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09.11.2019 | Original Article | Ausgabe 1/2020 Open Access

European Journal of Applied Physiology 1/2020

Hyperinsulinaemia and hyperglycaemia promote glucose utilization and storage during low- and high-intensity exercise

European Journal of Applied Physiology > Ausgabe 1/2020
Hamid Mohebbi, Iain T. Campbell, Marie A. Keegan, James J. Malone, Andrew T. Hulton, Don P. M. MacLaren
Wichtige Hinweise
Communicated by Philip D Chilibeck.

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The effect of hyperglycaemia with and without additional insulin was explored at a low and high intensity of exercise (40% vs 70% VO2peak) on glucose utilization (GUR), carbohydrate oxidation, non-oxidative glucose disposal (NOGD), and muscle glycogen.


Eight healthy trained males were exercised for 120 min in four trials, twice at 40% VO2peak and twice at 70% VO2peak, while glucose was infused intravenously (40%G; 70%G) at rates to “clamp” blood glucose at 10 mM. On one occasion at each exercise intensity, insulin was also infused at 40 mU/m2/per min (i.e. 40%GI and 70%GI). The glucose and insulin infusion began 30 min prior to exercise and throughout exercise. A muscle biopsy was taken at the end of exercise for glycogen analysis.


Hyperglycaemia significantly elevated plasma insulin concentration (p < 0.001), although no difference was observed between the exercise intensities. Insulin infusion during both mild and severe exercise resulted in increased insulin concentrations (p < 0.01) and GUR (p < 0.01) compared with glucose (40%GI by 25.2%; 70%GI by 26.2%), but failed to significantly affect carbohydrate, fat and protein oxidation. NOGD was significantly higher for GI trials at both intensities (p < 0.05) with storage occurring during both lower intensities (62.7 ± 19.6 g 40%GI; 127 ± 20.7 g 40%GI) and 70%GI (29.0 ± 20.0 g). Muscle glycogen concentrations were significantly depleted from rest (p < 0.01) after all four trials.


Hyperinsulinaemia in the presence of hyperglycaemia during both low- and high-intensity exercise promotes GUR and NOGD, but does not significantly affect substrate oxidation.

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