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Department of Zoology, Brigham Young University, Provo, Utah 84602; and Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri 63110
Muscle contraction causes an increase in activity of
5'-AMP-activated protein kinase (AMPK). This study was designed
to determine whether chronic chemical activation of AMPK will increase
mitochondrial enzymes, GLUT-4, and hexokinase in different types of
skeletal muscle of resting rats. In acute studies, rats were
subcutaneously injected with either
5-aminoimidazole-4-carboxamide-1-
-D-ribofuranoside (AICAR; 1 mg/g body wt) in 0.9% NaCl or with 0.9% NaCl alone and were
then anesthetized for collection and freezing of tissues. AMPK activity
increased in the superficial, white region of the quadriceps and in
soleus muscles but not in the deep, red region of the quadriceps
muscle. Acetyl-CoA carboxylase (ACC) activity, a target for AMPK,
decreased in all three muscle types in response to AICAR injection but
was lowest in the white quadriceps. In rats given daily, 1 mg/g body
wt, subcutaneous injections of AICAR for 4 wk, activities of citrate
synthase, succinate dehydrogenase, and malate dehydrogenase were
increased in white quadriceps and soleus but not in red quadriceps.
Cytochrome c and
-aminolevulinic acid synthase levels were
increased in white, but not red, quadriceps. Carnitine
palmitoyl-transferase and hydroxy-acyl-CoA dehydrogenase were not
significantly increased. Hexokinase was markedly increased in all three
muscles, and GLUT-4 was increased in red and white quadriceps. These
results suggest that chronic AMPK activation may mediate the effects of
muscle contraction on some, but not all, biochemical adaptations of
muscle to endurance exercise training.
-aminolevulinate synthase; carnitine palmitoyl transferase; citrate synthase; citric acid cycle enzymes; endurance training; GLUT-4; muscle mitochondria
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