were not observed in the effects of combined
exercise and L-NAME feeding on [125I]BMIPP
and [2-3H]DG uptakes. In the conscious mouse, exercise
and NOS inhibition produce distinct patterns of tissue-specific fatty
acid and glucose uptake; NOS is not required for important components
of exercise-associated metabolic signaling, or other mechanisms
compensate for the absence of this regulatory mechanism.
skeletal muscle; fuels; metabolism; lipid; carbohydrate; nitric oxide synthase
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