Association between fatigue and failure to preserve cerebral energy turnover during prolonged exercise
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Association between fatigue and failure to preserve cerebral energy turnover during prolonged exercise. / Nybo, Lars; Møller, Kirsten; Pedersen, Bente Klarlund; Nielsen, Bodil; Secher, Niels H.
In: Acta Physiologica Scandinavica, Vol. 179, No. 1, 31.12.2003, p. 67-74.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Association between fatigue and failure to preserve cerebral energy turnover during prolonged exercise
AU - Nybo, Lars
AU - Møller, Kirsten
AU - Pedersen, Bente Klarlund
AU - Nielsen, Bodil
AU - Secher, Niels H.
PY - 2003/12/31
Y1 - 2003/12/31
N2 - 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 micromol g(-1) min(-1), while the cerebral uptake of beta-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.
AB - 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 micromol g(-1) min(-1), while the cerebral uptake of beta-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.
M3 - Journal article
VL - 179
SP - 67
EP - 74
JO - Acta Physiologica Scandinavica
JF - Acta Physiologica Scandinavica
SN - 0001-6772
IS - 1
ER -
ID: 162990278