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Background: The Global Initiative for Obstructive Lung Disease (GOLD) does not promote diffusing capacity for carbon monoxide (Dlco) values in the evaluation of COPD. In GOLD spirometric stage I COPD patients, the clinical and prognostic impact of a low Dlco has not been explored.Research Question: Could a Dlco threshold help define an increased risk of death and a different clinical presentation in these patients?Study Design and Methods: GOLD stage I COPD patients (n = 360) were enrolled and followed over 109 ± 50 months. Age, sex, pack-years' history, BMI, dyspnea, lung function measurements, exercise capacity, BODE index, and history of exacerbations were recorded. A cutoff value for Dlco was identified for all-cause mortality and the clinical and physiological characteristics of patients above and below the threshold compared. Cox regression analysis explored the predictive power of that cutoff value for all-cause mortality.Results: A Dlco cutoff value of <60% predicted was associated with all-cause mortality (Dlco ≥ 60%: 9% vs Dlco < 60%: 23%, P = .01). At a same FEV1% predicted and Charlson score, patients with Dlco < 60% had lower BMI, more dyspnea, lower inspiratory capacity (IC)/total lung capacity (TLC) ratio, lower 6-min walk distance (6MWD), and higher BODE. Cox multiple regression analysis confirmed that after adjusting for age, sex, pack-years history, smoking status, and BMI, a Dlco < 60% is associated with all-cause mortality (hazard ratio [HR], 95% CI = 3.37, 1.35-8.39; P = .009) INTERPRETATION: In GOLD I COPD patients, a Dlco < 60% predicted is associated with increased risk of death and worse clinical presentation. What the cause(s) of this association are and whether they can be treated need to be determined. [ABSTRACT FROM AUTHOR]

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Context: Breast cancer survivors often experience activity-related dyspnea and exercise intolerance, but the underlying mechanisms remain unknown.Objectives: We evaluated physiological contributors to reduced peak oxygen uptake (VO2), with particular attention to the role of respiratory impairment.Methods: We compared symptom assessments, respiratory and peripheral muscle strength, pulmonary function, and ventilatory responses to symptom-limited incremental treadmill exercise in 29 women who had survived breast cancer and 29 age-matched healthy controls.Results: Peak VO2 was reduced more than 20%, on average, in the cancer group compared with controls (P < 0.001). Slopes of dyspnea intensity ratings over ventilation or VO2 were >50% greater in the cancer group compared to controls (P < 0.05). Women with breast cancer had lower lung diffusing capacity for carbon monoxide (DLCO), respiratory and limb muscle strength, and ventilatory thresholds during exercise compared with controls (all P < 0.05). During exercise, indices of ventilatory efficiency were similar to controls, but inspiratory capacity (IC) was lower and breathing pattern was more rapid and shallow in the cancer group (P < 0.05). The lower peak VO2 in the cancer group was associated with greater dyspnea intensity, and lower DLCO, IC and ventilatory threshold (all P < 0.05).Conclusion: Breast cancer survivors had greater peripheral and respiratory muscle weakness, greater reduction of IC, impaired lung diffusion, and evidence of deconditioning compared with controls. Exercise intolerance was multifactorial and correlated well with the combination of these factors as well as with exertional dyspnea. Individualized physiological testing in breast cancer survivors can identify important contributors to exercise intolerance which can be targeted for treatment. [ABSTRACT FROM AUTHOR]

Dyspnoea (perceived breathing discomfort) is the most common symptom experienced by patients with chronic obstructive pulmonary disease (COPD) and is associated with progressive physical inactivity and poor quality of life. Exertional dyspnoea ratings in COPD have been shown to consistently correlate with a number of physiological ratios that ultimately point to demand/capacity imbalance of the dynamic respiratory system.[1] These include ventilatory output, tidal oesophageal pressure and tidal diaphragmatic electromyography (EMG) (all expressed relative to respective maxima). Studies using bronchodilators or inspiratory muscle training (IMT) to relive dyspnoea have confirmed the importance of high IND in dyspnoea causation in COPD. [Extracted from the article]

Time to exercise limitation (Tlim) in response to constant work rate (CWR) is sensitive to interventions in chronic obstructive pulmonary disease (COPD). This is particularly true when the pre-intervention test lasts between 3 and 8 min (Tlim3′-8′). There is, however, no simple method to select a work rate which is consistently associated with Tlim3′-8′ across the spectrum of COPD severity. We assessed 59 GOLD stages II-IV patients who initially cycled to Tlim at 75% peak. In case of short (<3 min, low-endurance) or long (>8 min, high-endurance) tests, patients exercised after 60 min at 50% or 90%, respectively (CWR50%⇐75%⇒90%). Critical mechanical constraints and limiting dyspnea at 75% were reached within the desired timeframe in 27 “mid-endurance” patients (46%). Increasing work rate intensity to 90% hastened the mechanical-ventilatory responses leading to Tlim3′-8′ in 23/26 (88%) “high-endurance” patients; conversely, decreasing exercise intensity to 50% slowed those responses leading to Tlim3′-8′ in 5/6 (83%) “high-endurance” patients. Repeating the tests at higher (60%) or lower (80%) intensities fail to consistently produce Tlim3′-8′ in “low-” and “high-endurance”, respectively (p > 0.05). Compared to a fixed work rate at 75%, CWR50%⇐75%⇒90% significantly decreased Tlim's coefficient of variation; consequently, the required N to detect 100 s or 33% improvement in Tlim decreased from 82 to 26 and 41 to 14, respectively. This simplified approach to individualized work rate adjustment (CWR50%⇐75%⇒90%) might allow greater sensitivity in evaluating interventional efficacy in improving respiratory mechanics and exercise tolerance while simultaneously reducing sample size requirements in patients with COPD. [ABSTRACT FROM AUTHOR]

This randomized, double-blind, crossover study examined the physiological rationale for using a dual long-acting bronchodilator (umeclidinium/vilanterol (UME/VIL)) versus its muscarinic-antagonist component (UME) as treatment for dyspnea and exercise intolerance in moderate COPD. After each 4-week treatment period, subjects performed pulmonary function and symptom-limited constant-work rate cycling tests with diaphragm electromyogram (EMGdi), esophageal (Pes), gastric (Pga) and transdiaphragmatic (Pdi) pressure measurements. Fourteen subjects completed the study. Both treatments improved spirometry and airway resistance. UME/VIL had larger increases in FEV 1 (+0.14 ± 0.23 L, p < 0.05) but no added reduction in lung hyperinflation compared with UME. Isotime during exercise after UME/VIL versus UME (p < 0.05): “unpleasantness of breathing” fell 0.8 ± 1.3 Borg units; mean expiratory flow and ventilation increased; Pdi and Pga decreased. There were no treatment differences in endurance time, breathing pattern, operating lung volumes, inspiratory neural drive (EMGdi) or respiratory muscle effort (Pes swings) during exercise. UME/VIL compared with UME was associated with reduced breathing unpleasantness reflecting improved airway and respiratory muscle function during exercise. [ABSTRACT FROM AUTHOR]

