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Artykuły w czasopismach na temat "Inspiratory capacity"

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Reig, Rafael Peset, i Thomas W. van der Mark. "Inspiratory and Expiratory Vital Capacity". Chest 88, nr 5 (listopad 1985): 797–98. http://dx.doi.org/10.1378/chest.88.5.797b.

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McCool, F. D., M. B. Hershenson, G. E. Tzelepis, Y. Kikuchi i D. E. Leith. "Effect of fatigue on maximal inspiratory pressure-flow capacity". Journal of Applied Physiology 73, nr 1 (1.07.1992): 36–43. http://dx.doi.org/10.1152/jappl.1992.73.1.36.

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The inspiratory muscles can be fatigued by repetitive contractions characterized by high force (inspiratory resistive loads) or high velocities of shortening (hyperpnea). The effects of fatigue induced by inspiratory resistive loaded breathing (pressure tasks) or by eucapnic hyperpnea (flow tasks) on maximal inspiratory pressure-flow capacity and rib cage and diaphragm strength were examined in five healthy adult subjects. Tasks consisted of sustaining an assigned breathing frequency, duty cycle, and either a “pressure-time product” of esophageal pressure (for the pressure tasks) or peak inspiratory flow rate (for the flow tasks). Esophageal pressure was measured during maximal inspiratory efforts against a closed glottis (Pesmax), maximal transdiaphragmatic pressure was measured during open-glottis expulsive maneuvers (Pdimax), and maximal inspiratory flow (VImax) was measured during maximal inspiratory efforts with no added external resistance before and after fatiguing pressure and flow tasks. The reduction in Pesmax) with pressure fatigue (-25 +/- 7%) was significantly greater than the change in Pesmax with flow fatigue (-8 +/- 8%, P less than 0.01). In contrast, the reductions in Pdimax (-11 +/- 8%) and VImax (-16 +/- 3%) with flow fatigue were greater than the changes in Pdimax (-0.6 +/- 4%, P less than 0.05) or VImax (-3 +/- 4%, P less than 0.05) with pressure fatigue. We conclude that respiratory muscle performance is dependent not only on the presence of fatigue but whether fatigue was induced by pressure tasks or flow tasks. The specific impairment of Pesmax and not of Pdimax or flow with pressure fatigue may reflect selective fatigue of the rib cage muscles.(ABSTRACT TRUNCATED AT 250 WORDS)
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Begle, R. L., J. B. Skatrud i J. A. Dempsey. "Ventilatory compensation for changes in functional residual capacity during sleep". Journal of Applied Physiology 62, nr 3 (1.03.1987): 1299–306. http://dx.doi.org/10.1152/jappl.1987.62.3.1299.

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The role of conscious factors in the ventilatory compensation for shortened inspiratory muscle length and the potency of this compensatory response were studied in five normal subjects during non-rapid-eye-movement sleep. To shorten inspiratory muscles, functional residual capacity (FRC) was increased and maintained for 2–3 min at a constant level (range of increase 160–1,880 ml) by creating negative pressure within a tank respirator in which the subjects slept. Minute ventilation was maintained in all subjects over the entire range of increased FRC (mean change +/- SE = -3 +/- 1%) through preservation of tidal volume (-2 +/- 2%) despite slightly decreased breathing frequency (-6 +/- 2%). The decrease in frequency (-13 +/- 2%) was due to a prolongation in expiratory time. Inspiratory time shortened (-10 +/- 1%). Mean inspiratory flow increased 15 +/- 3% coincident with an increase in the slope of the moving time average of the integrated surface diaphragmatic electromyogram (67 +/- 21%). End-tidal CO2 did not rise. In two subjects, control tidal volume was increased 35–50% with CO2 breathing. This augmented tidal volume was still preserved when FRC was increased. We concluded that the compensatory response to inspiratory muscle shortening did not require factors associated with the conscious state. In addition, the potency of this response was demonstrated by preservation of tidal volume despite extreme shortening of the inspiratory muscles and increase in control tidal volumes caused by CO2 breathing. Finally, the timing changes we observed may be due to reflexes following shortening of inspiratory muscle length, increase in abdominal muscle length, or cardiovascular changes.
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Cohen, Judith, Dirkje S. Postma, Karin Vink-Klooster, Wim van der Bij, Erik Verschuuren, Nick H. T. ten Hacken, Gerard H. Koëter i W. Rob Douma. "FVC to Slow Inspiratory Vital Capacity Ratio". Chest 132, nr 4 (październik 2007): 1198–203. http://dx.doi.org/10.1378/chest.06-2763.

