Ventilatory inefficiency during exercise is a key pathophysiological feature of chronic obstructive pulmonary disease. Currently, it is unknown how this physiological marker relates to clinically relevant outcomes as resting ventilatory impairment progresses across disease stages.Slope and intercept of the linear region of the ventilation-carbon dioxide output relationship and the ratio between these variables, at the lowest point (nadir), were contrasted in 316 patients with Global Initiative for Chronic Obstructive Lung Disease (GOLD) stages 1-4 (forced expiratory volume in 1 s, ranging from 148% pred to 12% pred) and 69 aged-and gender-matched controls, Compared to controls, slope and intercept were higher in GOLD stages 1 and 2, leading to higher nadirs ( p<0.05). Despite even larger intercepts in GOLD stages 3 and 4, slopes diminished as disease evolved (from mean±SD 35±6 in GOLD stage 1 to 24±5 in GOLD stage 3, p<0.05). As a result, there were no significant differences in nadirs among patient groups. Higher intercepts, across all stages ( p<0.01), and to a lesser extent lower slopes in GOLD stages 2-4 ( p<0.05), were related to greater mechanical constraints, worsening pulmonary gas exchange, higher dyspnoea scores, and poorer exercise capacity.Increases in the ventilation intercept best indicate the progression of exercise ventilatory inefficiency across the whole spectrum of chronic obstructive pulmonary disease severity. @ERSpublications Exercise ventilatory inefficiency relates to dyspnoea and exercise intolerance across whole COPD severity spectrum

AimsThe effects of exercise training in chronic heart failure are well established, however, they have not been evaluated in Chagas cardiomyopathy (ChC). We sought to determine the effects of exercise training on functional capacity, health-related quality of life (HQoL), and brain natriuretic peptide (BNP) levels in patients with ChC. Methods and resultsThis randomized, controlled, single-blind trial included 40 patients with ChC (age 49.5 + 7.8 years, 57.5% male) who did not practice regular exercise. All patients were assessed, at baseline and at the end of the study, by exercise test (VO 2 and exercise time), six-minute walk test (6MWT), Goldman Specific Activity Scale (SAS), HQoL, and BNP levels. Patients were randomized to inactive control group (ICG ¼ 19) or exercise training group (ETG ¼ 21). Exercise training group patients underwent 12 weeks of exercise training: walking for up to 30 min (intensity 50-70% HR reserve + HR at rest) and warm-up and cooling-down exercising, three times a week. The data were analysed for delta values (D¼ end 2 baseline). After intervention, compared with the ICG, the ETG had significant increases in functional parameters including, DVO 2 (6.5 vs. 2.8 mL/kg/min, P ¼ 0.001), D exercise time (2.9 vs.1.1 min, P , 0.001), D6MWT distance (83.5 vs. 2.0 m, P ¼ 0.001) improved DSAS (8 vs. 1 patient, P ¼ 0.008), and HQoL: D domains vitality (7.5 vs. 0 points, P ¼ 0.013), D emotional aspects (16.7 vs. 0 points, P ¼ 0.012), and D mental health (16.1 vs. 0 points, P ¼ 0.031). There was no difference in BNP levels. ConclusionIn patients with ChC, exercise training was associated with a major improvement in functional capacity and HQoL without any adverse effects.--

Exercise ventilation (') relative to carbon dioxide output (' ) is particularly relevant to patients limited by the respiratory system, those with chronic obstructive pulmonary disease (COPD). High'-' (poor ventilatory efficiency) has been found to be a key physiological abnormality in symptomatic patients with largely preserved forced expiratory volume in 1 s (FEV). Establishing an association between high '-' and exertional dyspnoea in mild COPD provides evidence that exercise intolerance is not a mere consequence of detraining. As the disease evolves, poor ventilatory efficiency might help explaining "out-of-proportion" breathlessness (to FEV impairment). Regardless, disease severity, cardiocirculatory co-morbidities such as heart failure and pulmonary hypertension have been found to increase '-' In fact, a high '-' has been found to be a powerful predictor of poor outcome in lung resection surgery. Moreover, a high '-' has added value to resting lung hyperinflation in predicting all-cause and respiratory mortality across the spectrum of COPD severity. Documenting improved ventilatory efficiency after lung transplantation and lung volume reduction surgery provides objective evidence of treatment efficacy. Considering the usefulness of exercise ventilatory efficiency in different clinical scenarios, the '-' relationship should be valued in the interpretation of cardiopulmonary exercise tests in patients with mild-to-end-stage COPD.

Severity of resting functional impairment only partially predicts the increased risk of death in chronic obstructive pulmonary disease (COPD). Increased ventilation during exercise is associated with markers of disease progression and poor prognosis, including emphysema extension and pulmonary vascular impairment. Whether excess exercise ventilation would add to resting lung function in predicting mortality in COPD, however, is currently unknown. After an incremental cardiopulmonary exercise test, 288 patients (forced expiratory volume in one second ranging from 18% to 148% predicted) were followed for a median (interquartile range) of 57 (47) months. Increases in the lowest (nadir) ventilation to CO2 output (VCO2) ratio determined excess exercise ventilation. Seventy-seven patients (26.7%) died during follow-up: 30/77 (38.9%) deaths were due to respiratory causes. Deceased patients were older, leaner, had a greater co-morbidity burden (Charlson Index) and reported more daily life dyspnea. Moreover, they had poorer lung function and exercise tolerance (p < 0.05). A logistic regression analysis revealed that ventilation/VCO2 nadir was the only exercise variable that added to age, body mass index, Charlson Index and resting inspiratory capacity (IC)/total lung capacity (TLC) ratio to predict all-cause and respiratory mortality (p < 0.001). Kaplan-Meier analyses showed that survival time was particularly reduced when ventilation/VCO2 nadir > 34 was associated with IC/TLC ≤ 0.34 or IC/TLC ≤ 0.31 for all-cause and respiratory mortality, respectively (p < 0.001). Excess exercise ventilation is an independent prognostic marker across the spectrum of COPD severity. Physiological abnormalities beyond traditional airway dysfunction and lung mechanics are relevant in determining the course of the disease.

Heightened neural drive promoting a ventilatory response beyond that required to overcome an increased "wasted" ventilation led to hypocapnia and poor exercise ventilatory efficiency in chronic obstructive pulmonary disease-heart failure overlap. Excessive ventilation led to better arterial oxygenation but at the expense of earlier critical mechanical constraints and intolerable dyspnea.