Chronic obstructive pulmonary disease ( COPD) is a common and often progressive inflammatory disease of the airways, alveoli and microvasculature that is both preventable and treatable. It is well established that smokers with mild airway obstruction, as spirometrically defined, represent the vast majority of patients with COPD, yet this population has not been extensively studied. An insidious preclinical course means that mild COPD is both underdiagnosed and undertreated. In this context, recent studies have confirmed that even patients with mild COPD can have extensive physiological impairment, which contributes to poor perceived health status compared with non-smoking healthy controls. This review describes the heterogeneous pathophysiology that can exist in COPD patients with only mild airway obstruction on spirometry. It exposes the compensatory adaptations that develop in such patients to ensure that the respiratory system fulfils its primary task of maintaining adequate pulmonary gas exchange for the prevailing metabolic demand. It demonstrates that adaptations such as increased inspiratory neural drive to the diaphragm due to combined effects of increased mechanical loading and chemostimulation underscore the increased dyspnoea and exercise intolerance in this population. Finally, based on available evidence, we present what we believe is a sound physiological rationale for earlier diagnosis in this population. [ABSTRACT FROM AUTHOR]

The article highlights developments in understanding and management of dyspnea, which mostly came from findings disclosed by studies on patients with chronic obstructive pulmonary disease (COPD). Topics discussed include the influence of obesity with increased prevalence of dyspnea, the effectiveness of using optimal exercise modality to evaluate intensity of dyspnea and new medications and rehabilitation strategies addressing the symptom.

Background: To have a better understanding of the mechanisms of exercise limitation in mild-to-moderate chronic obstructive pulmonary disease (COPD), we compared detailed respiratory physiology in patients with COPD and healthy age- and sex-matched controls. Methods: Data were collected during the pre-treatment, patient characterization phase of a multicenter, randomized, double-blind, crossover study. Patients with COPD met Global Initiative for Chronic Obstructive Lung Disease (GOLD) 1 or 2 spirometric criteria, were symptomatic, and had evidence of gas trapping during exercise. All participants completed pulmonary function and symptom-limited incremental treadmill exercise tests. Results: Chronic activity-related dyspnea measured by Baseline Dyspnea Index was similarly increased in patients with GOLD 1 (n = 41) and 2 (n = 63) COPD compared with controls (n = 104). Plethysmographic lung volumes were increased and lung diffusing capacity was decreased in both GOLD groups. Peak oxygen uptake and work rate were reduced in both GOLD groups compared with controls (p<0.001). Submaximal ventilation, dyspnea, and leg discomfort ratings were higher for a given work rate in both GOLD groups compared with controls. Resting inspiratory capacity, peak ventilation, and tidal volume were reduced in patients with GOLD 2 COPD compared with patients with GOLD 1 COPD and controls (p<0.001). Conclusions: Lower exercise tolerance in patients with GOLD 1 and 2 COPD compared with controls was explained by greater mechanical abnormalities, greater ventilatory requirements, and increased subjective discomfort. Lower resting inspiratory capacity in patients with GOLD 2 COPD was associated with greater mechanical constraints and lower peak ventilation compared with patients with GOLD 1 COPD and controls. Trial Registration: ClinicalTrials.gov: NCT01072396 [ABSTRACT FROM AUTHOR]

The article provides information on a study which examined responses to symptom-limited cycle exercise in chronic obstructive pulmonary disease (COPD) patients to determine the interrelationship among disease severity, inspiratory capacity (IC), breathing pattern and dyspnea. Factors compared include spirometry, plethysmographic lung volumes, and responses to constant work rate (CWR) cycle exercise. It concludes that progressive reduction of resting IC was associated with dyspnea increase.

In many parts of the world, the prevalence of obesity is increasing at an alarming rate. The association between obesity, multiple comorbidities, and increased mortality is now firmly established in many epidemiological studies. However, the link between obesity and exercise intolerance is less well studied and is the focus of this paper. Although exercise limitation is likely to be multifactorial in obesity, it is widely believed that the respiratory mechanical constraints and the attendant dyspnea are important contributors. In this paper, we examined the evidence that critical ventilatory constraint is a proximate source of exercise limitation in individuals withmild-to-moderate obesity. We first reviewed existing information on exercise performance, including ventilatory and perceptual response patterns, in obese individuals who are otherwise healthy. We then considered the impact of obesity in patients with preexisting respiratory mechanical abnormalities due to chronic obstructive pulmonary disease (COPD), with particular reference to the effect on dyspnea and exercise performance. Our main conclusion, based on the existing and rather sparse literature on the subject, is that abnormalities of dynamic respiratory mechanics are not likely to be the dominant source of dyspnea and exercise intolerance in otherwise healthy individuals or in patients with COPD with mild-to-moderate obesity. [ABSTRACT FROM AUTHOR]

Abstract: We examined the effects of dead space loading (DSL) on ventilation , neural respiratory drive (EMGdi%max, diaphragm EMG expressed as a % of maximal EMGdi), contractile respiratory muscle effort (Pes,tidal%PImax, tidal esophageal pressure swing expressed as a % of maximal inspiratory Pes) and exertional dyspnea intensity ratings in 11 healthy adults with normal spirometry. Subjects completed, in random order, symptom-limited incremental cycle exercise tests under control (CTRL) and DSL (500ml) conditions. Compared with CTRL, DSL decreased exercise tolerance by 20–25%; increased exertional dyspnea intensity ratings in direct proportion to concurrent increases in EMGdi%max, Pes,tidal%PImax and ; and had little/no effect on the inter-relationships between EMGdi%max, Pes,tidal%PImax and during exercise. In conclusion, DSL was associated with an earlier onset of intolerable dyspnea; however, neuro-muscular and neuro-ventilatory coupling of the respiratory system remained relatively preserved during exercise in the presence of an increased external dead space. Under these circumstances, DSL-induced increases in exertional dyspnea intensity ratings reflected, at least in part, the awareness of increased neural respiratory drive, contractile respiratory muscle effort and ventilatory output. [Copyright &y& Elsevier]

The article discusses a study which investigated the impact of increasing body mass index (BMI) on static lung volumes and airway function in a cohort of 2,265 subjects. The researchers also evaluated the influence of severity of airway obstruction. It was found that subjects with airway obstruction had consistent reductions in lung hyperinflation with increasing BMI.

