ERS statement on standardisation of cardiopulmonary exercise testing in chronic lung diseases

The objective of this document was to standardise published cardiopulmonary exercise testing (CPET) protocols for improved interpretation in clinical settings and multicentre research projects. This document: 1) summarises the protocols and procedures used in published studies focusing on incremental CPET in chronic lung conditions; 2) presents standard incremental protocols for CPET on a stationary cycle ergometer and a treadmill; and 3) provides patients’ perspectives on CPET obtained through an online survey supported by the European Lung Foundation. We systematically reviewed published studies obtained from EMBASE, Medline, Scopus, Web of Science and the Cochrane Library from inception to January 2017. Of 7914 identified studies, 595 studies with 26 523 subjects were included. The literature supports a test protocol with a resting phase lasting at least 3 min, a 3-min unloaded phase, and an 8- to 12-min incremental phase with work rate increased linearly at least every minute, followed by a recovery phase of at least 2–3 min. Patients responding to the survey (n=295) perceived CPET as highly beneficial for their diagnostic assessment and informed the Task Force consensus. Future research should focus on the individualised estimation of optimal work rate increments across different lung diseases, and the collection of robust normative data.The document facilitates standardisation of conducting, reporting and interpreting cardiopulmonary exercise tests in chronic lung diseases for comparison of reference data, multi-centre studies and assessment of interventional efficacy. http://bit.ly/31SXeB

High-Performance Phototransistor Based on a 2D Polybenzimidazole Polymer

Photodetectors are fundamental components of modern optoelectronics, enabling the conversion of light into electrical signals. The development of high-performance phototransistors necessitates materials with both high charge carrier mobility and robust photoresponse. However, achieving both in a single material poses challenges due to inherent trade-offs. Herein, this study introduces a polybenzimidazole-(1,3-diazole)-based 2D polymer (2DPBI), synthesized as few-layer, crystalline films covering ≈28 cm2 on the water surface at room temperature, with large crystalline domain sizes ranging from 110 to 140 µm2. The 2DPBI incorporates a π-conjugated photoresponsive porphyrin motif through a 1,3-diazole linkage, exhibiting enhanced π-electron delocalization, a narrow direct band gap of ≈1.18 eV, a small reduced electron–hole effective mass (m* = 0.171 m0), and a very high resonant absorption coefficient of up to 106 cm−1. Terahertz spectroscopy reveals excellent short-range charge carrier mobility of ≈240 cm2 V−1 s−1. Temperature-dependent photoconductivity measurements and theoretical calculations confirm a band-like charge transport mechanism. Leveraging these features, 2DPBI-based phototransistors demonstrate an on/off ratio exceeding 108, photosensitivity of 1.08 × 107, response time of 1.1 ms, and detectivity of 2.0 × 1013 Jones, surpassing previously reported standalone few-layer 2D materials and are on par with silicon photodetectors. The unique characteristics of 2DPBI make it a promising foundation for future optoelectronic devices

Tailoring the Morphology of a Diketopyrrolopyrrole-based Polymer as Films or Wires for High-Performance OFETs using Solution Shearing

Conjugated polymers often show efficient charge carrier transport along their backbone which is a primary factor in the electrical behavior of Organic Field Effect Transistor (OFETs) devices fabricated from these materials. Herein, a solution shearing procedure is reported to fabricate micro/nano wires from a diketopyrrolopyrrole (DPP)-based polymer. Millimeter to nanometer long polymer wires orientated in the coating direction are developed after a thorough analysis of the deposition conditions. It shows several morphological regimes - film, transition, and wires and experimentally derive a phase diagram for the parameters coating speed and surface energy of the substrate. The as-fabricated wires are isolated, which is confirmed by optical, atomic force, and scanning electron microscopy. Beside the macroscopic alignment of wires, cross-polarized optical microscopy images show strong birefringence suggesting a high degree of molecular orientation. This is further substantiated by polarized UV-Vis-NIR spectroscopy, selected area electron diffraction transmission electron microscopy, and grazing-incidence wide-angle X-ray scattering. Finally, an enhanced electrical performance of single wire OFETs is observed with a 15-fold increase in effective charge carrier mobility to 1.57 cm2 V−1 s−1 over devices using films (0.1 cm2 V−1 s−1) with similar values for on/off current ratio and threshold voltage

Effects of Respiratory Muscle Training on Physiological and Psychological Aspects of Dyspnea Perception and Exercise Tolerance in Patients with COPD

