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Exercise in the heat increases the slope of the relation between minute ventilation and carbon dioxide elimination (V̇E/V̇co2 slope) in young healthy adults. An indispensable role for skin temperature in modulating the ventilatory response to exercise is noted, contradicting common belief that internal/core temperature acts independently as a controller of ventilation during hyperthermia.

After multiple waves of the COVID-19 pandemic, it has become clear that the impact of SARS-CoV-2 will carry on for years to come. Acutely infected patients show a broad range of disease severity, depending on virus variant, vaccination status, age and the presence of underlying medical and physical conditions, including obesity. Additionally, a large number of patients who have been infected with the virus present with post-COVID syndrome. In September 2020, the International Society for the Advancement of Respiratory Psychophysiology organized a virtual interest meeting on ‘Respiratory research in the age of COVID-19’, which aimed to discuss how research in respiratory psychophysiology could contribute to a better understanding of psychophysiological interactions in COVID-19. In the resulting current paper, we propose an interdisciplinary research agenda discussing selected research questions on acute and long-term neurobiological, physiological and psychological outcomes and mechanisms related to respiration and the airways in COVID-19, as well as research questions on comorbidity and potential treatment options, such as physical rehabilitation.

Heart failure with preserved ejection fraction (HFpEF) is associated with cardiopulmonary abnormalities that may increase physiological dead space to tidal volume (VD/VT) during exercise. However, studies have not corrected VD/VT for apparatus mechanical dead space (VDM), which may confound the accurate calculation of VD/VT. We evaluated whether calculating physiological dead space with (VD/VT(VDM)) and without (VD/VT) correcting for VDM impacts the interpretation of gas exchange efficiency during exercise in HFpEF. Fifteen HFpEF (age: 69 ± 6 yr; V̇o(2peak): 1.34 ± 0.45 L/min) and 12 controls (70 ± 3 yr; V̇o(2peak): 1.70 ± 0.51 L/min) were studied. Pulmonary gas exchange and arterial blood gases were analyzed at rest, submaximal (20 W for HFpEF and 40 W for controls), and peak exercise. VD/VT was calculated as [Formula: see text] – [Formula: see text] / [Formula: see text]. VD/VT(VDM) was calculated as [Formula: see text] – [Formula: see text] / [Formula: see text] – VDM/VT. VD/VT decreased from rest (HFpEF: 0.54 ± 0.07; controls: 0.32 ± 0.07) to submaximal exercise (HFpEF: 0.46 ± 0.07; controls: 0.25 ± 0.06) in both groups (P < 0.05), but remained stable (P > 0.05) thereafter to peak exercise (HFpEF: 0.46 ± 0.09; controls: 0.22 ± 0.05). In HFpEF, VD/VT(VDM) did not change (P = 0.58) from rest (0.29 ± 0.07) to submaximal exercise (0.29 ± 0.06), but increased (P = 0.02) thereafter to peak exercise (0.33 ± 0.06). In controls, VD/VT(VDM) remained stable such that no change was observed (P > 0.05) from rest (0.17 ± 0.06) to submaximal exercise (0.14 ± 0.06), or thereafter to peak exercise (0.14 ± 0.05). Calculating physiological dead space with and without a VDM correction yields quantitively and qualitatively different results, which could have impact on the interpretation of gas exchange efficiency in HFpEF. Further investigation is required to uncover the clinical consequences and the mechanism(s) explaining the increase in VD/VT(VDM) during exercise in HFpEF. NEW & NOTEWORTHY Calculating VD/VT with and without correcting for VDM yields quantitively and qualitatively different results, which could have an important impact on the interpretation of V/Q mismatch in HFpEF. The finding that V/Q mismatch and gas exchange efficiency worsened, as reflected by an increase in VD/VT(VDM) during exercise, has not been previously demonstrated in HFpEF. Thus, further studies are needed to investigate the mechanisms explaining the increase in VD/VT(VDM) during exercise in patients with HFpEF.

Background: Exercise intolerance is a defining characteristic of heart failure with preserved ejection fraction (HFpEF). A marked rise in pulmonary capillary wedge pressure (PCWP) during exertion is pathognomonic for HFpEF and is thought to be a key cause of exercise intolerance. If true, acutely lowering PCWP should improve exercise capacity. To test this hypothesis, we evaluated peak exercise capacity with and without nitroglycerin to acutely lower PCWP during exercise in patients with HFpEF. Methods: Thirty patients with HFpEF (70±6 years of age; 63% female) underwent 2 bouts of upright, seated cycle exercise dosed with sublingual nitroglycerin or placebo control every 15 minutes in a single-blind, randomized, crossover design. PCWP (right heart catheterization), oxygen uptake (breath × breath gas exchange), and cardiac output (direct Fick) were assessed at rest, 20 Watts (W), and peak exercise during both placebo and nitroglycerin conditions. Results: PCWP increased from 8±4 to 35±9 mm Hg from rest to peak exercise with placebo. With nitroglycerin, there was a graded decrease in PCWP compared with placebo at rest (–1±2 mm Hg), 20W (–5±5 mm Hg), and peak exercise (–7±6 mm Hg; drug × exercise stage P =0.004). Nitroglycerin did not affect oxygen uptake at rest, 20W, or peak (placebo, 1.34±0.48 versus nitroglycerin, 1.32±0.46 L/min; drug × exercise P =0.984). Compared with placebo, nitroglycerin lowered stroke volume at rest (–8±13 mL) and 20W (–7±11 mL), but not peak exercise (0±10 mL). Conclusions: Sublingual nitroglycerin lowered PCWP during submaximal and maximal exercise. Despite reduction in PCWP, peak oxygen uptake was not changed. These results suggest that acute reductions in PCWP are insufficient to improve exercise capacity, and further argue that high PCWP during exercise is not by itself a limiting factor for exercise performance in patients with HFpEF. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT04068844.