Abstract: We examined the impact of human pregnancy on breathlessness intensity at matched levels of ventilation during isoxic hyperoxic CO2 rebreathing and incremental cycle exercise tests in 21 healthy women in the third trimester (TM3) and again ∼5 months post-partum (PP). Pregnancy had no significant (P >0.05) effect on the slope or threshold of the breathlessness relationship during both exercise and rebreathing. By contrast, the slope of the breathlessness relationship was significantly higher, while the threshold of this relationship was consistently lower during rebreathing vs. exercise (both P <0.05), regardless of pregnancy status (P >0.05). As a result, breathlessness intensity was markedly higher at any given (e.g., by ∼4 Borg units at 40L/min) during rebreathing vs. exercise, regardless of pregnancy status. Inter-subject variation in breathlessness slopes during exercise was not associated with inter-subject variation in breathlessness slopes during rebreathing or with increased central chemoreflex responsiveness during pregnancy (both P >0.05). In conclusion, the intensity of perceived breathlessness for a given depends, at least in part, on the nature and source of increased central respiratory motor command output, independent of pregnancy status; and pregnancy-induced increases in activity-related breathlessness cannot be easily explained by increased central chemoreflex responsiveness. [Copyright &y& Elsevier]

We aimed to characterize gender differences in exercise endurance, operating lung volumes and symptoms limitation during exercise in patients with COPD. Ninety-three women and 93 men with COPD matched for age and disease severity were evaluated during symptom-limited constant-work rate cycle exercise at 75% of peak capacity. Breathing pattern, inspiratory capacity, dyspnoea and leg discomfort Borg scores were recorded during exercise. Endurance time was shorter in women compared to men. Inspiratory capacity decreased at a similar rate during exercise in women and men (0.71 vs. 0.81 ml· s- 1 for women and men respectively, p = 0.47) despite lower ventilation at end-exercise in women. At end-exercise, women showed lower inspiratory reserve volume (p < 0.005). Dyspnoea responses during exercise occurred with a steep rise near end-exercise, when inspiratory reserve volume approached a critical value, at 10% of total lung capacity, this onset of dyspnoea acceleration occurred earlier in women (p < 0.0001). At the same relative exercise intensity, women with COPD had lower endurance time than men. Compared to men, women with COPD were disadvantaged during exercise as they reached a critical inspiratory reserve volume earlier, leading to a steep increase in dyspnoea and to exercise termination. [ABSTRACT FROM AUTHOR]

Abstract: Progressive activity-related dyspnea dominates the clinical presentation of patients afflicted by chronic obstructive and restrictive lung diseases. This symptom invariably leads to activity limitation, global skeletal muscle deconditioning and an impoverished quality of life. The effective management of exertional dyspnea remains an elusive goal but our understanding of the nature and mechanisms of this distressing symptom continues to grow. Refinements in psychophysical measurement of the sensory intensity and quality of dyspnea during laboratory clinical cardiopulmonary exercise testing (CPET) have provided new insights into causation. In this review, we focus on what is known about the physiological mechanisms of dyspnea during physical exertion in patients with chronic obstructive pulmonary disease (COPD) and interstitial lung disease (ILD). Although these conditions are pathologically diverse, perceptual and ventilatory responses to exercise are remarkably similar among patients with these two conditions. In both patient groups, dyspnea intensity is increased at any given ventilation compared with age-matched healthy individuals; at the limits of tolerance, most patients predominantly select qualitative descriptors that allude to perceptions of “increased respiratory effort” and “unsatisfied inspiration.” Common abnormal physiological responses to CPET across conditions include: (1) increased central respiratory drive secondary to pulmonary gas exchange and metabolic derangements, (2) abnormal “restrictive” constraints on tidal volume expansion with earlier development of critical mechanical limitation of ventilation and (3) an increasing disparity (as exercise proceeds) between the magnitude of contractile respiratory muscle effort and the thoracic volume displacement achieved. Reductionist experimental approaches that attempt to partition, or isolate, the contribution of central and multiple peripheral sensory afferent systems to activity-induced dyspnea have met with limited success. Integrative approaches which explore the possible neurophysiological mechanisms involved in the two dominant qualitative descriptors of activity-related dyspnea in both diseases may prove to be more fruitful. In this review, we present a hypothetical model for exertional dyspnea that is based on current neurophysiological constructs that have been rigorously developed to explain the origins of perceptions of “effort,” “air hunger” and the accompanying affective “distress” response. [Copyright &y& Elsevier]

Dyspnea and activity limitation are the primary symptoms of chronic obstructive pulmonary disease and progress relentlessly as the disease advances. In COPD, dyspnea is multifactorial but abnormal dynamic ventilatory mechanics are believed to be important. Dynamic lung hyperinflation occurs during exercise in the majority of flow-limited patients with chronic obstructive pulmonary disease and may have serious sensory and mechanical consequences. This proposition is supported by several studies, which have shown a close correlation between indices of dynamic lung hyperinflation and measures of both exertional dyspnea and exercise performance. The strength of this association has been further confirmed by studies that have therapeutically manipulated this dependent variable. Relief of exertional dyspnea and improved exercise endurance following bronchodilator therapy correlate well with reduced lung hyperinflation. The mechanisms by which dynamic lung hyperinflation give rise to exertional dyspnea and exercise intolerance are complex. However, recent mechanistic studies suggest that dynamic lung hyperinflation-induced volume restriction and consequent neuromechanical uncoupling of the respiratory system are key mechanisms. This review examines, in some detail, the derangements of ventilatory mechanics that are peculiar to chronic obstructive pulmonary disease and attempts to provide a mechanistic rationale for the attendant respiratory discomfort and activity limitation. [ABSTRACT FROM AUTHOR]

Traditional spirometry, while of unquestionable diagnostic utility, provides imprecise information about the nature and extent of physiological impairment or the resultant clinical consequences in any given patient with chronic obstructive pulmonary disease (COPD). The corollary is that exclusive reliance on spirometric forced expiratory flow rates as the primary outcome measure for the evaluation of therapeutic efficacy can lead to significant underestimation of clinical benefit. Recognition of the limitations of routinely used physiological parameters has prompted a search for additional simple and reliable tests for use in clinical trials. Among these, the spirometric inspiratory capacity (IC) shows early promise as a useful, clinically relevant outcome measure that complements traditional expiratory flow measurements. Consistent improvements in IC after bronchodilator therapy signify reduction in lung hyperinflation and can occur in the setting of minimal or no change in maximal expiratory flow rates, particularly in patients with more severe disease. Moreover, improved IC has been shown to correlate well with improvement in important clinical outcomes such as dyspnea and exercise endurance in patients with moderate to severe COPD. This review charts the evolving experience with this novel parameter in the clinical trial setting. [ABSTRACT FROM AUTHOR]

Lung hyperinflation commonly accompanies expiratory flow-limitation in patients with Chronic Obstructive Pulmonary Disease (COPD) and contributes importantly to dyspnea and activity limitation. It is not surprising, therefore, that lung hyperinflation has become an important therapeutic target in symptomatic COPD patients. There is increasing evidence that acute dynamic increases in lung hyperinflation, under conditions of worsening expiratory flow-limitation and increased ventilatory demand (or both) can seriously stress cardiopulmonary reserves, particularly in patients with more advanced disease. Our understanding of the physiological mechanisms of dynamic lung hyperinflation during both physical activity and exacerbations in COPD continues to grow, together with an appreciation of its serious negative mechanical and sensory consequences. In this review, we will discuss the basic pathophysiology of COPD during rest, exercise and exacerbation so as to better understand how this can be pharmacologically manipulated for the patient's benefit. Finally, we will review current concepts of the mechanisms of symptom relief and improved exercise endurance following pharmacological lung volume reduction. [ABSTRACT FROM AUTHOR]

The article examines the effect of fluticasone propionate/salmeterol (FSC 250/50) on lung hyperinflation and exercise endurance in chronic obstructive pulmonary disease (COPD) patients. Predose and postdose spirometry, plethysmography and constant-load cycle cardiopulmonary exercises test evaluations have been compared. It was found that FSC 250/50 significantly reduced postdose functional residual capacity and increased inspiratory capacity compared with placebo.

