beta-endorphin (beta E) bolus (8.05 mg.kg(-1)) infusion (0.05 mg.kg(-1).h(-
1)) was previously shown in rats to attenuate the decline in plasma glucose
during exercise, Purpose: The present investigation compared beta E and sa
line infusion in rats without a bolus of beta E to determine whether 1) the
attenuation in the glucose decline was attributable to the type of adminis
tration (bolus beta E + continuous beta E infusion vs continuous beta E inf
usion), and 2) whether circulating catecholamines or FFAs were in part invo
lved in the glucose decline. Methods: Forty untrained Sprague-Dawley rats w
ere randomly assigned to one of four treatments: 1) beta E infusion at rest
(beta R), 2) beta E infusion during exercise (beta X), 3) saline infusion
at rest (SR), and 4) saline infusion during exercise (SX). Infusions (beta
E or saline) with running (22 m.min(-1), 0% grade) lasted 90 min. Results:
A 2 X 2 ANOVA indicated beta E infusion significantly attenuated the declin
e in plasma glucose due to exercise at 90 min (SX = 4.16 +/- 0.1 vs beta X
= 4.61 +/- 0.1 mM). beta E infusion elevated plasma beta E about 2.5-fold a
t rest compared with SR and two-fold after exercise beta X) compared with S
X. beta E infusion had no effect at rest on any of the other variables meas
ured. Exercise significantly increased catecholamines, FFAs and glucagon co
mpared with resting levels. PE infusion enhanced the glucagon response to e
xercise (SX = 577 +/- 67.5 vs PX = 913 + 153 ng.L-1, P < 0.02). Epinephrine
and norepinephrine and FFAs were similar with beta E infusion either at re
st or during exercise compared with saline infusion. Conclusion: These resu
lts suggest that beta E infusion independent of the beta E bolus can attenu
ate the decline in glucose during exercise by enhancing glucagon levels and
the SE infusion did not influence circulating catecholamines or FFA's resp
onse to exercise.