BackgroundThe 1-minute sit-to-stand (STS) test could be valuable to assess the level of exercise tolerance in chronic obstructive pulmonary disease (COPD). There is a need to provide the minimal important difference (MID) of this test in pulmonary rehabilitation (PR).MethodsCOPD patients undergoing the 1-minute STS test before PR were included. The test was performed at baseline and the end of PR, as well as the 6-minute walk test, and the quadriceps maximum voluntary contraction (QMVC). Home and community-based programs were conducted as recommended. Responsiveness to PR was determined by the difference in the 1-minute STS test between baseline and the end of PR. The MID was evaluated using distribution and anchor-based methods.ResultsForty-eight COPD patients were included. At baseline, the significant predictors of the number of 1-minute STS repetitions were the 6-minute walk distance (6MWD) (r=0.574; P<10−3), age (r=−0.453; P=0.001), being on long-term oxygen treatment (r=−0.454; P=0.017), and the QMVC (r=0.424; P=0.031). The multivariate analysis explained 75.8% of the variance of 1-minute STS repetitions. The improvement of the 1-minute STS repetitions at the end of PR was 3.8±4.2 (P<10−3). It was mainly correlated with the change in QMVC (r=0.572; P=0.004) and 6MWD (r=0.428; P=0.006). Using the distribution-based analysis, an MID of 1.9 (standard error of measurement method) or 3.1 (standard deviation method) was found. With the 6MWD as anchor, the receiver operating characteristic curve identified the MID for the change in 1-minute STS repetitions at 2.5 (sensibility: 80%, specificity: 60%) with area under curve of 0.716.ConclusionThe 1-minute STS test is simple and sensitive to measure the efficiency of PR. An improvement of at least three repetitions is consistent with physical benefits after PR.

Background: Sit-to-stand tests (STST) have recently been developed as easy-to-use field tests to evaluate exercise tolerance in COPD patients. As several modalities of the test exist, this review presents a synthesis of the advantages and limitations of these tools with the objective of helping health professionals to identify the STST modality most appropriate for their patients. Method: Seventeen original articles dealing with STST in COPD patients have been identified and analysed including eleven on 1min-STST and four other versions of the test (ranging from 5 to 10 repetitions and from 30 s to 3 min). In these studies the results obtained in sit-to-stand tests and the recorded physiological variables have been correlated with the results reported in other functional tests. Results: A good set of correlations was achieved between STST performances and the results reported in other functional tests, as well as quality of life scores and prognostic index. According to the different STST versions the processes involved in performance are different and consistent with more or less pronounced associations with various physical qualities. These tests are easy to use in a home environment, with excellent metrological properties and responsiveness to pulmonary rehabilitation, even though repetition of the same movement remains a fragmented and restrictive approach to overall physical evaluation. Conclusions: The STST appears to be a relevant and valid tool to assess functional status in COPD patients. While all versions of STST have been tested in COPD patients, they should not be considered as equivalent or interchangeable.

Parasympathetic respiratory control and nonautonomic mechanisms may influence the HF-peak shift during strenuous exercise. HRV and the usual indexes of sympathetic activity do not accurately reflect changes in autonomic modulation during exhaustive exercise.

