Uncertainties in the adaptation of alpine pastures to climate change based on remote sensing products and modelling.

Over the last century, the management of pastoral systems has undergone major changes to meet the livelihood needs of alpine communities. Faced with the changes induced by recent global warming, the ecological status of many pastoral systems has seriously deteriorated in the western alpine region. We assessed changes in pasture dynamics by integrating information from remote-sensing products and two process-based models, i.e. the grassland-specific, biogeochemical growth model PaSim and the generic crop-growth model DayCent. Meteorological observations and satellite-derived Normalised Difference Vegetation Index (NDVI) trajectories of three pasture macro-types (high, medium and low productivity classes) in two study areas - Parc National des Écrins (PNE) in France and Parco Nazionale Gran Paradiso (PNGP) in Italy - were used as a basis for the model calibration work. The performance of the models was satisfactory in reproducing pasture production dynamics (R2 = 0.52 to 0.83). Projected changes in alpine pastures due to climate-change impacts and adaptation strategies indicate that: i) the length of the growing season is expected to increase between 15 and 40 days, resulting in changes in the timing and amount of biomass production, ii) summer water stress could limit pasture productivity; iii) earlier onset of grazing could enhance pasture productivity; iv) higher livestock densities could increase the rate of biomass regrowth, but major uncertainties in modelling processes need to be considered; and v) the carbon sequestration potential of pastures could decrease under limited water availability and warming.

Effects of unsupported arm training on arm exercise-related perception in COPD patients.

We hypothesized that arm training might affect unsupported arm exercise-related perception by decreasing motor output to arm/torso muscles in patients with chronic obstructive pulmonary disease (COPD). Eleven patients were studied at 80% of peak incremental arm exercise, before and after unsupported arm training. Training increased endurance time, decreased respiratory effort and much more arm effort (by Borg scale) without affecting chest wall dynamic hyperinflation or configuration. Ventilatory response to carbon dioxide output was the same before and after training so that at isotime the reduction in ventilation correlated strongly with a simultaneous reduction in metabolic output. These changes reflect a reduced ventilatory drive. We conclude that: (i) a reduced level of ventilation, relative to a decrease in central motor output, is the contribution of arm training to symptom alleviation during unsupported arm exercise in COPD patients, and (ii) arm training improved patients' exercise-related perception without affecting chest wall operational volumes or configuration.

Chest wall kinematics, respiratory muscle action and dyspnoea during arm vs. leg exercise in humans.

AIM: We hypothesize that different patterns of chest wall (CW) kinematics and respiratory muscle coordination contribute to sensation of dyspnoea during unsupported arm exercise (UAE) and leg exercise (LE). METHODS: In six volunteer healthy subjects, we evaluated the volumes of chest wall (V(cw)) and its compartments, the pulmonary apposed rib cage (V(rc,p)), the diaphragm-abdomen apposed rib cage (V(rc,a)) and the abdomen (V(ab)), by optoelectronic plethysmography. Oesophageal, gastric and trans-diaphragmatic pressures were simultaneously measured. Chest wall relaxation line allowed the measure of peak rib cage inspiratory muscle, expiratory muscle and abdominal muscle pressures. The loop V(rc,p)/V(rc,a) allowed the calculation of rib cage distortion. Dyspnoea was assessed by a modified Borg scale. RESULTS: There were some differences and similarities between UAE and LE. Unlike LE with UAE: (i) V(cw) and V(rc,p) at end inspiration did not increase, whereas a decrease in V(rc,p) contributed to decreasing CW end expiratory volume; (ii) pressure production of inspiratory rib cage muscles did not significantly increase from quiet breathing. Not unlike LE, the diaphragm limited its inspiratory contribution to ventilation with UAE with no consistent difference in rib cage distortion between UAE and LE. Finally, changes in abdominal muscle pressure, and inspiratory rib cage muscle pressure predicted 62% and 41.4% of the variability in Borg score with UAE and LE, respectively (P < 0.01). CONCLUSION: Leg exercise and UAE are associated with different patterns of CW kinematics, respiratory muscle coordination, and production of dyspnoea.

Mechanisms of dyspnoea and its language in patients with asthma.

