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运动诱导的脂蛋白(a)升高。

Exercise-induced increase in lipoprotein (a).

作者信息

Holme I, Urdal P, Anderssen S, Hjermann I

机构信息

Ullevaal University Hospital, Life Insurance Companies' Institute for Medical Statistics, Oslo, Norway.

出版信息

Atherosclerosis. 1996 Apr 26;122(1):97-104. doi: 10.1016/0021-9150(95)05761-7.

Abstract

In the Oslo Diet and Exercise Study (ODES) 219 healthy middle-aged physically inactive persons with moderately deranged risk factor levels (increased bodyweight, diastolic blood pressure, serum cholesterol, triglycerides, decreased HDL-cholesterol) were randomized to 4 intervention groups: dietary intervention, exercise, diet + exercise and control. The purpose of the study was to test if these interventions maintained for a year, isolated or in combination, would change coronary risk factor levels as compared to control. One of the risk factors included was lipoprotein (a) (Lp(a)). The hypothesis to be tested was if physical exercise would be associated with increased levels of Lp(a) as a result of intervention. Those who exercised increased their Lp(a) levels with 15.4 (S.E. = 8.0) mg/l as compared to no exercise (P < 0.05). Also, dietary intervention tended to increase Lp(a), but the increase did not reach statistical significance. There was no detectable interaction on the effect on Lp(a) of the two intervention modalities. A dose-response relationship was found between change in the exercise-specific variables heart rate and peak oxygen uptake, and Lp(a)-change and this dose-response was most pronounced in the exercise group. Change in Lp(a) was associated to change in several lifestyle related variables such as alcohol intake and waist circumference, pointing to the possibility that Lp(a), at least in some subpopulations, is more amenable to change through lifestyle alterations than reported so far.

摘要

在奥斯陆饮食与运动研究(ODES)中,219名健康的中年体力活动不足者,其危险因素水平中度紊乱(体重增加、舒张压升高、血清胆固醇、甘油三酯升高,高密度脂蛋白胆固醇降低),被随机分为4个干预组:饮食干预组、运动组、饮食 + 运动组和对照组。该研究的目的是测试这些干预措施单独或联合进行一年,与对照组相比是否会改变冠状动脉危险因素水平。其中一个纳入的危险因素是脂蛋白(a)[Lp(a)]。要检验的假设是体育锻炼是否会因干预导致Lp(a)水平升高。与不运动者相比,运动者的Lp(a)水平升高了15.4(标准误 = 8.0)mg/l(P < 0.05)。此外,饮食干预也倾向于使Lp(a)升高,但升高未达到统计学显著性。两种干预方式对Lp(a)的影响未发现可检测到的相互作用。在运动特异性变量心率和峰值摄氧量的变化与Lp(a)的变化之间发现了剂量反应关系,且这种剂量反应在运动组中最为明显。Lp(a)的变化与一些生活方式相关变量的变化有关,如酒精摄入量和腰围,这表明至少在某些亚人群中,Lp(a)可能比目前报道的更易于通过生活方式改变而发生变化。

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