Oxygen supplementation during exercise improves leg muscle fatigue in chronic fibrotic interstitial lung disease.

Abstract

Exercise-induced hypoxaemia is a hallmark of chronic fibrotic interstitial lung disease (<i>f</i>-ILD). It remains unclear whether patients' severe hypoxaemia may exaggerate locomotor muscle fatigue and, if so, to what extent oxygen (O₂) 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 O₂ (42%±7%) for the same duration. Near-infrared spectroscopy assessed vastus lateralis oxyhaemoglobin concentration ((HbO₂)). Pre-exercise to postexercise variation in twitch force (∆Tw) induced by femoral nerve magnetic stimulation quantified muscle fatigue. Patients showed severe hypoxaemia (lowest O₂ saturation by pulse oximetry=80.0%±7.6%) which was associated with a blunted increase in muscle (HbO₂₎ 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 O₂ was associated with a significant increase in muscle (HbO₂₎, leading to a reduced decrease in ∆Tw in patients (-0.33±0.19 %/kJ; p<0.001 vs air). Supplemental O₂ significantly improved leg discomfort (p=0.005). O₂ supplementation during exercise improves leg muscle oxygenation and fatigue in <i>f</i>-ILD. Lessening peripheral muscle fatigue to enhance exercise tolerance is a neglected therapeutic target that deserves clinical attention in this patient population.