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运动诱发的动脉血氧不足对健康人股四头肌疲劳的影响。

Effect of exercise-induced arterial hypoxemia on quadriceps muscle fatigue in healthy humans.

作者信息

Romer Lee M, Haverkamp Hans C, Lovering Andrew T, Pegelow David F, Dempsey Jerome A

机构信息

Centre for Sports Medicine and Human Performance, Brunel University, Uxbridge, UK.

出版信息

Am J Physiol Regul Integr Comp Physiol. 2006 Feb;290(2):R365-75. doi: 10.1152/ajpregu.00332.2005. Epub 2005 Sep 15.

DOI:10.1152/ajpregu.00332.2005
PMID:16166208
Abstract

The effect of exercise-induced arterial hypoxemia (EIAH) on quadriceps muscle fatigue was assessed in 11 male endurance-trained subjects [peak O2 uptake (VO2 peak) = 56.4 +/- 2.8 ml x kg(-1) x min(-1); mean +/- SE]. Subjects exercised on a cycle ergometer at >or=90% VO2 peak) to exhaustion (13.2 +/- 0.8 min), during which time arterial O2 saturation (Sa(O2)) fell from 97.7 +/- 0.1% at rest to 91.9 +/- 0.9% (range 84-94%) at end exercise, primarily because of changes in blood pH (7.183 +/- 0.017) and body temperature (38.9 +/- 0.2 degrees C). On a separate occasion, subjects repeated the exercise, for the same duration and at the same power output as before, but breathed gas mixtures [inspired O2 fraction (Fi(O2)) = 0.25-0.31] that prevented EIAH (Sa(O2) = 97-99%). Quadriceps muscle fatigue was assessed via supramaximal paired magnetic stimuli of the femoral nerve (1-100 Hz). Immediately after exercise at Fi(O2) 0.21, the mean force response across 1-100 Hz decreased 33 +/- 5% compared with only 15 +/- 5% when EIAH was prevented (P < 0.05). In a subgroup of four less fit subjects, who showed minimal EIAH at Fi(O2) 0.21 (Sa(O2) = 95.3 +/- 0.7%), the decrease in evoked force was exacerbated by 35% (P < 0.05) in response to further desaturation induced via Fi(O2) 0.17 (Sa(O2) = 87.8 +/- 0.5%) for the same duration and intensity of exercise. We conclude that the arterial O2 desaturation that occurs in fit subjects during high-intensity exercise in normoxia (-6 +/- 1% DeltaSa(O2) from rest) contributes significantly toward quadriceps muscle fatigue via a peripheral mechanism.

摘要

在11名男性耐力训练受试者[峰值摄氧量(VO₂峰值)=56.4±2.8 ml·kg⁻¹·min⁻¹;均值±标准误]中评估了运动诱发的动脉低氧血症(EIAH)对股四头肌疲劳的影响。受试者在自行车测力计上以≥90%VO₂峰值的强度运动至力竭(13.2±0.8分钟),在此期间动脉血氧饱和度(Sa(O₂))从静息时的97.7±0.1%降至运动结束时的91.9±0.9%(范围84 - 94%),主要是由于血液pH值(7.183±0.017)和体温(38.9±0.2℃)的变化。在另一个时间点,受试者重复相同持续时间和相同功率输出的运动,但呼吸气体混合物[吸入氧分数(Fi(O₂))=0.25 - 0.31]以防止EIAH(Sa(O₂)=97 - 99%)。通过对股神经进行超最大配对磁刺激(1 - 100 Hz)来评估股四头肌疲劳。在Fi(O₂)为0.21的运动后立即测量,1 - 100 Hz范围内的平均力反应与防止EIAH时相比下降了33±5%,而防止EIAH时仅下降了15±5%(P<0.05)。在一个由四名身体状况较差的受试者组成的亚组中,他们在Fi(O₂)为0.21时表现出最小的EIAH(Sa(O₂)=95.3±0.7%),在相同持续时间和强度的运动中,通过Fi(O₂)为0.17进一步诱发血氧饱和度下降(Sa(O₂)=87.8±0.5%)后,诱发电力下降加剧了35%(P<0.05)。我们得出结论,在常氧下高强度运动期间健康受试者中发生的动脉血氧饱和度下降(相对于静息时ΔSa(O₂)为-6±1%)通过外周机制对股四头肌疲劳有显著影响。

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