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IntroductionSeveral studies report that pulmonary oxygen uptake (V̇O 2 ) at the respiratory compensation point (RCP) is equivalent to the V̇O 2 at critical power (CP), suggesting that the variables can be used interchangeably to demarcate the threshold between heavy and severe intensity domains. However, if RCP is a valid surrogate for CP, their values should correspond even when assessed in patients with chronic obstructive pulmonary disease (COPD) in whom the "normal" mechanisms linking CP and RCP are impeded. The aim of this study was to compare V̇O 2 at CP with V̇O 2 at RCP in patients with COPD.MethodsTwenty-two COPD patients (14 male/8 female; forced expiratory volume in 1 s, 46% ± 17% pred) performed ramp-incremental cycle ergometry to intolerance (5-10 W·min -1 ) for the determination of gas exchange threshold (GET) and RCP. CP was calculated from the asymptote of the hyperbolic power-duration relationship from 3-5 constant-power exercise tests to intolerance. CP was validated with a 20-min constant-power ride.ResultsGET was identified in 20 of 22 patients at a V̇O 2 of 0.93 ± 0.18 L·min -1 (75% ± 13% V̇O 2peak ), whereas RCP was identified in just 3 of 22 patients at a V̇O 2 of 1.40 ± 0.39 L·min -1 (85% ± 2% V̇O 2peak ). All patients completed constant-power trials with no difference in peak physiological responses relative to ramp-incremental exercise ( P > 0.05). CP was 46 ± 22 W, which elicited a V̇O 2 of 1.04 ± 0.29 L·min -1 (90% ± 9% V̇O 2peak ) during the validation ride. The difference in V̇O 2 at 15 and 20 min of the validation ride was 0.00 ± 0.04 L, which was not different from a hypothesized mean of 0 ( P = 0.856), thereby indicating a V̇O 2 steady state.ConclusionsIn COPD patients, who present with cardiopulmonary and/or respiratory-mechanical dysfunction, CP can be determined in the absence of RCP. Accordingly, CP and RCP are not equivalent in this group.

Exercise limitation is a characteristic feature of chronic respiratory diseases such as COPD and is associated with poor outcomes including decreased functional status and health-related quality of life and increased mortality. The mechanisms responsible for exercise limitation are complex and include ventilatory limitation, cardiovascular impairment, and skeletal muscle dysfunction. In addition, comor- bidities such as cardiovascular disease are common in this population and can further impact exercise capacity. Exercise training, a core component of pulmonary rehabilitation, improves exercise capacity by addressing many of these mechanisms that, in turn, can potentially slow the decline of lung function, reduce the frequency of exacerbations, and decrease mortality. This article will discuss the mechanisms of exercise limitation in individuals with chronic respiratory disease, primarily focusing on COPD, and provide an overview of exercise training and its benefits in this patient population. [ABSTRACT FROM AUTHOR]

Mehrdad Behnia,1 Kathy E Sietsema2 1Pulmonary and Critical Care, University of Central Florida, Orlando, FL, USA; 2The Lundquist Institute for Biomedical Innovation, Harbor-UCLA Medical Center, Torrance, CA, USACorrespondence: Mehrdad Behnia, Pulmonary and Critical Care, University of Central Florida, PO Box 953814, Lake Mary, FL, 32749, USA, Tel +1 706-339-8634, Email Mehrdad.behnia.md.phd@adventhelath.comAbstract: Chronic obstructive pulmonary disease (COPD) is a disease defined by airflow obstruction with a high morbidity and mortality and significant economic burden. Although pulmonary function testing is the cornerstone in diagnosis of COPD, it cannot fully characterize disease severity or cause of dyspnea because of disease heterogeneity and variable related and comorbid conditions affecting cardiac, vascular, and musculoskeletal systems. Cardiopulmonary exercise testing (CPET) is a valuable tool for assessing physical function in a wide range of clinical conditions, including COPD. Familiarity with measurements made during CPET and its potential to aid in clinical decision-making related to COPD can thus be useful to clinicians caring for this population. This review highlights pulmonary and extrapulmonary impairments that can contribute to exercise limitation in COPD. Key elements of CPET are identified with an emphasis on measurements most relevant to COPD. Finally, clinical applications of CPET demonstrated to be of value in the COPD setting are identified. These include quantifying functional capacity, differentiating among potential causes of symptoms and limitation, prognostication and risk assessment for operative procedures, and guiding exercise prescriptionKeywords: dyspnea, obstructive lung disease, exercise intolerance, exercise limitation

Patients with chronic obstructive pulmonary disease receive a range of treatments including but not limited to inhaled bronchodilators, inhaled and systemic corticosteroids, supplemental oxygen, and pulmonary rehabilitation. Pulmonary rehabilitation is a multidisciplinary intervention that seeks to combine patient education, exercise, and lifestyle changes into a comprehensive program. Programs 6 to 8 weeks in length have been shown to improve health, reduce dyspnea, increase exercise capacity, improve psychological well-being, and reduce healthcare utilization and hospitalization. Although the use of pulmonary rehabilitation is widely supported by the literature, controversy still exists regarding what should be included in the programs. The goal of this review was to summarize the evidence for pulmonary rehabilitation and identify the areas that hold promise in improving its utilization and effectiveness.

