Manipulation of dietary carbohydrate and muscle glycogen affects glucose uptake during exercise when fat oxidation is impaired by beta-adrenergic blockade.
We have recently reported that, during moderate intensity exercise, low muscle glycogen concentration and utilization caused by a high-fat diet is associated with a marked increase in fat oxidation with no effect on plasma glucose uptake (R(d) glucose). It is our hypothesis that this increase in fat oxidation compensates for low muscle glycogen, thus preventing an increase in R(d) glucose. Therefore, the purpose of this study was to determine whether low muscle glycogen availability increases R(d) glucose under conditions of impaired fat oxidation. Six cyclists exercised at 50% peak O(2) consumption (Vo(2 peak)) for 1 h after 2 days on either a high-fat (HF, 60% fat, 24% carbohydrate) or control (CON, 22% fat, 65% carbohydrate) diet to manipulate muscle glycogen to low and normal levels, respectively. Two hours before the start of exercise, subjects ingested 80 mg of propanolol (betaB), a nonselective beta-adrenergic receptor blocker, to impair fat oxidation during exercise. HF significantly decreased calculated muscle glycogen oxidation (P < 0.05), and this decrease was partly compensated for by an increase in fat oxidation (P < 0.05), accompanied by an increase in whole body lipolysis (P < 0.05), despite the presence of betaB. Although HF increased fat oxidation, plasma glucose appearance rate, R(d) glucose, and glucose clearance rate were also significantly increased by 13, 15, and 26%, respectively (all P < 0.05). In conclusion, when lipolysis and fat oxidation are impaired, in this case by betaB, fat oxidation cannot completely compensate for a reduction in muscle glycogen utilization, and consequently plasma glucose turnover increases. These findings suggest that there is a hierarchy of substrate compensation for reduced muscle glycogen availability after a high-fat, low-carbohydrate diet, with fat being the primary and plasma glucose the secondary compensatory substrate. This apparent hierarchy likely serves to protect against hypoglycemia when endogenous glucose availability is low.
Zderic
Theodore W
TW
Dept. of Kinesiology and Health Education, Bellmont Hall 222, The University of Texas at Austin, Austin, TX 78712, USA.
Schenk
Simon
S
Davidson
Christopher J
CJ
Byerley
Lauri O
LO
Coyle
Edward F
EF
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D001682:Biological Availability; D001786:Blood Glucose / Q000378:metabolism; D004040:Dietary Carbohydrates / Q000008:administration & dosage / Q000378:metabolism; D004041:Dietary Fats / Q000008:administration & dosage* / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D015444:Exercise / Q000502:physiology*; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005947:Glucose / Q000378:metabolism*; D005990:Glycerol / Q000378:metabolism; D006003:Glycogen / Q000378:metabolism*; D006801:Humans; D007328:Insulin / Q000097:blood; D050356:Lipid Metabolism; D008066:Lipolysis; D008297:Male; D018482:Muscle, Skeletal / Q000378:metabolism*; D010084:Oxidation-Reduction; D011433:Propranolol / Q000494:pharmacology*
D000319:Adrenergic beta-Antagonists; D001786:Blood Glucose; D004040:Dietary Carbohydrates; D004041:Dietary Fats; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D006003:Glycogen; D011433:Propranolol; D005947:Glucose; D005990:Glycerol