Association between fatigue and failure to preserve cerebral energy turnover during prolonged exercise
Article first published online: 26 AUG 2003
Acta Physiologica Scandinavica
Volume 179, Issue 1, pages 67–74, September 2003
How to Cite
Nybo, L., Møller, K., Pedersen, B. K., Nielsen, B. and Secher, N. H. (2003), Association between fatigue and failure to preserve cerebral energy turnover during prolonged exercise. Acta Physiologica Scandinavica, 179: 67–74. doi: 10.1046/j.1365-201X.2003.01175.x
- Issue published online: 26 AUG 2003
- Article first published online: 26 AUG 2003
- Received 5 February 2003, accepted 27 June 2003
Aim: This study evaluated if the fatigue and apathy arising during exercise with hypoglycaemia could relate to a lowering of the cerebral metabolic rates of glucose and oxygen.
Methods and results: Six males completed 3 h of cycling with or without glucose supplementation in random order. Cerebral blood flow, metabolism and interleukin-6 (IL-6) release were evaluated with the Kety–Schmidt technique. Blood glucose was maintained during the glucose trial, while it decreased from 5.2 ± 0.1 to 2.9 ± 0.3 mmol L−1 (mean ± SE) after 180 min of exercise in the placebo trial with a concomitant increase in perceived exertion (P < 0.05). During hypoglycaemia, the cerebral glucose uptake was reduced from 0.34 ± 0.05 to 0.28 ± 0.04 μmol g−1 min−1, while the cerebral uptake of β-hydroxybutyrate increased to 5 ± 1 pmol g−1 min−1 (P < 0.05). The reduced glucose uptake was accompanied by a lowering of the cerebral metabolic rate of oxygen from 1.84 ± 0.19 mmol g−1 min−1 during exercise with glucose supplementation to 1.60 ± 0.16 mmol g−1 min−1 during hypoglycaemia (P < 0.05). In addition, the cerebral IL-6 release was reduced from 0.4 ± 0.1 to 0.0 ± 0.1 pg g−1 min−1 (P < 0.05).
Conclusions: Exercise-induced hypoglycaemia limits the cerebral uptake of glucose, exacerbates exercise, reduces the cerebral metabolic rate of oxygen and attenuates the release of IL-6 from the brain.