Rationale: Obesity presents a mechanical load to the thorax, which could perturb the generation of minute ventilation (V̇e) during exercise. Because the respiratory effects of obesity are not homogenous among all individuals with obesity and obesity-related effects could vary depending on the magnitude of obesity, we hypothesized that the exercise ventilatory response (slope of the V̇e and carbon dioxide elimination [V̇co (2)] relationship) would manifest itself differently as the magnitude of obesity increases. Objectives: To investigate the V̇e/V̇co (2) slope in an obese population that spanned across a wide body mass index (BMI) range. Methods: A total of 533 patients who presented to a surgical weight loss center for pre–bariatric surgery testing performed an incremental maximal cycling test and were studied retrospectively. The V̇e/V̇co (2) slope was calculated up to the ventilatory threshold. Patients were examined in groups based on BMI (category 1: 30–39.9 kg/m(2), category 2: 40–49.9 kg/m(2), and category 3: ≥50 kg/m(2)). Because the respiratory effects of obesity could be sex and/or age specific, we further examined patients in groups by sex and age (younger

In children, obesity typically reduces functional residual capacity (FRC), which reduces airway caliber and increases airway resistance. Whether these obesity-related changes in respiratory function can alter bronchodilator responsiveness is unknown.To investigate bronchodilator responsiveness in nonasthmatic children with and without obesity.Seventy nonasthmatic children, 8-12 years old, without (n = 19) and with (n = 51) obesity, completed spirometry, impulse oscillometry, and airway resistance measurements through plethysmography pre/post 360 µg of inhaled albuterol. FRC was assessed pre albuterol. A two-way analysis of variance determined the effects of obesity (group) and inhaled albuterol (pre-post) on outcome measures.FRC (%total lung capacity) was 16% lower in children with obesity compared with those without obesity. There was no significant group by pre-post albuterol interaction on any outcome variables. Albuterol inhalation reduced total, central and peripheral airway resistance and increased airway reactance (i.e., less negative) to a similar degree in children with and without obesity. In children with obesity, airway resistance was increased whether measured by impulse oscillometry or plethysmography. However, once airway resistance was adjusted for lung volumes (i.e., specific airway resistance or sRIn nonasthmatic early pubescent children, obesity increases total, central, and peripheral respiratory system resistance. However, the added respiratory system resistance and low lung volume breathing with obesity are not sufficient to reduce bronchodilator responsiveness.

PURPOSE: Thoracic gas compression and exercise-induced bronchodilation can influence the assessment of expiratory flow limitation (EFL) during cardiopulmonary exercise tests. The purpose of this study was to examine the effect of thoracic gas compression and exercise-induced bronchodilation on assessment of EFL in children with and without obesity. METHODS: Forty children (10.7±1.0 years; 27 obese; 15 with EFL) completed pulmonary function tests and incremental exercise tests. Inspiratory capacity maneuvers were performed during the incremental exercise test for placement of tidal flow volume loops within the maximal expiratory flow volume (MEFV) loops and EFL was calculated as the overlap between the tidal and MEFV loops. MEFV loops were plotted with volume measured at the lung using plethysmography (MEFVp), volume measured at the mouth using spirometry concurrent with measurements in the plethysmograph (MEFVm) as well as from spirometry before (MEFVpre) and after (MEFVpost) the incremental exercise test. Only the MEFVp loops were corrected for thoracic gas compression. RESULTS: Not correcting for thoracic gas compression resulted in incorrect diagnosis of EFL in 23% of children at peak exercise. EFL was 26±15%V(T) higher for MEFVm compared with MEFVp (p

Patients with heart failure with preserved ejection fraction (HFpEF) exhibit many cardiopulmonary abnormalities that could result in V˙/Q˙ mismatch, manifesting as an increase in alveolar dead space (VDDo patients with HFpEF develop VDTwenty-three patients with HFpEF and 12 control participants were studied. Gas exchange (ventilation [V˙VDThese data suggest that the increase in V˙/Q˙ mismatch may be explained by increases in VD