Patients with chronic obstructive pulmonary disease receive a range of treatments including but not limited to inhaled bronchodilators, inhaled and systemic corticosteroids, supplemental oxygen, and pulmonary rehabilitation. Pulmonary rehabilitation is a multidisciplinary intervention that seeks to combine patient education, exercise, and lifestyle changes into a comprehensive program. Programs 6 to 8 weeks in length have been shown to improve health, reduce dyspnea, increase exercise capacity, improve psychological well-being, and reduce healthcare utilization and hospitalization. Although the use of pulmonary rehabilitation is widely supported by the literature, controversy still exists regarding what should be included in the programs. The goal of this review was to summarize the evidence for pulmonary rehabilitation and identify the areas that hold promise in improving its utilization and effectiveness.

Caroline Oliveira Ribeiro,1 Agnaldo José Lopes,2,3 Pedro Lopes de Melo1 1Biomedical Instrumentation Laboratory, Institute of Biology and Faculty of Engineering, State University of Rio de Janeiro, Rio de Janeiro, Brazil; 2Pulmonary Function Laboratory, State University of Rio de Janeiro, Rio de Janeiro, Brazil; 3Pulmonary Rehabilitation Laboratory, Augusto Motta University Center, Rio de Janeiro, BrazilCorrespondence: Pedro Lopes de Melo, Rua São Francisco Xavier 524, Pavilhão Haroldo Lisboa da Cunha, Sala 104, Maracanã, Rio de Janeiro, 20550-013, Brazil, Tel +55-21-2334-0705, Email plopes@uerj.brPurpose: Respiratory oscillometry has emerged as a powerful method for detecting respiratory abnormalities in COPD. However, this method has not been widely introduced into clinical practice. This limitation arises, at least in part, because the clinical meaning of the oscillometric parameters is not clear. In this paper, we evaluated the association of oscillometry with functional capacity and its ability to predict abnormal functional capacity in COPD.Patients and Methods: This cross-sectional study investigated a control group formed by 30 healthy subjects and 30 outpatients with COPD. The subjects were classified by the Glittre‑ADL test and handgrip strength according to the functional capacity.Results: This study has shown initially that subjects with abnormal functional capacity had a higher value for resistance (p < 0.05), reactance area (Ax, p < 0.01), impedance modulus (Z4, p < 0.05), and reduced dynamic compliance (Cdyn, p < 0.05) when compared with subjects with normal functional capacity. This resulted in significant and consistent correlations among resistive oscillometric parameters (R=− 0.43), Cdyn (R=− 0.40), Ax (R = 0.42), and Z4 (R = 0.41) with exercise performance. Additionally, the effects of exercise limitation in COPD were adequately predicted, as evaluated by the area under the curve (AUC) obtained by receiver operating characteristic analysis. The best parameters for this task were R4-R20 (AUC = 0.779) and Ax (AUC = 0.752).Conclusion: Respiratory oscillometry provides information related to functional capacity in COPD. This method is also able to predict low exercise tolerance in these patients. These findings elucidate the physiological and clinical meaning of the oscillometric parameters, improving the interpretation of these parameters in COPD patients.Keywords: chronic obstructive pulmonary disease, COPD physiopathology, forced oscillation technique, respiratory impedance, Glittre-ADL test, handgrip strength, exercise limitation

Abstract Unexplained exertional dyspnoea or fatigue can arise from a number of underlying disorders and shows only a weak correlation with resting functional or imaging tests. Noninvasive cardiopulmonary exercise testing (CPET) offers a unique, but still under-utilised and unrecognised, opportunity to study cardiopulmonary and metabolic changes simultaneously. CPET can distinguish between a normal and an abnormal exercise response and usually identifies which of multiple pathophysiological conditions alone or in combination is the leading cause of exercise intolerance. Therefore, it improves diagnostic accuracy and patient health care by directing more targeted diagnostics and facilitating treatment decisions. Consequently, CPET should be one of the early tests used to assess exercise intolerance. However, this test requires specific knowledge and there is still a major information gap for those physicians primarily interested in learning how to systematically analyse and interpret CPET findings. This article describes the underlying principles of exercise physiology and provides a practical guide to performing CPET and interpreting the results in adults.

Abstract Aims Peak exercise oxygen uptake (VO2) and cardiac output (CO) are strong prognostic indexes in heart failure (HF) but unrelated to real‐life physical activity, which is associated to submaximal effort. Methods and results We analysed maximal cardiopulmonary exercise test with rest, mid‐exercise, and peak exercise non‐invasive CO measurements (inert gas rebreathing) of 231 HF patients and 265 healthy volunteers. HF patients were grouped according to exercise capacity (peak VO2

Unexplained exertional dyspnoea or fatigue can arise from a number of underlying disorders and shows only a weak correlation with resting functional or imaging tests. Noninvasive cardiopulmonary exercise testing (CPET) offers a unique, but still under-utilised and unrecognised, opportunity to study cardiopulmonary and metabolic changes simultaneously. CPET can distinguish between a normal and an abnormal exercise response and usually identifies which of multiple pathophysiological conditions alone or in combination is the leading cause of exercise intolerance. Therefore, it improves diagnostic accuracy and patient health care by directing more targeted diagnostics and facilitating treatment decisions. Consequently, CPET should be one of the early tests used to assess exercise intolerance. However, this test requires specific knowledge and there is still a major information gap for those physicians primarily interested in learning how to systematically analyse and interpret CPET findings. This article describes the underlying principles of exercise physiology and provides a practical guide to performing CPET and interpreting the results in adults. [ABSTRACT FROM AUTHOR]