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O'Donnell, Denis E., Jordan A. Guenette, François Maltais i Katherine A. Webb. "Decline of Resting Inspiratory Capacity in COPD". Chest 141, nr 3 (marzec 2012): 753–62. http://dx.doi.org/10.1378/chest.11-0787.

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Yildirim, Yavuz Selim, Erol Senturk, Selahattin Tugrul i Orhan Ozturan. "Evaluation of the nasal contractility capacity in postmenopausal women". Rhinology journal 52, nr 4 (1.12.2014): 397–402. http://dx.doi.org/10.4193/rhino13.107.

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Background: The aim of this study was to objectively compare nasal contractility in premenopausal and postmenopausal patients by means of rhinomanometry, acoustic rhinometry, and peak inspiratory nasal flow. Methods: Design: prospective, clinical case-controlled study. Setting: university tertiary-care hospital, referral center. Participants: the study included 97 participants divided into two groups: 49 postmenopausal (the study group) and 48 premenopausal (control) females. Nasal evaluations were made utilizing anterior rhinoscopy, peak inspiratory nasal flow, acoustic rhinometry, and anterior rhinomanometry. Results: The differences between before and after decongestant application of Minimal Cross-sectional Area (MCA) 1, Minimal Cross-sectional Area (MCA) 2, Peak inspiratory nasal flow (PNIF), Rhinomanometry (RMM), Flow, and Volume values were been statistically significant in both postmenopausal and premenopausal group (control). Conclusion: Before and after all the subjects were administered nasal decongestant, nasal contractility was evaluated using objective nasal tests (acoustic rhinometry, rhinomanometry, and peak inspiratory nasal flow. Results showed that erectile tissues were not affected after menopause: postmenopausal women have the same nasal contractility capacity as premonopausal women.
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Hegazy, Fatma A., Sara M. Mohamed Kamel, Ahmed S. Abdelhamid, Emad A. Aboelnasr, Mahmoud Elshazly i Ali M. Hassan. "Effect of postoperative high load long duration inspiratory muscle training on pulmonary function and functional capacity after mitral valve replacement surgery: A randomized controlled trial with follow-up". PLOS ONE 16, nr 8 (27.08.2021): e0256609. http://dx.doi.org/10.1371/journal.pone.0256609.

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Objectives Although, pre-operative inspiratory muscle training has been investigated and reported to be an effective strategy to reduce postoperative pulmonary complications, the efficacy of postoperative inspiratory muscle training as well as the proper load, frequency, and duration necessary to reduce the postoperative pulmonary complications has not been fully investigated. This study was designed to investigate the effect of postoperative high-load long-duration inspiratory muscle training on pulmonary function, inspiratory muscle strength, and functional capacity after mitral valve replacement surgeries. Design Prospective randomized controlled trial. Methods A total of one hundred patients (mean age 38.3±3.29years) underwent mitral valve replacement surgery were randomized into experimental (n = 50) and control (n = 50) groups. The control group received conventional physiotherapy care, while experimental group received conventional care in addition to inspiratory muscle training, with 40% of the baseline maximal inspiratory pressure targeting a load of 80% by the end of the 8 weeks intervention protocol. Inspiratory muscle training started on the patient’s first day in the inpatient ward. Lung functions, inspiratory muscle strength, and functional capacity were evaluated using a computer-based spirometry system, maximal inspiratory pressure measurement and 6MWT respectively at 5 time points and a follow-up assessment was performed 6 months after surgery. Repeated measure ANOVA and post-hoc analyses were used (p <0.05). Results Group-time interactions were detected for all the studied variables (p<0.001). Between-group analysis revealed statistically significant postoperative improvements in all studied variables in the experimental group compared to the control group (p <0.001) with large effect size of η2 ˃0.14. Within-group analysis indicated substantial improvements in lung function, inspiratory pressure and functional capacity in the experimental group (p <0.05) over time, and these improvements were maintained at follow-up. Conclusion High intensity, long-duration postoperative inspiratory muscle training is highly effective in improving lung function, inspiratory muscle strength, and functional capacity after mitral valve replacement surgeries.
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Palau, Patricia, Eloy Domínguez, José María Ramón, Laura López, Antonio Ernesto Briatore, J. Pablo Tormo, Bruno Ventura, Francisco J. Chorro i Julio Núñez. "Home-based inspiratory muscle training for management of older patients with heart failure with preserved ejection fraction: does baseline inspiratory muscle pressure matter?" European Journal of Cardiovascular Nursing 18, nr 7 (31.05.2019): 621–27. http://dx.doi.org/10.1177/1474515119855183.

