Many patients with severe chronic obstructive pulmonary disease (COPD) develop hypoxaemia at rest when awake as their disease progresses. This may or may not be accompanied by hypercapnia but is a poor prognostic feature, independent of the forced expiratory volume in one second (FEV₁).1 For many years the scientific study of COPD was driven by the need to gain a greater understanding of the processes which led to these disorders of gas exchange. Ultimately this led to the introduction of effective treatment designed to increase the arterial oxygen tension beyond 8.0 kPa for at least 15 hours per day. The well known randomised controlled trials which confirmed the survival benefit of this treatment2 ,3 are also the cornerstone of evidence based oxygen prescribing.4 Since these results were published in the 1980s the costs of oxygen therapy have increased steadily in the UK and elsewhere5 and constitute one of the largest medical expenses, particularly in the care of patients with COPD. Over half of this money is spent on providing oxygen for indications other than continuous domiciliary care. The rationale for these other indications is less secure and certainly less studied. The publication of two papers addressing different aspects of this treatment in this issue ofThorax is a welcome addition to our information about this common therapeutic problem.6 ,7

The physiological basis of exercise limitation in COPD has been challenged in recent years with the observation that end expiratory lung volume rises during exercise and is closely related to the degree of breathlessness.8 ,9 Empirical studies have shown that supplementary oxygen increases the six minute walking distance compared with placebo in COPD,10 ,11 and that these effects are most marked when tests of endurance rather than maximum exercise …