Journal of Applied Physiology, Vol 66, Issue 5 2419-2422, Copyright © 1989 by American Physiological Society
Beta-adrenergic receptors are not responsible for exercise stimulation of glucose transport
E. Sternlicht, R. J. Barnard and G. K. Grimditch
Department of Kinesiology, University of California, Los Angeles 90024.
This study was designed to examine whether the increased glucose transport
after acute exercise in rat skeletal muscle is mediated via beta-adrenergic
receptor stimulation. Sarcolemmal (SL) membranes were isolated from three
groups: control (C), acute exercise (E), and exercise + propranolol (E+P).
The acute exercise bout was performed on a treadmill and consisted of a
45-min run until near exhaustion. E+P received an intravenous propranolol
injection (0.8 mg/kg) 10 min before the exercise session. Michaelis-Menten
kinetics at 1.5 s indicated that the Vmax for glucose transport was
increased after each perturbation compared with C but were not different
from each other (E, 4,334 +/- 377; E+P, 4,824 +/- 357; and C, 1,366 +/- 124
pmol.mg protein-1.s-1). The apparent Km's were similar in all groups.
Scatchard plots for the D-glucose inhibitable class of cytochalasin B
binding sites indicated no differences in either the total number of
binding sites in the SL vesicles (C, 5.5 +/- 0.3; E, 5.1 +/- 0.2, and E+P,
5.1 +/- 0.3 pmol/mg protein) or in their dissociation constant (Kd) (C, 46
+/- 3; E, 48 +/- 3; and E+P, 49 +/- 2 nM). The increase in Vmax for
transport was similar between E and E+P, indicating that exercise does not
stimulate glucose transport via the beta-adrenergic receptor.