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Background:Heart failure with preserved ejection fraction is a clinical syndrome characterised by reduced exercise capacity. Some evidence has shown that a simple and home-based programme of inspiratory muscle training offers promising results in terms of aerobic capacity improvement in patients with heart failure with preserved ejection fraction. This study aimed to investigate whether the baseline inspiratory muscle function predicts the changes in aerobic capacity (measured as peak oxygen uptake; peak VO2) after a 12-week home-based programme of inspiratory muscle training in patients with heart failure with preserved ejection fraction.Methods:A total of 45 stable symptomatic patients with heart failure with preserved ejection fraction and New York Heart Association II–III received a 12-week home-based programme of inspiratory muscle training between June 2015 and December 2016. They underwent cardiopulmonary exercise testing and measurements of maximum inspiratory pressure pre and post-inspiratory muscle training. Maximum inspiratory pressure and peak VO2were registered in both visits. Multivariate linear regression analysis was used to assess the association between changes in peak VO2(Δ-peakVO2) and baseline predicted maximum inspiratory pressure (pp-MIP).Results:The median (interquartile range) age was 73 (68–77) years, 47% were women and 35.6% displayed New York Heart Association III. The mean peak VO2at baseline and Δ-peakVO2post-training were 10.4±2.8 ml/min/kg and +2.2±1.3 ml/min/kg (+21.3%), respectively. The median (interquartile range) of pp-MIP and Δ-MIP were 71% (64–92) and 39.2 (26.7–80.4) cmH2O, respectively. After a multivariate analysis, baseline pp-MIP was not associated with Δ-peakVO2(β coefficient 0.005, 95% confidence interval −0.009–0.019, P=0.452).Conclusions:In symptomatic and deconditioned older patients with heart failure with preserved ejection fraction, a home-based inspiratory muscle training programme improves aerobic capacity regardless of the baseline maximum inspiratory pressure.
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Bauerle, O., i M. Younes. "Role of ventilatory response to exercise in determining exercise capacity in COPD". Journal of Applied Physiology 79, nr 6 (1.12.1995): 1870–77. http://dx.doi.org/10.1152/jappl.1995.79.6.1870.

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The progression of chronic obstructive pulmonary disease (COPD) is generally associated with decreased exercise capacity. Differences in forced expired volume in 1 s (FEV1) among patients account for only a fraction of the variability in maximal oxygen consumption (VO2max). We hypothesized that variability in ventilatory response to exercise and in inspiratory mechanics and body mass index contributes importantly to variability in VO2max in this disease. We analyzed the files of 53 patients with established diagnosis of COPD who underwent a recent symptom-limited exercise test. We used inspiratory capacity and maximum inspiratory flow as measures of variability in inspiratory mechanics. The minute ventilation (VE) at the subject's VO2max was divided by the predicted in a normal subject at the same VO2 to obtain a ratio (VE,max/VE,pred). The ventilatory response during exercise provided the best correlation with peak VO2 (r = 0.62). FEV1 and inspiratory capacity also correlated with peak oxygen consumption but not as well as the ventilatory response (r = 0.49 and r = 0.46, respectively). Maximum inspiratory flow and body mass index showed only weak positive correlations (r = 0.23, not significant). The stepwise analysis generated the following equation: VO2max (%predicted) = (77.26 x VE,pred/VE,max) + [0.45 x FEV1 (%predicted)] - 23.66; r = 0.76, P < 0.001. We conclude that variability in the ventilatory response during exercise is one of the main determinants of variability in exercise capacity in COPD patients.
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dos Santos, Tamires Daros, Sergio Nunes Pereira, Luiz Osório Cruz Portela, Marisa Bastos Pereira, Adriane Schmidt Pasqualoto, Aron Ferreira da Silveira i Isabella Martins de Albuquerque. "Influence of inspiratory muscle strength on exercise capacity before and after cardiac rehabilitation". International Journal of Therapy and Rehabilitation 28, nr 2 (2.02.2021): 1–12. http://dx.doi.org/10.12968/ijtr.2020.0027.

