Oxygen supplementation during exercise improves leg muscle fatigue in chronic fibrotic interstitial lung disease. Issue 7 (4th February 2021)

• Record Type: Journal Article
• Authors: Marillier, Mathieu; Bernard, Anne-Catherine; Verges, Samuel; Moran-Mendoza, Onofre; O'Donnell, Denis E; Neder, José Alberto
• Is Part Of: Thorax. Volume 76:Issue 7(2021)
• Page Start: 672
• Page End: 680
• Publication Date: 2021-02-04
• Subjects: exercise -- Long Term Oxygen Therapy (LTOT) -- interstitial fibrosis -- lung physiology -- pulmonary rehabilitation -- respiratory measurement -- short burst oxygen therapy; Chest -- Diseases -- Periodicals; Thorax; Chest -- Diseases; Periodicals; Periodicals; 617.54
• DOI: 10.1136/thoraxjnl-2020-215135
• Languages: English
• ISSNs: 0040-6376

Abstract

Abstract : Background: Exercise-induced hypoxaemia is a hallmark of chronic fibrotic interstitial lung disease ( f -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. Methods: 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. Results: 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). Conclusion: O2 supplementation during exercise improves leg muscle oxygenation and fatigue in f -ILD. Lessening peripheral muscle fatigue to enhance exercise tolerance is a neglected therapeutic target that deserves clinical attention in this patient population.