Pulmonary rehabilitation (PR) is undoubtedly a pivotal intervention in the management of patients with chronic respiratory diseases (CRD) with troublesome and persistent exertional symptoms and exercise intolerance. The majority of patients attending PR programmes in the modern era have chronic obstructive pulmonary disease (COPD), but we increasingly see expansions to include those with other CRD. The importance of the exercise training component of PR is appropriately recognized, but clearly, a sizeable fraction of patients with advanced CRD - many with significant co-morbidities - may not reach training thresholds where physiological benefits are consistently achieved. [Extracted from the article]

Objectives: Current criteria use FEV[sub 1] to assess bronchodilator responsiveness, despite its insensitivity and inability to predict improvement in symptoms or exercise tolerance. Response in lung volumes remains largely unexplored even though volume parameters, such as inspiratory capacity (IC), closely correlate with functional improvements. Therefore, we assessed the response of lung volumes (ie, by IC, total lung capacity [TLC], functional residual capacity [FRC], residual volume [RV], and FVC) to salbutamol and the relationship of these changes to improvements in the spirometry in these patients. Design: A retrospective review of data extracted from a large database of patients who were undergoing spirometry and static lung volume measurements before and after the administration of 200 µg salbutamol. Patients: Patients with an FEV[sub 1]/FVC ratio of < 85% of predicted values were defined as being severely hyperinflated (SH) if TLC was > 133% of predicted and as being moderately hyperinflated (MH) if TLC was 115 to 133% of predicted. Results: Two hundred eighty-one SH patients and 676 MH patients were identified. Salbutamol significantly reduced the mean (± SEM) TLC (SH patients, 222 ± 23 mL; MH patients, 150 ± 10 mL; p < 0.001), FRC (SH patients, 442 ± 26 mL; MH patients, 260 ± 39 mL; p < 0.001), and RV (SH patients, 510 ± 28 mL; MH patients, 300 ± 14 mL; p < 0.001) and increased both the 1C (SH patients, 220 ± 15 mL; MH patients, 110 ± 11 mL; p < 0.001) and FVC (SH patients, 336 ± 21 mL; MH patients, 204 ± 13 mL; p < 0.001). FEV[sub 1] improved in a minority of patients (SH patients, 33%; MH patients, 26%), but if lung volume measurements are also considered, the overall bronchodilator response may improve to up to 76% of the SH group and up to 62% of the MH group. Changes in volumes correlated poorly with changes in maximal airflows. Conclusions: Bronchodilators reduce... [ABSTRACT FROM AUTHOR]

Heightened sensation of leg effort contributes importantly to poor exercise tolerance in patient populations. We aim to provide a sex‐ and age‐adjusted frame of reference to judge symptom's normalcy across progressively higher exercise intensities during incremental exercise. Two‐hundred and seventy‐five non‐trained subjects (130 men) aged 19–85 prospectively underwent incremental cycle ergometry. After establishing centiles‐based norms for Borg leg effort scores (0–10 category‐ratio scale) versus work rate, exponential loss function identified the centile that best quantified the symptom's severity individually. Peak O2 uptake and work rate (% predicted) were used to threshold gradually higher symptom intensity categories. Leg effort‐work rate increased as a function of age; women typically reported higher scores at a given age, particularly in the younger groups (p < 0.05). For instance, "heavy" (5) scores at the 95th centile were reported at ~200 W (<40 years) and ~90 W (≥70 years) in men versus ~130 W and ~70 W in women, respectively. The following categories of leg effort severity were associated with progressively lower exercise capacity: ≤50th ("mild"), >50th to <75th ("moderate"), ≥75th to <95th ("severe"), and ≥ 95th ("very severe") (p < 0.05). Although most subjects reporting peak scores <5 were in "mild" range, higher scores were not predictive of the other categories (p > 0.05). This novel frame of reference for 0–10 Borg leg effort, which considers its cumulative burden across increasingly higher exercise intensities, might prove valuable to judging symptom's normalcy, quantifying its severity, and assessing the effects of interventions in clinical populations. [ABSTRACT FROM AUTHOR]

There is growing recognition that a sizable fraction of COPD patients with forced expiratory volume in one second (FEV1)/forced vital capacity ratio below the lower limit of normal but preserved FEV 1 reports out-of-proportion dyspnea relative to the severity of airflow limitation. Most physicians, however, assume that patients' breathlessness is unlikely to reflect the negative physiological consequences of COPD vis-à-vis FEV1 normalcy. This concise review integrates the findings of recent studies which uncovered the key pathophysiological features shared by these patients: poor pulmonary gas exchange efficiency (increased "wasted" ventilation) and gas trapping. These abnormalities are associated with two well-known causes of exertional dyspnea: heightened ventilation relative to metabolic demand and critically low inspiratory reserves, respectively. From a clinical standpoint, a low diffusion capacity associated with increased residual volume (RV) and/or RV/total lung capacity ratio might uncover these disturbances, identifying the subset of patients in whom exertional dyspnea is causally related to "mild" COPD. [ABSTRACT FROM AUTHOR]

The lung function laboratory frequently provides relevant information to the practice of pulmonology. Clinical interpretation of pulmonary function and exercise tests, however, has been complicated more recently by temporal changes in demographic characteristics (higher life expectancy), anthropometric attributes (increased obesity prevalence), and the surge of polypharmacy in a sedentary population with multiple chronic degenerative diseases. In this narrative review, we concisely discuss some key challenges to test interpretation that have been affected by these epidemiologic shifts: (a) the confounding effects of advanced age and severe obesity, (b) the contemporary controversies in the diagnosis of obstruction (including asthma and/or COPD), (c) the importance of considering the diffusing capacity of the lung for carbon monoxide (Dlco)/"accessible" alveolar volume (carbon monoxide transfer coefficient) in association with Dlco to uncover the causes of impaired gas exchange, and (d) the modern role of the pulmonary function laboratory (including cardiopulmonary exercise testing) in the investigation of undetermined dyspnea. Following a Bayesian perspective, we suggest interpretative algorithms that consider the pretest probability of abnormalities as indicated by additional clinical information. We, therefore, adopt a pragmatic approach to help the practicing pulmonologist to apply the information provided by the lung function laboratory to the care of individual patients. [ABSTRACT FROM AUTHOR]

