A randomised trial of pulmonary rehabilitation in the UK reported a similar mean increase of 71 m in stable disease. Selfreported dyspnoea on the Borg scale suggested a degree of desensitisation to exertional dyspnoea associated with this improvement. Alternatively, improvement in peripheral muscle function and hence lactate production, particularly from the quadriceps,32 33 could provide a physiological explanation for reduced ventilatory drive. Quadriceps endurance properties were not measured. No significant change in static pulmonary function was observed, but many patients struggled to perform adequate gas transfer or body plethysmography measurements following exacerbation. Dynamic inspiratory capacity measurements were not performed.34