title: Effects of beta-adrenergic receptor stimulation and blockade on substrate metabolism during submaximal exercise.
abstract: We used beta-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 VO(2 peak) 1) during a control trial (CON); 2) while epinephrine was intravenously infused at 0.015 microg. kg(-1) x min(-1) (beta-STIM); 3) after ingesting 80 mg of propranolol (beta-BLOCK); and 4) combining beta-BLOCK with intravenous infusion of Intralipid-heparin to restore plasma fatty acid (FFA) levels (beta-BLOCK+LIPID). beta-BLOCK suppressed lipolysis (i.e., glycerol rate of appearance) and fat oxidation while elevating carbohydrate oxidation above CON (135 +/- 11 vs. 113 +/- 10 micromol x kg(-1) x min(-1); P < 0.05) primarily by increasing rate of disappearance (R(d)) of glucose (36 +/- 2 vs. 22 +/- 2 micromol x kg(-1) x min(-1); P < 0.05). Plasma FFA restoration (beta-BLOCK+LIPID) attenuated the increase in R(d) glucose by more than one-half (28 +/- 3 micromol x kg(-1) x 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, beta-STIM markedly increased glycogen oxidation and reduced glucose clearance and fat oxidation despite elevating plasma FFA. Therefore, reduced plasma FFA availability with beta-BLOCK increased R(d) glucose, whereas beta-STIM increased glycogen oxidation, which reduced fat oxidation and glucose clearance. In summary, compared with control exercise at 45% VO(2 peak) (CON), both beta-BLOCK and beta-STIM reduced fat and increased carbohydrate oxidation, albeit through different mechanisms.
authors: The Human Performance Laboratory, Department of Kinesiology and Health Education, University of Texas at Austin, Austin, Texas 78712, USA.
authors: R
authors: R
authors: Mora-Rodriguez
authors: B J
authors: BJ
authors: Hodgkinson
authors: L O
authors: LO
authors: Byerley
authors: E F
authors: EF
authors: Coyle
mesh_terms: D000318:Adrenergic beta-Agonists / Q000097:blood / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000328:Adult; D001786:Blood Glucose / Q000032:analysis; D050260:Carbohydrate Metabolism; D004734:Energy Metabolism; D004837:Epinephrine / Q000097:blood / Q000494:pharmacology; D015444:Exercise / Q000502:physiology*; D005230:Fatty Acids, Nonesterified / Q000097:blood / Q000378:metabolism; D005260:Female; D005990:Glycerol / Q000097:blood; D006003:Glycogen / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000097:blood; D007700:Kinetics; D019344:Lactic Acid / Q000097:blood; D008297:Male; D008660:Metabolism / Q000187:drug effects* / Q000502:physiology*; D009638:Norepinephrine / Q000097:blood; D009994:Osmolar Concentration; D010084:Oxidation-Reduction; D011943:Receptors, Adrenergic, beta / Q000502:physiology*
chemical_list: D000318:Adrenergic beta-Agonists; D000319:Adrenergic beta-Antagonists; D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D011943:Receptors, Adrenergic, beta; D019344:Lactic Acid; D006003:Glycogen; D005990:Glycerol; D009638:Norepinephrine; D004837:Epinephrine