This study hypothesises that regardless of the global score of dyspnoea intensity, different descriptors may be selected by asthmatic patients during short cardiopulmonary exercise test (sCPET) and methacholine (Mch) inhalation. It also examines whether different qualitative dyspnoea sensations can help explain the underlying mechanisms of the symptom. Minute ventilation (V'E), tidal volume (VT) and inspiratory capacity (IC) were measured in 22 stable asthmatic patients, and the sensation of dyspnoea during Mch inhalation and sCPET was quantitatively (Borg scale) and qualitatively (descriptors) assessed. The work rate and oxygen uptake (V'O2) were also measured during sCPET. Airway obstruction and hyperinflation, as measured by IC reduction, were the best correlates for dyspnoea with Mch. During sCPET, changes in WR, V'O2, V'E and VT significantly correlated with Borg score, with V'E being the best predictor of dyspnoea; IC decreased in eight patients. Furthermore, chest tightness (68%) was the highest reported descriptor during Mch inhalation, whereas work/effort (72%) was the highest during sCPET. In conclusion, obstruction/hyperinflation and work rate are highly reliable predictors of Borg rating of dyspnoea during methacholine inhalation and short cardiopulmonary exercise testing, respectively. Regardless of the global score of intensity dyspnoea, different descriptors may be selected by patients during short cardiopulmonary exercise testing and methacholine inhalation. Various qualities of dyspnoea result from different pathophysiological abnormalities.

Understanding dyspnoea by its language.

Dyspnoea is a general term used to characterise a range of qualitatively distinct descriptors that vary in intensity. Based on the hypothesis that various qualities of respiratory discomfort result from different pathophysiological abnormalities, language could help to define one or more of the abnormalities responsible for breathing discomfort. The use of descriptors of dyspnoea may contribute to the understanding of the mechanisms of dyspnoea, and assist in identifying or predicting a specific diagnosis. Symptoms that can be reliably discriminated imply different pathophysiological mechanisms, whereas symptoms that cannot be reliably discriminated imply similar pathophysiological mechanisms. Since dyspnoea is a fundamental part of patient's clinical history, physicians should become more fluent in the language of dyspnoea.

Measures of perception of bronchoconstriction and clinical and functional data are not interrelated in asthma.

BACKGROUND: Sensitivity and absolute perceptual magnitude characterize the perception of bronchoconstriction (PB). OBJECTIVES: To define whether clinical and functional characteristics and level of bronchial hyperresponsiveness (BHR) correlate with these two PB indexes during bronchial challenge in asthma. METHODS: PB on both the Borg scale and the visual-analogue scale (VAS) was assessed in 45 consecutive asthmatics during a methacholine-induced decrease in forced expiratory volume in 1 s (FEV(1)) and specifically quantified as Borg and VAS slope, as a measure of sensitivity, whereas scores at a 20% FEV(1) decrease (PB(20)) were assessed as a measure of absolute perceptual magnitude. Clinical score and BHR were also assessed. RESULTS: PB(20) related to slope on both the Borg scale and the VAS (p < 0.0001). PB(20) and slope related neither to clinical score nor to baseline functional data on both scales. The relationship between the level of BHR and PB(20) on either scale was of questionable clinical significance (r(2) = 7%). CONCLUSIONS: Irrespective of the scale employed, our data indicate the need for directly assessing PB rather than deriving it from clinical and functional data and level of BHR.

Dyspnea, respiratory function and sputum profile in asthmatic patients during exacerbations.

Dyspnea is often used as a marker of asthma severity although a wide variation in dyspnea perception associated with bronchoconstriction (PB) has been described in asthmatic patients. Our hypothesis is that changes of airway inflammation, airway narrowing and hyperinflation may account for a part of the variability of breathlessness in spontaneous asthma attack. In asthmatic patients with exacerbation of the disease, we evaluated respiratory function, dyspnea (using visual Analogue Scale--VAS) and peak expiratory flow (PEF) values and variability (amplitude % mean), and sputum cellular and biochemical profile before (day I) and after (day II) therapy with i.v. corticosteroids and inhaled beta2-agonists, as appropriate. By day II, forced expiratory volume in 1 s (FEV1), inspiratory capacity (IC), PEF or VAS values and variability, sputum eosinophils and eosinophilic cationic protein (ECP) had improved. Improvement of dyspnea expressed as a decrease in VAS and reduction in variability of dyspnea sensation significantly correlated with increase in FEV1 %predicted value (%pv) (P=0.03; p=0.72 and P=0.02; p=0.74, respectively). No significant correlation was found between IC and VAS either in absolute values or as changes from days I and II, nor between sputum outcomes and PEF or VAS, regardless of how they were measured. We conclude that in acute asthmatic patients, dyspnea measurement, functional measurements and sputum analysis may be useful in monitoring disease activity, response to therapy and can provide different information on the state of the disease.

