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剧烈运动10至35分钟后,α-和β-血影蛋白改变引起的溶血。

Haemolysis caused by alterations of alpha- and beta-spectrin after 10 to 35 min of severe exercise.

作者信息

Beneke Ralph, Bihn Detlef, Hütler Matthias, Leithäuser Renate M

机构信息

Centre for Sports and Exercise Science, Department of Biological Sciences, University of Essex, Wivenhoe Park, Colchester, CO43SQ, England.

出版信息

Eur J Appl Physiol. 2005 Oct;95(4):307-12. doi: 10.1007/s00421-005-0010-y. Epub 2005 Oct 27.

Abstract

The pathophysiology of exercise related haemolysis is not thoroughly understood. We investigated whether exercise related haemolysis (1) is associated with alterations of red blood cell (RBC) membrane proteins similar to those found in inherited anaemic diseases, (2) can be induced with a non-running exercise mode, (3) is related to exercise intensity, and (4) coincides with indicators of oxidative stress. In ten triathletes [median (P25/P75-percentiles) age: 28.0 (26.3/28.5) years, height: 1.84 (1.78/1.87) m, body mass: 78.5 (74.8/80.8) kg, maximal oxygen uptake: 60.0 (57.3/64.8) ml kg(-1) min(-1)], haptoglobin, alpha- and beta-spectrin bands, malondialdehyde (MDA) and H2O2-induced chemiluminescence (H2O2-Chem) were determined immediately pre- and post-both, a 35 min low intensity and a high intensity cycling exercise [240 (218/253) vs 290 (270/300) W, P<0.05) requiring similar amounts of metabolic energy [28.3 (25.9/29.9) vs 24.9 (18.4/30.5) kJ kg(-1), P>0.05]. At high exercise intensity haptoglobin [1.10 (0.81/2.53) vs 1.01 (0.75/2.00) g l(-1)] decreased (P<0.05) whilst MDA [2.80 (2.65/3.20) vs 3.13 (2.78/3.31) nmol ml(-1)] and H2O2-Chem [29.70 (22.55/37.10) vs 37.25 (35.20/52.63) rel. U min] increased (P<0.05), coinciding with the disappearance of the spectrin bands in six out of ten gels. No corresponding changes were found at low intensity exercise. Ten to 35 min of non-running exercise in a regularly used intensity domain causes intra-vascular haemolysis associated with alterations in the RBC membrane proteins similar to those found after in vitro oxidative stress and in inherited anaemic diseases like Sphaerocytosis and Fanconi's anaemia.

摘要

运动相关性溶血的病理生理学尚未完全明确。我们研究了运动相关性溶血是否:(1)与红细胞(RBC)膜蛋白的改变有关,类似于遗传性贫血疾病中发现的改变;(2)可由非跑步运动模式诱发;(3)与运动强度有关;(4)与氧化应激指标相符。在10名铁人三项运动员中[年龄中位数(第25/75百分位数):28.0(26.3/28.5)岁,身高:1.84(1.78/1.87)米,体重:78.5(74.8/80.8)千克,最大摄氧量:60.0(57.3/64.8)毫升·千克⁻¹·分钟⁻¹],在35分钟的低强度和高强度自行车运动前及运动后即刻测定了触珠蛋白、α和β血影蛋白条带、丙二醛(MDA)以及H₂O₂诱导的化学发光(H₂O₂-Chem)[240(218/253)瓦对290(270/300)瓦,P<0.05],这两种运动消耗的代谢能量相似[28.3(25.9/29.9)对24.9(18.4/30.5)千焦·千克⁻¹,P>0.05]。在高强度运动时,触珠蛋白[1.10(0.81/2.53)对1.01(0.75/2.00)克/升]降低(P<0.05),而MDA[2.80(2.65/3.20)对3.13(2.78/3.31)纳摩尔/毫升]和H₂O₂-Chem[29.70(22.55/37.10)对37.25(35.20/52.63)相对单位·分钟]升高(P<0.05),同时在十分之六的凝胶中血影蛋白条带消失。在低强度运动时未发现相应变化。在常用强度范围内进行10至35分钟的非跑步运动可导致血管内溶血,并伴有RBC膜蛋白的改变,类似于体外氧化应激后以及遗传性贫血疾病(如球形红细胞增多症和范可尼贫血)中发现的改变。

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