Association between fatigue and failure to preserve cerebral energy turnover during prolonged exercise

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Standard

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.

I: Acta Physiologica Scandinavica, Bind 179, Nr. 1, 31.12.2003, s. 67-74.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Nybo, L, Møller, K, Pedersen, BK, Nielsen, B & Secher, NH 2003, 'Association between fatigue and failure to preserve cerebral energy turnover during prolonged exercise', Acta Physiologica Scandinavica, bind 179, nr. 1, s. 67-74.

APA

Nybo, L., Møller, K., Pedersen, B. K., Nielsen, B., & Secher, N. H. (2003). Association between fatigue and failure to preserve cerebral energy turnover during prolonged exercise. Acta Physiologica Scandinavica, 179(1), 67-74.

Vancouver

Nybo L, Møller K, Pedersen BK, Nielsen B, Secher NH. Association between fatigue and failure to preserve cerebral energy turnover during prolonged exercise. Acta Physiologica Scandinavica. 2003 dec. 31;179(1):67-74.

Author

Nybo, Lars ; Møller, Kirsten ; Pedersen, Bente Klarlund ; Nielsen, Bodil ; Secher, Niels H. / Association between fatigue and failure to preserve cerebral energy turnover during prolonged exercise. I: Acta Physiologica Scandinavica. 2003 ; Bind 179, Nr. 1. s. 67-74.

Bibtex

@article{6b5027ec3eac4a569353bfd8ff12842d,
title = "Association between fatigue and failure to preserve cerebral energy turnover during prolonged exercise",
abstract = "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. ",
author = "Lars Nybo and Kirsten M{\o}ller and Pedersen, {Bente Klarlund} and Bodil Nielsen and Secher, {Niels H.}",
year = "2003",
month = dec,
day = "31",
language = "English",
volume = "179",
pages = "67--74",
journal = "Acta Physiologica Scandinavica",
issn = "0001-6772",
publisher = "Blackwell Science Ltd.",
number = "1",

}

RIS

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