Chest wall kinematics during chemically stimulated breathing in healthy man.

Chest wall compartment kinematics and respiratory muscle coordinate activity, during either hypercapnia or hypoxia, have not been comparatively assessed in healthy humans. We assessed the displacement volume of the chest wall (Vcw) in 5 normal subjects during hypoxic-normocapnic and hypercapnic-hyperoxic rebreathing by using linearized magnetometers. Vcw was divided into displacement volumes of the rib cage (Vrc) and the abdomen (Vab). Esophageal (Pes) and gastric (Pga) pressures were simultaneously recorded and transdiaphragmatic pressure (Pdi) was calculated by subtracting Pes from Pga. Pressure swings (sw) from end expiration (EE) to end inspiration (EI) were also calculated. During both hypoxia and hypercapnia, from quiet breathing to 40 L/min VE, Vrc,EI increased consistently but Vrc,EE, and Vab,EI did not. Moreover, Vab,EE decreased significantly during hypercapnia and remained unchanged during hypoxia. PesEI decreased (more negative values) and PesEE increased (less negative values) during either stimulus, while PgaEE increased with hypercapnia. Pdisw, calculated as the difference between PdiEE and PdiEI, increased significantly with both hypercapnia and hypoxia ( p = 0.002 for both). On the plot of Pes vs Pga, the slope of a line from end expiratory to end inspiratory lung volume between 20 and 40 L/min VE progressively increased during hypercapnia indicating increasing rib cage muscle (RCM) contribution to inspiratory pressure swings relative to the diaphragm. From these results we conclude that in healthy man: (i) with both chemical stimuli RCM contribution accounts for increase in Vrc displacement; (ii) with hypercapnia, the decrease in Vab,EE displacement indicates abdominal muscle (ABM) contribution to tidal volume; (iii) RCM and ABM assist the diaphragmatic function during hypercapnic stimulation.

Perception of bronchoconstriction in smokers with airflow limitation.

To our knowledge, no data have been provided as to whether and to what extent dynamic hyperinflation, through its deleterious effect on inspiratory muscle function, affects the perception of dyspnoea during induced bronchoconstriction in patients with chronic airflow obstruction. We hypothesized that dynamic hyperinflation accounts in part for the variability in dyspnoea during acute bronchoconstriction. We therefore studied 39 consecutive clinically stable patients whose pulmonary function data were as follows (% of predicted value): vital capacity (VC), 97.8% (S.D. 16.0%); functional residual capacity, 105.0% (18.8%); actual forced expiratory volume in 1 s (FEV(1))/VC ratio, 56.1% (6.3%). Perception of dyspnoea using the Borg scale was assessed during a methacholine-induced fall in FEV(1). The clinical score and the treatment score, the level of bronchial hyper-responsiveness and the cytological sputum differential count were also assessed. In each patient, the percentage fall in FEV(1) and the concurrent Borg rating were linearly related, with the mean slope (PD slope) being 0.09 (0.06). The percentage fall in FEV(1) accounted for between 41% and 94% of the variation in the Borg score. At a 20% fall in FEV(1), the decrease in inspiratory capacity (Delta IC) was 0.156 (0.050) litres. Patients were divided into three subgroups according to the PD slope (arbitrary units/% fall in FEV(1)): subgroup I [eight hypoperceivers; PD slope 0.026 (0.005)], subgroup II [26 moderate perceivers; 0.090 (0.037)] and subgroup III [five hyperperceivers; 0.200 (0.044)]. By applying stepwise multiple regression analysis with the PD slope as the dependent variable, and other characteristics (demographic, clinical and functional characteristics, smoking history, level of bronchial hyper-responsiveness and sputum cytological profile) as independent variables, Delta IC (r(2)=45%, P<0.00001) and to a lesser extent treatment score (r(2)=17.3%, P<0.0006), and to an even lesser extent age (r(2)=3%, P<0.05), independently predicted a substantial amount (r(2)=65.27%, P<0.00001) of the variability in the Borg slope. Thus acute hyperinflation, and to a lesser extent treatment score and age, account in part for the variability in the perception of dyspnoea after accounting for changes in FEV(1) during bronchoconstriction in patients with chronic airflow obstruction.