Individuals with COPD and preserved ratio impaired spirometry (PRISm) findings in clinical settings have an increased risk of cardiovascular disease (CVD). Do individuals with mild to moderate or worse COPD and PRISm findings in community settings have a higher prevalence and incidence of CVD compared with individuals with normal spirometry findings? Can CVD risk scores be improved when impaired spirometry is added? The analysis was embedded in the Canadian Cohort Obstructive Lung Disease (CanCOLD). Prevalence of CVD (ischemic heart disease [IHD] and heart failure [HF]) and their incidence over 6.3 years were compared between groups with impaired and normal spirometry findings using logistic regression and Cox models, respectively, adjusting for covariables. Discrimination of the pooled cohort equations (PCE) and Framingham risk score (FRS) in predicting CVD were assessed with and without impaired spirometry. Participants (n = 1,561) included 726 people with normal spirometry findings and 835 people with impaired spirometry findings (COPD Global Initiative for Chronic Obstructive Lung Disease [GOLD] stage 1 disease, n = 408; GOLD stage ≥ 2, n = 331; PRISm findings, n = 96). Rates of undiagnosed COPD were 84% in GOLD stage 1 and 58% in GOLD stage ≥ 2 groups. Prevalence of CVD (IHD or HF) was significantly higher among individuals with impaired spirometry findings and COPD compared with those with normal spirometry findings, with ORs of 1.66 (95% CI, 1.13-2.43; P =.01∗) (∗ indicates statistical significane with P <.05) and 1.55 (95% CI, 1.04-2.31; P =.033∗), respectively. Prevalence of CVD was significantly higher in participants having PRISm findings and COPD GOLD stage ≥ 2, but not GOLD stage 1. CVD incidence was significantly higher, with hazard ratios of 2.07 (95% CI, 1.10-3.91; P =.024∗) for the impaired spirometry group and 2.09 (95% CI, 1.10-3.98; P =.024∗) for the COPD group compared to individuals with normal spirometry findings. The difference was significantly higher among individuals with COPD GOLD stage ≥ 2, but not GOLD stage 1. The discrimination for predicting CVD was low and limited when impaired spirometry findings were added to either risk score. Individuals with impaired spirometry findings, especially those with moderate or worse COPD and PRISm findings, have increased comorbid CVD compared with their peers with normal spirometry findings, and having COPD increases the risk of CVD developing. [ABSTRACT FROM AUTHOR]

Reduced lung diffusing capacity for carbon monoxide (DLCO) at rest and increased ventilation (⩒E)-carbon dioxide output (⩒CO2) during exercise are frequent findings in dyspneic smokers with largely preserved FEV1. It remains unclear whether low DLCO and high ⩒E-⩒CO2 are mere reflections of alveolar destruction (i.e. emphysema) or impaired pulmonary perfusion in non-emphysematous tissue contributes to these functional abnormalities. Sixty-four smokers (41 males, FEV1= 84 ± 13%predicted) underwent pulmonary function tests, an incremental exercise test, and quantitative chest computed tomography. Total pulmonary vascular volume (TPVV) was calculated for the entire segmented vascular tree (VIDA Vision™). Using the median % low attenuation area (-950 HU), participants were dichotomized into “Trace” or “Mild” emphysema (E), each group classified into preserved versus reduced DLCO. Within each emphysema subgroup, participants with abnormally low DLCO showed lower TPVV, higher ⩒E-⩒CO2, and exertional dyspnea than those with preserved DLCO (p < 0.05). TPVV (r = 0.34; p = 0.01), but not emphysema (r = −0.05; p = 0.67), correlated with lower DLCO after adjusting for age and height. Despite lower emphysema burden, Trace-E participants with reduced DLCO had lower TPVV, higher dyspnea, and lower peak work rate than the Mild-E with preserved DLCO (p < 0.05). Interestingly, TPVV (but not emphysema) correlated inversely with both dyspnea-work rate (r = −0.36, p = 0.004) and dyspnea-⩒E slopes (r = −0.40, p = 0.001). Reduced pulmonary vascular volume adjusted by emphysema extent is associated with low DLCO and heightened exertional ventilation in dyspneic smokers with minor emphysema. Impaired perfusion of non-emphysematous regions of the lungs has greater functional and clinical consequences than hitherto assumed in these subjects. [ABSTRACT FROM AUTHOR]

Background: Single-point measurements of maximal inspiratory pressure (MIP) are frequently used to suggest muscle weakness in clinical practice. Although there is a large variability in "mean" predicted MIP depending on the chosen reference values, it remains unclear whether those discrepancies actually impact on the prevalence of weakness, that is, MIP below the lower limit of normal.Methods: A total of 1,729 subjects (50.1% men, aged 20 to 94 years) who underwent MIP measurements in a clinical laboratory comprised the study group. MIP was predicted according to the most frequently cited regression equations as of August 2015. Pretest probability of weakness was defined by a cluster of clinical and physiologic variables.Results: Prevalence of weakness ranged from 33.4 to 66.9%. Set 2 equations agreed well in indicating weakness (κ [95% CI] ranging from 0.81 [0.79-0.83] to 0.83 [0.81-0.85]; P < .01). There was closer agreement between higher pretest probability of weakness and low MIP according to set 2 equations compared with set 1 equations. Thus, a significant fraction of subjects with abnormal MIP according to set 1 equations but preserved MIP according to set 2 equations had higher pretest probability of weakness (P < .05).Conclusions: The choice of MIP reference values strongly impacts on the prevalence of weakness. Some specific equations relate better to clinical and physiologic indicators of weakness, suggesting that they might be particularly useful to screen subjects for advanced respiratory neuromuscular assessment. [ABSTRACT FROM AUTHOR]

Background: The COPD Assessment Test (CAT) is a valid disease-specific questionnaire measuring health status. However, knowledge concerning its use regarding patient and disease characteristics remains limited. Our main objective was to assess the degree to which the CAT score varies and can discriminate between specific patient population groups.Methods: The Canadian Cohort Obstructive Lung Disease (CanCOLD) is a random-sampled, population-based, multicenter, prospective cohort that includes subjects with COPD (Global Initiative for Chronic Obstructive Lung Disease [GOLD] classifications 1 to 3). The CAT questionnaire was administered at three visits (baseline, 1.5 years, and 3 years). The CAT total score was determined for sex, age groups, smoking status, GOLD classification, exacerbations, and comorbidities.Results: A total of 716 subjects with COPD were included in the analysis. The majority of subjects (72.5%) were not previously diagnosed with COPD. The mean FEV1/FVC ratio was 61.1 ± 8.1%, with a mean FEV1 % predicted of 82.3 ± 19.3%. The mean CAT scores were 5.8 ± 5.0, 9.6 ± 6.7, and 16.1 ± 10.0 for GOLD 1, 2, and 3+ classifications, respectively. Higher CAT scores were observed in women, current smokers, ever-smokers, and subjects with a previous diagnosis of COPD. The CAT was also able to distinguish between subjects who experience exacerbations vs those who had no exacerbation.Conclusions: These results suggest that the CAT, originally designed for use in clinically symptomatic patients with COPD, can also be used in individuals with mild airflow obstruction and newly diagnosed COPD. In addition, the CAT was able to discriminate between sexes and subjects who experience frequent and infrequent exacerbations.Trial Registry: ClinicalTrials.gov; No.: NCT00920348; Study ID No.: IRO-93326. [ABSTRACT FROM AUTHOR]

