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1 Department of Kinesiology and Applied Physiology, University of Colorado, Boulder, Colorado 80309; and 2 Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio 44106
The purpose of this study was to
examine the effect of acute (24 h) and chronic (5 wk) hypobaric hypoxic
exposure equivalent to a simulated altitude of 4,300 m (446 mmHg) on
the enzymes of fat metabolism. Heart, liver, and skeletal muscle were
taken from 32 male Sprague-Dawley rats. Altitude exposure did not
affect the activity of citrate synthase in any of the tissues,
suggesting that mitochondrial content was unchanged. Carnitine
palmitoyltransferase-I (CPT-I) activity was significantly reduced in
the heart by both acute and chronic high altitude exposure compared
with controls. A similar reduction was found for CPT-I activity in
extensor digitorum longus after acute and chronic exposure
compared with control animals. CPT-I activity was not affected by
altitude exposure in the soleus muscle or the liver. 3-Hydroxyacyl-CoA
dehydrogenase (
-HAD) activity was significantly depressed in the
hearts of chronically exposed animals compared with controls. No
difference between acute and control animals was found in the heart for
-HAD activity. Liver
-HAD activity was also significantly
decreased in the acclimatized as well as in the acute animals compared
with the control group. Quadriceps
-HAD activity was reduced for the chronic animals only compared with controls. These data suggest that
acclimatization to high altitude selectively decreases key enzymes in
fat utilization and oxidation in the heart, liver, and select skeletal muscles.
hypobaric hypoxia; 3-hydroxyacyl-CoA dehydrogenase; carnitine palmitoyltransferase-I
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