Do inhaled corticosteroids affect perception of dyspnea during bronchoconstriction in asthma?

BACKGROUND: Some of the disagreements on the perception of dyspnea (PD) during bronchoconstriction in asthma patients could depend on the interrelationships among the following: (1) the influence of baseline airflow obstruction on the patient's ability to detect any further increase in airway resistance; (2) the effect of eosinophilic inflammation on the airway; (3) bronchial hyperresponsiveness (BHR); and (4) the effect of inhaled corticosteroids (ICSs). OBJECTIVE: We hypothesized that if the inflammation of the airway wall influences to some extent and in some way the PD in asthma patients, ICSs reverse the effect of airway inflammation on the PD. METHODS: We studied 100 asthma patients who were divided into the following four groups: patients with obstruction who were either ICS-naive (group I) or were treated with ICSs (group II); and nonobstructed patients who were either ICS-naive (group III) or were treated with ICSs (group IV). PD on the visual analog scale (VAS) was assessed during a methacholine-induced FEV(1) decrease and specifically was quantified as the VAS slope and score at an FEV(1) decrease of 5 to 20%. BHR was assessed in terms of the provocative concentration of methacholine causing a 20% fall in FEV(1) (PC(20)). Eosinophil counts in induced sputum samples also were performed. Regression analysis, univariate analysis of variance, and factor analysis were applied for statistical evaluation. RESULTS: For a 5 to 20% fall in FEV(1) from the lowest point after saline solution induction, VAS score was lowest in group II, slightly higher in group I, slightly higher still in group IV, and the highest in group III. In the patients as a whole, BHR related to PD, but age, clinical score, duration of the disease, and presence of baseline airway obstruction did not. In patients with obstruction who were treated with ICSs, eosinophil counts related to PD negatively. Factor analysis yielded the following four factors that accounted for 70% of the variance in the data: ICS; eosinophil counts; FEV(1); and PC(20) loaded on separated factors with PD loading on the same factors as PC(20). The post hoc analysis carried out dividing the patients into ICS-treated and ICS-naive, showed that in the former group eosinophil counts and BHR proved to be factors negatively associated with PD, while in the latter group eosinophil counts were positively associated with PD. CONCLUSIONS: We have shown that eosinophilic inflammation of the airway wall may increase PD and that the association of eosinophil counts with ICSs may result in lessening the PD.

Pharmacological treatment of exercise dyspnoea.

A better understanding of the mechanisms of dyspnoea improves the clinician's ability to treat patients with shortness of breath. Any intervention that: 1) reduces ventilatory demands; 2) reduces ventilatory impedance; or 3) improves inspiratory muscle function, may relieve dyspnoea. Reduced ventilatory demand may be obtained by reducing metabolic load. Supplemental oxygen during exercise reduces exertional breathlessness and improves exercise tolerance, the decrease in dyspnoea being proportional to decrease in minute ventilation. Reduced ventilatory demand may also be obtained by decreasing the central drive. Opiates have been shown to decrease minute ventilation at rest and during submaximal exercise. They can alter the central processing of neural signals within the central nervous system to reduce sensations associated with breathing. Contrastingly, no consistent improvement in dyspnoea (versus placebo) has been shown with anxolytics. Decreasing central drive may also be obtained by altering pulmonary afferent information. Interventions that alter transmittal of afferent information to the central controller, potentially reduce dyspnoea. Reduction of ventilatory impedance is obtained by administering B2, anticholinergics or theophylline. B2 and anticholinergics act by modulating the increase in operational lung volumes and the inspiratory muscle effort during exercise. The mechanism by which theophylline relieves dyspnoea is probably related to a mechanism other than its bronchodilation alone. Alterations in respiratory muscle function are currently being detected in patients with chronic obstructive pulmonary disease, due to alteration in respiratory muscle energy balance. Nutritional repletion may improve respiratory muscle function but uncertainty remains as to whether nutritional repletion may relieve dyspnoea. The cumulative benefit of interventions targeting the pathophysiologic mechanism of dyspnoea must be identified for optimum treatment of patients with shortness of breath.