Background: Reduced exercise capacity has been reported previously in patients with OSA hypopnea syndrome (OSAHS), although the underlying mechanisms are unclear.Research Question: What are the underlying mechanisms of reduced exercise capacity in untreated patients with OSAHS? Is there a role for systemic or pulmonary vascular abnormalities?Study Design and Methods: This was a cross-sectional observational study in which 14 patients with moderate to severe OSAHS and 10 control participants (matched for age, BMI, smoking history, and FEV1) underwent spirometry, incremental cycle cardiopulmonary exercise testing (CPET) with arterial line, resting echocardiography, and assessment of arterial stiffness (pulse wave velocity [PWV] and augmentation index [AIx]).Results: Patients (mean ± SD age, 50 ± 11 years; mean ± SD BMI, 30.5 ± 2.7 kg/m2; mean ± SD smoking history, 2.4 ± 4.0 pack-years; mean ± SD FEV1 to FVC ratio, 0.78 ± 0.04%; mean ± SD FEV1, 85 ± 14% predicted) showed mean ± SD apnea hypopnea index of 43 ± 19/h. At rest, PWV, AIx, and mean pulmonary artery pressure (PAP) were higher in patients vs control participants (P < .05). During CPET, patients showed lower peak work rate (WR) and oxygen uptake and greater dyspnea ratings compared with control participants (P < .05 for all). Minute ventilation (V·E), ventilatory equivalent for CO2 output (V·E/V·CO2), and dead space ventilation (VD) to tidal volume (VT) ratio were greater in patients vs control participants during exercise (P < .05 for all). Reduction in VD to VT ratio from rest to peak exercise was greater in control participants compared with patients (0.24 ± 0.08 vs 0.04 ± 0.14, respectively; P = .001). Dyspnea intensity at the highest equivalent WR correlated with corresponding values of V·E/V·CO2 (r = 0.65; P = .002), and VD (r = 0.70; P = .001). Age, PWV, and mean PAP explained approximately 70% of the variance in peak WR, whereas predictors of dyspnea during CPET were rest-to-peak change in VD to VT ratio and PWV (R2 = 0.50; P < .001).Interpretation: Patients with OSAHS showed evidence of pulmonary gas exchange abnormalities during exercise (in the form of increased dead space) and resting systemic vascular dysfunction that may explain reduced exercise capacity and increased exertional dyspnea intensity. [ABSTRACT FROM AUTHOR]

In people with COPD, pulmonary gas-exchange efficiency may be impaired because of abnormal alveolar ventilation (V˙A), capillary perfusion (Q˙c), or both. Both have been reported in early and mild stages of the disease. Such derangements often accompany significant clinical consequences such as activity-related dyspnea and exercise intolerance. Although much attention has been paid to pharmacologic treatment of mechanical abnormalities in COPD (eg, bronchodilators to deflate the lungs), increasing neurochemical afferent activity, secondary to gas-exchange inefficiency, has remained elusive as a therapeutic target. Hence, in this invited review, we first summarize how dyspnea, leading to poor exercise tolerance in COPD, may be explained by an increased venous admixture resulting from low V˙A/Q˙c, or wasted ventilation related to high V˙A/Q˙c, or both. We review the conflicting evidence supporting current treatments for gas-exchange inefficiency and exercise tolerance that act primarily on V˙A (bronchodilators, antiinflammatory medications) or Q˙c (oral and inhaled vasodilators, almitrine, and supplemental oxygen). Finally, to address the current knowledge and health care gaps, we propose two independent clinical research foci that may lead to a better understanding of the role of pulmonary gas-exchange inefficiency and activity-related dyspnea in COPD: (1) enhanced and deeper phenotyping of patients with COPD with V˙A/Q˙c abnormalities and (2) evaluation of existing and novel pharmacologic treatments to improve gas-exchange inefficiency, exertional dyspnea, and exercise tolerance across the spectrum of COPD severity. [ABSTRACT FROM AUTHOR]

The article discusses the effect of ventilatory assist on exercise performance in cardiopulmonary disease. Patients with cardiopulmonary diseases stop exercise primarily because of severe exertional symptoms of dyspnea and leg discomfort before reaching the physiological limits dictated by their respiratory and cardiovascular systems.

In patients with chronic obstructive pulmonary disease (COPD), exertional dyspnoea generally arises when there is imbalance between ventilatory demand and capacity, but the neurophysiological mechanisms are unclear. We therefore determined if disparity between elevated inspiratory neural drive (IND) and tidal volume (VT) responses (neuromechanical dissociation) impacted dyspnoea intensity and quality during exercise, across the COPD severity spectrum. In this two‐centre, cross‐sectional observational study, 89 participants with COPD divided into tertiles of FEV1 %predicted (Tertile 1 = FEV1 = 87 ± 9%, Tertile 2 = 60 ± 9%, Tertile 3 = 32 ± 8%) and 18 non‐smoking controls, completed a symptom‐limited cardiopulmonary exercise test (CPET) with measurement of IND by diaphragm electromyography (EMGdi (%max)). The association between increasing dyspnoea intensity and EMGdi (%max) during CPET was strong (r = 0.730, P < 0.001) and not different between the four groups who showed marked heterogeneity in pulmonary gas exchange and mechanical abnormalities. Significant inspiratory constraints (tidal volume/inspiratory capacity (VT/IC) ≥ 70%) and onset of neuromechanical dissociation (EMGdi (%max):VT/IC > 0.75) occurred at progressively lower minute ventilation (V̇E${\dot{V}}_{{\rm{E}}}$) from Control to Tertile 3. Lower resting IC meant earlier onset of neuromechanical dissociation, heightened dyspnoea intensity and greater propensity (93% in Tertile 3) to select qualitative descriptors of 'unsatisfied inspiration'. We concluded that, regardless of marked variation in mechanical and pulmonary gas exchange abnormalities in our study sample, exertional dyspnoea intensity was linked to the magnitude of EMGdi (%max). Moreover, onset of critical inspiratory constraints and attendant neuromechanical dissociation amplified dyspnoea intensity at higher exercise intensities. Simple measurements of IC and breathing pattern during CPET provide useful insights into mechanisms of dyspnoea and exercise intolerance in individuals with COPD. Key points: Dyspnoea during exercise is a common and troublesome symptom reported by patients with chronic obstructive pulmonary disease (COPD) and is linked to an elevated inspiratory neural drive (IND). The precise mechanisms of elevated IND and dyspnoea across the continuum of airflow obstruction severity in COPD remains unclear.The present study sought to determine the mechanisms of elevated IND (by diaphragm EMG, EMGdi (%max)) and dyspnoea during cardiopulmonary exercise testing (CPET) across the continuum of COPD severity.There was a strong association between increasing dyspnoea intensity and EMGdi (%max) during CPET across the COPD continuum despite significant heterogeneity in underlying pulmonary gas exchange and respiratory mechanical impairments.Critical inspiratory constraints occurred at progressively lower ventilation during exercise with worsening severity of COPD. This was associated with the progressively lower resting inspiratory capacity with worsening disease severity.Earlier critical inspiratory constraint was associated with earlier neuromechanical dissociation and greater likelihood of reporting the sensation of 'unsatisfied inspiration'. [ABSTRACT FROM AUTHOR]

