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This study aimed to investigate the walking economy and possible factors influencing self-selected walking speed (SSWS) in patients with fibrotic interstitial lung disease (ILD) compared to controls. In this study, 10 patients with ILD (mean age: 63.8 ± 9.2 years, forced expiratory volume in the first second: 56 ± 7% of predicted) and 10 healthy controls underwent resting pulmonary function tests, cardiopulmonary exercise, and submaximal treadmill walking tests at different speeds. The walking economy was assessed by calculating the cost-of-transport (CoT). Dynamic stability was assessed by stride-to-stride fluctuations using video recordings. Patients with ILD showed reduced peak oxygen uptake with a tachypneic breathing pattern and significant oxygen desaturation during exercise. The CoT did not differ between the groups (p = 0.680), but dyspnea and SpO 2 were higher and lower, respectively, in patients with ILD at the same relative speeds. SSWS was reduced in ILD patients (2.6 ± 0.9 vs. 4.2 ± 0.4 km h -1 p = 0.001) and did not correspond to the energetically optimal walking speed. Dynamic stability was significantly lower in patients with ILD than in healthy controls, mainly at lower speeds. Patients with ILD presented a similar cost of transport compared to healthy controls; however, they chose lower SSWS despite higher walking energy expenditure. Although walking stability and dyspnea were negatively affected, these factors were not associated with the slower walking speed chosen by individuals with ILD.

Introduction: Inspiratory muscle weakness (IMW) is a potential cause of exertional dyspnea frequently under-appreciated in clinical practice. Cardiopulmonary exercise testing (CPET) is usually requested as part of the work-up for unexplained breathlessness, but the specific pattern of exercise responses ascribed to IMW is insufficiently characterized., Objectives: To identify the physiological and sensorial responses to progressive exercise in dyspneic patients with IMW without concomitant cardiorespiratory or neuromuscular diseases., Methods: Twenty-three subjects (18 females, 55.2 ± 16.9 years) complaining of chronic daily life dyspnea (mMRC = 3 [2-3]) plus maximal inspiratory pressure < the lower limit of normal and 12 matched controls performed incremental cycling CPET. FEV 1 /FVC<0.7, significant abnormalities in chest CT or echocardiography, and/or an established diagnosis of neuromuscular disease were among the exclusion criteria., Results and Conclusion: Patients presented with reduced aerobic capacity (peak V̇O 2 : 79 ± 26 vs 116 ± 21 %predicted), a tachypneic breathing pattern (peak breathing frequency/tidal volume = 38.4 ± 22.7 vs 21.7 ± 14.2 breaths/min/L) and exercise-induced inspiratory capacity reduction (-0.17 ± 0.33 vs 0.10 ± 0.30 L) (all P < .05) compared to controls. In addition, higher ventilatory response (ΔV̇ E /ΔV̇CO 2 = 34.1 ± 6.7 vs 27.0 ± 2.3 L/L) and symptomatic burden (dyspnea and leg discomfort) to the imposed workload were observed in patients. Of note, pulse oximetry was similar between groups. Reduced aerobic capacity in the context of a tachypneic breathing pattern, inspiratory capacity reduction and preserved oxygen exchange during progressive exercise should raise the suspicion of inspiratory muscle weakness in subjects with otherwise unexplained breathlessness., (© 2020 John Wiley & Sons Ltd.)