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Background/Aims Coronary artery bypass grafting is a complex procedure that triggers a series of clinical and functional complications. The reduction of inspiratory muscle strength that persists during the late postoperative period has been suggested as an important determinant of functional capacity after coronary artery bypass grafting. The aim of this study was to investigate whether inspiratory muscle strength, functional capacity and quality of life are determinants of exercise capacity before and after a short-term phase II cardiac rehabilitation programme in patients who have had coronary artery bypass graft surgery. Methods A prospective quasi-experimental study was undertaken with 20 patients who had recevied coronary artery bypass surgery. All patients completed a short-term, moderate-to-high intensity inspiratory muscle training programme, followed by aerobic and resistance exercise, two times a week for 12 weeks, totalling 24 sessions, under the direct supervision of a physical therapist. Results Pre-intervention, peak oxygen consumption (peak VO2) was associated with maximum inspiratory pressure (β=0.037; 95% confidence interval 0.01–0.06; P=0.002). Post-intervention, peak VO2 was associated with maximum inspiratory pressure (β=0.03; 95% confidence interval 0.007–0.053; P=0.014) and the 6-Minute Walk Test (β=0.007; 95% confidence interval, 0.001–0.013; P=0.024). Conclusions Inspiratory muscle strength influences exercise capacity before and after a short-term cardiac rehabilitation programme in patients who have had coronary artery bypass graft surgery.
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Rozprawy doktorskie na temat "Inspiratory capacity"

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Plachi, Franciele. "Investigação da hiperinsuflação pulmonar dinâmica durante o exercício e sua relação com a força dos músculos inspiratórios em pacientes com insuficiência cardíaca". reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2017. http://hdl.handle.net/10183/158307.

