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Manipulation of dietary carbohydrate and muscle glycogen affects glucose uptake during exercise when fat oxidation is impaired by -adrenergic blockade

¹Department of Kinesiology and Health Education, The University of Texas at Austin, Austin, Texas 78712; and ²Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, Louisiana 78080

Submitted 9 July 2004 ; accepted in final form 10 August 2004

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 O₂ consumption (O_{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 (B), a nonselective -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 B. 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 B, 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.

lipolysis; glycerol rate of appearance; free fatty acids; glucose rate of appearance

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