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长时间运动期间疲劳与脑能量代谢维持失败之间的关联。

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

作者信息

Nybo L, Møller K, Pedersen B K, Nielsen B, Secher N H

机构信息

Department of Human Physiology, Institute of Exercise and Sport Sciences, University of Copenhagen, Copenhagen, Denmark.

出版信息

Acta Physiol Scand. 2003 Sep;179(1):67-74. doi: 10.1046/j.1365-201X.2003.01175.x.

DOI:10.1046/j.1365-201X.2003.01175.x
PMID:12940940
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.

摘要

目的

本研究评估运动期间出现低血糖时产生的疲劳和冷漠是否可能与脑葡萄糖代谢率和氧代谢率降低有关。

方法与结果

六名男性按随机顺序完成了3小时的骑行,期间有或没有补充葡萄糖。采用凯蒂-施密特技术评估脑血流量、代谢及白细胞介素-6(IL-6)释放。在葡萄糖试验期间血糖得以维持,而在安慰剂试验中,运动180分钟后血糖从5.2±0.1降至2.9±0.3毫摩尔/升(平均值±标准误),同时自觉用力程度增加(P<0.05)。在低血糖期间,脑葡萄糖摄取量从0.34±0.05微摩尔/克(-1)分钟(-1)降至0.28±0.04微摩尔/克(-1)分钟(-1),而脑β-羟基丁酸摄取量增加至5±1皮摩尔/克(-1)分钟(-1)(P<0.05)。葡萄糖摄取量减少伴随着脑氧代谢率从补充葡萄糖运动期间的1.84±0.19毫摩尔/克(-1)分钟(-1)降至低血糖期间的1.60±0.16毫摩尔/克(-1)分钟(-1)(P<0.05)。此外,脑IL-6释放量从0.4±0.1皮克/克(-1)分钟(-1)降至0.0±0.1皮克/克(-1)分钟(-1)(P<0.05)。

结论

运动诱发的低血糖限制了脑葡萄糖摄取,加剧了运动疲劳,降低了脑氧代谢率,并减弱了脑IL-6的释放。

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