长期COVID中运动不耐受的潜在机制:多系统功能障碍的累积
Alexandra Jamieson1, Lamia Al Saikhan2, Lamis Alghamdi1,2
1MRC Unit for Lifelong Health & Ageing at UCL, University College London, London, UK.
Physiological reports
|February 12, 2024
概括
长期COVID患者的运动表现和骨肌肉容量下降,表明潜在的线粒体问题. 自主神经系统的失调也导致了这些人的运动不耐受.
科学领域:
- 生理学 生理学 生理学
- 病理学 病理学 病理学
- 运动科学 运动科学
背景情况:
- 长期COVID,在SARS-CoV-2感染后,呈现出无法解释的运动不耐受和疲劳.
- 这些症状的潜在机制尚未完全理解.
- 了解这些机制对于开发有效治疗方法至关重要.
研究的目的:
- 调查长期COVID中运动不耐症的生理基础.
- 在长期COVID患者和健康对照者之间比较运动表现,心肺功能,血管健康,骨肌氧化能力和自主神经系统功能.
- 确定在长期COVID中减弱运动耐受性的潜在促成因素.
主要方法:
- 招募了32名长期COVID患者和19名年龄/性别匹配的健康对照.
- 评估运动表现,肺和心脏功能,血管健康,骨肌氧化能力 (使用近红外光谱),以及自主神经系统功能.
- 群体之间的生理测量和对准值的比较,调整为混因素.
主要成果:
- 与健康对照组相比,长期COVID患者的氧气吸收效率斜率和厌氧值显著降低.
- 长期COVID患者的骨肌氧化能力较低.
- 在39%的长期COVID病例中,自主神经系统的测量异常,低于正常限度.
结论:
- 长期的COVID与运动性能和骨肌肉氧化能力的降低有关,这表明线粒体病理.
- 微血管功能障碍的缺失表明存在固有肌肉问题.
- 自主神经系统的调节障碍很普遍,可能导致运动耐受性受损.
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