Resting humans transport ~ 100 quintillion (1018) oxygen (O2) molecules every second to tissues for consumption. The final, short distance (< 50 µm) from capillary to the most distant mitochondria, in skeletal muscle where exercising O2 demands may increase 100-fold, challenges our understanding of O2 transport. To power cellular energetics O2 reaches its muscle mitochondrial target by dissociating from hemoglobin, crossing the red cell membrane, plasma, endothelial surface layer, endothelial cell, interstitial space, myocyte sarcolemma and a variable expanse of cytoplasm before traversing the mitochondrial outer/inner membranes and reacting with reduced cytochrome c and protons. This past century our understanding of O2's passage across the body's final O2 frontier has been completely revised. This review considers the latest structural and functional data, challenging the following entrenched notions: (1) That O2 moves freely across blood cell membranes. (2) The Krogh–Erlang model whereby O2 pressure decreases systematically from capillary to mitochondria. (3) Whether intramyocyte diffusion distances matter. (4) That mitochondria are separate organelles rather than coordinated and highly plastic syncytia. (5) The roles of free versus myoglobin-facilitated O2 diffusion. (6) That myocytes develop anoxic loci. These questions, and the intriguing notions that (1) cellular membranes, including interconnected mitochondrial membranes, act as low resistance conduits for O2, lipids and H+-electrochemical transport and (2) that myoglobin oxy/deoxygenation state controls mitochondrial oxidative function via nitric oxide, challenge established tenets of muscle metabolic control. These elements redefine muscle O2 transport models essential for the development of effective therapeutic countermeasures to pathological decrements in O2 supply and physical performance. [ABSTRACT FROM AUTHOR]

Patients with chronic obstructive pulmonary disease receive a range of treatments including but not limited to inhaled bronchodilators, inhaled and systemic corticosteroids, supplemental oxygen, and pulmonary rehabilitation. Pulmonary rehabilitation is a multidisciplinary intervention that seeks to combine patient education, exercise, and lifestyle changes into a comprehensive program. Programs 6 to 8 weeks in length have been shown to improve health, reduce dyspnea, increase exercise capacity, improve psychological well-being, and reduce healthcare utilization and hospitalization. Although the use of pulmonary rehabilitation is widely supported by the literature, controversy still exists regarding what should be included in the programs. The goal of this review was to summarize the evidence for pulmonary rehabilitation and identify the areas that hold promise in improving its utilization and effectiveness.

Although various determinants of exercise limitation in Fontan patients have been studied, most research has been performed in patients who underwent different surgical procedures with differing haemodynamic characteristics. The aim of the current study was to evaluate non-invasively measured cardiovascular parameters and their influence on exercise performance in paediatric Fontan patients with an extracardiac conduit and moderate-good systolic ventricular function. Fontan patients, between 8 and 18 years of age, with moderate to good systolic ventricular function and an extracardiac conduit were included. Exercise performance and cardiovascular assessment, comprising echocardiography, aortic stiffness measurement and ambulatory measurement of cardiac autonomous nervous activity were performed on the same day. Healthy subjects served as controls. Thirty-six Fontan patients (age 14.0 years) and thirty-five healthy subjects (age 12.8 years) were included. Compared to controls, Fontan patients had reduced diastolic ventricular function and increased arterial stiffness. No differences were found in heart rate (HR) and cardiac parasympathetic nervous activity. In Fontan patients, maximal as well as submaximal exercise capacity was impaired, with the percentage of predicted capacity ranging between 54 and 72%. Chronotropic competence, however, was good with a peak HR of 174 (94% of predicted). Lower maximal and submaximal exercise capacity was correlated with a higher HR at rest, higher pulse wave velocity of the aorta and a lower ratio of early and late diastolic flow velocity. Contemporary paediatric Fontan patients have an impaired exercise capacity with preserved chronotropic competence. Exercise performance correlates with heart rate at rest, diastolic function and aortic stiffness. • Although exercise capacity was impaired, chronotropic competence was preserved. • Exercise capacity relates to heart rate, diastolic function and aortic stiffness. • Further research is warranted to determine the prognostic values of these markers. [ABSTRACT FROM AUTHOR]