No abstract

Using simultaneous nitric oxide and carbon monoxide lung transfer measurements (T LNO and T LCO ), the membrane transfer capacity (D m ) and capillary lung volume (V c ) as well as the dimensionless ratio T LNO /T LCO can be calculated. The significance of this ratio is yet unclear. Theoretically, the T LNO /T LCO ratio should be inversely related to the product of both lung alveolar capillary membrane (μ) and blood sheet thicknesses (K ). NO and CO transfers were measured in healthy subjects in various conditions likely to be associated with changes in K and/or μ. Experimentally, deflation of the lung from 7.4 to 4.8 l decreased the T LNO /T LCO ratio from 4.9 to 4.2 (n = 25) which was consistent mainly with a thickening of the blood sheet. Compared with continuous negative pressure breathing, continuous positive pressure breathing increased this ratio suggesting a thinning of the capillary sheet. It was also observed with 12 healthy subjects that slight haemodilution that may thicken the blood sheet decreased the T LNO /T LCO ratio from 4.85 to 4.52. In conclusion, the T LNO /T LCO ratio is related to the thickness of the alveolar blood barrier. This ratio provides novel information for the analysis of the diffusion properties. Diffusion of gases between the alveolar space of the lung and blood is usually described with Roughton and Forster's model (Forster et al. 1957). In this model, key factors affecting gas transfer include two components: (a) the membrane which is supposed to be homogenous and characterized by its conductance (D m ) and (b) the product of red cell conductance for a given gas (θ ) and pulmonary capillary volume (V c ). D m is considered to be an independent variable to V c .In order to calculate D m and V c the NO/CO transfer method (T LNO /T LCO ) was introduced in the lung function testing of humans in 1987 (Guénard et al. 1987). As the in vivo conductance of NO in blood is very high, the only limitation to its transfer through the barrier is the membrane. CO transfer (T LCO ) depends on D m , V c and haemoglobin concentration. T LCO also varies with pulmonary capillary oxygen tension since θ CO is inversely proportional to this pressure. The ratio of NO to CO transfer (T LNO /T LCO ) should therefore provide some insight into the relative properties of the membrane and capillaries.The surface area of the alveolar membrane and capillary are identical or closely related and by consequence, D m and V c should be directly correlated. The hypothesis of this study is based on the assumption that V c and D m are dependent parameters.Under this assumption, this study is designed to identify the significance of the T LNO /T LCO ratio through both theoretical and experimental approaches with the expectations that the new model would be relevant for physiological or clinical purposes. Specifically, we have shown that the T LNO /T LCO ratio is independent of membrane surface area and inversely proportional to the product of alveolar membrane and capillary blood layer thicknesses. Methods Theoretica...

de Bisschop C, Martinot J, Leurquin-Sterk G, Faoro V, Guénard H, Naeije R. Improvement in lung diffusion by endothelin A receptor blockade at high altitude. J Appl Physiol 112: 20 -25, 2012. First published October 6, 2011 doi:10.1152/japplphysiol.00670.2011.-Lung diffusing capacity has been reported variably in high-altitude newcomers and may be in relation to different pulmonary vascular resistance (PVR). Twenty-two healthy volunteers were investigated at sea level and at 5,050 m before and after random double-blind intake of the endothelin A receptor blocker sitaxsentan (100 mg/day) vs. a placebo during 1 wk. PVR was estimated by Doppler echocardiography, and exercise capacity by maximal oxygen uptake (V O2 max). The diffusing capacities for nitric oxide (DLNO) and carbon monoxide (DLCO) were measured using a single-breath method before and 30 min after maximal exercise. The membrane component of DLCO (Dm) and capillary volume (Vc) was calculated with corrections for hemoglobin, alveolar volume, and barometric pressure. Altitude exposure was associated with unchanged DLCO, DLNO, and Dm but a slight decrease in Vc. Exercise at altitude decreased DLNO and Dm. Sitaxsentan intake improved V O2 max together with an increase in resting and postexercise DLNO and Dm. Sitaxsentan-induced decrease in PVR was inversely correlated to DLNO. Both DLCO and DLNO were correlated to V O2 max at sea level (r ϭ 0.41-0.42, P Ͻ 0.1) and more so at altitude (r ϭ 0.56 -0.59, P Ͻ 0.05). Pharmacological pulmonary vasodilation improves the membrane component of lung diffusion in high-altitude newcomers, which may contribute to exercise capacity. altitude; hypoxia; lung diffusion; gas exchange; exercise capacity; pulmonary vascular resistance; pulmonary capillary pressure; pulmonary hypertension BOTH THE MEMBRANE AND THE capillary components of lung diffusing capacity have been shown to be increased in highaltitude residents (10,13,15,25). Increased lung diffusing capacity at high altitude allows for the preservation of gas exchange in the presence of a decreased ventilatory response at exercise (15). High-altitude newcomers do not benefit from this adaptation (10,15,25) and, accordingly, depend on increased ventilation to maintain pulmonary gas exchange (15,45).Previous studies on lung diffusing capacity at high altitudes calculated the membrane and capillary components of alveolocapillary transfer of carbon monoxide (CO) using measurements at ambient air and increased inspired PO 2 (10,13,15,25). This approach rests on the PO 2 dependence of , the blood's specific transfer conductance of CO, in the Roughton and Forster equation, which states that 1/DL CO ϭ 1/Dm ϩ 1/ Vc where DL CO is the diffusing capacity of the lung for CO, Dm its membrane component, and Vc the capillary blood volume (37). Thus changing as by increasing or decreasing inspired PO 2 allows for the calculation of Dm and Vc from a simple system of two equations with two unknowns. However, changing inspired PO 2 might also change pulmonary vascular tone, cardiac output, ...