Assessment of dyspnoea severity during incremental cardiopulmonary exercise testing (CPET) has long been hampered by the lack of reference ranges as a function of work rate (WR) and ventilation ( V' E ). This is particularly relevant to cycling, a testing modality which overtaxes the leg muscles leading to a heightened sensation of leg discomfort.Reference ranges based on dyspnoea percentiles (0-10 Borg scale) at standardised work rates and V' E were established in 275 apparently healthy subjects aged 20-85 years (131 men). They were compared with values recorded in a randomly selected "validation" sample (n=451; 224 men). Their usefulness in properly uncovering the severity of exertional dyspnoea were tested in 167 subjects under investigation for chronic dyspnoea ("testing sample") who terminated CPET due to leg discomfort (86 men).Iso-work rate and, to a lesser extent, iso- V' E reference ranges (5th-25th, 25th-50th, 50-75th and 75th-95th percentiles) increased as a function of age, being systematically higher in women (p<0.01). There were no significant differences in percentiles distribution between "reference" and "validation" samples (p>0.05). Submaximal dyspnoea-work rate scores fell within the 75th-95th or >95th percentiles in 108 out of 118 (91.5%) subjects of the "testing" sample who showed physiological abnormalities known to elicit exertional dyspnoea, i.e. ventilatory inefficiency and/or critical inspiratory constraints. In contrast, dyspnoea scores typically fell in the 5th-50th range in subjects without those abnormalities (p<0.001).This frame of reference might prove useful to uncover the severity of exertional dyspnoea in subjects who otherwise would be labelled as "non-dyspnoeic" while providing mechanistic insights into the genesis of this distressing symptom., Competing Interests: Conflict of interest: J.A. Neder has nothing to disclose. Conflict of interest: D.C. Berton has nothing to disclose. Conflict of interest: L.E. Nery has nothing to disclose. Conflict of interest: W.C. Tan reports grants from Canadian Respiratory Research Network, AstraZeneca Canada Ltd, Boehringer Ingelheim Canada Ltd, GlaxoSmithKline Canada Ltd, Novartis, Canadian Institutes of Health Research, Respiratory Health Network of the Fonds de la recherche en santé du Québec, Merck, Nycomed, Pfizer Canada Ltd and Theratechnologies, during the conduct of the study. Conflict of interest: J. Bourbeau reports grants from CIHR, Canadian Respiratory Research Network (CRRN), Foundation of the MUHC and Aerocrine, personal fees for consultancy and lectures from Canadian Thoracic Society and CHEST, grants and personal fees for advisory board work and lectures from AstraZeneca, Boehringer Ingelheim, Grifols, GlaxoSmithKline, Novartis and Trudell, outside the submitted work. Conflict of interest: D.E. O'Donnell has nothing to disclose., (Copyright ©ERS 2020.)

Background: Exertional dyspnea increases when the mechanical output of the respiratory muscles becomes uncoupled from increases in neural respiratory drive. Combining measurements of inspiratory constraints and ventilatory inefficiency may better uncover the role of mechanical-ventilatory abnormalities on exertional dyspnea than the currently-recommended approach, i.e., a low breathing reserve., Methods: We determined the presence of a low breathing reserve (1-(peak ventilation (V̇E)/estimated maximal voluntary ventilation) x 100 < 15%), critical inspiratory constraints (tidal volume (VT)/exercise inspiratory capacity (IC dyn ) > 0.7) and ventilatory inefficiency (V̇E/CO 2 output (V̇CO 2 ) nadir>34) in 284 subjects (161 males) with "disproportionate dyspnea" (N = 148), "dyspnea with multiple potential causes" (N = 93) and "dyspnea without an apparent cause., Results: The agreement between breathing reserve and assessment of inspiratory constraints was only "fair" (kappa [confidence interval (CI)] = 0.264 [0.169-0.358]). Attainment of critical inspiratory constraints and an upward inflection in dyspnea ratings systematically preceded a low breathing reserve. Of note, ~55% (93/167) of subjects with normal breathing reserve showed critical inspiratory constraints despite largely preserved lung function. Regardless of the breathing reserve, subjects showing critical inspiratory constraints and/or poor ventilatory efficiency reported higher dyspnea and more impaired exercise tolerance compared to their counterparts (p < 0.05). Poor ventilatory efficiency strongly predicted a high dyspnea/work rate in subjects without critical inspiratory constraints regardless of the breathing reserve (odds ratio [95% CI] = 4.21 [2.01-6.42; p < 0.001)., Conclusion: An integrated analysis of inspiratory constraints and ventilatory inefficiency is key to uncover physiological abnormalities germane to dyspnea in clinical populations in whom the origins of this distressing symptom are uncertain., (Copyright © 2019. Published by Elsevier Ltd.)

