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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 (   \documentclass[12pt]{minimal} 				\usepackage{amsmath} 				\usepackage{wasysym}  				\usepackage{amsfonts}  				\usepackage{amssymb}  				\usepackage{amsbsy} 				\usepackage{mathrsfs} 				\usepackage{upgreek} 				\setlength{\oddsidemargin}{-69pt} 				\begin{document}$$ \overset{.}{V} $$\end{document}    V  .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    \documentclass[12pt]{minimal} 				\usepackage{amsmath} 				\usepackage{wasysym}  				\usepackage{amsfonts}  				\usepackage{amssymb}  				\usepackage{amsbsy} 				\usepackage{mathrsfs} 				\usepackage{upgreek} 				\setlength{\oddsidemargin}{-69pt} 				\begin{document}$$ \overset{.}{V} $$\end{document}    V  .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 (   \documentclass[12pt]{minimal} 				\usepackage{amsmath} 				\usepackage{wasysym}  				\usepackage{amsfonts}  				\usepackage{amssymb}  				\usepackage{amsbsy} 				\usepackage{mathrsfs} 				\usepackage{upgreek} 				\setlength{\oddsidemargin}{-69pt} 				\begin{document}$$ \overset{.}{V} $$\end{document}    V  .O 2 , [HHb]) or without (HR) a time delay.    Results  The    \documentclass[12pt]{minimal} 				\usepackage{amsmath} 				\usepackage{wasysym}  				\usepackage{amsfonts}  				\usepackage{amssymb}  				\usepackage{amsbsy} 				\usepackage{mathrsfs} 				\usepackage{upgreek} 				\setlength{\oddsidemargin}{-69pt} 				\begin{document}$$ \overset{.}{V} $$\end{document}    V  .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    \documentclass[12pt]{minimal} 				\usepackage{amsmath} 				\usepackage{wasysym}  				\usepackage{amsfonts}  				\usepackage{amssymb}  				\usepackage{amsbsy} 				\usepackage{mathrsfs} 				\usepackage{upgreek} 				\setlength{\oddsidemargin}{-69pt} 				\begin{document}$$ \overset{.}{V} $$\end{document}    V  .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.

bmc pulmonary medicine

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