A cardiopulmonary exercise test (CPET) is ideally suited to quantify exercise tolerance and evaluate the pathophysiological mechanism(s) of dyspnea and exercise limitation in people with chronic respiratory disease. Although there are several statements on CPET and many outstanding resources detailing the cardiorespiratory and perceptual responses to exercise, limited information is available to support the health care provider in conducting a practical CPET evaluation. This article provides the health care provider with practical and timely information on how to use CPET data to understand dyspnea and exercise intolerance in people with chronic respiratory diseases. Information on CPET protocol, as well as how to evaluate maximal patient effort, peak rate of oxygen consumption, ventilatory demand, pulmonary gas exchange, ventilatory reserve, operating lung volumes, and exertional dyspnea, is presented. Two case examples are also described to highlight how these parameters are evaluated to provide a clinical interpretation of CPET data. [ABSTRACT FROM AUTHOR]

Background: Chronic obstructive pulmonary disease (COPD) is mostly managed within primary care, but there is little Canadian evidence from this setting. This study was undertaken to determine the prevalence of physician-diagnosed COPD in primary care practices, and the degree of comorbidity with other chronic conditions, and to assess patterns of medication prescribing. Methods: The Canadian Primary Care Sentinel Surveillance Network is a national "network of networks" whose member practices use electronic medical records (EMRs). At the time of the study, it included data from 444 physicians from 10 networks in 8 provinces. We conducted an epidemiologic cohort study of all patients who had EMR data collected by the network at the end of 2012. Validated case-finding algorithms were used to identify cases of COPD. We used descriptive statistics and multivariate modelling analyses to calculate the prevalence of COPD, its association with key demographic factors and comorbidities, and patterns of medication prescribing. Results: The observed prevalence of COPD was 4.0% (10 043/250 346), which represents a population prevalence of 3.4% using age-sex standardization. Comorbidity was common, with prevalence ratios ranging from 1.1 for the presence of a single comorbid condition to 1.9 for 4 or more comorbid conditions. Anticholinergic agents (63%), short- (48%) and long-acting (38%) β-agonists and inhaled corticosteroids (41%) were the most commonly used medications. Interpretation: The prevalence of physician-diagnosed COPD in Canadian primary care practices was similar to that reported in other practice-based studies at about 3%-4%. Most patients had comorbid conditions and were taking multiple medications. EMR data may be useful to assess both the epidemiology and management of COPD in primary care practices. [ABSTRACT FROM AUTHOR]

Purpose: To assess whether night-time increases in mechanical loading negatively impact respiratory muscle function in COPD and whether compensatory increases in inspiratory neural drive (IND) are adequate to stabilize ventilatory output and arterial oxygen saturation, especially during sleep when wakefulness drive is withdrawn. Methods: 21 patients with moderate-to-severe COPD and 20 age-/sex-matched healthy controls (CTRL) participated in a prospective, cross-sectional, one-night study to assess the impact of COPD on serial awake, supine inspiratory capacity (IC) measurements and continuous dynamic respiratory muscle function (esophageal manometry) and IND (diaphragm electromyography, EMGdi) in supine sleep. Results: Supine inspiratory effort and EMGdi were consistently twice as high in COPD versus CTRL (p < 0.05). Despite overnight increases in awake total airways resistance and dynamic lung hyperinflation in COPD (p < 0.05; not in CTRL), elevated awake EMGdi and respiratory effort were unaltered in COPD overnight. At sleep onset (non-rapid eye movement sleep, N2), EMGdi was decreased versus wakefulness in COPD (− 43 ± 36%; p < 0.05) while unaffected in CTRL (p = 0.11); however, respiratory effort and arterial oxygen saturation (SpO2) were unchanged. Similarly, in rapid eye movement (stage R), sleep EMGdi was decreased (− 38 ± 32%, p < 0.05) versus wakefulness in COPD, with preserved respiratory effort and minor (2%) reduction in SpO2. Conclusions: Despite progressive mechanical loading overnight and marked decreases in wakefulness drive, inspiratory effort and SpO2 were well maintained during sleep in COPD. Preserved high inspiratory effort during sleep, despite reduced EMGdi, suggests continued (or increased) efferent activation of extra-diaphragmatic muscles, even in stage R sleep. Clinical trial information: The COPD data reported herein were secondary data (Placebo arm only) obtained through the following Clinical Trial: "Effect of Aclidinium/Formoterol on Nighttime Lung Function and Morning Symptoms in Chronic Obstructive Pulmonary Disease" (https://clinicaltrials.gov/ct2/show/NCT02429765; NCT02429765). [ABSTRACT FROM AUTHOR]

Introduction: Evaluation of the intensity and quality of activity-related dyspnea is potentially useful in people with chronic obstructive pulmonary disease (COPD). The present study sought to examine associations between qualitative dyspnea descriptors, dyspnea intensity ratings, dynamic respiratory mechanics, and exercise capacity during cardiopulmonary exercise testing (CPET) in COPD and healthy controls. Methods : In this cross-sectional study, 261 patients with mild-to-very severe COPD (forced expiratory volume in 1 s, 62 +/- 25%pred) and 94 age-matched controls (forced expiratory volume in 1 s, 114 +/- 14%pred) completed an incremental cycle CPET to determine peak oxygen uptake (V[spacing dot above]O2peak). Throughout exercise, expired gases, operating lung volumes, and dyspnea intensity were assessed. At peak exercise, dyspnea quality was assessed using a modified 15-item questionnaire. Results : Logistic regression analysis revealed that among 15 dyspnea descriptors, only those alluding to the cluster "unsatisfied inspiration" were consistently associated with an increased likelihood for both critical inspiratory mechanical constraint (end-inspiratory lung volume/total lung capacity ratio >=0.9) during exercise and reduced exercise capacity (V[spacing dot above]O2peak < lower limit of normal) in COPD (odds ratio (95% confidence interval), 3.26 (1.40-7.60) and 3.04 (1.24-7.45), respectively; both, P < 0.05). Thus, patients reporting "unsatisfied inspiration" (n = 177 (68%)) had an increased relative frequency of critical inspiratory mechanical constraint and low exercise capacity compared with those who did not select this descriptor, regardless of COPD severity or peak dyspnea intensity scores. Conclusions : In patients with COPD, regardless of disease severity, reporting descriptors in the unsatisfied inspiration cluster complemented traditional assessments of dyspnea during CPET and helped identify patients with critical mechanical abnormalities germane to exercise intolerance. [ABSTRACT FROM AUTHOR]