Objectives: Coronavirus disease 2019 (COVID-19) is a global pandemic affecting individuals to varying degrees. There is emerging evidence that even patients with mild symptoms will suffer from prolonged physical impairment.Methods: In this prospective observational study, lung function, and cardiopulmonary exercise testing have been performed in 100 patients for 3–6 months after COVID-19 diagnosis (post-CoVG). Depending on the severity of severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) infection, patients were divided into asymptomatic, or mild to moderate (mild post-CoVG), and severe post-CoVG [hospitalization with or without intensive care unit/non-invasive ventilation (ICU/NIV)]. Results have been compared with age, sex, and body mass index (BMI) matched control group (CG, N = 50).Results: Both lung function (resting) and exercise capacity (peak workload, Wpeak and peak oxygen uptake, VO2 peak - % predicted) were considerably affected in patients with severe post-CoV (81.7 ± 27.6 and 86.1 ± 20.6%), compared to the mild post-CoVG (104.8 ± 24.0%, p = 0.001 and 100.4 ± 24.8; p = 0.003). In addition, also the submaximal exercise performance was significantly reduced in the severe post-CoVG (predicted VT1/VO2 peak; p = 0.013 and VT2/VO2 peak; p = 0.001). Multiple linear regression analyses revealed that 74 % (adjusted R2) of the variance in relative VO2 peak of patients who had CoV could be explained by the following variables: lower age, male sex, lower BMI, higher DLCO, higher predicted heart rate (HR) peak, lower breathing reserve (BR), and lower SaO2 peak, which were related to higher relative VO2 peak values. Higher NT-proBNP and lower creatinine kinase (CK) values were seen in severe cases compared to patients who experienced mild CoV.Discussion: Maximal and submaximal exercise performance in patients recovering from severe COVID-19 remain negatively affected for 3–6 months after COVID-19 diagnosis. The presented findings reveal that impaired pulmonary, cardiac, and skeletal muscle function contributed to the limitation of VO2 peak in those patients, which may have important implications on rehabilitation programs.

Aims: Peak exercise oxygen uptake (VO2) and cardiac output (CO) are strong prognostic indexes in heart failure (HF) but unrelated to real‐life physical activity, which is associated to submaximal effort. Methods and results: We analysed maximal cardiopulmonary exercise test with rest, mid‐exercise, and peak exercise non‐invasive CO measurements (inert gas rebreathing) of 231 HF patients and 265 healthy volunteers. HF patients were grouped according to exercise capacity (peak VO2 < 50% and ≥50% pred, Groups 1 and 2). To account for observed differences, data regarding VO2, CO, stroke volume (SV), and artero‐venous O2 content difference [ΔC(a‐v)O2] were adjusted by age, gender, and body mass index. A multiple regression analysis was performed to predict peak VO2 from mid‐exercise cardiopulmonary exercise test and CO parameters among HF patients. Rest VO2 was lower in HF compared with healthy subjects; meanwhile, Group 1 patients had the lowest CO and highest ΔC(a‐v)O2. At mid‐exercise, Group 1 patients achieved a lower VO2, CO, and SV [0.69 (interquartile range 0.57–0.80) L/min; 5.59 (4.83–6.67) L/min; 62 (51–73) mL] than Group 2 [0.94 (0.83–1.1) L/min; 7.6 (6.56–9.01) L/min; 77 (66–92) mL] and healthy subjects [1.15 (0.93–1.30) L/min; 9.33 (8.07–10.81) L/min; 87 (77–102) mL]. Rest to mid‐exercise SV increase was lower in Group 1 than Group 2 (P = 0.001) and healthy subjects (P < 0.001). At mid‐exercise, ΔC(a‐v)O2 was higher in Group 2 [13.6 (11.8–15.4) mL/100 mL] vs. healthy patients [11.6 (10.4–13.2) mL/100 mL] (P = 0.002) but not different from Group 1 [13.6 (12.0–14.9) mL/100 mL]. At peak exercise, Group 1 patients achieved a lower VO2, CO, and SV than Group 2 and healthy subjects. ΔC(a‐v)O2 was the highest in Group 2. At multivariate analysis, a model comprising mid‐exercise VO2, carbon dioxide production (VCO2), CO, haemoglobin, and weight predicted peak VO2, P < 0.001. Mid‐exercise VO2 and CO, haemoglobin, and weight added statistically significantly to the prediction, P < 0.050. Conclusions: Mid‐exercise VO2 and CO portend peak exercise values and identify severe HF patients. Their evaluation could be clinically useful. [ABSTRACT FROM AUTHOR]

Objective: In children with congenital heart defects (CHD), a sedentary lifestyle should be avoided and usually WHO recommendations on physical activity (PA) are supposed to be followed. In order to obtain representative data of the actual amount of PA (and potential influencing factors) in children with CHD we performed a nationwide online survey.Methods: All patients aged 6–17 years registered in the German National Register for CHD were contacted by email and asked to participate in the survey using the comprehensive questionnaire of the “Motorik-Modul” from the German Health Interview and Examination Survey for Children and Adolescents (KiGGS), thus allowing the comparison with a representative age-matched subset of 3.385 participants of the KiGGS study. The questionnaire for CHD-patients was amended by specific questions regarding medical care, sports recommendations and PA restrictions.Results: Complete datasets of 1.198 patients (mean age of 11.6 ± 3.1 years) were available for evaluation. Compared to the reference group, CHD patients significantly less frequently reached the WHO recommended level of 60 min of daily PA (8.8 vs. 12%; p < 0.001). Enjoyment in sports was almost equally distributed across CHD and reference groups, and strongly correlated with the level of PA (r = 0.41; p < 0.001). Remarkably, 49.2% of children with complex CHD, 31.7% with moderate, and even 13.1% with simple CHD were advised by their physician to restrict PA.Conclusions: According to this nationwide survey, PA is markedly reduced in children with CHD. An important reason for this might be an unexpected high rate of physician-recommended restrictions on levels of PA.

