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-adrenergic receptor stimulation and blockade
on substrate metabolism during submaximal exercise
1 The Human Performance Laboratory, Department of Kinesiology and Health Education, University of Texas at Austin, Austin, Texas 78712; 2 University of Castilla-la Mancha at Toledo, Toledo 45071, Spain; and 3 Pennington Biomedical Research Center, Baton Rouge, Louisiana 70808
We used
-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
O2 peak 1) during a control trial (CON); 2) while
epinephrine was intravenously infused at 0.015 µg · kg
1 · min
1
(
-STIM); 3) after ingesting 80 mg of propranolol
(
-BLOCK); and 4) combining
-BLOCK with intravenous
infusion of Intralipid-heparin to restore plasma fatty acid (FFA)
levels (
-BLOCK+LIPID).
-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
1 · min
1;
P < 0.05) primarily by increasing rate of
disappearance (Rd) of glucose (36 ± 2 vs. 22 ± 2 µmol · kg
1 · min
1;
P < 0.05). Plasma FFA restoration (
-BLOCK+LIPID)
attenuated the increase in Rd glucose by more than one-half
(28 ± 3 µmol · kg
1 · min
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,
-STIM markedly increased glycogen
oxidation and reduced glucose clearance and fat oxidation despite
elevating plasma FFA. Therefore, reduced plasma FFA availability with
-BLOCK increased Rd glucose, whereas
-STIM increased
glycogen oxidation, which reduced fat oxidation and glucose clearance.
In summary, compared with control exercise at 45%
O2 peak (CON), both
-BLOCK and
-STIM reduced fat and increased carbohydrate oxidation, albeit
through different mechanisms.
lipid; glucose; propranolol; epinephrine; stable isotopes
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