Combining measurements of impaired lung mechanics (inspiratory constraints) with an index of increased respiratory stimuli to metabolic demand (poor ventilatory efficiency) might enhance the ability of cardiopulmonary exercise testing (CPET) in exposing a mechanistic role for ventilation on exertional dyspnea in COPD. In addition to the standard approach to suggest ventilatory limitation to exercise - a low breathing reserve (1-(peak ventilation (V̇E)/maximal voluntary ventilation × 100 < 20%) - we assessed the presence of critical inspiratory constraints (end-inspiratory lung volume (EILV)/total lung capacity (TLC) ≥ 0.9) and ventilatory inefficiency (V̇E/CO 2 output (V̇CO 2 ) nadir > 34) in 288 patients with mild to very severe COPD (FEV 1 ranging from 18 to 121% predicted). We found that ∼50% of the patients with preserved breathing reserve developed critical inspiratory constraints. A low breathing reserve was weakly related to a lower peak O 2 uptake (V̇O 2 ) and/or a higher dyspnea burden; for instance, patients with low breathing reserve but without critical inspiratory constraints had similar dyspnea and peak V̇O 2 than those with preserved breathing reserve ( p  > 0.05). In contrast, critical inspiratory constraints and ventilatory inefficiency were strongly associated with a negative outcome (likelihood ratio = 42.3 and 47.7, respectively; p  < 0.001). A multiple logistic regression analysis revealed that only EILV/TLC ≥ 0.9 and V̇E/V̇CO 2 nadir >34 predicted a severely reduced peak V̇O 2 due to a high dyspnea burden ( p  < 0.001). Measurements of dynamic mechanical constraints and ventilatory inefficiency during incremental CPET are key to determine the impact of COPD on dyspnea and exercise tolerance across the spectrum of disease severity.

We aimed to assess detailed ventilatory and sensory responses to exercise contrasting subjects with and without PAH. 20 non-smoking patients with PAH (37.5 ± 12.1 ys; FEV 1 /FVC = 0.77 ± 0.04; mPAP by heart catheterization = 50.6 ± 18.1 mmHg) and 10 matched controls performed cycling cardiopulmonary exercise test with serial assessments of dyspnea, airway occlusion pressure during the first 0.1 s (P0.1) of tidal volume and inspiratory capacity (IC). Patients showed lower spirometric variables compared to controls. Dyspnea and ventilation (V E ) were significantly higher in patients for a given work rate. Dyspnea persisted more intense in patients even when expressed as a function of V E . Lower IC at rest (in non-hyperinflators; n = 10) or exercise-induced reduction in IC (in hyperinflators) predisposed patients to achieve earlier and at lower workloads a critical inspiratory reserve volume (IRV). At this point, there was a sudden rise in P0.1 and dyspnea perception. Attainment of a critical IRV at premature workloads leads to neuromechanical dissociation with an abrupt increment in exertional dyspnea., (Copyright © 2019 Elsevier B.V. All rights reserved.)

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 (Tlim 3'-8' ). There is, however, no simple method to select a work rate which is consistently associated with Tlim 3'-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 (CWR 50%⇐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 Tlim 3'-8' in 23/26 (88%) "high-endurance" patients; conversely, decreasing exercise intensity to 50% slowed those responses leading to Tlim 3'-8' in 5/6 (83%) "high-endurance" patients. Repeating the tests at higher (60%) or lower (80%) intensities fail to consistently produce Tlim 3'-8' in "low-" and "high-endurance", respectively (p > 0.05). Compared to a fixed work rate at 75%, CWR 50%⇐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 (CWR 50%⇐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.