It has been suggested that increased pulmonary vascular reserve, as defined by reduced pulmonary vascular resistance (PVR) and increased pulmonary transit of agitated contrast measured by echocardiography, might be associated with increased exercise capacity. Thus, at altitude, where PVR is increased because of hypoxic vasoconstriction, a reduced pulmonary vascular reserve could contribute to reduced exercise capacity. Furthermore, a lower PVR could be associated with higher capillary blood volume and an increased lung diffusing capacity. We reviewed echocardiographic estimates of PVR and measurements of lung diffusing capacity for nitric oxide (DL(NO)) and for carbon monoxide (DL(CO)) at rest, and incremental cardiopulmonary exercise tests in 64 healthy subjects at sea level and during 4 different medical expeditions at altitudes around 5000 m. Altitude exposure was associated with a decrease in maximum oxygen uptake (VO2max), from 42±10 to 32±8 mL/min/kg and increases in PVR, ventilatory equivalents for CO2 (V(E)/VCO2), DL(NO), and DL(CO). By univariate linear regression VO2max at sea level and at altitude was associated with V(E)/VCO2 (p<0.001), mean pulmonary artery pressure (mPpa, p<0.05), stroke volume index (SVI, p<0.05), DL(NO) (p<0.02), and DL(CO) (p=0.05). By multivariable analysis, VO2max at sea level and at altitude was associated with V(E)/VCO2, mPpa, SVI, and DL(NO). The multivariable analysis also showed that the altitude-related decrease in VO2max was associated with increased PVR and V(E)/VCO2. These results suggest that pulmonary vascular reserve, defined by a combination of decreased PVR and increased DL(NO), allows for superior aerobic exercise capacity at a lower ventilatory cost, at sea level and at high altitude.

Tibetans have been reported to present with a unique phenotypic adaptation to high altitude characterized by higher resting ventilation and arterial oxygen saturation, no excessive polycythemia, and lower pulmonary arterial pressures (Ppa) compared with other high-altitude populations. How this affects exercise capacity is not exactly known. We measured aerobic exercise capacity during an incremental cardiopulmonary exercise test, lung diffusing capacity for carbon monoxide (DL(CO)) and nitric oxide (DL(NO)) at rest, and mean Ppa (mPpa) and cardiac output by echocardiography at rest and at exercise in 13 Sherpas and in 13 acclimatized lowlander controls at the altitude of 5,050 m in Nepal. In Sherpas vs. lowlanders, arterial oxygen saturation was 86 ± 1 vs. 83 ± 2% (mean ± SE; P = nonsignificant), mPpa at rest 19 ± 1 vs. 23 ± 1 mmHg (P < 0.05), DL(CO) corrected for hemoglobin 61 ± 4 vs. 37 ± 2 ml · min(-1) · mmHg(-1) (P < 0.001), DL(NO) 226 ± 18 vs. 153 ± 9 ml · min(-1) · mmHg(-1) (P < 0.001), maximum oxygen uptake 32 ± 3 vs. 28 ± 1 ml · kg(-1) · min(-1) (P = nonsignificant), and ventilatory equivalent for carbon dioxide at anaerobic threshold 40 ± 2 vs. 48 ± 2 (P < 0.001). Maximum oxygen uptake was correlated directly to DL(CO) and inversely to the slope of mPpa-cardiac index relationships in both Sherpas and acclimatized lowlanders. We conclude that Sherpas compared with acclimatized lowlanders have an unremarkable aerobic exercise capacity, but with less pronounced pulmonary hypertension, lower ventilatory responses, and higher lung diffusing capacity.