Key points: Heart failure patients with reduced ejection fraction (HFrEF) exhibit severe limitations in exercise capacity (V̇O2 peak).One of the primary peripheral mechanisms suggested to underlie exercise intolerance in HFrEF is excessive locomotor muscle group III/IV afferent feedback; however, this has never been investigated in human heart failure.HFrEF patients and controls performed an incremental exercise test to volitional exhaustion to determine V̇O2 peak with lumbar intrathecal fentanyl or placebo. During exercise, cardiac output, leg blood flow and radial artery and femoral venous blood gases were measured.With fentanyl, compared with placebo, patients with HFrEF achieved a higher peak workload, V̇O2 peak, cardiac output, stroke volume and leg blood flow.These findings suggest that locomotor muscle group III/IV afferent feedback in HFrEF leads to increased systemic vascular resistance, which constrains stroke volume, cardiac output and O2 delivery thereby impairing V̇O2 peak and thus exercise capacity. To better understand the underlying mechanisms contributing to exercise limitation in heart failure with reduced ejection fraction (HFrEF), we investigated the influence of locomotor muscle group III/IV afferent inhibition via lumbar intrathecal fentanyl on peak exercise capacity (V̇O2 peak) and the contributory mechanisms. Eleven HFrEF patients and eight healthy matched controls were recruited. The participants performed an incremental exercise test to volitional exhaustion to determine V̇O2 peak with lumbar intrathecal fentanyl or placebo. During exercise, cardiac output and leg blood flow (Q̇L) were measured via open‐circuit acetylene wash‐in technique and constant infusion thermodilution, respectively. Radial artery and femoral venous blood gases were measured. V̇O2 peak was 15% greater with fentanyl compared with placebo for HFrEF (P < 0.01), while no different in the controls. During peak exercise with fentanyl, cardiac output was 12% greater in HFrEF secondary to significant decreases in systemic vascular resistance and increases in stroke volume compared with placebo (all, P < 0.01). From placebo to fentanyl, leg V̇O2, Q̇L and O2 delivery were greater for HFrEF during peak exercise (all, P < 0.01), but not control. These findings indicate that locomotor muscle group III/IV afferent feedback in patients with HFrEF leads to increased systemic vascular resistance, which constrains stroke volume, cardiac output and O2 delivery, thereby impairing V̇O2 peak and thus exercise capacity. These findings have important clinical implications as V̇O2 peak is highly predictive of morbidity and mortality in HF. Key points: Heart failure patients with reduced ejection fraction (HFrEF) exhibit severe limitations in exercise capacity (V̇O2 peak).One of the primary peripheral mechanisms suggested to underlie exercise intolerance in HFrEF is excessive locomotor muscle group III/IV afferent feedback; however, this has never been investigated in human heart failure.HFrEF patients and controls performed an incremental exercise test to volitional exhaustion to determine V̇O2 peak with lumbar intrathecal fentanyl or placebo. During exercise, cardiac output, leg blood flow and radial artery and femoral venous blood gases were measured.With fentanyl, compared with placebo, patients with HFrEF achieved a higher peak workload, V̇O2 peak, cardiac output, stroke volume and leg blood flow.These findings suggest that locomotor muscle group III/IV afferent feedback in HFrEF leads to increased systemic vascular resistance, which constrains stroke volume, cardiac output and O2 delivery thereby impairing V̇O2 peak and thus exercise capacity. [ABSTRACT FROM AUTHOR]

We sought to investigate the role of group III/IV muscle afferents in limiting endurance exercise performance, independently of their role in optimizing locomotor muscleO2delivery. While breathing 100%O2to ensure a similar arterialO2content (CaO2) in both trials, eight male cyclists performed 5-km time trials under control conditions (HCTRL) and with lumbar intrathecal fentanyl (HFENT) impairing neural feedback from the lower limbs. After each time trial, common femoral artery blood flow (FBF) was quantified (Doppler ultrasound) during constant-load cycling performed at the average power of the preceding time trial. The assessment of end-tidal gases, hemoglobin content and saturation, and FBF facilitated the calculation of legO2delivery. Locomotor muscle activation during cycling was estimated from vastus lateralis EMG. With electrical femoral nerve stimulation, peripheral and central fatigue were quantified by pre- to postexercise decreases in quadriceps twitch torque (ΔQtw) and voluntary activation (ΔVA), respectively. FBF (~16 mL·min-1·W-1; P = 0.6), CaO2 (~24 mL O2/dL; P = 0.9), and legO2delivery (~0.38 mL O2·min-1·W-1; P = 0.9) were not different during HCTRL and HFENT. Mean power output and time to completion were significantly improved by 9% (~310 W vs. ~288 W) and 3% (~479 s vs. ~463 s), respectively, during HFENT compared with HCTRL. Quadriceps muscle activation was 9 ± 7% higher during HFENT compared with HCTRL (P < 0.05). ΔQtw was significantly greater in HFENT compared with HCTRL (54 ± 8% vs. 39 ± 9%), whereas ΔVA was not different (~5%; P = 0.3) in both trials. These findings reveal that group III/IV muscle afferent feedback limits whole body endurance exercise performance and peripheral fatigue by restricting neural activation of locomotor muscle. [ABSTRACT FROM AUTHOR]