What is the central question of the study? What are the sex differences in ventilatory responses during exercise in adults with obesity? What is the main finding and its importance? Tidal volume and expiratory flows are lower in females when compared with males at higher levels of ventilation despite small increases in end-expiratory lung volumes. Since dyspnoea on exertion is a frequent complaint, particularly in females with obesity, careful attention should be paid to unpleasant respiratory symptoms and mechanical ventilatory constraints while prescribing exercise.Obesity is associated with altered ventilatory responses, which may be exacerbated in females due to the functional consequences of sex-related morphological differences in the respiratory system. This study examined sex differences in ventilatory responses during exercise in adults with obesity. Healthy adults with obesity (n = 73; 48 females) underwent pulmonary function testing, underwater weighing, magnetic resonance imaging (MRI), a graded exercise test to exhaustion, and two constant work rate exercise tests; one at a fixed work rate (60 W for females and 105 W for males) and one at a relative intensity (50% of peak oxygen uptake

Introduction: Heart failure with preserved ejection fraction (HFpEF) patients exhibit a marked rise in PCWP during exercise, which may contribute to ventilation-perfusion (V/Q) mismatch and manifest as an increase in alveolar dead space (alveolar V D ) and alveolar-arterial PO 2 difference (AaPO 2 ). Nitrates reduce PCWP during exercise in HFpEF, but whether nitrates also reduce V/Q mismatch during exercise is unknown. Hypothesis: The increase in PCWP and V/Q mismatch during exercise would be attenuated with acute nitroglycerin (NTG) treatment compared with placebo in HFpEF patients. Methods: 13 patients performed a 6min cycling test at 20W and an incremental cycling test (with right-heart and arterial catheterization) with placebo and NTG treatment. The physiologic dead space to tidal volume (V D /V T ) was calculated using the Enghoff modification of the Bohr equation. Alveolar V D was calculated as: V D /V T x V T - anatomic dead space (anatomic V D , estimated as 2mL/kg lean body mass). AaPO 2 was calculated using the alveolar gas equation. Data were analyzed using a 2-way ANOVA. Results: PCWP decreased with NTG at 20W (placebo: 21.1±6.2 vs. NTG: 16.5±6.1mmHg, p=0.02) and peak exercise (placebo: 33.7±7.1 vs. NTG: 26.2±5.6mmHg, pD did not differ between treatments at rest (placebo: 0.11±0.07 vs. NTG:0.12±0.06L/breath, p=0.91), 20W (placebo: 0.22±0.09 vs. NTG: 0.24±0.10L/breath, p=0.62), or peak exercise (placebo: 0.34±0.14 vs. NTG:0.36±0.16L/breath, p=0.83). Nor did AaPO 2 differ between treatments at rest (placebo: 17.6±4.3 vs. NTG: 18.3±5.7mmHg, p=0.76), 20W (placebo: 22.0±6.9 vs. NTG: 22.1±8.1mmHg, p=0.99), or peak exercise (placebo: 25.1±9.1 vs. NTG: 27.8±9.9mmHg, p=0.41). No significant exercise-by-treatment interaction was detected for V D /V T (p=0.80). Conclusions: This study showed that NTG attenuated the increase in PCWP, but had no effect on the increase in alveolar V D or AaPO 2 during exercise. These findings suggest that the exercise-induced increase in V/Q mismatch may not be exclusively related to abnormal exercise hemodynamics. Further study is required to determine the clinical consequences and the mechanism(s) responsible for the progressive increase in V/Q mismatch during exercise in HFpEF patients.

Patients with heart failure with preserved ejection fraction (HFpEF) exhibit cardiopulmonary abnormalities that could affect the predictability of exercise [Formula: see text] from the Jones corrected partial pressure of end-tidal CO(2) (PJ(CO(2))) equation (PJ(CO(2)) = 5.5 + 0.9 × [Formula: see text] − 2.1 × V(T)). Since the dead space to tidal volume (V(D)/V(T)) calculation also includes [Formula: see text] measurements, estimates of V(D)/V(T) from PJ(CO(2)) may also be affected. Because using noninvasive estimates of [Formula: see text] and V(D)/V(T) could save patient discomfort, time, and cost, we examined whether partial pressure of end-tidal CO(2) ([Formula: see text]) and PJ(CO(2)) can be used to estimate [Formula: see text] and V(D)/V(T) in 13 patients with HFpEF. [Formula: see text] was measured from expired gases measured simultaneously with radial arterial blood gases at rest, constant-load (20 W), and peak exercise. V(D)/V(T[art]) was calculated using the Enghoff modification of the Bohr equation, and estimates of V(D)/V(T) were calculated using [Formula: see text] (V(D)/V(T[ET])) and PJ(CO(2)) (V(D)/V(T[J])) in place of [Formula: see text]. [Formula: see text] was similar to [Formula: see text] at rest (−1.46 ± 2.63, P = 0.112) and peak exercise (0.66 ± 2.56, P = 0.392), but overestimated [Formula: see text] at 20 W (−2.09 ± 2.55, P = 0.020). PJ(CO(2)) was similar to [Formula: see text] at rest (−1.29 ± 2.57, P = 0.119) and 20 W (−1.06 ± 2.29, P = 0.154), but underestimated [Formula: see text] at peak exercise (1.90 ± 2.13, P = 0.009). V(D)/V(T[ET]) was similar to V(D)/V(T[art]) at rest (−0.01 ± 0.03, P = 0.127) and peak exercise (0.01 ± 0.04, P = 0.210), but overestimated V(D)/V(T[art]) at 20 W (−0.02 ± 0.03, P = 0.025). Although V(D)/V(T[J]) was similar to V(D)/V(T[art]) at rest (−0.01 ± 0.03, P = 0.156) and 20 W (−0.01 ± 0.03, P = 0.133), V(D)/V(T[J]) underestimated V(D)/V(T[art]) at peak exercise (0.03 ± 0.04, P = 0.013). Exercise [Formula: see text] and V(D)/V(T[ET]) provides better estimates of [Formula: see text] and V(D)/V(T[art]) than PJ(CO(2)) and V(D)/V(T[J]) does at peak exercise. Thus, estimates of [Formula: see text] and V(D)/V(T) should only be used if sampling arterial blood during CPET is not feasible. NEW & NOTEWORTHY [Formula: see text] provides a better estimate of [Formula: see text] than PJ(CO(2)) at peak exercise, and V(D)/V(T[ET]) provides a better estimate of V(D)/V(T[art]) than V(D)/V(T[J]) at peak exercise. Although we reported significant correlations, we did not find an identity between [Formula: see text] and estimates of [Formula: see text] , nor did we find an identity between V(D)/V(T[art]) and estimates of V(D)/V(T[art]). Thus, caution should be taken and estimates of [Formula: see text] and V(D)/V(T) should only be used if sampling arterial blood during CPET is not feasible.

