Influence of acute exercise on human platelet responsiveness: possible involvement of exercise-induced oxidative stress
Influence of acute exercise on human platelet responsiveness: possible involvement of exercise-induced oxidative stress
复制标题
急性运动对人体血小板反应性的影响：可能涉及运动诱发的氧化应激
DOI：
10.1007/s00421-001-0542-8
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发表时间：
2001
影响因子：
3
通讯作者：
C. Di Massimo
中科院分区：
文献类型：
--
作者：
M. Tozzi;M. Penco;C. Di Massimo
抽象的。本研究的目的是评估久坐的男性受试者急性剧烈和适度运动对离体血小板反应性的影响及其与运动相关的氧化剂-抗氧化状态改变的可能关系。在力竭运动后观察到 ADP 和胶原诱发的血小板聚集增加，这与膜流动性和离子稳态的改变有关。适度运动后，我们发现低浓度激动剂引起血小板聚集减少。剧烈运动（而非中等强度的运动）会导致脂质过氧化次级产物的积累增加，总抗氧化能力降低，包括超氧化物歧化酶活性降低，以及低密度脂蛋白（LDL）对体外氧化的敏感性增加。每次体能测试后，观察到血浆亚硝酸盐/硝酸盐（NOX）含量急剧升高，而血小板NOX含量在剧烈运动后下降，在适度运动后增加。本研究的结果表明，急性剧烈运动引起的氧化应激可能会干扰血小板反应性，最有可能是通过促进氧化低密度脂蛋白介导的血小板活化以及降低血浆和血小板衍生的一氧化氮（NO）生物活性。此外，我们的结果进一步表明，急性中度物理应激源后血小板的反应性可能取决于血浆和血小板内NO使血小板对激动剂刺激脱敏的效率。
Abstract. The aim of this study was to evaluate in sedentary male subjects the effects of an acute bout of strenuous and moderate exercise on ex vivo platelet responsiveness and its possible relationship with exercise-associated modifications of oxidant-antioxidant status. An increased ADP- and collagen-evoked platelet aggregation associated with modified membrane fluidity and ion homeostasis was observed after exhaustive exercise. After moderate exercise, we found a decrease of platelet aggregation evoked by low concentrations of agonists. Strenuous exercise, but not moderate exertion, resulted in the enhanced accumulation of secondary products of lipid peroxidation, decreased total antioxidant capacity, including a diminished superoxide dismutase activity, and increased susceptibility of low-density lipoprotein (LDL) to in vitro oxidation. Acute elevation of plasma nitrite/nitrate (NOX) content was observed following each single session of physical test, whilst the platelet NOX content was decreased after strenuous exercise and increased after moderate exercise. Findings of the present study suggest that oxidative stress induced by acute strenuous exercise may interfere with platelet responsiveness most likely by promoting oxidized LDL-mediated platelet activation and by decreasing plasma and platelet-derived nitric oxide (NO) bioactivity. Moreover, our results further suggest that platelet responsiveness following an acute moderate physical stressor may depend on the efficiency of plasma and intraplatelet NO to desensitize platelets to agonist stimulation.