INTRODUCTION:Fatiguing of respiratory muscles reduces peripheral muscle perfusion. Further, acute hypoxia enhances respiratory muscle fatigue. This study investigated the effects of inspiratory muscle loading (IML) on resting locomotor muscle perfusion in hypoxia compared to normoxia. METHODS:Ten subjects completed two study days of fatiguing IML (blinded, randomized) in normobaric hypoxia (targeted oxygen saturation 80%) and normoxia, respectively. Contrast-enhanced ultrasound (CEUS) of the gastrocnemius muscle and popliteal doppler ultrasonography were used to monitor muscle perfusion. Based on CEUS and monitored cardiac output, perfusion surrogate parameters (CLPaer and CLPap) were established. RESULTS:Muscle perfusion declines early during IML in normoxia (CLPaer: -54±25%, p<0.01; CLPap: -58±32%, p<0.01) and hypoxia (CLPaer: -43±23%, p<0.01; CLPap: -41±20%, p<0.01). Hypoxia compared to normoxia increased cardiac output before (+23±19%, p<0.01 ANOVA) and during (+22±20%, p<0.01 ANOVA) IML, while local muscle perfusion during IML remained unchanged (CLPaer: p=0.41 ANOVA; CLPap: p=0.29 ANOVA). CONCLUSION:Acute hypoxia compared to normoxia does not affect locomotor muscle perfusion during fatiguing IML.

译文

引言:呼吸肌疲劳会减少周围肌肉的灌注。此外,急性缺氧会增强呼吸肌疲劳。这项研究调查了吸氧量(IML)与低氧相比低氧对静息运动肌灌注的影响。
方法:十名受试者分别在常压低氧(目标血氧饱和度为80%)和常氧下完成了对IML(盲,随机)疲劳训练的两个研究日。腓肠肌的造影增强超声(CEUS)和pop肌多普勒超声检查可监测肌肉灌注情况。基于CEUS和监测的心输出量,建立灌注替代参数(CLPaer和CLPap)。
结果:常氧(CLPaer:-54±25%,p <0.01; CLPap:-58±32%,p <0.01)和缺氧(CLPaer:-43±23%,p <0.01)在IML早期肌肉灌注下降。 CLPap:-41±20%,p <0.01)。与常氧相比,低氧增加了IML之前(23±19%,p <0.01 ANOVA)和期间(22±20%,p <0.01 ANOVA)的心输出量,而IML期间的局部肌肉灌注保持不变(CLPaer:p = 0.41 ANOVA; CLPap:p = 0.29 ANOVA)。
结论:与常氧相比,急性缺氧并不影响IML疲劳期间运动肌的灌注。

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