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INTRODUÇÃO: Estudos prévios demonstram que pacientes com insuficiência cardíaca (IC) podem apresentar redução dinâmica na capacidade inspiratória (CI) durante o exercício associada à redução da capacidade aeróbia. Poucas informações estão disponíveis atualmente sobre se esta redução está relacionada a anormalidades da mecânica ventilatória ou à disfunção muscular inspiratória. OBJETIVOS: Comparar a atividade muscular inspiratória e a intensidade da dispneia durante o exercício em pacientes com IC estável que apresente (Grupo 1) ou não (Grupo 2) redução da CI durante o exercício. MÉTODOS: Foram avaliados 16 pacientes com IC clinicamente estáveis (11 homens, 30 ± 5% de fração de ejeção) e não obesos tratados de acordo com diretrizes baseadas em evidências, sem outras doenças sistêmicas ou evidência espirométrica de obstrução do fluxo aéreo (VEF1/CVF = 83 ± 5%). Os pacientes realizaram teste de exercício cardiopulmonar incremental com medidas seriadas de CI, percepção de dispneia (Borg) e monitoramento contínuo das pressões esofágica (Pes) e gástrica (Pga). A pressão transdiafragmática (Pdi) foi obtida a partir de Pga–Pges. As manobras de Sniff e pressão inspiratória máxima (PImax) foram comparadas em repouso e imediatamente após o exercício. RESULTADOS: Quatro pacientes (25%, Grupo 1) apresentaram redução da CI durante o exercício (-0,18 ± 0,01 vs 0,28 ± 0,05L, p < 0,05). Não houve diferença significativa entre os grupos na função pulmonar e variáveis ecocardiográficas, exceto por uma menor capacidade residual funcional no Grupo 1 (72 ± 9 vs 97 ± 17%; p < 0,05) e menor PImax no Grupo 2 (-101± 25 vs 67 ± 24 cmH2O, p < 0,05). Pes,Sniff (Grupo 1: -77,9 ± 8,7 a -79,6 ± 8,8; Grupo 2: -63,3 ± 4,8 a -66,3 ± 3,8 cmH2O) e Pdi,Sniff (Grupo 1: 116,3 ± 13,9 a 118,3 ± 14,2; Grupo 2: 92,3 ± 5,6 a 98,0 ± 6,0 cmH2O) não diminuíram significativamente com o exercício, assim como Pes,PImax (Grupo 1: -90,5 ± 6,2 a 90,0 ± 9,7; Grupo 2: -64,5 ± 7,3 a 62,3 ± 7,5 cmH2O) e Pdi,PImax (Grupo 1: 140,0 ± 14,0 a 129,3 ± 15,1; Grupo 2: 102,1 ± 15,4 a 90,4 ± 11,4 cmH2O). Apesar de Pga e Pdi terem reduzido ao longo das manobras seriadas de CI durante o exercício no Grupo 1, a Pes não diferiu entre os grupos. A dispneia também foi semelhante entre os grupos. Por fim, o Grupo 1 apresentou volume de reserva inspiratório menor que o Grupo 2 somente no pico do exercício (0,90 ± 0,08 vs 1,47 ± 0,21L; p <0,05). CONCLUSÃO: A redução da CI durante o exercício em alguns pacientes com IC parece ser acompanhada por queda da força diafragmática que é totalmente compensada pelos músculos inspiratórios acessórios. O Grupo 1 apresentou dispneia similar em relação ao grupo 2, provavelmente, pelo fato de o exercício ter sido interrompido antes de os pacientes atingirem limiares ventilatórios críticos para expansão do volume corrente.
BACKGROUNG: It has been described that patients with chronic heart failure (CHF) may present with dynamic reduction in inspiratory capacity (IC), which was associated with low peak aerobic capacity. Little information is currently available about whether this reduction is related to respiratory mechanics abnormalities or to impaired inspiratory muscle function. OBJECTIVE: To compare inspiratory muscle activity and intensity of dyspnea during exercise in stable patients with CHF presenting (Group 1) or not (Group 2) with dynamic reduction in IC. METHODS: We studied 16 clinically stable, non obese patients with CHF (11 males, 30 ± 5% ejection fraction) treated according to current evidence-based guidelines with no other systemic diseases or spirometric evidence of airflow obstruction (FEV1/FVC = 83 ± 5%). They performed incremental cardiopulmonary cycle exercise test with serial measurements of IC, dyspnea rating (Borg), and continuous monitoring of esophageal (Pes) and gastric (Pga) pressures. Transdiaphragmatic pressure (Pdi) was obtained from Pga–Pes. Sniff and maximal inspiratory pressure (MIP) maneuvers were compared at rest and immediately post exercise. RESULTS: Four patients (25%, Group 1) showed IC reduction during exercise (-0.18 ± 0.02 vs 0.28 ± 0.19L; p<0.05). There were no significant between-groups differences in lung function and echocardiographic variables, except for a lower functional residual capacity (72 ± 9 vs 97 ± 17%; p < 0.05) in Group 1 and a lower MIP (-101 ± 25 vs 67 ± 24 cm H2O; p < 0.05) in Group 2. Pes,Sniff (Group 1: -77.9 ± 8.7 to -79.6 ± 8.8; Group 2: -63.3 ± 4.8 to -66.3 ± 3.8 cmH2O) and Pdi,Sniff (Group 1: 116.3 ± 13.9 to 118.3 ± 14.2; Group 2: 92.3 ± 5.6 to 98.0 ± 6.0 cmH2O) did not significantly decrease with exercise. Despite Pga and Pdi felt along successive IC maneuvers in Group 1, Pes did not differ between groups. Dyspnea was also similar between groups. Finally, inspiratory reserve volume was lower in Group 1 only at peak exercise (0.90 ± 0.08 vs 1.47 ± 0.21L; p <0.05). CONCLUSIONS: Decrements in exercise IC in some patients with CHF seems accompanied by a dynamic impairment in diaphragm strength that is fully compensated by other inspiratory rib cage muscles. Group 1 presented similar dyspnea compared to Group 2 probably because they stopped exercise before reaching critical ventilatory constraints to tidal volume expansion.
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Gazzana, Marcelo Basso. "Investigação da hiperinsuflação pulmonar dinâmica durante o exercício e sua relação com a força dos músculos inspiratórios em pacientes com hipertensão arterial pulmonar". reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2015. http://hdl.handle.net/10183/119416.

