Wang Jong-Shyan, Chow Shu-Er
Graduate Institute of Rehabilitation Science and Department of Physiology, Chang Gung University, Taoyuan, Taiwan.
Arch Phys Med Rehabil. 2004 Sep;85(9):1531-7. doi: 10.1016/j.apmr.2003.08.112.
To investigate how exercise training and detraining affect oxidized low-density lipoprotein (Ox-LDL)-potentiated platelet function in men.
Cohort study.
Department of physical medicine and rehabilitation.
Ten sedentary men (mean age +/- standard error of the mean, 21.6+/-0.2 y) who did not engage in any regular physical activity for at least 1 year before the study.
Subjects cycled on an ergometer at about 50% of maximal oxygen consumption for 30 minutes daily, 5 days a week, for 8 weeks, then detrained for 12 weeks.
During the experimental period, blood samples from the subjects were collected before and immediately after a progressive exercise test (ie, strenuous, acute exercise) every 4 weeks. The following measurements were taken when the subjects were at rest and immediately after exercise: plasma lipid profile, plasma Ox-LDL level, and platelet aggregation and intracellular calcium concentration ([Ca2+]i) elevation induced by adenosine disphosphate (ADP) alone or simultaneous ADP and Ox-LDL addition.
Analytical results indicated that: (1) plasma total cholesterol and LDL levels were reduced after exercise training from 151+/-7 mg/dL and 58+/-2 mg/dL to 133+/-6 mg/dL and 46+/-2 mg/dL (P<.05), respectively, whereas the plasma Ox-LDL level remained unchanged; (2) platelet aggregation and [Ca2+]i elevation promoted by 100 microg/mL of Ox-LDL were significantly increased from 70%+/-5% and 91%+/-7% of resting level to 108%+/-4% and 125%+/-3% after strenuous, acute exercise (P<.05); (3) exercise training decreased resting and postexercise 100 microg/mL Ox-LDL-potentiated platelet aggregation (ie, 31%+/-4% and 82%+/-4%, respectively; P<.05) and [Ca2+]i elevation (ie, 35%+/-6% and 71%+/-4%, respectively; P<.05); (4) detraining reversed the training effects on lipid profile and platelet function; and (5) treating the platelet with L-arginine-inhibited Ox-LDL-potentiated platelet activation during the experimental period.
Our results suggest that 8 weeks of exercise training decreased the plasma LDL level, but failed to influence production of plasma Ox-LDL. Importantly, resting and exercise-induced Ox-LDL-potentiated platelet activation was decreased by exercise training. However, this was reversed by detraining to the pretraining level.
研究运动训练和停训如何影响男性氧化型低密度脂蛋白(Ox-LDL)增强的血小板功能。
队列研究。
物理医学与康复科。
10名久坐不动的男性(平均年龄±平均标准误差,21.6±0.2岁),在研究前至少1年未进行任何规律的体育活动。
受试者每周5天,每天在测力计上以约最大耗氧量的50%进行30分钟的骑行,持续8周,然后停训12周。
在实验期间,每4周在进行递增运动试验(即剧烈、急性运动)之前和之后立即采集受试者的血样。在受试者休息时和运动后立即进行以下测量:血浆脂质谱、血浆Ox-LDL水平,以及单独使用二磷酸腺苷(ADP)或同时添加ADP和Ox-LDL诱导的血小板聚集和细胞内钙浓度([Ca2+]i)升高。
分析结果表明:(1)运动训练后血浆总胆固醇和低密度脂蛋白水平分别从151±7mg/dL和58±2mg/dL降至133±6mg/dL和46±2mg/dL(P<0.05),而血浆Ox-LDL水平保持不变;(2)在剧烈急性运动后,由100μg/mL Ox-LDL促进的血小板聚集和[Ca2+]i升高从静息水平的70%±5%和91%±7%显著增加至108%±4%和125%±3%(P<0.05);(3)运动训练降低了静息和运动后100μg/mL Ox-LDL增强的血小板聚集(分别为31%±4%和82%±4%;P<0.05)和[Ca2+]i升高(分别为35%±6%和71%±4%;P<0.05);(4)停训逆转了训练对脂质谱和血小板功能的影响;(5)在实验期间用L-精氨酸处理血小板可抑制Ox-LDL增强的血小板活化。
我们的结果表明,8周的运动训练降低了血浆低密度脂蛋白水平,但未能影响血浆Ox-LDL的产生。重要的是,运动训练降低了静息和运动诱导的Ox-LDL增强的血小板活化。然而,停训使其恢复到训练前水平。