PURPOSE: Without consideration for the effects of fat mass, there could be an underestimation of cardiorespiratory fitness in children with obesity leading to a clinical diagnosis of deconditioning and resulting in unrealistic training goals and limitation of physical activities. The purpose of this study was to identity methods of quantifying cardiorespiratory fitness that were less influenced by fat mass. METHODS: Fifty-three children, 27 with obesity (10.9 ± 1.0 yr) and 26 without obesity (11.0 ± 1.0 yr), volunteered for this study. Maximal oxygen uptake, an indicator of cardiorespiratory fitness, was referenced to lean body mass, body mass, and predicted body mass at the 50th and 85th body mass index percentiles. RESULTS: Children with obesity carried 18 kg more fat mass and 7 kg more lean body mass compared with children without obesity. Cardiorespiratory fitness based on lean body mass, body mass, and predicted body mass at the 85th percentile was lower in children with obesity compared with children without obesity (P 0.37). CONCLUSION: Quantifying cardiorespiratory fitness based on lean body mass or predicted body mass at the 50th percentile could be useful for estimating fitness levels in children with obesity.

We hypothesized that weight loss would ameliorate dyspnea on exertion (DOE) and feelings of unpleasantness related to the DOE in obese men. Eighteen men (34±7yr, 35±4kg/m(2) BMI, mean±SD) participated in a 12-week weight loss program. Body composition, pulmonary function, cardiorespiratory measures, DOE, and unpleasantness (visual analog scale) were assessed before and after weight loss. Subjects were grouped by Ratings of Perceived Breathlessness (RPB, Borg 0–10 scale) during submaximal cycling: Ten men rated RPB≥4 (+DOE), eight rated RPB≤2 (–DOE). Subjects lost 10.3±5.6kg (9.2±4.5%) of body weight (n=18). RPB during submaximal cycling was significantly improved in both groups (+DOE: 4.1±0.3 to 2.8±1.1; –DOE: 1.3±0.7 to 0.8±0.6, p0.05). Moderate weight loss appears to be an effective option to ameliorate DOE and unpleasantness related to DOE in obese men.

While the 0-10 Borg scale to rate perceived breathlessness (RPB) is widely used to assess dyspnea on exertion, the repeatability of RPB in women with obesity is unknown. We examined the repeatability of RPB in women with obesity during submaximal constant-load cycling following at least 10 weeks of normal daily life. Seventeen women (37 ± 7 yr; 34.6 ± 4.5 kg/m

Obesity alters chest wall mechanics, reduces lung volumes, and increases airway resistance. In addition, the luminal area of the larger conducting airways is smaller in women than in men when matched for lung size. We examined whether differences in pulmonary mechanics with obesity and sex were associated with the dysanapsis ratio (DR), an estimate of airway size when the expiratory flow is maximal, in men and women with and without obesity. In addition, we examined the ability to estimate DR using predicted versus measured static recoil pressure at 50% forced vital capacity (FVC; Pst(50FVC)). Participants completed pulmonary function testing and measurements of pulmonary mechanics. Flow, volume, and transpulmonary pressure were recorded while completing forced vital capacity (FVC) maneuvers in a body plethysmograph. Static compliance curves were collected using the occlusion technique. DR was calculated using measured values of forced midexpiratory flow and Pst(50FVC). DR was also calculated using Pst predicted from previously reported data. There was no significant group (lean vs. obese) by sex interaction or main effect of group on DR. However, women displayed significantly larger DR compared with men. Predicted Pst(50FVC) was significantly greater than measured Pst(50FVC). DR calculated from measured Pst was significantly greater than when using predicted Pst. In conclusion, although obesity does not appear to alter airway size, women may have larger airways compared with men when midexpiratory flow is maximal. In addition, DR estimated using predicted Pst should be used with caution. NEW & NOTEWORTHY It is unclear whether obesity in combination with sex influences the dysanapsis ratio (DR). These data indicate that DR is unaltered in adults with obesity and is greater in women than in men but similar between sexes when matched for lung volume. We also report a significant difference between predicted and measured static recoil pressure. Thus, we caution against predicting static recoil pressure in the calculation of DR.

