Abnormalities in lung mechanics (restriction) and pulmonary gas exchange (hypoxaemia) may jointly conspire to elicit exertional dyspnoea and decrease exercise tolerance in patients with fibrosing interstitial lung disease (f-ILD) [1]. Obesity (body mass index (BMI) ≥30 kg·m^–2), a prevalent comorbidity of f-ILD [2], may negatively impact on "static" (e.g. total lung capacity (TLC)) and dynamic (forced vital capacity (FVC)) lung volumes relevant to dyspnoea genesis [3]. Arterial oxygenation decreases as obesity worsens, particularly on exertion when poorly ventilated areas are perfused with less oxygenated mixed venous blood [4]. Mass loading in the thorax increases the elastic work of breathing [5], and heightened ventilation in response to high metabolic demands [6] contributes to breathlessness and exercise intolerance in a "dose" (weight)-response fashion [7]. It is conceivable, therefore, that the functional and sensory consequences of moderate-to-severe obesity (BMI ≥35 kg·m^–2) may confound the assessment of disease severity and stability in these patients.

肺力学（限制）和肺气体交换（低氧血症）的异常可能共同引起纤维化间质性肺疾病（f-ILD）患者的劳力性呼吸困难和运动耐量降低[1]。肥胖（体重指数 (BMI) ≥30 kg·m ^–2）是 f-ILD 的常见合并症[2]，可能对“静态”（例如总肺活量（TLC））和动态（用力肺活量）产生负面影响。 (FVC)) 与呼吸困难发生相关的肺容量 [3]。动脉氧合随着肥胖的恶化而降低，尤其是在通气不良的区域灌注含氧量较低的混合静脉血时用力时[4]。胸部的质量负荷增加了呼吸的弹性功[5]，并且响应高代谢需求而加强通气[6]以“剂量”（体重）反应方式导致呼吸困难和运动不耐受[7]。因此，可以想象，中度至重度肥胖（BMI≥35 kg·m ^–2）的功能和感觉后果可能会混淆这些患者疾病严重程度和稳定性的评估。