title: Pulmonary oxygen uptake and muscle deoxygenation kinetics during heavy intensity cycling exercise in patients with emphysema and idiopathic pulmonary fibrosis.
abstract: 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] O2) 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] O2and 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 ([Formula: see text] O2, [HHb]) or without (HR) a time delay.
  
  
  RESULTS
  The [Formula: see text] O2phase 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]:O2ratio differed between patient groups.
  
  
  CONCLUSIONS
  The slower [Formula: see text] O2kinetics in emphysema and IPF may reflect poorer matching of O2delivery-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.
authors.affiliation: A-STEM, College of Engineering, Swansea University, Swansea, UK. m.mcnarry@swansea.ac.uk.
authors.forename: Melitta A
authors.initials: MA
authors.lastname: McNarry
authors.affiliation: College of Medicine, Swansea University, Swansea, UK.|Respiratory Unit, Morriston Hospital, Swansea, UK.
authors.forename: Nicholas K
authors.initials: NK
authors.lastname: Harrison
authors.affiliation: A-STEM, College of Engineering, Swansea University, Swansea, UK.
authors.forename: Tom
authors.initials: T
authors.lastname: Withers
authors.affiliation: Respiratory Unit, Morriston Hospital, Swansea, UK.
authors.forename: Narendra
authors.initials: N
authors.lastname: Chinnappa
authors.affiliation: A-STEM, College of Engineering, Swansea University, Swansea, UK.
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Lewis
mesh_terms: D000222:Adaptation, Physiological; D000368:Aged; D016022:Case-Control Studies; D005080:Exercise Test; D017079:Exercise Tolerance; D005260:Female; D006339:Heart Rate; D006801:Humans; D054990:Idiopathic Pulmonary Fibrosis / Q000503:physiopathology*; D007700:Kinetics; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000378:metabolism; D010101:Oxygen Consumption; D010865:Pilot Projects; D011656:Pulmonary Emphysema / Q000503:physiopathology*; D011659:Pulmonary Gas Exchange; D012044:Regression Analysis
keywords: Cycle; NIRS; O2 kinetics; Respiratory disease