Temporal responses of ratings of perceived breathlessness (RBP) during constant-load and incremental exercise, and during voluntary hyperpnea (EVH) were examined in women with obesity. Following 6 min of constant-load (60W) cycling, 34 women rated RPB≥4 (+DOE) and 22 women rated RPB≤2 (–DOE). Both groups completed an incremental cycling test and an EVH test at 40 and 60L/min; RPB was assessed each minute of incremental cycling and at the end of each EVH trial. RPB increased with ventilation during constant-load (+DOE: R2=0.86; –DOE: R2=0.82) and incremental (+DOE: R2=0.91; –DOE: R2=0.92) exercise, but + DOE had a greater y-intercept than –DOE (60W: -0.16±1.53 vs. -0.73±0.55; incremental: -0.50±1.40 vs. -1.71±0.84). Despite matching ventilation, RPB was greater in + DOE at baseline (0.97±1.14 vs. 0.14±0.28), 40L/min (2.50±1.43 vs. 0.98±0.91), and 60L/min (3.94±2.19 vs. 2.07±1.32) during EVH. These findings show that despite linear associations between RPB and ventilation during exercise and voluntary hyperpnea, breathlessness perception at a given ventilatory demand is heightened in +DOE compared with –DOE.

Forced mid-expiratory flow (i.e., isoFEF(25-75)) may increase with a short-acting β(2)-agonist in nonasthmatic children without bronchodilator responsiveness. This could also increase estimated ventilatory capacity along mid-expiration ([Formula: see text] ecap(25-75)), especially in vulnerable children with obesity who exhibit altered breathing mechanics. We estimated [Formula: see text] ecap(25-75) pre- and post-albuterol treatment in 8-12yo children without (n=28) and with (n=46) obesity. A two-way ANOVA was performed to determine effects of an inhaled bronchodilator (pre-post) and obesity (group) on isoFEF(25-75) and [Formula: see text] ecap(25-75). There was no group by bronchodilator interaction or main group effect on outcome variables. However, a significant main effect of the bronchodilator was detected in spirometry parameters, including a substantial increase in isoFEF(25-75) (17.1±18.0%) and only a slight (non-clinical) but significant increase in FEV(1) (2.4±4.3%). [Formula: see text] ecap(25-75) significantly increased with albuterol (+11.7±10.6L/min; +15.8±13.9%). These findings imply potentially important increases in ventilatory reserve with a bronchodilator in nonasthmatic children without and with obesity, which could potentially influence respiratory function at rest and during exercise.

PURPOSE: While dyspnea on exertion (DOE) is a common complaint in otherwise healthy obese women, less is known about feelings of unpleasantness and/or negative emotions provoked by DOE. We examined whether ratings of perceived breathlessness (RPB) during exercise were associated with ratings of unpleasantness and negative emotions (depression, anxiety, frustration, anger, and fear) in obese women. METHODS: Seventy-four women (34 ± 7 yrs, 36 ± 4 kg/m(2), 46 ± 5% body fat) performed 6 minutes of constant-load cycling (60 W); RPB (0–10 scale), and unpleasantness and negative emotions (visual analog scales, 10 cm) were assessed at the end. RESULTS: RPB were significantly correlated with unpleasantness and negative emotions (p < 0.05). The strongest correlations were between RPB and unpleasantness (r = 0.61, p < 0.001), and RPB and anxiety (r = 0.50, p < 0.001). CONCLUSIONS: DOE can significantly provoke unpleasantness and negative emotions during exercise in obese women. This may affect their willingness to engage in regular physical activity.

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Obesity is a common comorbidity of chronic obstructive pulmonary disease (COPD) and has been associated with worse outcomes. However, it is unknown whether the interaction between obesity and COPD modulates diaphragm shape and consequently its function. The body mass index (BMI) has been used as a correlate of obesity. We tested the hypothesis that the shape of the diaphragm muscle and size of the ring of its insertion in non-COPD and COPD subjects are modulated by BMI. We recruited 48 COPD patients with postbronchiodilator forced expiratory volume in 1 s (FEV1)-to-forced vital capacity (FVC) < 0.7 and 29 age-matched smoker/exsmoker control (non-COPD) subjects, who underwent chest computed tomography (CT) at lung volumes ranging from functional residual capacity (FRC) to total lung capacity (TLC). We then computed maximum principal diaphragm curvature in the midcostal region of the left hemidiaphragm at the end of inspiration during quiet breathing (EI) and at TLC. The radius of maximum curvature of diaphragm muscle increased with BMI in both COPD and non-COPD subjects. The size of diaphragm ring of insertion on the chest wall also increased significantly with increasing BMI. Surprisingly, COPD severity did not appear to cause significant alteration in diaphragm shape except in normal-weight subjects at TLC. Our data uncovered important factors such as BMI, the size of the diaphragm ring of insertion, and disease severity that modulate the structure of the ventilatory pump in non-COPD and COPD subjects.

