To assess the 1-min sit-to-stand test (1STS) test-retest reliability and construct validity and its associated cardiorespiratory response in comparison to the 6-min walk test (6MWT) and ...symptom-limited cycling cardiopulmonary exercise test (CPET) in people with interstitial lung disease (ILD).
Fifteen participants with ILD performed two 1STS tests, a 6MWT and a CPET. The three tests were administered on three separate visits, and cardiorespiratory parameters were continuously recorded during the tests.
The number of repetitions during both 1STS tests was 22 ± 4 and 22 ± 4 (mean difference of 0.53 ± 2.00 repetitions, P = 0.32) with an intraclass correlation of 0.937 (95% confidence interval, 0.811-0.979) and a minimal detectable change of 2.9 repetitions. The number of 1STS repetitions was highly correlated with the 6MWT distance (r = 0.823, P < 0.001) and with the peak cycling power output expressed in % predicted values (r = 0.706, P < 0.003). Oxygen consumption (V˙O2) peak during the 1STS reached 83% and 78% of V˙O2 peak during 6MWT and CPET, respectively. Peak 1STS HR, minute ventilation (V˙E,), V˙O2 values, as well as nadir SpO2 were achieved during the recovery phase of the test, whereas peak 6MWT and CPET HR, V˙E, V˙O2 and nadir SpO2 always occurred at the end of the test. The three tests elicited a similar fall in SpO2 ranging between 8% and 12%. Symptom scores after the 1STS were similar to those seen at the end of the 6MWT but lower than those of CPET.
The 1STS showed excellent test-retest reliability in patients with ILD in whom it elicited a substantial, but submaximal cardiorespiratory response. Our data also support the construct validity of the 1STS to assess functional exercise capacity in patients with ILD and to detect exercise-induced O2 desaturation.
SARS-CoV-2 infection causing the novel coronavirus disease 2019 (COVID-19) has been responsible for more than 2.8 million deaths and nearly 125 million infections worldwide as of March 2021. In March ...2020, the World Health Organization determined that the COVID-19 outbreak is a global pandemic. The urgency and magnitude of this pandemic demanded immediate action and coordination between local, regional, national, and international actors. In that mission, researchers require access to high-quality biological materials and data from SARS-CoV-2 infected and uninfected patients, covering the spectrum of disease manifestations. The "Biobanque québécoise de la COVID-19" (BQC19) is a pan-provincial initiative undertaken in Québec, Canada to enable the collection, storage and sharing of samples and data related to the COVID-19 crisis. As a disease-oriented biobank based on high-quality biosamples and clinical data of hospitalized and non-hospitalized SARS-CoV-2 PCR positive and negative individuals. The BQC19 follows a legal and ethical management framework approved by local health authorities. The biosamples include plasma, serum, peripheral blood mononuclear cells and DNA and RNA isolated from whole blood. In addition to the clinical variables, BQC19 will provide in-depth analytical data derived from the biosamples including whole genome and transcriptome sequencing, proteome and metabolome analyses, multiplex measurements of key circulating markers as well as anti-SARS-CoV-2 antibody responses. BQC19 will provide the scientific and medical communities access to data and samples to better understand, manage and ultimately limit, the impact of COVID-19. In this paper we present BQC19, describe the process according to which it is governed and organized, and address opportunities for future research collaborations. BQC19 aims to be a part of a global communal effort addressing the challenges of COVID-19.
Limb muscle dysfunction is prevalent in chronic obstructive pulmonary disease (COPD) and it has important clinical implications, such as reduced exercise tolerance, quality of life, and even ...survival. Since the previous American Thoracic Society/European Respiratory Society (ATS/ERS) statement on limb muscle dysfunction, important progress has been made on the characterization of this problem and on our understanding of its pathophysiology and clinical implications.
The purpose of this document is to update the 1999 ATS/ERS statement on limb muscle dysfunction in COPD.
An interdisciplinary committee of experts from the ATS and ERS Pulmonary Rehabilitation and Clinical Problems assemblies determined that the scope of this document should be limited to limb muscles. Committee members conducted focused reviews of the literature on several topics. A librarian also performed a literature search. An ATS methodologist provided advice to the committee, ensuring that the methodological approach was consistent with ATS standards.
We identified important advances in our understanding of the extent and nature of the structural alterations in limb muscles in patients with COPD. Since the last update, landmark studies were published on the mechanisms of development of limb muscle dysfunction in COPD and on the treatment of this condition. We now have a better understanding of the clinical implications of limb muscle dysfunction. Although exercise training is the most potent intervention to address this condition, other therapies, such as neuromuscular electrical stimulation, are emerging. Assessment of limb muscle function can identify patients who are at increased risk of poor clinical outcomes, such as exercise intolerance and premature mortality.
