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Journal of Applied Physiology, Vol 66, Issue 1 377-383, Copyright © 1989 by American Physiological Society
ARTICLES |
M. E. Bracken, D. R. Bracken, W. W. Winder and R. K. Conlee
Department of Physical Education, Brigham Young University, Provo, Utah 84602.
To determine the effects of a variety of doses of cocaine on endurance capacity, rats were injected intraperitoneally with either 0.1, 0.5, 2.5, 12.5, or 20 mg/kg body wt 20 min before running to exhaustion at 26 m/min up a 10% grade. Animals given saline ran 116 +/- 9 (SE) min. At doses of 12.5 and 20 mg/kg, cocaine reduced endurance time significantly (34 and 74%, respectively). At rest the drug had no effect on liver or fast-twitch muscle glycogen but significantly reduced (20-40%) soleus glycogen at the two highest doses. However, at exhaustion, the quantity of glycogen depleted in the fast-twitch red and white vastus muscles was similar in all groups despite the reduced run times of the animals receiving a higher dose implying a greater rate of glycogenolysis due to cocaine. Blood lactate in the 20 mg/kg group (9.9 +/- 1.2 mM) at exhaustion was nearly twice that of the saline controls at exhaustion (5.1 +/- 0.6). Before exercise plasma norepinephrine (at doses of 2.5, 12.5 and 20 mg/kg) was higher than saline controls and remained higher (20 mg/kg groups) at exhaustion. We conclude that high doses of cocaine cause rapid muscle glycogen depletion and early fatigue. The mechanism by which cocaine causes these effects is not clear.
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R. K. Conlee, K. P. Kelly, E. O. Ojuka, and R. L. Hammer Cocaine and exercise: alpha -1 receptor blockade does not alter muscle glycogenolysis or blood lactacidosis J Appl Physiol, January 1, 2000; 88(1): 77 - 81. [Abstract] [Full Text] [PDF] |
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