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Introdução: A redução da capacidade inspiratória (CI) induzida pelo exercício observada em alguns pacientes com hipertensão arterial pulmonar (HAP) poderia potencialmente ser influenciada por disfunção muscular respiratória. Objetivos: Investigar se há alguma relação entre CI e força muscular respiratória antes e após o exercício máximo e estudar o papel da pressão muscular respiratória e da CI na dispneia e na capacidade de exercício em pacientes com HAP. Métodos: 27 pacientes com HAP e 12 controles saudáveis pareados foram comparados. Todos os participantes foram submetidos a teste de exercício cardiopulmonar (TECP) com determinação seriada da CI. As pressões inspiratória e expiratória máximas (PImáx e PEmáx, respectivamente) foram medidas antes, no pico e após o exercício. Resultados: Os pacientes tiveram menor volume expiratório forçado no primeiro segundo (VEF1), capacidade vital forçada (CVF) (com relação VEF1/CVF semelhante) e capacidade aeróbia máxima e maior dispneia no exercício. A PImáx e a PEmáx foram significativamente menores nos pacientes com HAP que nos controles. Entretanto, a variação pós exercício em relação ao repouso não foi significativamente diferente nos dois grupos. Os pacientes apresentaram redução significativa da CI do repouso ao pico do exercício em comparação aos controles. 17/27 pacientes (63%) apresentaram redução da CI durante o exercício. Considerando-se apenas os pacientes, não houve associação entre CI e PImáx ou PEmáx (pré, pós exercício ou mudança do repouso). Comparando-se os pacientes com e sem redução da CI, não houve diferença na proporção de pacientes que apresentaram redução da PImáx (41 vs 44%) ou da PEmáx (76 vs 89%) após o exercício. Da mesma forma, nenhuma diferença na PImáx ou PEmáx foi observada no exercício comparando estes subgrupos. Conclusões: Em resumo, a força muscular respiratória foi significativamente menor em pacientes com HAP em comparação com controles e uma proporção significativa de pacientes com HAP apresentaram redução da CI durante o exercício. No entanto, não foram observadas associações entre CI e alterações de força muscular respiratória com o exercício, sugerindo que ocorra verdadeira hiperinsuflação dinâmica. Além disso, o único parâmetro relacionado com a dispneia induzida pelo exercício foi a CI no repouso e com capacidade aeróbia no pico foi a magnitude da redução da PEmáx após o exercício.
Rationale: The exercise induced inspiratory capacity (IC) reduction observed in some patients with pulmonary arterial hypertension (PAH) could potentially be influenced by respiratory muscle dysfunction. Aims: To investigate if there is any relationship between IC and respiratory muscle strength before and after maximal exercise and to study the contribution of respiratory muscle pressure and IC in exercise dyspnea and capacity in PAH patients. Methods: 27 patients with PAH and 12 healthy matched controls were compared. All participants underwent cardiopulmonary exercise test (CPET) with serial IC measurements. Inspiratory and expiratory maximal mouth pressure (PImax and PEmax, respectively) were measured before and at peak/post exercise. Results: Patients had lower forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) (with similar FEV1/FVC ratio) and peak aerobic capacity and higher exercise dyspnea. PImax and PEmax were significantly lower in PAH patients compared to controls. However, post exercise variations from rest were not significant different in either group. Patients presented significant rest-to-peak reduction in IC compared to controls. 17/27 patients (63%) exhibited IC reduction during exercise. Considering only patients, there was no association between IC and PImax or PEmax (pre, post exercise or change from rest). Comparing patients with and without IC reduction, there was no difference in the proportion of patients presenting inspiratory (41 vs 44%) or expiratory (76 vs 89%) pressure reduction after exercise, respectively. In the same way, no difference in both inspiratory and expiratory respiratory pressure change with exercise was observed comparing these subgroups. Conclusions: In summary, respiratory muscle strength was significantly lower in PAH patients compared to controls and a significant proportion of PAH presented IC reduction during exercise. Nonetheless, no associations between IC and respiratory muscle strength changes with exercise were observed, suggesting a true dynamic lung hyperinflation. Additionally, the only parameter associated with exercise induced dyspnea was resting IC and with peak aerobic capacity was the magnitude of PEmax reduction after exercise.
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Sehlin, Maria. "Resistance breathing with PEP and CPAP : effects on respiratory parameters". Doctoral thesis, Umeå universitet, Anestesiologi och intensivvård, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-94650.

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Background: Positive expiratory pressure (PEP) and continuous positive airway pressure (CPAP) are two forms of resistance breathing used in spontaneously breathing patients. With a threshold resistor or a flow resistor, both PEP and CPAP provide a positive (elevated) pressure level during the expiratory phase. With PEP, inspiratory pressure is negative, i.e. lower than ambient air pressure, as during a normal inspiration, but with CPAP, the inspiratory pressure is positive, i.e. higher than ambient air pressure. Methods: This thesis is based on four separate studies in which four different breathing devices, a PEP-bottle (threshold resistor device), a PEP-mask (flow resistor device), a threshold resistor CPAP and a flow resistor device were investigated. Paper I, II and III are based on studies in healthy volunteers. Paper IV is a bench study performed in a hypobaric chamber. Paper I examined differences between two PEP devices, the PEP-bottle and the PEP-mask. Paper II evaluated the performance of a flow resistor CPAP device, (Boussignac CPAP). Paper III investigated the effect of two PEP-devices, a PEP-bottle and a PEP-mask and two CPAP devices, a threshold resistor CPAP and a flow resistor CPAP, on inspiratory capacity (IC). In paper IV, the effect of changes in ambient pressure on preset CPAP levels in two different CPAP devices was compared. Results: With the PEP bottle, both expiration and inspiration began with a zero-flow period during which airway pressure changed rapidly. With the PEP-mask, the zero-flow period was very short and the change in airway pressure almost non-existent (paper I). During normal breathing with the Boussignac CPAP, changes in airway pressure were never large enough to reduce airway pressure below zero. During forced breathing, as airflow increased, both the drop in inspiratory airway pressure and the increase in expiratory airway pressure were potentiated (paper II). IC decreased significantly with three of the breathing devices, the PEP-mask and the two CPAP devices (paper III). With the threshold resistor CPAP, measured pressure levels were close to the preset CPAP level. With the flow resistor CPAP, as the altitude increased CPAP produced pressure levels increased (paper IV). Conclusion: The effect on airway pressure, airflow, IC and the effect of changes in ambient air pressure differ between different kinds of resistance breathing devices. These differences in device performance should be taken into consideration when choosing the optimal resistance breathing device for each patient.
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Dumke, Anelise. "Efeitos da facilitação neuromuscular proprioceptiva aplicada à musculatura acessória da respiração sobre variáveis pulmonares e ativação muscular em pacientes com DPOC". reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2012. http://hdl.handle.net/10183/60763.

