Pulmonary oxygen uptake and muscle deoxygenation kinetics during heavy intensity cycling exercise in patients with emphysema and idiopathic pulmonary fibrosis

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 ([Formula: see text] 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 [Formula: see text] O(2) and the gas exchange threshold, six emphysema (66 ± 7 years; FEV(1,) 36 ± 16%), five IPF (65 ± 12 years; FEV(1), 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 ([Formula: see text] O(2), [HHb]) or without (HR) a time delay. RESULTS: The [Formula: see text] O(2) phase II time-constant (τ) 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 τ 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] τ nor [HHb]:O(2) ratio differed between patient groups. CONCLUSIONS: The slower [Formula: see text] 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.