The purpose of this study was to characterize exercise-induced arterial hypoxaemia (EIAH), pulmonary gas exchange and respiratory mechanics during exercise, in young healthy women. We defined EIAH as a >10 mmHg decrease in arterial oxygen tension () during exercise compared to rest. We used a heliox inspirate to test the hypothesis that mechanical constraints contribute to EIAH. Subjects with a spectrum of aerobic capacities (n= 30; maximal oxygen consumption () = 49 ± 1, range 28–62 ml kg−1 min−1) completed a stepwise treadmill test and a subset (n= 18 with EIAH) completed a constant load test (∼85%) with heliox gas. Throughout exercise arterial blood gases, oxyhaemoglobin saturation (), the work of breathing (WOB) and expiratory flow limitation (EFL) were assessed. Twenty of the 30 women developed EIAH with a nadir and ranging from 58 to 88 mmHg and 87 to 96%, respectively. At maximal exercise, was inversely related to (r=–0.57, P < 0.05) with notable exceptions where some subjects with low aerobic fitness levels demonstrated EIAH. Subjects with EIAH had a greater (51 ± 1 vs. 43 ± 2 ml kg−1 min−1), lower end-exercise (93.2 ± 0.5 vs. 96.1 ± 0.3%) and a greater maximal energetic WOB (324 ± 19 vs. 247 ± 23 J min−1), but had similar resting pulmonary function compared to those without EIAH. Most subjects developed EIAH at submaximal exercise intensities, with distinct patterns of hypoxaemia. In some subjects with varying aerobic fitness levels, mechanical ventilatory constraints (i.e. EFL) were the primary mechanism associated with the hypoxaemia during the maximal test. Mechanical ventilatory constraints also prevented adequate compensatory alveolar hyperventilation in most EIAH subjects. Minimizing mechanical ventilatory constraints with heliox inspiration partially reversed EIAH in subjects who developed EFL. In conclusion, healthy women of all aerobic fitness levels can develop EIAH and begin to do so at submaximal intensities. Mechanical ventilatory constraints are a primary mechanism for EIAH in some healthy women and prevent reversal of hypoxaemia in women for whom it is not the primary mechanism.
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机译:这项研究的目的是表征年轻健康妇女在运动过程中运动诱发的动脉低氧血症(EIAH),肺气体交换和呼吸力学。我们将EIAH定义为与休息相比,运动期间动脉血氧张力降低(> 10 mmHg)。我们使用了氦氧混合气吸气器来检验机械约束有助于EIAH的假设。有氧能力谱的受试者(n = 30;最大耗氧量()= 49±1,范围28-62 ml kg -1 min -1 sup>)分步式跑步机测试和一个子集(对于EIAH,n = 18)使用氦氧混合气完成了恒定负载测试(〜85%)。在整个运动过程中,对动脉血气,氧合血红蛋白饱和度(),呼吸功(WOB)和呼气流量限制(EFL)进行了评估。 30名妇女中有20名患上了最低点的EIAH,分别为58至88 mmHg和87至96%。在最大运动量时,与(r = –0.57,P <0.05)呈负相关,但有一些例外,其中一些有氧健身水平低的受试者表现出EIAH。接受EIAH的受试者运动量更大(51±1 vs. 43±2 ml kg −1 sup> min −1 sup>),下肢运动能力较低(93.2±0.5 vs. 96.1± 0.3%)和更高的最大能量WOB(324±19 vs. 247±23 J min -1 sup>),但与没有EIAH的患者相比,其静息肺功能相似。大多数受试者在运动强度不足的情况下发展为EIAH,低氧血症的模式不同。在有氧健身水平各不相同的某些受试者中,最大通气测试期间,机械通气限制(即EFL)是与低氧血症相关的主要机制。机械通气限制也阻止了大多数EIAH受试者进行充分的代偿性肺泡过度换气。利用氦氧混合气吸气使机械通气限制减至最小,可部分逆转发生EFL的受试者的EIAH。总之,所有有氧健身水平的健康女性都可以发展出EIAH,并开始以最大强度进行运动。机械通气限制是一些健康女性的EIAH的主要机制,并且可以防止不是主要机制的女性逆转低氧血症。
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