Pulmonary arterial hypertension (PAH) is a chronic disease that is associated with a significant and progressive limitation of exercise tolerance. The pathophysiological mechanisms of exercise intolerance during exercise are complex, multifactorial, and in fact not limited to the pulmonary circulation and the right ventricle. Disturbance of autonomic nervous function leads to an enhanced chemosensitivity, as well as respiratory and peripheral muscle weakness, and systemic endothelial dysfunction, which together play important roles in PAH pathophysiology and symptomatology. This article is focused on the different pathophysiological mechanisms of exercise intolerance in PAH, their interactions, and their relevance for clinical practice. [ABSTRACT FROM AUTHOR]

Dyspnea on exertion is a commonly encountered problem in clinical practice. It is usually investigated by resting tests such as pulmonary function tests and echocardiogram, which may at times can be non-diagnostic. Cardiopulmonary exercise testing (CPET) measures physiologic parameters during exercise which can enable accurate identification of the cause of dyspnea. Though CPET has been around for decades and provides valuable and pertinent physiologic information on the integrated cardiopulmonary responses to exercise, it remains underutilized. The objective of this review is to provide a comprehensible overview of the underlying principles of exercise physiology, indications and contraindications of CPET, methodology and interpretative strategies involved and thereby increase the understanding of the insights that can be gained from the use of CPET.

Neuromuscular fatigue compromises exercise performance and is determined by central and peripheral mechanisms. Interactions between the two components of fatigue can occur via neural pathways, including feedback and feedforward processes. This brief review discusses the influence of feedback and feedforward mechanisms on exercise limitation. In terms of feedback mechanisms, particular attention is given to group III/IV sensory neurons which link limb muscle with the central nervous system. Central corollary discharge, a copy of the neural drive from the brain to the working muscles, provides a signal from the motor system to sensory systems and is considered a feedforward mechanism that might influence fatigue and consequently exercise performance. We highlight findings from studies supporting the existence of a ‘critical threshold of peripheral fatigue’, a previously proposed hypothesis based on the idea that a negative feedback loop operates to protect the exercising limb muscle from severe threats to homeostasis during whole-body exercise. While the threshold theory remains to be disproven within a given task, it is not generalisable across different exercise modalities. The ‘sensory tolerance limit’, a more theoretical concept, may address this issue and explain exercise tolerance in more global terms and across exercise modalities. The ‘sensory tolerance limit’ can be viewed as a negative feedback loop which accounts for the sum of all feedback (locomotor muscles, respiratory muscles, organs, and muscles not directly involved in exercise) and feedforward signals processed within the central nervous system with the purpose of regulating the intensity of exercise to ensure that voluntary activity remains tolerable. [ABSTRACT FROM PUBLISHER]

Study Design: A prospective evaluation of cardiorespiratory function following spinal fusion in adolescent idiopathic scoliosis (AIS).Objective: To evaluate the cardiopulmonary function during exercise in patients with severe AIS, before and 2 years after undergoing a posterior spinal fusion.Summary Of Background Data: After surgical correction of scoliosis, a greater cardiorespiratory adaptation to exercise would be expected from correction of the rib cage associated with the spine deformity. However, there is no clear evidence regarding whether tolerance to maximum exercise improves in the medium term after surgery in patients with severe curves.Methods: We include patients with AIS proposed for posterior surgical correction aging between 12 and 17 years. Every patient had a Cobb angle >45° and a Lenke type 1A scoliosis. Cardiac and respiratory functional measures, such as heart rate and blood pressure, maximum oxygen consumption (VO2max), eliminated volume of carbon dioxide (VCO2), quotient between ventilation and volume of exhaled carbon dioxide (VE/CO2), respiratory exchange rate, ventilatory capacity at maximal exercise (VEmax), were recorded before and 2 years after surgery.Results: Twenty patients were included in our study, 15 girls and 5 boys, with an average age of 13 years. The main scoliotic curve was corrected in the coronal plane in an average of 71.9%. The maximal aerobic power expressed by body weight normalized VO2max was found preoperatively to have an average of 30.9 ± 6.2 mL/kg/minute, indicating a poor aerobic capacity, which did not improve at final follow-up, decreasing to a mean value of 29.3 ± 5.7 but without statistical significance. However, the percentages of curve correction showed a statistically significant correlation with VO2max (r = 0.534; P < 0.05).Conclusion: Patients with severe adolescent idiopathic scoliosis Lenke type 1A showed limited cardiorespiratory tolerance to maximum exercise that did not improve 2 years after surgery.Level Of Evidence: 3. [ABSTRACT FROM AUTHOR]

Interstitial lung disease (ILD) is a group of chronic respiratory diseases characterized by dyspnoea on exertion and decline in health-related quality of life (HRQL). People with ILD experience significant exercise limitation with contributors that include ventilatory limitation, impaired gas exchange, decreased cardiac function and skeletal muscle dysfunction. Pulmonary rehabilitation (PR) is well established in patients with chronic obstructive pulmonary disease (COPD) as a means to overcome exercise limitation and improve activity-related dyspnoea. There is increasing evidence for similar effects of PR in people with ILD. This review discusses the evidence for PR in ILD, outlines the essential components of PR in this population, and highlights special considerations for exercise training in people with ILD. Possible future directions for PR research in people with ILD are explored. [ABSTRACT FROM AUTHOR]