Interval exercise delays critical mechanical-ventilatory constraints with positive consequences on Dyspnoea and exercise tolerance in COPD. We hypothesized that those advantages of interval exercise would be partially off-set in patients showing excessive ventilation (V˙E) to metabolic demand (V˙CO 2 ). Sixteen men (FEV 1  = 42.3 ± 8.9%) performed, on different days, 30 s and 60 s bouts at 100% peak (on) interspersed by moderate exercise at 40% (off). Nine patients did not sustain exercise for 30 min irrespective of on duration. They presented with higher V˙E/V˙CO 2 nadir (35 ± 3 vs. 30 ± 5) and dead space/tidal volume (0.39 ± 0.05 vs. 0.34 ± 0.06) compared to their counterparts (p < 0.05). [Lactate], operating lung volumes and symptom burden (dyspnoea and leg effort) were also higher (p < 0.05). Unloading off decreased the metabolic-ventilatory demands, thereby allowing 7/9 patients to exercise for 30 min. Increased wasted ventilation accelerates the rate at which critical mechanical constraints and limiting dyspnoea are reached during interval exercise in patients with COPD., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Rationale: An increased ventilatory response to exertional metabolic demand (high [Formula: see text]e/[Formula: see text]co 2 relationship) is a common finding in patients with coexistent chronic obstructive pulmonary disease and heart failure., Objectives: We aimed to determine the mechanisms underlying high [Formula: see text]e/[Formula: see text]co 2 and its impact on operating lung volumes, dyspnea, and exercise tolerance in these patients., Methods: Twenty-two ex-smokers with combined chronic obstructive pulmonary disease and heart failure with reduced left ventricular ejection fraction undertook, after careful treatment optimization, a progressive cycle exercise test with capillary (c) blood gas collection., Measurements and Main Results: Regardless of the chosen metric (increased [Formula: see text]e-[Formula: see text]co 2 slope, [Formula: see text]e/[Formula: see text]co 2 nadir, or end-exercise [Formula: see text]e/[Formula: see text]co 2 ), ventilatory inefficiency was closely related to Pc CO 2 (r values from -0.80 to -0.84; P < 0.001) but not dead space/tidal volume ratio. Ten patients consistently maintained exercise Pc CO 2 less than or equal to 35 mm Hg (hypocapnia). These patients had particularly poor ventilatory efficiency compared with patients without hypocapnia (P < 0.05). Despite the lack of between-group differences in spirometry, lung volumes, and left ventricular ejection fraction, patients with hypocapnia had lower resting Pa CO 2 and lung diffusing capacity (P < 0.01). Excessive ventilatory response in this group was associated with higher exertional Pc O 2 . The group with hypocapnia, however, had worse mechanical inspiratory constraints and higher dyspnea scores for a given work rate leading to poorer exercise tolerance compared with their counterparts (P < 0.05)., Conclusions: 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.

Introduction: The application of expiratory positive airway pressure (EPAP) in patients with COPD during exercise may reduce dynamic hyperinflation, while, on the other hand, it can increase the resistive work of breathing. Therefore, we evaluated the effects of 2 intensities of EPAP during exercise on tolerance, dynamic hyperinflation, and dyspnea in subjects with moderate to very severe COPD., Methods: We performed a cross-sectional, experimental, 4-visit study. In visit 1, subjects performed symptom-limited cycling incremental cardiopulmonary exercise test (CPET). In visits 2-4, at least 48 h apart, in a randomized order, subjects performed constant CPET without EPAP, EPAP with 5 cm H 2 O (EPAP5), or EPAP with 10 cm H 2 O (EPAP10)., Results: The study included 15 non-hypoxemic subjects ranging from moderate to very severe COPD (mean FEV 1 = 35 ± 11% predicted). Increasing intensities of EPAP during constant CPET tended to cause progressive reduction in exercise tolerance ( P = .11). Of note, 10 of 15 subjects demonstrated significantly shorter average exercise duration with EPAP10 compared to the test without EPAP (-151 ± 105 s, P = .03 or -41 ± 26%). Minute ventilation increment was constrained by EPAP, secondary to a limited increase in tidal volume ( P = .01). Finally, dyspnea sensation and serial measurements of inspiratory capacity during exercise were similar when comparing the three interventions at isotime and at end-constant CPETs., Conclusions: The application of EPAP5 or EPAP10 during exercise tended to cause a progressive reduction in exercise tolerance in subjects with COPD without improvement in dyspnea or dynamic hyperinflation at equivalent exercise duration., (Copyright © 2017 by Daedalus Enterprises.)

