Durstine J L, Davis P G, Ferguson M A, Alderson N L, Trost S G
Department of Exercise Science, University of South Carolina, Columbia, SC 29208, USA.
Med Sci Sports Exerc. 2001 Sep;33(9):1511-6. doi: 10.1097/00005768-200109000-00014.
Most studies that use either a single exercise session, exercise training, or a cross-sectional design have failed to find a relationship between exercise and plasma lipoprotein(a) [Lp(a)] concentrations. However, a few studies investigating the effects of longer and/or more strenuous exercise have shown elevated Lp(a) concentrations, possibly as an acute-phase reactant to muscle damage. Based on the assumption that greater muscle damage would occur with exercise of longer duration, the purpose of the present study was to determine whether exercise of longer duration would increase Lp(a) concentration and creatine kinase (CK) activity more than exercise of shorter duration.
Ten endurance-trained men (mean +/- SD: age, 27 +/- 6 yr; maximal oxygen consumption [VO(2max)], 57 +/- 7 mL x kg(-1) x min(-1)) completed two separate exercise sessions at 70% VO(2max). One session required 800 kcal of energy expenditure (60 +/- 6 min), and the other required 1500 kcal (112 +/- 12 min). Fasted blood samples were taken immediately before (0-pre), immediately after (0-post), 1 d after (1-post), and 2 d after (2-post) each exercise session.
CK activity increased after both exercise sessions (mean +/- SE; 800 kcal: 0-pre 55 +/- 11, 1-post 168 +/- 64 U x L(-1) x min(-1); 1500 kcal: 0-pre 51 +/- 5, 1-post 187 +/- 30, 2-post 123 +/- 19 U x L(-1) x min(-1); P < 0.05). However, median Lp(a) concentrations were not altered by either exercise session (800 kcal: 0-pre 5.0 mg x dL(-1), 0-post 3.2 mg x dL(-1), 1-post 4.0 mg x dL(-1), 2-post 3.4 mg x dL(-1); 1500 kcal: 0-pre 5.8 mg x dL(-1), 0-post 4.3 mg x dL(-1), 1-post 3.2 mg x dL(-1), 2-post 5.3 mg x dL(-1)). In addition, no relationship existed between exercise-induced changes in CK activity and Lp(a) concentration (800 kcal: r = -0.26; 1500 kcal: r = -0.02).
These results suggest that plasma Lp(a) concentration will not increase in response to minor exercise-induced muscle damage in endurance-trained runners.
大多数采用单次运动、运动训练或横断面设计的研究未能发现运动与血浆脂蛋白(a)[Lp(a)]浓度之间的关系。然而，一些研究调查了更长时间和/或更剧烈运动的影响，结果显示Lp(a)浓度升高，这可能是对肌肉损伤的一种急性期反应。基于持续时间更长的运动将导致更大肌肉损伤的假设，本研究的目的是确定持续时间更长的运动是否比持续时间较短的运动更能增加Lp(a)浓度和肌酸激酶(CK)活性。
10名耐力训练男性(平均±标准差：年龄，27±6岁；最大摄氧量[VO(2max)]，57±7 mL·kg(-1)·min(-1))在70%VO(2max)强度下完成了两次单独的运动。一次运动需要消耗800千卡能量(60±6分钟)，另一次需要消耗1500千卡(112±12分钟)。在每次运动前(0-前)、运动后即刻(0-后)、运动后1天(1-后)和运动后2天(2-后)采集空腹血样。
两次运动后CK活性均增加(平均±标准误；800千卡：0-前55±11，1-后168±64 U·L(-1)·min(-1)；1500千卡：0-前51±5，1-后187±30，2-后123±19 U·L(-1)·min(-1)；P<0.05)。然而，两次运动均未改变Lp(a)浓度中位数(800千卡：0-前5.0 mg·dL(-1)，0-后3.2 mg·dL(-1)，1-后4.0 mg·dL(-1)，2-后3.4 mg·dL(-1)；1500千卡：0-前5.8 mg·dL(-1)，0-后4.3 mg·dL(-1)，1-后3.2 mg·dL(-1)，2-后5.3 mg·dL(-1))。此外，运动引起的CK活性变化与Lp(a)浓度之间不存在相关性(800千卡：r=-0.26；1500千卡：r=-0.02)。
这些结果表明，在耐力训练型跑步者中，轻微运动引起的肌肉损伤不会导致血浆Lp(a)浓度升高。