Limb muscle dysfunction is a key systemic consequence of COPD. However, there are still important gaps in our knowledge about the mechanisms of development of this problem. Strategies for early detection and specific treatments for this condition are also needed.
This study aimed to assess the cardiorespiratory response during a 1-min sit-to-stand test (1STS) in comparison with cycling cardiopulmonary exercise test (CPET) in people with chronic obstructive ...pulmonary disease (COPD) and in healthy subjects and to evaluate whether 1STS may induce leg fatigue in these individuals.
Fourteen people with severe COPD and 12 healthy subjects performed a 1STS and a CPET during which cardiorespiratory response, perception of dyspnea, and leg fatigue were assessed. Quadriceps strength was assessed before and after 1STS, and contractile fatigue was defined as a postexercise fall in quadriceps twitch force greater than 15% of resting values.
In COPD, peak V˙O2, V˙E, and HR achieved during 1STS reached 113%, 103%, and 93% of the corresponding values during CPET, respectively. Decrease in SpO2 from preexercise to peak exercise and the magnitude of dynamic hyperinflation were similar between 1STS and CPET. Borg dyspnea and leg fatigue scores were higher for CPET than 1STS. In healthy subjects, peak cardiorespiratory demand and symptom scores were higher during CPET compared with 1STS. A V˙O2 overshoot during recovery was observed only in people with COPD. After 1STS, the V˙O2 half-time recovery of COPD was 152 ± 25 s compared with 74 ± 18 in healthy subjects (P < 0.01). Ten people with COPD and five healthy subjects were considered as fatiguers.
The 1STS induced a similar cardiorespiratory stress to that of CPET and was associated with contractile quadriceps fatigue in people with severe COPD. The V˙O2 overshoot and slower recovery time of cardiorespiratory variables seen in COPD demonstrate the clinical relevance of monitoring the recovery phase of exercise.
Exercising small muscle groups at a time allows higher muscle specific workloads compared with whole body aerobic exercises in people with chronic obstructive pulmonary disease (COPD). Whether ...similar effects also occur with partitioning exercise during low load/high-repetition resistance exercises is uncertain.
To investigate the acute effects of partitioning exercise on exercise workload, exertional symptoms and quadriceps muscle fatigue during low load/high-repetition resistance exercises in people with COPD and healthy controls.
We compared the acute physiological effects of single-limb (SL) versus two-limb (TL) execution of isokinetic knee extension and of six low load/high-repetition elastic resistance exercises in 20 people with COPD (forced expiratory volume in 1 s = 38% predicted) and 15 healthy controls.
Among people with COPD, SL exercises resulted in higher exercise workloads during isokinetic knee extension (17% ± 31%, P < 0.05) and elastic exercises (rowing, 17% ± 23%; leg curl, 23% ± 21%; elbow flexion, 19% ± 26%; chest press, 14% ± 15%; shoulder flexion, 33% ± 24%; and knee extension, 24% ± 18%, all P < 0.05). Muscle fatigue ratings were similar during SL compared with TL exercises, whereas dyspnea ratings were similar between conditions during isokinetic exercises and lower during SL compared with TL elastic exercises (P < 0.05). In COPD, SL knee extension resulted in greater quadriceps fatigue than TL knee extension as evidenced by a greater fall in quadriceps potentiated twitch force after the former exercise (-24% ± 10% vs -16% ± 8%, P = 0.025). In healthy controls, partitioning exercise with SL exercise did not modify workload, quadriceps fatigue nor dyspnea achieved during the various exercises.
Partitioning exercise by exercising using an SL allowed higher muscle localized exercise workloads, larger amount of quadriceps muscle fatigue with lower, or similar level of exertional symptoms during low load/high-repetition resistance exercises in people with advanced COPD.
Limb muscle dysfunction is documented in pulmonary arterial hypertension (PAH), but little is known regarding muscle oxygen (O2) supply and its possible effects on exercise tolerance in PAH.
Ten ...patients with PAH and 10 matched controls underwent progressive maximal cardiopulmonary exercise test, voluntary and nonvolitional dominant quadriceps muscle strength measures, and nondominant quadriceps biopsy to assess maximal oxygen uptake, muscle function, and lower limb fiber type and capillarity, respectively. Both groups then performed normoxic and hyperoxic submaximal intensity exercise protocol at the same absolute workload during which muscle O2 supply was assessed by measuring changes in myoglobin-deoxyhemoglobin level (ΔMb-HHb) and tissue oxygenation index in the dominant quadriceps using near-infrared spectroscopy. Changes in cardiac output, estimated systemic O2 delivery, and systemic O2 saturation were also assessed noninvasively throughout both submaximal exercises.