Exertional dyspnea is present across the spectrum of chronic obstructive pulmonary disease (COPD) severity. However, without realizing it themselves, patients may decrease daily physical activity to avoid distressing respiratory sensations. Dyspnea also may be associated with deconditioning. Cardiopulmonary exercise testing can uncover exertional dyspnea and its physiological determinants in patients with preserved or only mildly reduced FEV 1 . Dyspnea in mild COPD can largely be explained by increased "wasted" ventilation in the physiological dead space, which heightens the drive to breathe and worsens the inspiratory mechanical constraints. During incremental exercise testing, this is readily identified as an excessive ventilation-to-metabolic demand, that is, a high ventilation ([Formula: see text]e) to carbon dioxide output ([Formula: see text]co 2 ) relationship. Linking increases in [Formula: see text]e/[Formula: see text]co 2 to exertional dyspnea may provide objective evidence that a patient's poor exercise tolerance is not just a consequence of deconditioning. This information should prompt a proactive therapeutic approach to increase the available ventilatory reserve by, for example, giving inhaled bronchodilators. Considering that the structural determinants of ventilatory inefficiency (early emphysema, ventilation-perfusion mismatching, and microvascular disease) may progress despite only modest changes in FEV 1 , serial [Formula: see text]e/[Formula: see text]co 2 measurements might also prove valuable to track disease progression in these symptomatic patients.

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., (Copyright © 2016 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.)

Background: Exercise oscillatory ventilation (EOV) is associated with poor ventilatory efficiency and higher operating lung volumes in heart failure. These abnormalities may be particularly deleterious to dyspnea and exercise tolerance in mechanically-limited patients, e.g. those with coexistent COPD., Methods: Ventilatory, gas exchange and sensory responses to incremental exercise were contrasted in 68 heart failure-COPD patients (12 EOV+). EOV was established by standard criteria., Results: Compared to EOV-, EOV+ had lower exercise capacity, worse ventilatory inefficiency and higher peak dyspnea scores (p<0.05). Peak capillary PCO 2 (PcCO 2 ) was higher and end-tidal CO 2 (PETCO 2 ) was lower in EOV+. Thus, greater (i.e., more positive) P(c-ET)CO 2 and dead space/tidal volume values were found in these patients compared to EOV- (p<0.05). Ventilatory inefficiency was related to increased dead space/tidal volume in EOV+ (r=0.74; p<0.01). Owing to higher operating lung volumes, inspiratory reserve volume (IRV) decreased to a greater extent in EOV+. Tidal volume oscillations consistently ceased when a "critical" IRV was reached (~0.3-0.5L); thereafter, PcCO 2 stabilized or increased and dyspnea scores rose sharply. Exercise capacity was closely related to IRV decrements and peak dyspnea in EOV+ (r=-0.78 and 0.84, respectively; p<0.01)., Conclusions: Dyspnea and exercise tolerance are negatively influenced by EOV in heart failure patients presenting with COPD as co-morbidity. Pharmacological and non-pharmacological interventions known to decrease EOV might prove particularly valuable to mitigate symptom burden and exercise intolerance in this specific heart failure group., (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)

A 56-year-old white woman was referred to the pulmonary clinic for evaluation of unexplained shortness of breath. She enjoyed good health until 3 months prior to this visit when she reported experiencing recurrent episodes of shortness of breath and oppressive retrosternal chest discomfort with radiation to the neck. Episodes lasting 5 to 10 min often occurred at rest and were inconsistently related to physical activity. These symptoms became progressively worse and were often associated with light-headedness and presyncope. Her past medical history was uneventful apart from a prior diagnosis of breast cysts and suspected prolactinoma. Her symptoms escalated to such a level that she was forced to seek urgent medical attention at our institutional ED on two separate occasions in the preceding weeks. These visits precipitated a number of investigations and, eventually, a referral to the pulmonary clinic., (Copyright © 2016 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.)