Purpose: The purpose of this study was to examine whether a supramaximal constant-load verification test at 105% of the highest work rate would yield a higher V˙O2max when compared with an incremental test in 10- to 12-yr-old nonobese and obese children. Methods: Nine nonobese (body mass index percentile = 57.5 ± 23.2) and nine obese (body mass index percentile = 97.9 ± 1.4) children completed a two-test protocol that included an incremental test followed 15 min later by a supramaximal constant-load verification test. Results: The V˙O2max achieved in verification testing (nonobese = 1.71 ± 0.31 L·min−1 and obese = 1.94 ± 0.47 L·min−1) was significantly higher than that achieved during the incremental test (nonobese = 1.57 ± 0.27 L·min−1 and obese = 1.84 ± 0.48 L·min−1; P < 0.001). There was no significant group (i.e., nonobese vs obese)–test (i.e., incremental vs verification) interaction, suggesting that there was no effect of obesity on the difference between verification and incremental V˙O2max (P = 0.747). Conclusion: A verification test yielded significantly higher values of V˙O2max when compared with the incremental test in obese children. Similar results were observed in nonobese children. Supramaximal constant-load verification is a time-efficient and well-tolerated method for identifying the highest V˙O2 in nonobese and obese children.

Background Pediatric patients with pulmonary embolism (PE) suffer from exercise intolerance and dyspnea on exertion, often without right heart dysfunction or pulmonary hypertension - at least at rest. The pathophysiology of the exercise limitation following pediatric PE therefore remains incompletely understood. Objectives To extend our understanding of exercise intolerance in pediatric patients with PE by examining ventilatory and hemodynamic responses to exercise. Methods To accomplish our goal, we instituted a standardized institutional protocol to systematically assess exercise capacity in pediatric PE patients in the first 3 months following diagnosis. Between February 2019- June 2020, 15 patients underwent resting pulmonary function tests and an incremental symptom-limited cardiopulmonary exercise testing (CPET) to obtain peak exercise in 8-12 minutes. All patients had received anticoagulation for at least 3 months. In all patients, right and left ventricular systolic and/or diastolic dysfunction at rest was ruled out by transthoracic echocardiography. Continuous measurements were made of minute ventilation (VE), oxygen uptake (VO2), carbon dioxide production (VCO2), heart rate (HR), and blood pressure. Predicted values for peak VO2 and work rate were generated from predictive equations. Patients with impaired exercise capacity, defined as Results Baseline, clinical characteristics, and CPET data are shown in Tables 1 and 2. Forced Vital Capacity was normal without signs of airway obstruction. Three patients failed to reach their predicted physiologic limits during exercise, and CPET was terminated by the patient prematurely (e.g., muscular exertion, fatigue, & dyspnea, respectively). The mean exercise duration was 9.85 min. The mean ventilatory reserve was within normal limits (>15%) in all but 1 patient. VO2/work rate was normal with normal VO2 at the anaerobic threshold (mean 1541ml/kg/min, SD:731). Exercise capacity, as measured by peak VO2 was reduced, that is, 35) in three of the five patients with decreased exercise capacity. The O2 pulse was attenuated in patients with decreased exercise capacity when compared to those with normal exercise capacity (7.5 mL.beat -1 vs. 12.9-1; p=0.037). Of the two patients who underwent exCMR; one showed reduced right ventricular ejection fraction (38%), abnormal RV strain (-11.3%), elevated right sided pressures signified by interventricular flattening upon inspiration during free breathing scan and an uncoupled RV to the pulmonary circulation. Conclusions Reduced exercise capacity is common after PE and not evident by resting evaluations. Pediatric PE patients with low exercise capacity and dyspnea seem to be characterized by either an abnormal pulmonary vascular response to exercise or decreased ventilatory efficiency. Larger studies are needed to better understand exercise pathophysiology after pediatric PE. Disclosures No relevant conflicts of interest to declare.

Assessing respiratory mechanics and muscle function is critical for both clinical practice and research purposes. Several methodological developments over the past two decades have enhanced our understanding of respiratory muscle function and responses to interventions across the spectrum of health and disease. They are especially useful in diagnosing, phenotyping and assessing treatment efficacy in patients with respiratory symptoms and neuromuscular diseases. Considerable research has been undertaken over the past 17 years, since the publication of the previous American Thoracic Society (ATS)/European Respiratory Society (ERS) statement on respiratory muscle testing in 2002. Key advances have been made in the field of mechanics of breathing, respiratory muscle neurophysiology (electromyography, electroencephalography and transcranial magnetic stimulation) and on respiratory muscle imaging (ultrasound, optoelectronic plethysmography and structured light plethysmography). Accordingly, this ERS task force reviewed the field of respiratory muscle testing in health and disease, with particular reference to data obtained since the previous ATS/ERS statement. It summarises the most recent scientific and methodological developments regarding respiratory mechanics and respiratory muscle assessment by addressing the validity, precision, reproducibility, prognostic value and responsiveness to interventions of various methods. A particular emphasis is placed on assessment during exercise, which is a useful condition to stress the respiratory system. ispartof: EUROPEAN RESPIRATORY JOURNAL vol:53 issue:6 ispartof: location:England status: published

