Comparison of these results with those of studies comparing healthy glycolytic with oxidative muscle suggests that these differences may be attributable to greater type II fiber expression in COPD muscle, as mitochondria within this fiber type have respiratory function similar to that of mitochondria from type I fibers, and yet are intrinsically prone to greater release of H(2)O(2) and more resistant to PTP opening. These results thus argue against the presence of pathological mitochondrial alterations in this category of patients with COPD.

Evidence exists for locomotor muscle impairment in patients with chronic obstructive pulmonary disease (COPD), including fiber type alterations and reduced mitochondrial oxidative capacity. In this study high-resolution respirometry was used to quantify oxygen flux in permeabilized fibres from biopsies of the vastus lateralis muscle in patients with COPD and compared to healthy control subjects. The main findings of this study were that (i) routine state 2 respiration was higher in COPD; (ii) state 3 respiration in the presence of ADP was similar in both groups with substrate supply of electrons to complex I (COPD 38·28 ± 3·58 versus control 42·85 ± 3·10 pmol s(-1) mg tissue(-1) ), but O(2) flux with addition of succinate was lower in COPD patients (COPD 63·72 ± 6·33 versus control 95·73 ± 6·53 pmol s(-1) mg tissue(-1) ); (iii) excess capacity of cytochrome c oxidase in COPD patients was only ~50% that of control subjects. These results indicate that quadriceps muscle mitochondrial function is altered in patients with COPD. The regulatory mechanisms underlying these functional abnormalities remain to be uncovered.

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Rationale.Interest in the measurement of exercise cardiac output (Qc) in patients with Chronic Obstructive Pulmonary Disease (COPD) has resurged due to the recent proposition that dynamic hyperinflation may result in blood trapping within the pulmonary circulation, thereby limiting oxygen delivery and exercise capacity. To date, the ability to measure Qc non-invasively in these patients is constrained by techniques dependent upon appropriate ventilation: perfusion for adequate pulmonary blood-gas diffusion. The technique of thoracic bioimpedance presents an interesting alternative as it does not depend on gas lung transfer factors, provides continuous measurement from rest to peak exercise and is free of patient interaction, unlike rebreathing methods. This study reports on the reliability of thoracic bioimpedance (Physioflow ®) compared to standard CO -rebreathing and inert-gas rebreathing (Innocor ®) techniques for use in test-restest submaximal 2 steady state exercise. Methods.Stable COPD patients (N=8; 66±4 yrs; FEV = 56±6% pred.) were assessed on 2 occasions separated by at least 2 days. Qc was measured 1 using the 3 techniques at the end of 5-minute steady-state cycling at 20, 35, 50 and 65%peak power bouts. The reported Qc was the average of 2 consecutive measures at each workload. Results.All techniques provided measurements in a physiologically acceptable range for the power output and showed good reproducibility with no difference in test-retest mean values. CO rebreathing resulted in systematically higher values both at rest and during exercise as 2 compared to Physioflow® (mean Δ L/min: 0.5 rest; 0.7, 0.3, 0.8 at 20, 35, 50% peak power). In contrast, Innocor® resulted in systematically lower rest and exercise values as compared to Physioflow® (mean Δ L/min: 1.6 rest; 1.6, 1.2, 1.8 at 20, 35, 50% peak power). Results also showed the coefficient of reproducibility calculated on test-restest to be highest in Physioflow® (R = 0.80) compared with Innocor® and 2 CO rebreathing (R = 0.72 and 0.53) 2 2 Conclusions.These preliminary results suggest that thoracic bioimpedance presents a valuable tool to monitor Qc in COPD under resting and moderate exercise conditions resulting in significant hyperventilation and moderate dynamic hyperinflation.This abstract is funded by:

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