Background: It is currently unclear whether the additive effects of a long-acting beta(2)-agonist (LABA) and the antimuscarinic tiotropium bromide (TIO) on resting lung function are translated into lower operating lung volumes and improved exercise tolerance in patients with chronic obstructive pulmonary disease (COPD)., Methods: On a double-blind and cross-over study, 33 patients (FEV(1) = 47.4 +/- 12.9% predicted) were randomly allocated to 2-wk formoterol fumarate 12 microg twice-daily (FOR) plus TIO 18 microg once-daily or FOR plus placebo (PLA). Inspiratory capacity (IC) was obtained on constant-speed treadmill tests to the limit of tolerance (Tlim)., Results: FOR-TIO was superior to FOR-PLA in increasing post-treatment FEV(1) and Tlim (1.34 +/- 0.42 L vs. 1.25 +/- 0.39 L and 124 +/- 27% vs. 68 +/- 14%, respectively; p < 0.05). FOR-TIO slowed the rate of decrement in exercise IC compared to FOR-PLA (Deltaisotime-rest = -0.27 +/- 0.40 L vs. -0.45 +/- 0.36 L, p < 0.05). In addition, end-expiratory lung volume (% total lung capacity) was further reduced with FOR-TIO (p < 0.05). Of note, patients showing greater increases in Tlim with FOR-TIO (16/26, 61.6%) had more severe airways obstruction and lower exercise capacity at baseline. Improvement in Tlim with FOR-TIO was also related to larger increases in FEV(1) (p < 0.05)., Conclusions: Compared to FOR monotherapy, FOR-TIO further improved effort-induced dynamic hyperinflation and exercise endurance in patients with moderate-to-severe COPD. These beneficial consequences were more likely to be found in severely-disabled patients with larger resting functional responses to the combination therapy., Trial Registration: Clinicaltrials.gov Identifier: NCT00680056 [ClinicalTrials.gov].

BACKGROUND: Continuous monitoring of pulse oximetry (...) is recommended during the 6-min walk test (6MWT) to ensure that the lowest ... is recorded. In this case, severe exercise-induced desaturation (EID; ... < 80%) triggers walking interruption by the examiner. Our main objective was to assess the impact of this approach on 6MWT distance in patients with chronic respiratory diseases and, second, to evaluate the safety of the test without interruption due to severe EID. METHODS: 6MWTs with continuous monitoring of ... were prospectively performed in subjects with chronic respiratory disease. The participants were randomly allocated to walk with or without ... real-time assessment. ... visualization during the test execution was available only in the first group, and walking interruption was requested by the examiner if ... < 80%. RESULTS: One hundred forty-five participants were included in each group (68.6% females, 62 [52-69] y old) without differences in demographic and resting lung function parameters between them. The main respiratory conditions were COPD (n = 101), asthma (n = 73), pulmonary hypertension (n = 47), and interstitial lung disease (n = 39). The walked distance was similar comparing groups (349.5 ± 117.5 m vs 351.2 ± 105.4 m). Twenty-five subjects presented with severe EID in the group with real-time ... assessment, and 20 subjects had severe EID in the group without real-time assessment respectively (overall prevalence of 15.5%). The 23 participants who had their test interrupted by the examiner due to severe EID in the first group (2 subjects stopped by themselves due to excessive symptoms) walked a shorter distance compared to the 11 subjects with severe EID without test interruption in the second group (9 subjects stopped by themselves due to excessive symptoms): 240.6 ± 100.2 m versus 345.9 ± 73.4 m. No exercise-related serious adverse events were observed. CONCLUSIONS: Interruption driven by severe EID reduced the walked distance during the 6MWT. No serious adverse event, in turn, was observed in subjects with severe desaturation without real-time ... assessment. [ABSTRACT FROM AUTHOR]

