CNS Fatigue and Prolonged Exercise: Effect of Glucose Supplementation

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Ingestion of carbohydrates during prolonged exercise may improve endurance, whereas an insufficient supply of glucose results in hypoglycemia and fatigue. Fatigue, defined as a loss of force-generating capacity, may develop for a variety of reasons and involve both central and peripheral factors. This study investigated whether CNS activation of the skeletal muscles was affected by prolonged exercise with or without glucose supplementation.


Voluntary force production and central activation ratios, assessed by the twitch interpolation technique, were determined during a 2-min sustained maximal knee extension in eight endurance-trained males in a baseline condition and immediately after 3 h of cycling randomized to be with or without glucose supplementation.


The exercise bout without glucose supplementation (placebo trial) reduced the blood glucose concentration from 4.5 ± 0.2 to 3.0 ± 0.2 mM, whereas blood glucose homeostasis was maintained during the glucose trial. The average force during the sustained maximal voluntary muscle contraction was 248 ± 23 N at baseline, 222 ± 20 N in the glucose trial, and 197 ± 21 N in the placebo trial (P < 0.05 between conditions). In the placebo trial, the lowered force production was accompanied by a reduced level of CNS activation compared with the other two conditions (P < 0.05), whereas the central activation ratios were similar in the glucose trial as compared with baseline.


Exercise-induced hypoglycemia attenuates CNS activation during a sustained maximal muscle contraction, whereas central activation appears to be unaffected by 3 h of moderately intense exercise in endurance-trained athletes when euglycemia is maintained by carbohydrate ingestion.

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