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急性缺氧后静息能量消耗的持续抑制

Persistent suppression of resting energy expenditure after acute hypoxia.

作者信息

Oltmanns Kerstin M, Gehring Hartmut, Rudolf Sebastian, Schultes Bernd, Schweiger Ulrich, Born Jan, Fehm Horst L, Peters Achim

机构信息

Department of Psychiatry, University of Luebeck, 23538 Luebeck, Germany.

出版信息

Metabolism. 2006 May;55(5):669-75. doi: 10.1016/j.metabol.2006.01.004.

DOI:10.1016/j.metabol.2006.01.004
PMID:16631445
Abstract

Resting energy expenditure (REE) is known to be influenced by various ambient conditions such as oxygen supply. Investigations in healthy subjects during acute hypoxia revealed a drop in REE, but persistent effects after hypoxia had ended have not been examined so far. Although indirect calorimetry is a well-established method to measure REE, it may lead to false conclusions when hyperventilation, rise in lactate or catecholamines, and decrease of food intake accompany hypoxia. Therefore, we determined REE in healthy men after hypoxia had ended and under conditions of controlled energy supply during a glucose clamp. In a double-blind crossover study design, we induced hypoxia for 30 minutes by decreasing oxygen saturation to 75% (vs 96% in a control session) in 13 healthy men. Indirect calorimetry was performed at baseline and 150 minutes after hypoxia had ended. Plasma glucose was held stable between 4.5 and 5.5 mmol/L, and lactate as well as catecholamine concentrations were monitored. In parallel, we measured alterations in hormones of the hypothalamic-pituitary-thyroid axis, which is one known factor mediating changes in REE. Resting energy expenditure was decreased after hypoxia (from 1656+/-80 to 1564+/-97 kcal/d) as compared with the normoxic control condition (1700+/-82 to 1749+/-79 kcal/d, P=.037), whereas the respiratory quotient remained stable (P=.79). Plasma lactate, catecholamine levels, and the pituitary thyroid secretory activity were unchanged after hypoxia (P>.2). Our data demonstrate that the REE decrease persists 150 minutes after acute hypoxia, indicating an adaptation of energy metabolism. This should be valued as an additive pathogenic factor in diseases with disturbed energy metabolism.

摘要

静息能量消耗(REE)已知会受到各种环境条件的影响,如氧气供应。对健康受试者在急性缺氧期间的研究显示REE下降,但缺氧结束后的持续影响迄今尚未得到研究。尽管间接测热法是一种成熟的测量REE的方法,但当缺氧伴有过度通气、乳酸或儿茶酚胺升高以及食物摄入量减少时,可能会得出错误的结论。因此,我们在缺氧结束后且在葡萄糖钳夹期间能量供应受控的条件下,测定了健康男性的REE。在一项双盲交叉研究设计中,我们通过将13名健康男性的氧饱和度降至75%(对照时段为96%)诱导缺氧30分钟。在基线和缺氧结束后150分钟进行间接测热法。将血浆葡萄糖维持在4.5至5.5 mmol/L之间,并监测乳酸以及儿茶酚胺浓度。同时,我们测量了下丘脑 - 垂体 - 甲状腺轴激素的变化,这是已知介导REE变化的一个因素。与常氧对照条件(1700±82至1749±79 kcal/d,P = 0.037)相比,缺氧后静息能量消耗降低(从1656±八十至1564±97 kcal/d),而呼吸商保持稳定(P = 0.79)。缺氧后血浆乳酸、儿茶酚胺水平以及垂体甲状腺分泌活性未发生变化(P>0.2)。我们的数据表明,急性缺氧后150分钟REE下降持续存在,表明能量代谢发生了适应性变化。这应被视为能量代谢紊乱疾病中的一个附加致病因素。

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