Exercise intolerance, skeletal muscle dysfunction, and reduced daily activity are central in COPD patients and closely related to quality of life and prognosis. Studies assessing muscle exercise have revealed an increase in sympathetic outflow as a link to muscle hypoperfusion and exercise limitation. Our primary hypothesis was that muscle sympathetic nerve activity (MSNA) correlates with exercise limitation in COPD. MSNA was evaluated at rest and during dynamic or static handgrip exercise. Additionally, we assessed heart rate, blood pressure, CO2 tension, oxygen saturation (SpO2), and breathing frequency. Ergospirometry was performed to evaluate exercise capacity. We assessed MSNA of 14 COPD patients and 8 controls. In patients, MSNA was negatively correlated with peak oxygen uptake (VO2% pred) (r = −0.597;p= 0.040). During dynamic or static handgrip exercise, patients exhibited a significant increase in MSNA, which was not observed in the control group. The increase in MSNA during dynamic handgrip was highly negatively correlated with peak exercise capacity in Watts (w) and peak oxygen uptake (VO2/kg) (r = −0.853; p = 0.002 and r = −0.881; p = 0.002, respectively). Our study reveals an association between increased MSNA and limited exercise capacity in patients with COPD. Furthermore, we found an increased sympathetic response to moderate physical exercise (handgrip), which may contribute to exercise intolerance in COPD. [ABSTRACT FROM PUBLISHER]

The purpose of this study was to evaluate cardiorespiratory fitness and reasons for exercise curtailment in a contemporary adult cystic fibrosis (CF) cohort with mild lung disease. Adults with mild CF (n = 19, forced expiratory volume in 1 s = 95 ± 17% predicted) were age-, sex-, ethnicity-, and body mass index-matched to healthy controls (n = 19) and underwent a detailed cardiopulmonary cycle exercise test. While CF subjects had a reduced peak oxygen uptake compared with controls, the values were normal when expressed as %predicted in 14/19 (74%) of subjects. Both groups demonstrated a normal cardiovascular limitation to exercise and stopped exercise primarily because of leg fatigue. Despite not being exercise-limited by respiratory factors, there was some evidence of ventilatory abnormalities as patients with mild CF had increased end-inspiratory lung volumes and reached an inflection/plateau in tidal volume relative to minute ventilation at lower exercise intensities compared with controls. Subjects with CF were not more likely to demonstrate expiratory flow limitation compared with controls and did not have evidence of dynamic hyperinflation during exercise. Despite increased end-inspiratory lung volumes and an earlier tidal volume inflection/plateau, CF subjects did not experience higher levels of dyspnea. In an exploratory analysis, a significant inverse correlation was observed between sweat chloride and peak work rate. Adult CF subjects with relatively well preserved spirometry have normal exercise performance relative to reference values and are primarily limited by nonrespiratory factors. However, ventilatory abnormalities were detected even in this mild CF cohort and should be evaluated in future therapeutic trials focused on diseasemodifying therapies in mild CF. [ABSTRACT FROM AUTHOR]

Background: Sarcoidosis patients suffer from fatigue and exercise limitation. The aim of this study was to establish whether a physical training program improves these and other outcomes important to sarcoidosis patients. Methods: From 11/2012 to 9/2014, 201 sarcoidosis patients were referred to the ild care expertise team, Ede, the Netherlands. In our center, all patients are routinely recommended to undergo testing at baseline to determine their physical functioning and encouraged to complete a 12-week, supervised physical training program. Ninety patients underwent baseline testing and returned for repeat testing at 3 months in the interim, 49 completed the training program (Group I) and 41 chose not to participate (Group II). Change over time (from baseline to 3 months) in fatigue, exercise capacity, and skeletal muscle strength were assessed between the two groups. Results: At baseline, there were no between-group differences for fatigue, DLCO %, FVC %, or exercise capacity [assessed by percent predicted six-minute walk distance (6MWD %) and Steep Ramp Test (SRT)]. The 6MWD for Group I improved between baseline and 3 months, while the 6MWD remained the same in Group II ( F = 72.2, p < 0.001). Group I showed a significantly larger decrease of fatigue compared with Group II ( F = 6.27, p = 0.014). Lung function tests did not change in either group. Conclusion: A supervised physical training program improves exercise capacity and fatigue among sarcoidosis patients and should be included in their management regimen. [ABSTRACT FROM AUTHOR]

Dyspnea on exertion is a commonly encountered problem in clinical practice. It is usually investigated by resting tests such as pulmonary function tests and echocardiogram, which may at times can be non-diagnostic. Cardiopulmonary exercise testing (CPET) measures physiologic parameters during exercise which can enable accurate identification of the cause of dyspnea. Though CPET has been around for decades and provides valuable and pertinent physiologic information on the integrated cardiopulmonary responses to exercise, it remains underutilized. The objective of this review is to provide a comprehensible overview of the underlying principles of exercise physiology, indications and contraindications of CPET, methodology and interpretative strategies involved and thereby increase the understanding of the insights that can be gained from the use of CPE [ABSTRACT FROM AUTHOR]

