title: Does correction of exercise-induced desaturation by O(2) always improve exercise tolerance in COPD? A preliminary study.
abstract: BACKGROUND
  This study sought to investigate whether correction of exercise-induced desaturation by oxygen supply (O(2)) systematically improves exercise tolerance and cardiorespiratory adaptations in COPD patients.
  
  
  METHODS
  Twenty-five COPD patients [FEV(1)=52+/-2.5% pred] exhibiting exercise-induced desaturation performed cyclo-ergometer endurance exercise at 60%of their maximal workload in two randomized conditions: air vs. O(2). O(2) was adjusted to ensure 90 < or = SpO(2) < or = 95%. Endurance time (Tlim), dyspnoea, ventilation (V (E)), breathing frequency (fb), tidal volume (V(T)), cardiac output (CO), heart rate (HR) and arterio-venous difference in oxygen (AVD) were compared between conditions.
  
  
  RESULTS
  The comparison of whole group performance between conditions revealed no differences, but individual analysis showed that O(2) increased Tlim for 14 patients [+68%; p<0.01; (positive responders)], decreased it for seven [-36%; p<0.05; (negative responders)] and induced no change for four (non-responders). For positive responders, improved performance was supported by reduced dyspnoea, V (E), fb, HR and CO and increased AVD. For negative responders, hyperoxia resulted in increased dyspnoea and fb without change in V (E) or cardiovascular parameters.
  
  
  CONCLUSIONS
  For comparable correction of exercise desaturation, O(2) does not induce similar effects on exercise responses in all patients. These results were confirmed in complementary study with 11 consecutives patients at higher exercise intensity. For R+, we recorded the classic and expected O(2) effects on cardiorespiratory adaptations (i.e. reduced ventilatory demand and cardiac output). In the other group, exercise breathing frequency and dyspnoea were paradoxically increased despite desaturation correction. However, this study must be considered as pilot study, which will need to be confirmed in future studies conducted on a larger case series.
authors.affiliation: EA 2991, Laboratory of Motor Efficiency and Deficiency, University of Montpellier 1, 700 Av. du Pic Saint Loup, 34090 Montpellier, France. nelly.heraud@fontalvie.fr
authors.forename: Nelly
authors.initials: N
authors.lastname: Héraud
authors.forename: Christian
authors.initials: C
authors.lastname: Préfaut
authors.forename: Fabienne
authors.initials: F
authors.lastname: Durand
authors.forename: Alain
authors.initials: A
authors.lastname: Varray
mesh_terms: D000368:Aged; D000704:Analysis of Variance; D002306:Cardiac Volume; D005081:Exercise Therapy / Q000379:methods; D017079:Exercise Tolerance; D005260:Female; D006339:Heart Rate; D006801:Humans; D008168:Lung / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D010100:Oxygen / Q000097:blood / Q000627:therapeutic use*; D010101:Oxygen Consumption / Q000502:physiology; D029424:Pulmonary Disease, Chronic Obstructive / Q000097:blood / Q000503:physiopathology* / Q000628:therapy; D012044:Regression Analysis; D012129:Respiratory Function Tests; D013318:Stroke Volume
chemical_list: D010100:Oxygen