beta-adrenergic blockade augments glucose utilization in horses during graded exercise.
To examine the role of beta-adrenergic mechanisms in the regulation of endogenous glucose (Glu) production [rate of appearance (R(a))] and utilization [rate of disappearance (R(d))] and carbohydrate (CHO) metabolism, six horses completed consecutive 30-min bouts of exercise at approximately 30% (Lo) and approximately 60% (Hi) of estimated maximum O(2) uptake with (P) and without (C) prior administration of the beta-blocker propranolol (0.22 mg/kg iv). All horses completed exercise in C; exercise duration in P was 49.9 +/- 1.2 (SE) min. Plasma Glu was unchanged in C during Lo but increased progressively in Hi. In P, plasma Glu rose steadily during Lo and Hi and was higher (P < 0.05) than in C throughout exercise. Plasma insulin declined during exercise in P but not in C; beta-blockade attenuated (P < 0.05) the rise in plasma glucagon and free fatty acids and exaggerated the increases in epinephrine and norepinephrine. Glu R(a) was 8.1 +/- 0.8 and 8.4 +/- 1.0 micromol. kg(-1). min(-1) at rest and 30.5 +/- 3.6 and 42.8 +/- 4.1 micromol. kg(-1). min(-1) at the end of Lo in C and P, respectively. During Hi, Glu R(a) increased to 54.4 +/- 4.4 and 73.8 +/- 4.7 micromol. kg(-1). min(-1) in C and P, respectively. Similarly, Glu R(d) was approximately 40% higher in P than in C during Lo (27.3 +/- 2.0 and 39.5 +/- 3.3 micromol. kg(-1). min(-1) in C and P, respectively) and Hi (37.4 +/- 2.6 and 61.5 +/- 5.3 micromol. kg(-1). min(-1) in C and P, respectively). beta-Blockade augmented CHO oxidation (CHO(ox)) with a concomitant reduction in fat oxidation. Inasmuch as estimated muscle glycogen utilization was similar between trials, the increase in CHO(ox) in P was due to increased use of plasma Glu. We conclude that beta-blockade increases Glu R(a) and R(d) and CHO(ox) in horses during exercise. The increase in Glu R(d) under beta-blockade suggests that beta-adrenergic mechanisms restrain Glu R(d) during exercise.
Geor
R J
RJ
Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus, Ohio 43210, USA. rgeor@ker.com
Hinchcliff
K W
KW
Sams
R A
RA
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D001798:Blood Proteins / Q000032:analysis; D050260:Carbohydrate Metabolism; D004837:Epinephrine / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D005947:Glucose / Q000378:metabolism*; D005990:Glycerol / Q000097:blood; D006400:Hematocrit; D006728:Hormones / Q000097:blood; D006736:Horses / Q000378:metabolism*; D007700:Kinetics; D019344:Lactic Acid / Q000097:blood; D008297:Male; D009043:Motor Activity / Q000502:physiology*; D009638:Norepinephrine / Q000378:metabolism; D010084:Oxidation-Reduction; D011433:Propranolol / Q000494:pharmacology*; D011659:Pulmonary Gas Exchange
D000319:Adrenergic beta-Antagonists; D001786:Blood Glucose; D001798:Blood Proteins; D005230:Fatty Acids, Nonesterified; D006728:Hormones; D019344:Lactic Acid; D011433:Propranolol; D005947:Glucose; D005990:Glycerol; D009638:Norepinephrine; D004837:Epinephrine