The objective of this study was to examine the effects of obesity on the oxygen (O2) cost of breathing using the eucapnic voluntary hyperpnea (EVH) technique in 10- and 11-year-old children. Seventeen children (8 without and 9 with obesity) underwent EVH trials at two levels of ventilation for assessing the O2 cost of breathing (slope of oxygen uptake, V ˙ O 2 vs. minute ventilation) and a dual energy x-ray absorptiometry scan. Resting and EVH V ˙ O 2 was higher in children with obesity when compared with children without obesity (P = 0.0096). The O2 cost of breathing did not statistically differ between children without (2.09 ± 0.46 mL/L) and with obesity (2.08 ± 0.64 mL/L, P = 0.99), but the intercept was significantly greater in children with obesity. Chest mass explained 85 % of the variance in resting V ˙ O 2 in children with obesity. Higher resting energy requirements, attributable to increased chest mass, can increase the absolute metabolic costs of exercise and hyperpnea in children with obesity.

We investigated the contributions of obesity on multidimensional aspects of dyspnea on exertion (DOE) in patients referred for clinical cardiopulmonary exercise testing (CPET). Ratings of perceived breathlessness (RPB, Borg scale 0–10) were collected in obese (BMI ≥ 30; n = 47) and nonobese (BMI ≤ 25; n = 27) patients during two (one lower: ~30 W; and one higher: ~50 W) 4–6 min constant load cycling bouts. Multidimensional dyspnea profiles (MDP) were collected in the final 26 obese and 14 nonobese patients of the sample. RPB was greater (p < 0.05) in obese (3.3 ± 2.2 vs 2.4 ± 1.4) at lower work rates, but similar at higher work rates (4.9 ± 2.2 vs 4.4 ± 1.8). MDP sensory score including unpleasantness was 4.3 ± 2.2 in obese vs 2.5 ± 1.9 in nonobese (p < 0.001). The affective score was 1.9 ± 2.2 vs 0.7 ± 0.7, respectively (p < 0.01). Breathing sensations including ‘air hunger’, ‘effort’, and ‘breathing at lot’ were greater (p < 0.05) in obese, making these patients more frustrated/angry (p < 0.05). Obesity should be considered as a potential independent influencing factor that provokes DOE and unpleasantness when assessing breathlessness during CPET.

Most diagnostic tests assess the function of a single organ or organ system at rest. Conversely, exercise requires the integrated function of multiple systems under stress, including the cardiovascular, pulmonary, and musculoskeletal systems. The physical stress of exercise can expose physiological limitations not otherwise apparent at rest. This is particularly relevant for patients with respiratory and/or heart diseases in whom the increased physical demands of exercise quickly exhaust their reduced functional reserves, leading to the disabling symptoms of dyspnea, leg discomfort, and fatigue. The present chapter provides a framework for CPET performance and interpretation aimed at maximizing its clinical relevance. This approach underscores the principle that measurement of exertional symptoms, using validated scales and parameters of ventilatory control and dynamic respiratory mechanics, should be routinely used to optimize clinical CPET interpretation.

During constant-load exercise, some otherwise healthy obese women report substantially more dyspnea on exertion (DOE) than do others. The objective of this study was to investigate whether qualitative differences exist between the sensations of dyspnea felt by these women.Seventy-eight women were categorized based on their ratings of perceived breathlessness (RPBs) (Borg 0-10 scale) after 6 min of 60-W cycling. Thirty-four women rated RPB ≥ 4 (+DOE) (34 ± 7 years, 36 ± 5 kg/m² BMI), and 22 women rated RPB ≤ 2 (-DOE) (32 ± 7 years, 37 ± 4 kg/m² BMI). Twenty-two women rated RPB as 3 (RPB = 3) (34 ± 7 years, 34 ± 4 kg/m² BMI) and were grouped separately to allow for a better delineation of the +DOE and the -DOE groups. After the exercise test, subjects were asked to pick three of 15 statements that best described their respiratory sensations.The +DOE and the -DOE groups were characterized differentially (P.05) by the respiratory clusters "Breathing more" (82% of -DOE vs 41% of +DOE), "Shallow" (36% vs 6%), and "Heavy" (14% vs 53%). All four descriptors in the cluster "Work/Effort" were chosen more frequently by women in the +DOE group than by women in the -DOE group. Although relative exercise intensity was higher in the +DOE women (75% ± 13% vs 67% ± 10% of oxygen uptake at peak exercise, 41 ± 10 L/min vs 31 ± 8 L/min as % maximal voluntary ventilation, 83% ± 7% vs 76% ± 7% of peak heart rate), none of these variables was significantly associated with RPB.Not only is the intensity of dyspnea significantly different between the +DOE and the -DOE groups, but so are the self-reported qualitative aspects of their dyspnea. Women in the +DOE group reported an increased sensation of the work of breathing relative to women in the -DOE group, which may be associated with the elevated RPB.