Purpose: This study aimed to document the matching of muscle O2 delivery to O2 use in young patients with cystic fibrosis (CF) from muscle deoxygenation (HHb) dynamics during ramp exercise. Methods: Ten patients with stable, mild-to-moderate CF (12.7 ± 2.8 yr) and 10 healthy controls (CON, 12.8 ± 2.8 yr) completed a combined ramp and supramaximal cycling test to determine maximal O2 uptake (VO2max). Changes in gas exchange and ventilation, HR, andm. vastus lateralis HHb (near-infrared spectroscopy) were assessed. Δ[HHb]-work rate and Δ[HHb]-VO2 profiles were normalized and fit using a sigmoid function. Results: Aerobic function was impaired in CF, indicated by very likely reduced fat-free mass-normalized VO2max (mean difference, ±90% confidence interval: −7.9 mL•kg−1•min−1, ±6.1), very likely lower VO2 gain (−1.44 mL•min−1•W−1, ±1.12), and a likely slower VO2 mean response time (11 s, ±13). An unclear effect was found upon the absolute and relative work rate (−14 W, ±44, and −0.7% peak power output, ±12.0, respectively) and the absolute and percentage (−0.10 L•min−1, ±0.43, and 3.3% VO2max, ±6.0) VO2 corresponding to 50% Δ[HHb] amplitude, respectively, between groups. However, arterial oxygen saturation (SpO2) was very likely lower in CF (−1%, ±1) and demonstrated moderate-to–very large relations with parameters of aerobic function. Conclusions: Young patients with mild-to-moderate CF present with impaired aerobic function during ramp incremental cycling exercise. Because the rate of fractional O2 extraction during ramp cycling exercise was not altered by CF, yet SpO2 was lower, the present findings support the notion of centrally mediated oxygen delivery to principally limit the aerobic function of pediatric patients with CF during ramp incremental cycling exercise. [ABSTRACT FROM AUTHOR]

INTRODUCTION: There is growing evidence that exercise-induced variation in lung volumes is an important source of ventilatory limitation and is linked to exercise intolerance in COPD. The aim of this study was to compare the correlations of walk distance and lung volumes measured before and after a 6-min walk test (6MWT) in subjects with COPD. METHODS: Forty-five subjects with stable COPD (mean pre-bronchodilator FEV1: 47 ± 18% predicted) underwent a 6MWT. Body plethysmography was performed immediately pre- and post-6MWT. RESULTS: Correlations were generally stronger between 6-min walk distance and post-6MWT lung volumes than between 6-min walk distance and pre-6MWT lung volumes, except for FEV1. These differences in Pearson correlation coefficients were significant for residual volume expressed as percent of total lung capacity (-0.67 vs -0.58, P = .043), percent of predicted residual volume expressed as percent of total lung capacity (-0.68 vs -0.59, P = .026), inspiratory vital capacity (0.65 vs 0.54, P = .019), percent of predicted inspiratory vital capacity (0.49 vs 0.38, P = .037), and percent of predicted functional residual capacity (0.62 vs 0.47, P = .023). CONCLUSIONS: In subjects with stable COPD, lung volumes measured immediately after 6MWT are more closely related to exercise limitation than baseline lung volumes measured before 6MWT, except for FEV1. Therefore, pulmonary function testing immediately after exercise should be included in future studies on COPD for the assessment of exercise-induced ventilatory constraints to physical performance that cannot be adequately assessed from baseline pulmonary function testing at rest. [ABSTRACT FROM AUTHOR]

Background context Exercise limitation has been described in patients with adolescent idiopathic scoliosis (AIS); however, whether the walking performance is impaired in these patients should be elucidated. Purpose Thus, we aimed to evaluate the physiologic responses to the incremental shuttle walk test (ISWT) in patients with AIS. Study design/setting Cross-sectional study. Patient sample Twenty-nine patients with AIS and 20 healthy adolescents aged between 11 and 18 years old. Outcome measures Oxygen uptake (VO 2 ), incremental shuttle walk distance (ISWD), ΔVO 2 /Δwalking velocity, ΔHR/ΔVO 2 , ΔVE/ΔVCO 2 , and linearized Δtidal volume (VT)/ΔlnVE, forced expiratory volume in the first second of expiration (FEV 1 ), and forced vital capacity (FVC). Methods We performed two ISWTs, and the data used were acquired in the second test. We also evaluated the lung function and respiratory muscle strength through spirometry test and manovacuometry, respectively. All authors confirm that there are no conflicts of interest. To compare the means or medians of variables between patients and healthy subjects, we used the unpaired t test or Mann-Whitney U test, respectively. The correlations were assessed by Pearson or Spearman coefficients according to the distribution of the studied variables. The probability of alpha error was set at 5% for all analyses. Results Adolescent idiopathic scoliosis patients showed significant lower values of ISWD, VO 2 , and ventilation at the end of the ISWT, as well as lower FEV 1 and FVC; they also presented significantly shallower slope of ΔVT/ΔlnVE, whereas VO 2 related significantly with ISWD (r=0.80), FVC (r=0.78), FEV 1 (r=0.73), and ΔVT/ΔlnVE (r=0.58). Conclusions Adolescent idiopathic scoliosis correlated to walking limitation and was associated to reduced pulmonary function and worse breathing pattern during exercise. Our results suggest that walking-based aerobic exercises should be encouraged in these patients. [ABSTRACT FROM AUTHOR]