Rationale: Ventilatory demand-capacity imbalance, as inferred based on a low ventilatory reserve, is currently assessed only at peak cardiopulmonary exercise testing (CPET). Peak ventilatory reserve, however, is poorly sensitive to the submaximal, dynamic mechanical ventilatory abnormalities that are key to dyspnea genesis and exercise intolerance. Objectives: After establishing sex- and age-corrected norms for dynamic ventilatory reserve at progressively higher work rates, we compared peak and dynamic ventilatory reserve for their ability to expose increased exertional dyspnea and poor exercise tolerance in mild to very severe chronic obstructive pulmonary disease (COPD). Methods: We analyzed resting functional and incremental CPET data from 275 controls (130 men, aged 19-85 yr) and 359 Global Initiative for Chronic Obstructive Lung Disease patients with stage 1-4 obstruction (203 men) who were prospectively recruited for previous ethically approved studies in three research centers. In addition to peak and dynamic ventilatory reserve (12[ventilation / estimated maximal voluntary ventilation]3100), operating lung volumes and dyspnea scores (0-10 on the Borg scale) were obtained. Results: Dynamic ventilatory reserve was asymmetrically distributed in controls; thus, we calculated its centile distribution at every 20 W. The lower limit of normal (lower than the fifth centile) was consistently lower in women and older subjects. Peak and dynamic ventilatory reserve disagreed significantly in indicating an abnormally low test result in patients: whereas approximately 50% of those with a normal peak ventilatory reserve showed a reduced dynamic ventilatory reserve, the opposite was found in approximately 15% (P,0.001). Irrespective of peak ventilatory reserve and COPD severity, patients who had a dynamic ventilatory reserve below the lower limit of normal at an isowork rate of 40W had greater ventilatory requirements, prompting earlier attainment of critically low inspiratory reserve. Consequently, they reported higher dyspnea scores, showing poorer exercise tolerance compared with those with preserved dynamic ventilatory reserve. Conversely, patients with preserved dynamic ventilatory reserve but reduced peak ventilatory reserve reported the lowest dyspnea scores, showing the best exercise tolerance. Conclusions: Reduced submaximal dynamic ventilatory reserve, even in the setting of preserved peak ventilatory reserve, is a powerful predictor of exertional dyspnea and exercise intolerance in COPD. This new parameter of ventilatory demand-capacity mismatch may enhance the yield of clinical CPET in the investigation of activity-related breathlessness in individual patients with COPD and other prevalent cardiopulmonary diseases. [ABSTRACT FROM AUTHOR]

Activity-related dyspnea in chronic lung disease is centrally related to dynamic (dyn) inspiratory constraints to tidal volume expansion. Lack of reference values for exertional inspiratory reserve (IR) has limited the yield of cardiopulmonary exercise testing in exposing the underpinnings of this disabling symptom. One hundred fifty apparently healthy subjects (82 males) aged 40–85 underwent incremental cycle ergometry. Based on exercise inspiratory capacity (IC dyn), we generated centile-based reference values for the following metrics of IR as a function of absolute ventilation: IR dyn1 ([1-(tidal volume/IC dyn)] x 100) and IR dyn2 ([1-(end-inspiratory lung volume/total lung capacity] x 100). IR dyn1 and IR dyn2 standards were typically lower in females and older subjects (p <0.05 for sex and age versus ventilation interactions). Low IR dyn1 and IR dyn2 significantly predicted the burden of exertional dyspnea in both sexes (p <0.01). Using these sex and age-adjusted limits of reference, the clinician can adequately judge the presence and severity of abnormally low inspiratory reserves in dyspneic subjects undergoing cardiopulmonary exercise testing. • Proper interpretation of exertional inspiratory constraints requires reference values. • Females and older subjects showed higher inspiratory constraints at iso-ventilation. • Sex- and age-adjusted standards are provided for clinical use. • These norms might improve the yield of CPET in assessing exertional dyspnea. [ABSTRACT FROM AUTHOR]