Relevance of dyspnoea and respiratory function measurements in monitoring of asthma: a factor analysis.

Previous studies in patients with stable chronic obstructive pulmonary disease have demonstrated that objective measures (lung volumes and respiratory muscle force) and clinical or subjective measures (symptoms of breathlessness and exercise tolerance) are quantities that independently characterize the conditions of these patients. Such an evaluation has not been previously applied in patients with stable bronchial asthma. Sixty-nine patients with stable chronic asthma underwent evaluation of static (functional residual capacity, FRC) and dynamic [forced expiratory volume in 1 sec (FEV1) and forced vital capacity, FVC] lung volumes; respiratory muscle strength (RMS), by measuring maximal inspiratory and expiratory pressures, and exercise capacity by means of the 6-min walking distance (6MWD). Chronic exertional dyspnoea was assessed by the Baseline Dyspnoea Index (BDI) focal score and by the Medical Research Council (MRC) scale. Statistical evaluation was performed by applying factor analysis. Three factors accounted for 78% of the total variance in the data: FEV1, FVC loaded on a factor I; RMS, FRC and 6MWD loaded on a factor II; dyspnoea ratings loaded on a factor III. Post-hoc analysis by randomly dividing the patients into two subgroups gave the same results. In asthmatic patients, airway obstruction appeared as an independent dimension or factor. Dyspnoea independently characterized the condition of asthma. Submaximal exercise tolerance could not be associated with the symptom of breathlessness. Evidence of independent factors support the validity of routine, multi-factorial assessment and the primary goal of treatment to alleviate symptoms and improve functional capacity in stable asthmatics.

Mechanisms involved in airway obstruction: the role of smooth muscle.

Structural changes in the airway walls that are probably driven by mediators released as a consequence of chronic allergic inflammation are prominent features of asthma. However, it is not clear how each of the many changes that occur in the airway wall contribute to altered airway function in asthma. Collagen deposition in the subepithelial matrix, around and inside the smooth muscle, would be expected to oppose the effect of smooth-muscle contraction. Conversely, geometric factors would result in exaggerated airway narrowing for a given degree of smooth-muscle shortening; decreased airway wall stiffness and increased airway narrowing for a given amount of force generated by the smooth muscle. Degradation of the matrix may alter the coupling between muscle and lung recoil, allowing exaggerated smooth-muscle shortening. Increase in muscle mass associated with preservation of its contractile capacity could be the most important contributor to exaggerated airway narrowing.

Perception of bronchoconstriction and bronchial hyper-responsiveness in asthma.

The inter-relationship between the perception of bronchoconstriction, bronchial hyper-responsiveness and temporal adaptation in asthma is still a matter of debate. In a total of 52 stable asthmatic patients, 32 without airway obstruction ¿forced expiratory volume in 1 s (FEV(1))/vital capacity (VC) 84.1% (S.D. 7.9%), and 20 with airway obstruction [FEV(1)/VC 60% (4%)], we assessed the perception of bronchoconstriction during methacholine inhalation by using: (i) the slope and intercept of the Borg and VAS (Visual Analog Scale) scores against the decrease in FEV(1), expressed as a percentage of the predicted value; and (ii) the Borg and VAS scores at a 20% decrease in FEV(1) from the lowest post-saline level (PB(20)). Bronchial hyper-responsiveness was assessed as the provocative concentration of methacholine causing a 20% fall in FEV(1) (PC(20)FEV(1)). The reduction in FEV(1) was significantly related to the Borg and VAS scores, with values for the group mean slope and intercept of this relationship of 0.13 (S.D. 0.08) and -1.1 (3.02) for Borg, and 1.5 (1.19) and -12.01 (35) for VAS. PB(20) was 3 (1.75) with Borg scores and 34.6 (20.5) with VAS scores. Compared with the subgroup without airway obstruction, the obstructed subgroup exhibited similar slopes, but lower Borg and VAS intercepts. For similar decreases in FEV(1) (5-20% decreases from the lowest post-saline values), the Borg and VAS scores were lower in the non-obstructed than in the obstructed subgroup. PC(20)FEV(1) was significantly related to both Borg PB(20) and VAS PB(20) when considering all patients. When assessing the subgroups, PC(20)FEV(1) was related to Borg PB(20) and VAS PB(20) in the non-obstructed subjects, but not in the obstructed subjects. In neither subgroup was the log of the cumulative dose related to the Borg and VAS scores at the end of the test. We conclude that, unlike in previous studies, the ability to perceive acute bronchoconstriction may be reduced as background airflow obstruction increases in asthma. Bronchial hyper-responsiveness did not play a major role in perceived breathlessness in patients without airway obstruction, and even less of a role in patients with obstruction. The cumulative dose of agonist did not appear to influence the perception of bronchoconstriction.