Abstract: We tested the hypothesis that the magnitude of the pregnancy-induced increase in exercise hyperpnea is predictable based on the level at which is regulated at rest. We performed a detailed retrospective analysis of previous data from 25 healthy young women who performed exercise and rebreathing tests in the third trimester (TM3; 36.5±0.2 weeks gestation; mean±SEM) and again 20.4±1.7 weeks post-partum (PP). At rest, arterialized venous blood was obtained for the estimation of , [H+] and [HCO3 −]; and serum progesterone ([P4]) and 17β-estradiol ([E2]) concentrations. Duffin''s modified hyperoxic rebreathing procedure was used to evaluate changes in central ventilatory chemoreflex control characteristics at rest. Breath-by-breath ventilatory and gas exchange variables were measured at rest and during symptom-limited incremental cycle exercise tests. At rest in TM3 compared with PP: , [H+], [HCO3 −] and the central chemoreflex ventilatory recruitment threshold for () decreased, while ventilation (), [P4], [E2] and central chemoreflex sensitivity () increased (all p ≤0.001). The slope of the linear relation between and during exercise was significantly higher in TM3 vs. PP (31.2±0.6 vs. 27.5±0.5, p <0.001). The magnitude of this change in the slope correlated significantly with concurrent reductions in each of the (R 2 =0.619, p <0.001), (R 2 =0.203, p =0.024) and [HCO3 −] (R 2 =0.189, p =0.030); and was independent (p >0.05) of changes in [P4], [E2] and . In conclusion, the increased ventilatory response to exercise in pregnancy can be explained, in large part, by reductions in the respiratory control system''s resting equilibrium point as manifest primarily by reductions in the . [Copyright &y& Elsevier]

Abstract: The healthy human respiratory system has impressive ventilatory reserve and can easily meet the demands placed upon it by strenuous exercise. Several acute physiological adaptations during exercise ensure harmonious neuromechanical coupling of the respiratory system, which allow healthy humans to reach high levels of ventilation without perceiving undue respiratory discomfort (breathlessness). However, in certain circumstances, such as pregnancy, obesity and natural aging, ventilatory reserve becomes diminished and exertional breathlessness is present. In this review, we focus on what is known about the mechanisms of increased activity-related breathlessness in these populations. Notwithstanding the obvious physiological differences between the three conditions, they share some common perceptual and ventilatory responses to exercise. Breathlessness intensity ratings (described as an increased “sense of effort”) are consistently higher than normal at any given submaximal power output; and central motor drive to the respiratory muscles is consistently increased, reflecting increased ventilatory stimulation. The increased contractile respiratory muscle effort required to support the increased ventilatory requirements of exercise remains the most plausible source of increased activity-related breathlessness in pregnant, obese and elderly humans. In all three conditions, static and dynamic respiratory mechanical/muscular function is, to some extent, altered or impaired. Nevertheless, breathlessness intensity ratings are not significantly increased (compared to normal) at any given exercise ventilation in any of these three conditions. This strongly suggests that respiratory mechanical/muscular factors, per se, may be less important in the genesis of breathlessness. Moreover, in pregnancy and obesity, we present evidence that effective physiological adjustments exist to counterbalance the potentially negative sensory consequences of the altered respiratory mechanical/muscular function peculiar to these conditions. [Copyright &y& Elsevier]

The article presents a study that analyzes the relationship between respiratory symptom intensity and quality and dynamic lung hyperinflation (DH) during episodes of bronchoconstriction of asthma. There were 116 subjects with asthma who received baseline spirometry and lung volume measurement and high-dose methacholine challenge testing (MCT). DH accompanied mild bronchoconstriction during MCT in asthma made the mechanisms separation of chest tightness from other respiratory sensation uneasy.

Patients with mild chronic obstructive pulmonary disease (COPD) and lower resting diffusing capacity for carbon monoxide (DLCO) often report troublesome dyspnea during exercise although the mechanisms are not clear. We postulated that in such individuals, exertional dyspnea is linked to relatively high inspiratory neural drive (IND) due, in part, to the effects of reduced ventilatory efficiency. This cross-sectional study included 28 patients with GOLD I COPD stratified into two groups with (n = 15) and without (n = 13) DLCO less than the lower limit of normal (

Background and objective: The combination of both reduced resting diffusing capacity of the lung for carbon monoxide (DLCO) and ventilatory efficiency (increased ventilatory requirement for CO2 clearance [V˙E/V˙CO2]) has been linked to exertional dyspnoea and exercise intolerance in chronic obstructive pulmonary disease (COPD) but the underlying mechanisms are poorly understood. The current study examined if low resting DLCO and higher exercise ventilatory requirements were associated with earlier critical dynamic mechanical constraints, dyspnoea and exercise limitation in patients with mild COPD. Methods: In this retrospective analysis, we compared V˙E/V˙CO2, dynamic inspiratory reserve volume (IRV), dyspnoea and exercise capacity in groups of patients with Global Initiative for Chronic Obstructive Lung Disease stage 1 COPD with (1) a resting DLCO at or greater than the lower limit of normal (≥LLN; Global Lung Function Initiative reference equations [n = 44]) or (2) below the

• People with COPD had higher levels of all breathlessness sensations during exercise. • Intensity of breathlessness sensations was related to inspiratory reserve volume. • Critically low levels of inspiratory reserve volume occurred at low minute ventilation in COPD. • All groups rated work/effort of breathing higher than unsatisfied inspiration. • Only people with COPD reported moderate breathlessness-related fear and anxiety. This study compared the multidimensional breathlessness response to incremental cardiopulmonary cycle exercise testing (CPET) in people with chronic obstructive pulmonary disease (COPD; n = 14, aged 69 ± 9 years, forced expiratory volume in 1-sec = 54 ± 16 % predicted) and healthy older (OA) (n = 35, aged 68 ± 5 years) and younger (YA) (n = 19, aged 28 ± 8 years) adults. Participants performed CPET and successively rated overall breathlessness intensity, unsatisfied inspiration, breathing too shallow, work/effort of breathing, and breathlessness-related unpleasantness, fear, and anxiety using the 0−10 Borg scale. At any given percent predicted peak minute ventilation, people with COPD rated all breathlessness sensations higher than OA and YAs, who were similar. Most between group differences disappeared when examined in relation to inspiratory reserve volume, except people with COPD reported higher levels of unsatisfied inspiration and breathing too shallow (vs YA), and breathlessness-related fear and anxiety (vs OA and YAs). Multidimensional ratings of breathlessness sensations during CPET provides further insight into differences in exertional symptom perceptions among people with COPD and without COPD. [ABSTRACT FROM AUTHOR]