Effects of ß-adrenergic receptor stimulation and blockade on substrate metabolism
during submaximal exercise.
Rodriguez, Ricardo Mora, Bradley J. Hodgkinson, Lauri O. Byerley, and Edward F.
Coyle.
1The Human Performance Laboratory, Department of Kinesiology and Health
Education, University of Texas at Austin, Austin, Texas 78712; 2University of Castilla-la
Mancha at Toledo, Toledo 45071, Spain; and 3Pennington Biomedical Research Center,
Baton Rouge, Louisiana 70808
APStracts 8:0024E, 2001.
We used ß-adrenergic receptor stimulation and blockade as a tool to study substrate
metabolism during exercise. Eight moderately trained subjects cycled for 60 min at 45%
of «vo2peak»; 1) during a control trial (CON); 2) while epinephrine was intravenously
infused at 0.015 µg•kg«minus»1•min«minus»1 (ß-STIM); 3) after ingesting 80 mg of
propranolol (ß-BLOCK); and 4) combining ß-BLOCK with intravenous infusion of
Intralipid-heparin to restore plasma fatty acid (FFA) levels (ß-BLOCK+LIPID). ß-
BLOCK suppressed lipolysis (i.e., glycerol rate of appearance) and fat oxidation while
elevating carbohydrate oxidation above CON (135 ± 11 vs. 113 ± 10
µmol•kg«minus»1•min«minus»1; P < 0.05) primarily by increasing rate of
disappearance (Rd) of glucose (36 ± 2 vs. 22 ± 2 µmol•kg«minus»1•min«minus»1; P <
0.05). Plasma FFA restoration (ß-BLOCK+LIPID) attenuated the increase in Rd glucose
by more than one-half (28 ± 3 µmol•kg«minus»1•min«minus»1; P < 0.05), suggesting
that part of the compensatory increase in muscle glucose uptake is due to reduced energy
from fatty acids. On the other hand, ß-STIM markedly increased glycogen oxidation and
reduced glucose clearance and fat oxidation despite elevating plasma FFA. Therefore,
reduced plasma FFA availability with ß-BLOCK increased Rd glucose, whereas ß-STIM
increased glycogen oxidation, which reduced fat oxidation and glucose clearance. In
summary, compared with control exercise at 45% «vo2peak» (CON), both ß-BLOCK and
ß-STIM reduced fat and increased carbohydrate oxidation, albeit through different
mechanisms.
Received 18 August 2000; accepted in final form 26 January 2001
APS Manuscript Number E389-0.
Article publication pending Am J Physiol Endocrinol Metab
ISSN 1080-4757 Copyright 2001 The American Physiological Society.
Published in APStracts on 27 February 2001