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INTRODUÇÃO: A desvantagem mecânica induzida pela hiperinsuflação leva os pacientes com doença pulmonar obstrutiva crônica (DPOC) a usar a musculatura acessória da respiração. Os efeitos do alongamento destes músculos em pacientes com DPOC não são bem conhecidos. OBJETIVOS: a) Comparar a ativação dos músculos acessórios da respiração em pacientes com DPOC e controles e estudar a relação entre a ativação muscular e a capacidade inspiratória (CI); b) avaliar os efeitos de uma técnica de facilitação neuromuscular proprioceptiva (FNP) sobre os músculos acessórios da respiração em pacientes com DPOC. MÉTODOS: Foram estudados 30 homens com DPOC e 30 controles com espirometria normal. Todos os indivíduos realizaram espirometria, medida das pressões inspiratória e expiratória máxima (PImáx, PEmáx) e avaliação da ativação muscular através da eletromiografia de superfície (EMGs). Os pacientes com DPOC foram randomizados para FNP dos músculos acessórios da respiração ou contração isotônica do bíceps (tratamento simulado, TS). Capacidade vital forçada (CVF), CI, PImáx, PEmáx, oximetria de pulso (SpO2) e mobilidade torácica foram medidos antes e após a intervenção. RESULTADOS: Os valores basais dos pacientes com DPOC foram: CVF 2,69 ± 0,6 L, VEF1 1,07 ± 0,23 L (34,9 ± 8,2%), CI 2,25 ± 0,5 L, PImáx -71,8 ± 19,8 cmH2O e PEmáx 106,1 ± 29,9 cmH2O. No grupo controle os valores funcionais basais foram normais. Pacientes com DPOC apresentaram maior ativação dos músculos escalenos e intercostal direito no repouso e do músculo escaleno e intercostal esquerdo durante a manobra da CI (p<0,05). Foi observada correlação moderada entre CI e atividade muscular do esternocleidomastoideo direito (r=-0,41;p=0,026) e do escaleno esquerdo (r=- 0,40;p=0,031) em pacientes com DPOC. Nenhuma associação foi verificada no grupo controle. A CI variou (OCI) 0,083 ± 0,04 L após FNP e -0,029 ± 0,015 L após TS (p=0,03). A PEmáx aumentou de 102,4 ± 20,6 cmH2O para 112,4 ± 24,5 cmH2O (p=0,02) após FNP e não variou significativamente após TS. Observou-se um aumento significativo da SpO2 com a FNP (p=0,02). Não houve alteração da CV, da PImáx e da mobilidade torácica após a FNP. Não houve alteração no sinal EMG após FNP ou TS. CONCLUSÕES: Nossos resultados sugerem que pacientes com DPOC apresentam maior ativação dos músculos acessórios da respiração no repouso e durante a realização da CI em comparação com controles e que esta ativação está inversamente associada com a CI. Nosso estudo também demonstrou que uma sessão de FNP dos músculos acessórios da respiração em pacientes com DPOC aumentou a CI, a PEmáx e a SpO2, sem alteração no sinal EMG. Estudos adicionais são necessários para avaliar os efeitos da técnica de FNP em longo prazo em pacientes com DPOC.
BACKGROUND: The mechanical disadvantage induced by hyperinflation forces chronic obstructive pulmonary disease (COPD) patients to use their accessory respiratory muscles. In COPD patients the effects of applying stretching techniques to these muscles are not well understood. AIM: The aims of our study were: a) to compare the activation of accessory respiratory muscles in patients with COPD and control subjects and study the relationship between muscle activation and inspiratory capacity (IC); b) to analyze the effects of a proprioceptive neuromuscular facilitation (PNF) stretching technique applied to the accessory respiratory muscles on patients with COPD. METHODS: We studied 30 male COPD and 30 control subjects. All subjects underwent spirometry, measurement of maximal inspiratory and expiratory pressures (MIP, MEP) and assessment of muscle activation by surface electromyography (sEMG). COPD patients were randomized for PNF of accessory respiratory muscles or isometric contraction of the biceps (sham treatment; ST). Mean forced vital capacity (FVC), IC, MIP, MEP, pulse oximetry (SpO2) and thoracic expansion were measured before and after intervention. RESULTS: Baseline values of COPD patients were: FVC 2.69 ± 0.6 l, FEV1 1.07 ± 0.23 l (34.9 ± 8.2%), IC 2.25 ± 0.5l, PImax -71.8 ± 19.8 cmH2O and PEmax 106.1 ± 29.9 cmH2O. Control subjects had all baseline values normal. Patients with COPD showed higher activation of both scalene and right intercostal muscles at rest and of left intercostal and left scalene muscle during the IC maneuver (p <0.05). Moderate correlation was observed between CI and the right sternocleidomastoid muscle activity (r = -0.41, p = 0.026) and left scalene (r = -0.40, p = 0.031) in patients with COPD. No association was observed in the control group. CI varied (OCI) 0.083 ± 0.04 l after PNF and -0.029 ± 0.015 l after ST (p = 0.03). The MEP increased from 102.4 ± 20.6 to 112.4 ± 24.5 cmH2O (p = 0.02) after PNF and did not change significantly after TS. There was a significant increase in the SpO2 with PNF (p=0.02). There was no change in FVC, MIP or thoracic mobility after PNF. There was no change in EMG after PNF or TS. CONCLUSIONS: Our results showed that patients with COPD have greater activation of accessory respiratory muscles at rest and during CI compared with controls, and that this activation is inversely associated with CI. Our study also demonstrated that a session of PNF applied to the accessory respiratory muscles in patients with COPD increased CI, MEP and SpO2, with no change in the sEMG signal. Additional studies are needed to evaluate the long-term effects of PNF applied to the acessory respiratory muscles on patients with COPD.
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Borile, Suellen. "Resposta cardiovascular do exercício agudo da musculatura inspiratória em pacientes com cardiomiopatia hipertensiva ou chagásica". Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/5/5160/tde-04112010-114159/.