Patients with PAH displayed lower maximal oxygen uptake (P < 0.01), skeletal muscle strength (P < 0.05), and capillarity (P = 0.01). Throughout the normoxic submaximal exercise protocol, ΔMb-HHb (P < 0.01) was higher whereas changes in tissue oxygenation index (P < 0.01) and systemic O2 saturation (P = 0.01) were lower in patients with PAH compared with those in controls. Conversely, changes in cardiac output and estimated systemic O2 delivery were similar between groups. Muscle oxygenation remained unchanged with O2 supplementation. Among variables known to influence tissue oxygenation, only quadriceps capillarity density correlated with ΔMb-HHb (r = -0.66, P < 0.01), which in turn correlated with maximal oxygen uptake (r = -0.64, P < 0.01), 6-min walked distance (r = -0.74, P = 0.01), and both voluntary (r = -0.46, P = 0.04) and nonvolitional (r = -0.50, P = 0.02) quadriceps strength.
Capillary rarefaction within the skeletal muscle influences exercise tolerance and quadriceps strength at least partly through impaired muscle oxygen supply in PAH.
Outdoor air pollution is a potential risk factor for lower lung function and chronic obstructive pulmonary disease (COPD). Little is known about how airway abnormalities and lung growth might modify ...this relationship.
To evaluate the associations of ambient air pollution exposure with lung function and COPD and examine possible interactions with dysanapsis.
We made use of cross-sectional postbronchodilator spirometry data from 1,452 individuals enrolled in the CanCOLD (Canadian Cohort Obstructive Lung Disease) study with linked ambient fine particulate matter (PM
) and nitrogen dioxide (NO
) air pollution estimates. Dysanapsis, or the ratio of the airway-to-lung volume calculated from thoracic computed tomography images, was used to examine possible interactions.
In adjusted models, 101.7 ml (95% confidence interval CI, -166.2 to -37.2) and 115.0 ml (95% CI, -196.5 to -33.4) lower FEV
were demonstrated per increase of 2.4 ug/m
PM
and 9.2 ppb NO
, respectively. Interaction between air pollution and dysanapsis was not statistically significant when modeling the airway-to-lung ratio as a continuous variable. However, a 109.8 ml (95% CI, -209.0 to -10.5 lower FEV
and an 87% (95% CI, 12% to 213%) higher odds of COPD were observed among individuals in the lowest, relative to highest, airway-to-lung ratio, per 2.4 μg/m
increment of PM
.
Ambient air pollution exposure was associated with lower lung function, even at relatively low concentrations. Individuals with dysanaptic lung growth might be particularly susceptible to inhaled ambient air pollutants, especially those at the extremes of dysanapsis.
COPD increases susceptibility to sleep disturbances, which may in turn predispose to increased respiratory symptoms. The objective of this study was to evaluate, in a population-based sample, the ...relationship between subjective sleep quality and risk of COPD exacerbations.
Data were obtained from the Canadian Cohort Obstructive Lung Disease (CanCOLD) study. Participants with COPD who had completed 18 months of follow-up were included. Sleep quality was measured with the Pittsburgh Sleep Quality Index (PSQI) and a three-factor analysis. Symptom-based (dyspnea or sputum change ≥ 48 h) and event-based (symptoms plus medication or unscheduled health services use) exacerbations were assessed. Association of PSQI with exacerbation rate was assessed by using negative binomial regression. Exacerbation-free survival was also assessed.
A total of 480 participants with COPD were studied, including 185 with one or more exacerbations during follow-up and 203 with poor baseline sleep quality (PSQI score > 5). Participants with subsequent symptom-based exacerbations had higher median baseline PSQI scores than those without (6.0 interquartile range, 3.0-8.0 vs 5.0 interquartile range, 2.0-7.0; P = .01), and they were more likely to have baseline PSQI scores > 5 (50.3% vs 37.3%; P = .01). Higher PSQI scores were associated with increased symptom-based exacerbation risk (adjusted rate ratio, 1.09; 95% CI, 1.01-1.18; P = .02) and event-based exacerbation risk (adjusted rate ratio, 1.10; 95% CI, 1.00-1.21; P = .048). The association occurred mainly in those with undiagnosed COPD. Strongest associations were with Factor 3 (sleep disturbances and daytime dysfunction). Time to symptom-based exacerbation was shorter in participants with poor sleep quality (adjusted hazard ratio, 1.49; 95% CI, 1.09-2.03).
Higher baseline PSQI scores were associated with increased risk of COPD exacerbation over 18 months' prospective follow-up.
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.