Background Little is known about the mechanistic basis for the exercise intolerance characteristic of patients with respiratory disease; a lack of clearly defined, distinct patient groups limits interpretation of many studies. The purpose of this pilot study was to investigate the pulmonary oxygen uptake ((V)over dot O-2) response, and its potential determinants, in patients with emphysema and idiopathic pulmonary fibrosis (IPF). Methods Following a ramp incremental test for the determination of peak (V)over dot O-2 and the gas exchange threshold, six emphysema (66 +/- 7 years; FEV1, 36 +/- 16%), five IPF (65 +/- 12 years; FEV1, 82 +/- 11%) and ten healthy control participants (63 +/- 6 years) completed three repeat, heavy-intensity exercise transitions on a cycle ergometer. Throughout each transition, pulmonary gas exchange, heart rate and muscle deoxygenation ([HHb], patients only) were assessed continuously and subsequently modelled using a mono-exponential with ((V)over dot O-2, [HHb]) or without (HR) a time delay. Results The (V)over dot O-2 phase II time-constant (tau) did not differ between IPF and emphysema, with both groups significantly slower than healthy controls (Emphysema, 65 +/- 11; IPF, 69 +/- 7; Control, 31 +/- 7 s; P < 0.05). The HR t was slower in emphysema relative to IPF, with both groups significantly slower than controls (Emphysema, 87 +/- 19; IPF, 119 +/- 20; Control, 58 +/- 11 s; P < 0.05). In contrast, neither the [HHb] tau nor [HHb]:O-2 ratio differed between patient groups. Conclusions The slower (V)over dot O-2 kinetics in emphysema and IPF may reflect poorer matching of O-2 delivery-to-utilisation. Our findings extend our understanding of the exercise dysfunction in patients with respiratory disease and may help to inform the development of appropriately targeted rehabilitation strategies.