The aim of the present study was to calculate reference equations for carbon monoxide and nitric oxide transfer, measured in two distinct populations.The transfer factor of the lung for nitric oxide (TL,NO) and carbon monoxide (TL,CO) were measured in 303 people aged 18-94 yrs. Measurements were similarly made in two distant cities, using the single-breath technique. Capillary lung volume (Vc) and membrane conductance, the diffusing capacity of the membrane (Dm), for carbon monoxide (Dm,CO) were derived.The transfer of both gases appeared to depend upon age, height, sex and localisation. The rate of decrease in both transfers increased after the age of 59 yrs. TL,NO/alveolar volume (VA) and TL,CO/VA were only age-dependent. The mean TL,NO/TL,CO was 4.75 and the mean Dm/Vc was 6.17 min ; these parameters were independent of any covariate. Vc and Dm,CO calculations depend upon the choice of coefficients included in the Roughton-Forster equation. Values of 1.97 for Dm,NO/Dm,CO ratio and 12.86 min?kPa -1 for 1/red cell CO conductance are recommended.The scatter of transfer reference values in the literature, including the current study, is wide. The present results suggest that differences might be due to the populations themselves and not the methods alone.KEYWORDS: Ageing, capillary lung volume, carbon monoxide, diffusion, nitric oxide, pollution T he measurement of the transfer of gases through the lung is one of the few tests aimed at investigating alveolar function. The 1957 model and equation of ROUGHTON and FORSTER [1] permitted the transfer of carbon monoxide through the aveolocapillary structure to be split into two resistances, one for the alveolar membrane (1/membrane conductance, the diffusing capacity of the membrane (Dm), for carbon monoxide (Dm,CO)) and the other for the blood reacting with the gas (1/HCOVc), where HCO is the red cell conductance at a concentration, set by the pioneers of the method, of 14.9 g?dL -1 [2] and Vc the capillary lung volume:where TL,CO is the transfer factor of the lung for carbon monoxide. The first technique used to solve this equation with two unknowns, Dm and Vc, was to measure two transfers of CO, one under conditions of normoxia the other under hyperoxia. Breathing O 2 , by reducing HCO, lowers the TL,CO. GUENARD et al.[3] first published measurements of Dm and Vc using transfer factor of the lung for nitric oxide (TL,NO) and TL,CO and assuming HNO to be infinity, i.e. TL,NO5Dm,NO.The transfer of CO is dependant upon both Dm and Vc with HCO as a finite value.The relationship between Dm for nitric oxide (Dm,NO) and Dm,CO introduces a constant a: Dm,NO5aDm,CO. Therefore, the measurement of NO transfer alone permits the calculation of Dm,CO and, by introducing the latter into the CO transfer equation, of Vc.Most published reference values for Dm and Vc have been derived from the first two-step technique; one used the NO/CO method in a population of 127 healthy adults with a mean¡SD age of ,40¡12 yrs [4] and another focused on NO transfer in a population of 1...

The functional work capacity of chronic obstructive pulmonary disease (COPD) patients is usually assessed with walk tests such as the 6-minute walk test (6MWT) or the shuttle test. Because these exercise modalities require a controlled environment which limits their use by pulmonologists and severely restricts their use among general practitioners, different modalities of a short (1 minute or less) sit-to-stand test were recently proposed. In this study, we evaluated a new modality of a semipaced 3-minute chair rise test (3CRT) in 40 patients with COPD, and compared the reproducibility of physiological responses and symptoms during the 3CRT and their interchangeability with the 6MWT. The results demonstrate that physiological variables, heart rate, pulse oxygen saturation, work done, and symptoms (Borg dyspnea and fatigue scores), during the 3CRT were highly reproducible, and that the physiological responses and symptoms obtained during the 3CRT and the 6MWT were interchangeable for most patients. Moreover, these preliminary data suggest that patients able to perform more than 50 rises during 3 minutes had no significant disability. The simplicity and ease of execution of the 3CRT will facilitate the assessment of exercise symptoms and disability in COPD patients during routine consultations with pulmonologists and general practitioners, and will thus contribute to the improved management of COPD patients.

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Some recent studies of competitive athletes have shown exercise-induced hypoxemia to begin in submaximal exercise. We examined the role of ventilatory factors in the submaximal exercise gas exchange disturbance (GED) of healthy men involved in regular work-related exercise but not in competitive activities. From the 38 national mountain rescue workers evaluated (36 +/- 1 yr), 14 were classified as GED and were compared with 14 subjects matched for age, height, weight, and maximal oxygen uptake (VO2 max; 3.61 +/- 0.12 l/min) and showing a normal response (N). Mean arterial PO2 was already lower than N (P = 0.05) at 40% VO2 max and continued to fall until VO2 max (GED: 80.2 +/- 1.6 vs. N: 91.7 +/- 1.3 Torr). A parallel upward shift in the alveolar-arterial oxygen difference vs. %VO2 max relationship was observed in GED compared with N from the onset throughout the incremental protocol. At submaximal intensities, ideal alveolar PO2, tidal volume, respiratory frequency, and dead space-to-tidal volume ratio were identical between groups. As per the higher arterial PCO2 of GED at VO2 max, subjects with an exaggerated submaximal alveolar-arterial oxygen difference also showed a relative maximal hypoventilation. Results thus suggest the existence of a common denominator that contributes to the GED of submaximal exercise and affects the maximal ventilatory response.

We have previously reported a reduction in exercise-induced hypoxaemia following polyunsaturated fatty acid supplementation (PUFA). Although this might have been explained by increases in membrane fluidity, a clear explanation could not be provided due to potentially confounding influences of series-2 prosta- glandin mediated effects resulting from PUFA. In this investigation, ten master athletes [mean age 48.1 (SEM 6) years, maximal oxygen uptake (VO2max) 3.39 (SEM 0.21) l x min(-1)] completed a maximal cycling test (Ctrl) which was repeated after the administration of 150 mg of indomethacin to inhibit prostaglandin synthesis, both before and after 6 weeks of 3.66-g PUFA x day(-1). Cardiorespiratory parameters were obtained simultaneously with brachial arterial blood sampling for partial pressure of oxygen in arterial blood (PaO2), partial pressure of carbon dioxide in arterial blood (PaCO2), pH, oxygen saturation in arterial blood and lactate concentration determinations. A significant decrease in PaO2 (mmHg) from rest [93 (SEM 1.5)] was observed for exercise intensities of more than 40% VO2max in Ctrl reaching 75.9 (SEM 2.1) at VO2max. PUFA resulted in a 5.0 (SEM 0.68) mmHg upward shift (P < 0.05) in the PaO2-oxygen uptake relationship, reducing the difference in partial pressure of oxygen between alveolar air and arterial blood (P(A-a)O2) at VO2max [Ctrl 36 (SEM 1.6) vs PUFA 33 (SEM 2.2) mmHg] while PaCO2, remained unchanged. Indomethacin had no effect on either PaO2, ideal partial pressure of oxygen in alveolar gas or P(A-a)O2 in either Ctrl or after PUFA. In contrast, the fall in pH was significantly reduced after indomethacin while VCO2, PaCO2 and lactacidaemia remained unchanged. These observations confirm an effect of PUFA on exercise PaO2 behaviour which does not appear to be mediated by the influence of a series-2 prostaglandin.