Reduction in bronchodilation following a deep inhalation is poorly related to airway inflammation in asthma.

In patients with bronchial asthma, forced expiratory flows are differently sensitive to a previous volume history. A reduced ability of a deep inhalation (DI) to dilate obstructed airways has been hypothesized to be a physiological marker for the degree of airway responsiveness and to relate to the presence and magnitude of inflammation in the lung, even in mild stable asthma. However, there are at present doubts as to whether functional changes could be used as a substitute for airway inflammation studies. In order to investigate the interrelations among airway inflammation, bronchial hyperresponsiveness and effects of volume history, 58 consecutive asthmatics with mild to moderate asthma were studied. The effects of DI were assessed as the isovolumic ratio of flows from forced expiratory manoeuvres started from maximal (M) or partial (P) lung inflation. Airway inflammation was assessed by using induced sputum. Sputum was analysed for total and differential cell counts, and levels of eosinophil cationic protein (ECP) which reflects eosinophil activation. Airway responsiveness was assessed as the provocative concentration of histamine which caused a 20% fall in forced expiratory volume in one second (FEV1) from control (PC20). The M/P ratio was significantly related to ECP (r=-0.31, p<0.03) and eosinophils (r=-0.29, p<0.03), FEV1/vital capacity (VC) (r=0.32; p<0.01), clinical score (r=-0.33; p<0.03) and age (r=-0.41; p<0.0001). In a stepwise multiple regression analysis including age, score, baseline lung function, ECP, number of eosinophils and the response to beta2-agonist, age (p<0.037) predicted a small amount of the variance in M/P ratio (r2=0.12). It is concluded that volume history response is substantially independent of both sputum outcomes (inflammatory cell number and eosinophil cationic protein) and bronchial hyperresponsiveness; rather it seems to be associated with anthropometric characteristics. Functional aspects do not provide information on eosinophilic, probably central, airway inflammation.

Respiratory muscles in internal medicine.

This review provides evidence that respiratory muscle abnormalities are present in many illnesses of internal medicine and emphasizes that clinicians should look for respiratory muscle weakness in many circumstances, particularly immunological disorders. Controversial results in hormonal diseases, metabolic diseases and abdominal disorders indicate areas for further research.

Do sputum eosinophils and ECP relate to the severity of asthma?

There is much evidence that eosinophils play an important role in bronchial epithelial damage in asthma by releasing cationic proteins. However, the extent to which eosinophil inflammation relates to indices of asthma severity in chronic stable asthma is still a matter of debate. We studied 46 clinically stable patients with mild to severe chronic asthma (forced expiratory volume in one second (FEV1) 50-126% of predicted value). The clinical severity of asthma was graded from 1 to 4 according to the Aas scoring system. Twelve normal subjects were also studied as controls. Induction of sputum was performed by hypertonic saline to determine differential cell count, and eosinophil cationic protein (ECP) by the so-called "plug technique". The concentration of ECP was measured by a fluoroimmunoassay. Bronchial hyperresponsiveness was recorded by inhaling progressive concentrations of histamine, and the concentration that caused a 20% decrease in FEV1 (PC20) was calculated. Sputum eosinophils (range 0-61%), sputum ECP (range 24-10,800 microg x L[-1]) and serum ECP (range 4-61 microg x L[-1]) were significantly greater in asthmatics than in normal subjects, and distinguished the most severe group with the highest Aas score from the others. Sputum eosinophils and sputum ECP were strongly related to each other. The relationships between sputum or serum ECP and PC20 (range 0.016-7.5 mg x mL[-1]), and between sputum ECP and FEV1 were found to be weak. In conclusion, sputum outcomes of eosinophil activation and serum eosinophilic cationic protein appear to be useful indicators of disease. They do not accurately reflect current clinical or functional indices of asthma severity in chronic stable patients, and might therefore provide complementary data disease monitoring.