Several shortcomings on cardiopulmonary exercise testing (CPET) interpretation have shed a negative light on the test as a clinically useful tool. For instance, the reader should recognize patterns of dysfunction based on clusters of variables rather than relying on rigid interpretative algorithms. Correct display of key graphical data is of foremost relevance: prolixity and redundancy should be avoided. Submaximal dyspnea ratings should be plotted as a function of work rate (WR) and ventilatory demand. Increased work of breathing and/or obesity may normalize peak oxygen uptake (V̇O2) despite a low peak WR. Among the determinants of V̇O2, only heart rate is measured during non-invasive CPET. It follows that in the absence of findings suggestive of severe impairment in O2 delivery, the boundaries between inactivity and early cardiovascular disease are blurred in individual subjects. A preserved breathing reserve should not be viewed as evidence that "the lungs" are not limiting the subject. In this context, measurements of dynamic inspiratory capacity are key to uncover abnormalities germane to exertional dyspnea. A low end-tidal partial pressure for carbon dioxide may indicate either increased "wasted" ventilation or alveolar hyperventilation; thus, direct measurements of arterial (or arterialized) PO2 might be warranted. Differentiating a chaotic breathing pattern from the normal breath-by-breath noise might be complex if the plotted data are not adequately smoothed. A sober recognition of these limitations, associated with an interpretation report free from technicalities and convoluted terminology, is crucial to enhance the credibility of CPET in the eyes of the practicing physician. [ABSTRACT FROM AUTHOR]

The article describes how forced expiratory volume in one second/forced vital capacity (FEV1/FVC) ratio discordance relates to functional outcomes relevant to subjects' daily functioning. Topics include the fixed FEV1/FVC ratio cutoff can result in over diagnosis of Chronic obstructive pulmonary disease (COPD) in older individuals; and a discordant FEV1/FVC ratio should be individually interpreted in light of clinical data.

Dyspnea and exercise limitation are among the most common symptoms experienced by patients with various chronic lung diseases and are linked to poor quality of life. Our understanding of the source and nature of perceived respiratory discomfort and exercise intolerance in chronic lung diseases has increased substantially in recent years. These new mechanistic insights are the primary focus of the current review. Cardiopulmonary exercise testing (CPET) provides a unique opportunity to objectively evaluate the ability of the respiratory system to respond to imposed incremental physiological stress. In addition to measuring aerobic capacity and quantifying an individual's cardiac and ventilatory reserves, we have expanded the role of CPET to include evaluation of symptom intensity, together with a simple "non-invasive" assessment of relevant ventilatory control parameters and dynamic respiratory mechanics during standardized incremental tests to tolerance. This review explores the application of the new advances in the clinical evaluation of the pathophysiology of exercise intolerance in chronic obstructive pulmonary disease (COPD), chronic asthma, interstitial lung disease (ILD) and pulmonary arterial hypertension (PAH). We hope to demonstrate how this novel approach to CPET interpretation, which includes a quantification of activity-related dyspnea and evaluation of its underlying mechanisms, enhances our ability to meaningfully intervene to improve quality of life in these pathologically-distinct conditions. [ABSTRACT FROM AUTHOR]

Reduction in inspiratory capacity (IC) during exercise has been reported in chronic heart failure (CHF). Since inspiratory muscle dysfunction may be present to a variable degree, the assumption that IC reduction during exercise represents an increase in end-expiratory lung volume must be made with caution. This interpretation is flawed if patients develop dynamic inspiratory muscle strength reduction, i.e., progressively lower esophageal (Pes) pressures as the IC maneuvers are repeated. Sixteen CHF patients and 9 age-matched controls performed an incremental exercise test with serial IC and respiratory pressure measurements. Regardless whether IC decreased or not with exercise (N = 4 and N = 12, respectively), Pes,IC remained stable. This was confirmed by similar Pes,sniff immediately upon exercise cessation (p > .05). No association was found between changes in IC and related Pes from rest to peak exercise. Owing to the lack of dynamic inspiratory muscle weakness, non-invasive indexes of lung mechanics can be reliably obtained from exercise IC in CHF. [ABSTRACT FROM AUTHOR]