Chronic obstructive pulmonary disease (COPD) is a highly prevalent chronic health condition leading to increased disability, morbidity and mortality. COPD is a treatable and preventable disease but the significant health care costs related to the medical treatment of the condition constitute a global financial burden (1, 2). Dyspnea or breathlessness is the main symptom in many COPD patients and contributes to limitations in daily activities including exercise. Respiratory muscle weakness contributes to symptoms of dyspnea in patients with COPD (3-5). Due to dynamic hyperinflation COPD patients are forced to breathe at higher lung volumes during activities. The diaphragm (main inspiratory muscle) is adapted to chronic increases of resting lung volume (static hyperinflation) but not to the acute changes in lung volume during activities (dynamic hyperinflation) which puts it at a mechanical disadvantage. The increased elastic loading at higher lung volumes forces the inspiratory muscles to generate higher inspiratory pressures (i.e. perform more work for a given volume change) while the pressure generating capacity of the diaphragm and the other muscles of inspiration is reduced (because of muscle shortening). Simultaneously contraction velocity is increased when higher inspiratory flow rates are generated with increased ventilatory needs resulting in further functional weakening (6-11). During exercise the somatosensory cortex calibrates and interprets an appropriate muscular-mechanical response to the central respiratory motor drive. It has been shown that dyspnea varies directly with an awareness of the magnitude of central motor command output (12). When the load on the diaphragm is increased and force generating capacity is reduced during exercise induced dynamic hyperinflation an imbalance between drive and response occurs, which has been shown to intensify the sensation of breathlessness or dyspnea (13, 14). Improving inspiratory muscle strength could potentially reduce respiratory neural drive, perceived effort of breathing and dyspnea during exercise (10). Indeed, in previous studies significant improvements in inspiratory muscle function (strength and endurance) dyspnea and exercise capacity have been observed after inspiratory muscle training (IMT) (15, 16). Ventilatory muscle recruitment (VMR) in COPD patients is altered in comparison with healthy subjects. Due to both static and dynamic hyperinflation the inspiratory muscles of the ribcage are recruited more while the diaphragm contribution is reduced (17-19). Also at rest the motor unit recruitment of intercostal muscles, scalenes and diaphragm is higher in COPD patients compared to normal subjects, the neural drive to the sternomastoids is higher and for expiration the transversus abdominis is activated (20). These changes are all related to the mechanical disadvantage of the diaphragm. Potential changes of the VMR pattern in COPD patients in response to inspiratory muscle training have not yet been studied. Previous studies have mostly focused on diaphragmatic activity. It has been shown that during periods of increased respiratory muscle work, a so called 'metaboreflex' leads to sympathetically induced vasoconstriction of limb locomotor muscles (less blood and oxygen supply to active limbs muscle) resulting in locomotor muscle fatigue and reduced endurance performance (21). Previous studies applying both loading and unloading of respiratory muscles in COPD patients have shown effects of these procedures on limb blood flow (peripheral muscle oxygenation) (22, 23) and locomotor fatigue (24) during exercise. The effects of IMT on these mechanisms have however not yet been studied. Within this PhD project both physiological and psychological mechanisms of dyspnea reduction in response to inspiratory muscle training will be studied in COPD patients with pronounced inspiratory muscle weakness. The sensory aspects of dyspnea (intensity and quality) and affective perception of dyspnea (unpleasantness of the sensation for a given intensity) will be assessed and compared between patients who participated in either a sham-training or in an active IMT intervention. Also the changes in respiratory muscle recruitment patterns and changes of electromyogram of diaphragm and accessory inspiratory muscles (reflecting neural drive) will be compared between shame and IMT. The inter-relationships between the post-intervention changes in dyspnea (intensity and unpleasantness) and changes in relevant measures of respiratory muscle performance will be explored as well as the activation/connectivity patterns of regions of the central nervous system in response to a standardized dyspnea provoking stimulus (EEG measurements will be conducted to evaluate the affective perception). Moreover an evaluation of the impact of IMT on blood flow distribution and locomotor muscle function during exercise will be performed. A better understanding of the underlying mechanisms of dyspnea in response to inspiratory muscle training will provide better insights on the potential of this intervention to improve, exercise performance, participation in physical activities, and quality of life in patients with COPD 1. Halpin DM, Miravitlles M. Chronic obstructive pulmonary disease: the disease and its burden to society. Proceedings of the American Thoracic Society. 