一种建模方法来解开限制吸烟者肌肉氧化的因素
Hans Degens1,2, Tomas Venckunas3, Rob Cl Wüst4
1Department of Life Sciences, Research Centre for Musculoskeletal Science and Sports Medicine, Manchester Metropolitan University, John Dalton Building, Chester Street, Manchester, M1 5GD, UK. h.degens@mmu.ac.uk.
European journal of applied physiology
|August 6, 2023
概括
吸烟会降低运动能力,主要是由于慢性吸烟者的线粒体呼吸功能受损. 碳氧血球蛋白 (HbCO) 有助于减少氧气的运输,但线粒体功能障碍是减少肌肉氧气提取的关键.
科学领域:
- 运动生理学 运动生理学
- 呼吸系统医学 呼吸系统医学
- 细胞生物学 细胞生物学
背景情况:
- 吸烟与减少运动能力和肌肉疲劳有关.
- 吸烟者的碳氧血红蛋白 (HbCO) 降低了氧气的运输和组织的氧化.
- 线粒体功能障碍也可能损害氧气的吸收和利用.
研究的目的:
- 为了确定吸烟者的运动能力下降主要是由于HbCO或线粒体呼吸功能受损.
- 量化HbCO和线粒体功能障碍对肌肉氧化的影响.
主要方法:
- 利用现有关于肌肉毛细化,肌球蛋白和吸烟者和非吸烟者的最大氧气消耗的数据.
- 采用Krogh扩展组织氧化模型来模拟氧气的输送和利用.
- 通过酸脱酶染色,分析了来自横向巨大的肌肉组织.
主要成果:
- 6%和20%HbCO的吸烟者显示肌肉氧化分别减少了1.9%和7.2%.
- 在最大线粒体呼吸量减少29%时,肌肉氧化增加了13.3%.
- 与非吸烟者相比,组合的线粒体功能障碍和20%的HbCO使肌肉氧化正常化.
结论:
- 在慢性吸烟者中,线粒体呼吸受损是减少运动能力的主要驱动因素.
- HbCO有助于吸烟后立即的运动限制,但线粒体功能障碍在长期内更为显著.
- 血红蛋白分离曲线由HbCO向左移动在慢性吸烟者的运动能力降低方面起不大作用.
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