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  • Title: Beta-adrenergic receptors are not responsible for exercise stimulation of glucose transport.
    Author: Sternlicht E, Barnard RJ, Grimditch GK.
    Journal: J Appl Physiol (1985); 1989 May; 66(5):2419-22. PubMed ID: 2545659.
    Abstract:
    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.
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