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Articles in PresS, published online ahead of print May 21, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00098.2002
Submitted on March 4, 2002
Accepted on May 13, 2002
1 Health Sciences, Deakin University, Burwood, VIC, Australia
* To whom correspondence should be addressed. E-mail: mharg{at}deakin.edu.au.
This study examined the role of epinephrine on glucose disposal during moderate exercise when glycogenolytic flux was limited by low pre-exercise skeletal muscle glycogen availability. Six male subjects cycled for 40 min at 59 ± 1% VO2 peak on two occasions, either without (CON) or with (EPI) epinephrine infusion starting after 20 min of exercise. On the day prior to each experimental trial subjects completed fatiguing exercise and then maintained a low carbohydrate diet to lower muscle glycogen. Muscle samples were obtained after 20 and 40 min of exercise and glucose kinetics were measured using 6,6-2H glucose. Exercise increased plasma epinephrine above resting concentrations in both trials and plasma epinephrine was higher (P<0.05) during the final 20 min in EPI compared with CON. Muscle glycogen levels were low after 20 min of exercise (CON, 117 ± 25; EPI, 122 ± 20 mmol.kg-1 dm) and net muscle glycogen breakdown and muscle glucose 6-phosphate levels during the subsequent 20 min of exercise were unaffected by epinephrine infusion. Plasma glucose increased with epinephrine infusion (ie: 20-40 min) and this was due to a decrease in glucose Rd (40 min: CON, 33.8 ± 3; EPI, 20.9 ± 4.9 µmol*kg-1*min-1, P<0.05), since the exercise-induced rise in glucose Ra was similar in both trials. These results show that glucose Rd during exercise is reduced by elevated plasma epinephrine, even when muscle glycogen availability and utilisation are low. This suggests that the effect of epinephrine does not appear to be mediated by increased glucose 6-phosphate, secondary to enhanced muscle glycogenolysis, but may be linked to a direct effect of epinephrine on sarcolemmal glucose transport.
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