Division of Respirology, Department of Medicine, Queen's University, Kingston, Ontario, Canada.
2HP2 Laboratory, INSERM U1042, Grenoble Alpes University, Grenoble, Isere, France.
Thorax. 2021 Jul;76(7):672-680. doi: 10.1136/thoraxjnl-2020-215135. Epub 2021 Feb 4.
Exercise-induced hypoxaemia is a hallmark of chronic fibrotic interstitial lung disease (-ILD). It remains unclear whether patients' severe hypoxaemia may exaggerate locomotor muscle fatigue and, if so, to what extent oxygen (O) supplementation can ameliorate these abnormalities.
Fifteen patients (12 males, 9 with idiopathic pulmonary fibrosis) performed a constant-load (60% peak work rate) cycle test to symptom limitation (Tlim) while breathing medical air. Fifteen age-matched and sex-matched controls cycled up to patients' Tlim. Patients repeated the exercise test on supplemental O (42%±7%) for the same duration. Near-infrared spectroscopy assessed vastus lateralis oxyhaemoglobin concentration ((HbO)). Pre-exercise to postexercise variation in twitch force (∆Tw) induced by femoral nerve magnetic stimulation quantified muscle fatigue.
Patients showed severe hypoxaemia (lowest O saturation by pulse oximetry=80.0%±7.6%) which was associated with a blunted increase in muscle (HbO during exercise vs controls (+1.3±0.3 µmol vs +4.4±0.4 µmol, respectively; p<0.001). Despite exercising at work rates ∼ one-third lower than controls (42±13 W vs 66±13 W), ∆Tw was greater in patients (∆Tw/external work performed by the leg muscles=-0.59±0.21 %/kJ vs -0.25±0.19 %/kJ; p<0.001). Reversal of exertional hypoxaemia with supplemental O was associated with a significant increase in muscle (HbO, leading to a reduced decrease in ∆Tw in patients (-0.33±0.19 %/kJ; p<0.001 vs air). Supplemental O significantly improved leg discomfort (p=0.005).
O supplementation during exercise improves leg muscle oxygenation and fatigue in -ILD. Lessening peripheral muscle fatigue to enhance exercise tolerance is a neglected therapeutic target that deserves clinical attention in this patient population.
运动诱导性低氧血症是慢性纤维化间质性肺疾病（ILD）的标志。目前尚不清楚患者的严重低氧血症是否会加剧运动肌肉疲劳，如果是这样，那么氧（O）补充能在多大程度上改善这些异常。
15 名患者（12 名男性，9 名特发性肺纤维化）在呼吸医用空气的情况下，以恒定负荷（60%峰值工作率）进行直至症状限制（Tlim）的踏车试验。15 名年龄和性别匹配的对照者踏车至患者的 Tlim。患者在相同时间内接受 42%±7%的补充 O 进行重复运动测试。近红外光谱评估股外侧肌的氧合血红蛋白浓度（(HbO)。通过股神经磁刺激引起的强直收缩力（Tw）的预运动后变化来量化肌肉疲劳。
患者表现出严重的低氧血症（脉搏血氧饱和度最低=80.0%±7.6%），这与肌肉（HbO 在运动期间的增加减弱有关，与对照组相比（分别增加+1.3±0.3 µmol 和+4.4±0.4 µmol；p<0.001）。尽管患者的工作率比对照组低约三分之一（42±13 W 与 66±13 W），但患者的 ∆Tw 更大（∆Tw/腿部肌肉所做的外部功=-0.59±0.21 %/kJ 与-0.25±0.19 %/kJ；p<0.001）。用补充 O 逆转运动性低氧血症与肌肉（HbO 显著增加有关，导致患者的 ∆Tw 减少（-0.33±0.19 %/kJ；p<0.001 与空气）。补充 O 显著改善腿部不适（p=0.005）。
运动期间补充 O 可改善ILD 患者腿部肌肉的氧合和疲劳。减轻外周肌肉疲劳以提高运动耐量是一个被忽视的治疗靶点，值得在这一患者群体中引起临床关注。
