Cocaine and exercise: alteration in carbohydrate metabolism in
adrenodemedullated rats.
Ojuka, Edward O., John D. Bell, Gilbert W. Fellingham, and Robert K.
Conlee.
Departments of Physical Education, Zoology, and Statistics, Brigham
Young University, Provo, Utah 84602
APStracts 2:0381A, 1995.
The combined treatment of cocaine-exercise (CE) causes an exaggerated
catecholamine (CAT) response, a rapid depletion of muscle glycogen,
and accumulation of lactic acid. To assess the contribution of the
adrenal medulla in the CAT response and to determine the role of
epinephrine (EPI) on carbohydrate metabolism, cocaine (20 mg/kg, ip)
or saline was injected into sham operated (SHAM) or
adrenodemedullated (ADM) rats, which then ran for 5 min at 56 m/min,
0% grade. In SHAM, CE caused plasma EPI values (x +/- sem) to rise to
27.7 +/- 6.9 nM compared to 13.3 +/- 1.5 nM in saline-exercise (SE)
and 0.8 +/- 0.2 nM in both ADM-CE and ADM-SE (P < 0.05). With
minimal EPI in ADM, CE still caused glycogen to fall to lower levels
(25.4 +/- 3.0 NMol/g vs 40.5 +/- 2.4 NMol/g) and lactate to rise to
higher levels (17 +/- 3 vs 9 +/- 1 mMol/kg) in white vastus muscle
than SE (P< 0.05). CE had no significant effect on soleus and
red vastus glycogenolysis, but it did cause lactate accumulation in
red vastus. As a result plasma lactate levels were also higher after
CE compared to SE in ADM (17.9 +/- 2.0 vs 8.5 +/- 0.5 mM,
P<0.05). We conclude that during CE 1) EPI is not essential to
the alteration in carbohydrate metabolism, 2) the latter may be
related to the other CAT, 3) the adrenal medulla is the only source
of EPI, and 4) the adrenal medulla is not the source of the increased
levels of norepinephrine or dopamine.
Received 12 January 1995; accepted in final form 22 August 1995.
APS Manuscript Number A37-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 15 September 1995.