Simulated haemorrhage, e.g. lower body negative pressure (LBNP), reduces central blood volume and mean arterial pressure, while ventilation increases. Passive whole-body heat stress likewise increases ventilation. The objective of this project was to test the hypothesis that ventilatory responses to reductions in central blood volume and arterial pressure during simulated haemorrhage are enhanced when individuals are heat stressed rather than normothermic. Eight healthy men (34 ± 9 years old, 176 ± 6 cm tall and 80.2 ± 4.2 kg body weight) underwent a simulated haemorrhagic challenge via LBNP until presyncope on two separate occasions, namely normothermic control and whole-body heat-stress trials. Baseline ventilation and core and mean skin temperatures were not different between trials (all P > 0.05). Prior to LBNP, heat stress increased core (from 36.8 ± 0.2 to 38.2 ± 0.2°C, P 0.05). These data suggest that the increase in ventilation during simulated haemorrhage induced via LBNP is not altered in heat-stressed humans.

Background The ventilatory response to exercise can be transiently adjusted in response to environmentally (e.g., breathing apparatus) or physiologically altered conditions (e.g., respiratory disease), maintaining constant relative arterial PCO2 regulation from rest to exercise (Mitchell and Babb, 2006); this augmentation is called short-term modulation (STM) of the exercise ventilatory response. Obesity and/or obstructive sleep apnea could affect the exercise ventilatory response and the capacity for STM due to chronically increased mechanical and/or ventilatory loads on the respiratory system, and/or recurrent (chronic) intermittent hypoxia experienced during sleep. We hypothesized that: (1) the exercise ventilatory response is augmented in obese OSA patients compared with obese non-OSA adults, and (2) the capacity for STM with added dead space is diminished in obese OSA patients. Methods Nine obese adults with OSA (age: 39 ± 6 yr, BMI: 40 ± 5 kg/m2, AHI: 25 ± 24 events/h [range 6–73], mean ± SD) and 8 obese adults without OSA (age: 38 ± 10 yr, BMI: 37 ± 6 kg/m2, AHI: 1 ± 2) completed three, 20-min bouts of constant-load submaximal cycling exercise (8 min rest, 6 min at 10 and 30 W) with or without added external dead space (200 or 400 mL; 20 min rest between bouts). Steady-state measurements were made of ventilation ( V ˙ E), oxygen consumption V ˙ O2), carbon dioxide production ( V ˙ CO2), and end-tidal PCO2 (PETCO2). The exercise ventilatory response was defined as the slope of the V ˙ E- V ˙ CO2 relationship (Δ V ˙ E/Δ V ˙ CO2). Results In control (i.e. no added dead space), the exercise ventilatory response was not significantly different between non-OSA and OSA groups (Δ V ˙ E/Δ V ˙ CO2 slope: 30.5 ± 4.2 vs 30.5 ± 3.8, p > 0.05); PETCO2 regulation from rest to exercise did not differ between groups (p > 0.05). In trials with added external dead space, Δ V ˙ E/Δ V ˙ CO2 increased with increased dead space (p Conclusions Contrary to our hypotheses: (1) the exercise ventilatory response is not increased in obese OSA patients compared with obese non-OSA adults, and (2) the capacity for STM with added dead space is preserved in obese OSA and non-OSA adults.

The quantification and interpretation of cardiorespiratory fitness (CRF) in obesity is important for adequately assessing cardiovascular conditioning, underlying comorbidities, and properly evaluating disease risk. We retrospectively compared peak oxygen uptake (VO(2)peak) (ie, CRF) in absolute terms, and relative terms (% predicted) using three currently suggested prediction equations (Equations R, W, and G).There were 19 nonobese and 66 obese participants. Subjects underwent hydrostatic weighing and incremental cycling to exhaustion. Subject characteristics were analyzed by independent t test, and % predicted VO(2)peak by a two-way analysis of variance (group and equation) with repeated measures on one factor (equation).VO(2)peak (L/min) was not different between nonobese and obese adults (2.35 ± 0.80 [SD] vs 2.39 ± 0.68 L/min). VO(2)peak was higher (P.02) relative to body mass and lean body mass in the nonobese (34 ± 8 mL/min/kg vs 22 ± 5 mL/min/kg, 42 ± 9 mL/min/lean body mass vs 37 ± 6 mL/min/lean body mass). Cardiorespiratory fitness assessed as % predicted was not different in the nonobese and obese (91% ± 17% predicted vs 95% ± 15% predicted) using Equation R, while using Equation W and G, CRF was lower (P.05) but within normal limits in the obese (94 ± 15 vs 87 ± 11; 101% ± 17% predicted vs 90% ± 12% predicted, respectively), depending somewhat on sex.Traditional methods of reporting VO(2)peak do not allow adequate assessment and quantification of CRF in obese adults. Predicted VO(2)peak does allow a normalized evaluation of CRF in the obese, although care must be taken in selecting the most appropriate prediction equation, especially in women. In general, otherwise healthy obese are not grossly deconditioned as is commonly believed, although CRF may be slightly higher in nonobese subjects depending on the uniqueness of the prediction equation.