2006;3(7):619-23. 2. The burden of lung disease. 2013. In: The European Lung White Book Respiratory Health and Disease in Europe. [Internet]. The European Respiratory Society [2-14]. Available from: http://www.erswhitebook.org/chapters/the-burden-of-lung-disease/. 3. Gosselink R, Troosters T, Decramer M. Peripheral muscle weakness contributes to exercise limitation in COPD. Am J Respir Crit Care Med. 1996;153(3):976-80. 4. Hamilton AL, Killian KJ, Summers E, Jones NL. Muscle strength, symptom intensity, and exercise capacity in patients with cardiorespiratory disorders. Am J Respir Crit Care Med. 1995;152(6):2021-31. 5. Rennard S, Decramer M, Calverley PMA, Pride NB, Soriano JB, Vermeire PA, et al. Impact of COPD in North America and Europe in 2000: subjects' perspective of Confronting COPD International Survey. European Respiratory Journal. 2002;20(4):799-805. 6. De Troyer A, Wilson TA. Effect of acute inflation on the mechanics of the inspiratory muscles. J Appl Physiol. 2009;107(1):315-23. 7. Decramer M. Effects of hyperinflation on the respiratory muscles. Eur Respir J. 1989;2(4):299-302. 8. Decramer M. Respiratory muscles in COPD: regulation of trophical status. Verh K Acad Geneeskd Belg. 2001;63(6):577-602; discussion -4. 9. Decramer M. Response of the respiratory muscles to rehabilitation in COPD. J Appl Physiol. 2009;107(3):971-6. 10. Leblanc P, Bowie DM, Summers E, Jones NL, Killian KJ. Breathlessness and exercise in patients with cardiorespiratory disease. Am Rev Respir Dis. 1986;133(1):21-5. 11. Polkey MI, Hamnegård C-H, Hughes PD, Rafferty GF, Green M, Moxham J. Influence of acute lung volume change on contractile properties of human diaphragm. J Appl Physiol. 1998;85(4):1322-8. 12. Parshall MB, Schwartzstein RM, Adams L, Banzett RB, Manning HL, Bourbeau J, et al. An official American Thoracic Society statement: update on the mechanisms, assessment, and management of dyspnea. Am J Respir Crit Care Med. 2012;185(4):435-52. 13. Moxham J, Jolley C. Breathlessness, fatigue and the respiratory muscles. Clin Med. 2009;9(5):448-52. 14. O'Donnell DE, Ora J, Webb KA, Laveneziana P, Jensen D. Mechanisms of activity-related dyspnea in pulmonary diseases. Respir Physiol Neurobiol. 2009;167(1):116-32. 15. Geddes EL, O'Brien K, Reid WD, Brooks D, Crowe J. Inspiratory muscle training in adults with chronic obstructive pulmonary disease: an update of a systematic review. Respir Med. 2008;102(12):1715-29. 16. Gosselink R, De Vos J, van den Heuvel SP, Segers J, Decramer M, Kwakkel G. Impact of inspiratory muscle training in patients with COPD: what is the evidence? Eur Respir J. 2011;37(2):416-25. 17. Martinez FJ, Couser JI, Celli BR. Factors influencing ventilatory muscle recruitment in patients with chronic airflow obstruction. Am Rev Respir Dis. 1990;142(2):276-82. 18. Montes de Oca M, Celli BR. Respiratory muscle recruitment and exercise performance in eucapnic and hypercapnic severe chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2000;161(3 Pt 1):880-5. 19. Ora J, Laveneziana P, Wadell K, Preston M, Webb KA, O'Donnell DE. Effect of obesity on respiratory mechanics during rest and exercise in COPD. J Appl Physiol (1985). 2011;111(1):10-9. 20. Marchand E, Decramer M. Respiratory muscle function and drive in chronic obstructive pulmonary disease. Clin Chest Med. 2000;21(4):679-92. 21. Dempsey JA, Romer L, Rodman J, Miller J, Smith C. Consequences of exercise-induced respiratory muscle work. Respir Physiol Neurobiol. 2006;151(2-3):242-50. 22. Borghi-Silva A, Oliveira CC, Carrascosa C, Maia J, Berton DC, Queiroga F, Jr., et al. Respiratory muscle unloading improves leg muscle oxygenation during exercise in patients with COPD. Thorax. 2008;63(10):910-5. 23. Chiappa GR, Queiroga F, Jr., Meda E, Ferreira LF, Diefenthaeler F, Nunes M, et al. Heliox improves oxygen delivery and utilization during dynamic exercise in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2009;179(11):1004-10. 24. Amann M, Regan MS, Kobitary M, Eldridge MW, Boutellier U, Pegelow DF, et al. Impact of pulmonary system limitations on locomotor muscle fatigue in patients with COPD. Am J Physiol Regul Integr Comp Physiol. 2010;299(1):R314-24..status: publishe

Effect of an Inspiratory Muscle Training (IMT) Program on Respiratory Muscle Function, Symptoms of Dyspnea, Respiratory Muscle Activation and Tissue Oxygen Delivery During Exercise Breathing in a Patient with Idiopathic Unilateral Diaphragmatic Paralysis: A Case Report

This abstract is funded by: UZ Leuven/KU Leuve

Effect of an Inspiratory Muscle Training (IMT) Program on Respiratory Muscle Function, Symptoms of Dyspnea, Respiratory Muscle Activation and Tissue Oxygen Delivery During Exercise Breathing in a Patient with Idiopathic Unilateral Diaphragmatic Paralysis: A Case Report

This abstract is funded by: UZ Leuven/KU Leuve