调节红细胞氧化合成酶酸化在休息和运动的人类前臂
Jeffrey A Leo1, Surendran Sabapathy1, Lennart Kuck2
1Exercise and Sport, School of Health Sciences and Social Work, Griffith University, Gold Coast, Queensland, Australia.
概括
运动和低氧化增加红细胞氧化合成酶 (RBC-NOS) 酸化在血清1177上,增强RBC-NOS活性. 这种酸化与增加的血流和细胞变形性有关,揭示了体力活动和氧气水平在体内如何影响RBC-NOS.
科学领域:
- 生理学 生理学 生理学
- 生物化学 生物化学
- 心血管科学 心血管科学
背景情况:
- 人体红细胞具有功能性内皮氧化合成酶 (NOS) 异型,称为RBC-NOS,能够合成氧化.
- 红细胞-NOS在血清1177的酸化是一个关键的调节机制.
- 低氧症会影响局部血流,剪切应力和氧化的可用性,可能会影响红细胞-NOS活动.
研究的目的:
- 测试RBC-NOS在血清1177的酸化是否被放大在血液排泄活跃的骨肌肉中.
- 为了研究正常氧与缺氧对RBC-NOS酸化和运动期间红细胞功能的影响.
主要方法:
- 九名健康的志愿者在正常和低氧 (动脉氧和率约80%) 的情况下进行了节奏握手运动.
- 测量了手臂动脉的血流量,血管电导率,平均动脉压和血液粘度.
- 红细胞分析了酸化的红细胞-NOS水平和细胞变形性.
主要成果:
- 在normoxia下的前臂运动显著增加了血液流动,血管导电性,剪切应力,RBC-NOS酸化 (2.7倍) 和红细胞可变性.
- 休息时的低氧化症增加了血管导电性,剪切应力,红细胞变形性和RBC-NOS酸化,与normoxia相比.
- 低血运动进一步增强了血管导电性,剪切应力和细胞变形性,在RBC-NOS酸化中具有特定对象的反应.
结论:
- 血液动力学力量,如运动期间增加剪切应力,显著增强RBC-NOS酸化和红细胞可变性.
- 缺氧增强了这些效应,增加了血管导电性和RBC-NOS酸化,表明氧张力和机械刺激之间的复杂相互作用.
- 这些发现为体育炼和氧气供应相关的生理因素对红细胞-NOS的体内调节提供了新的见解.
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