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Pacientes com insuficiência cardíaca (IC) podem apresentar fraqueza da musculatura inspiratória. O treinamento da musculatura inspiratória (TMI) vem sendo utilizado nesta população para melhorar a capacidade cardiorrespiratória, porém, não se conhece a segurança e as alterações hemodinâmicas que possam ocorrer durante uma sessão deste modelo de exercício. Portanto, nosso objetivo foi avaliar a resposta cardiovascular durante o exercício agudo da musculatura inspiratória (ExAMI) em pacientes com IC associada a cardiomiopatia hipertensiva (CMHAS) ou chagásica (CMCH). Inicialmente, os pacientes responderam ao Questionário de Qualidade de Vida de Minnesota e na seqüência realizaram teste de força muscular respiratória por meio do equipamento manovacuômetro digital MVD300. Os pacientes que apresentaram fraqueza da musculatura inspiratória (valores 70% do predito da pressão inspiratória máxima - Pimáx) realizaram o ExAMI. Durante os momentos basal (repouso) e ExAMI registramos de forma indireta e não-invasiva, curvas da pressão arterial (PA) batimento a batimento com o equipamento Finometer. Também monitoramos o ritmo cardíaco por meio do eletrocardiograma e a frequência respiratória com uso da cinta respiratória. O protocolo foi realizado com todos os pacientes sentados e teve duração de 25 minutos (10 min basal, 10 min ExAMI e 5 min de recuperação). O exercício foi executado com o equipamento Threshold inspiratório com carga de 30% da Pimáx. O protocolo do ExAMI foi realizado por 27 pacientes com CMHAS e 9 pacientes com CMCH (FEVE<45%), porém, 7 pacientes (26%) do grupo CMHAS não finalizaram o protocolo por apresentarem elevação da PA sistólica > 20mmHg e referirem exaustão. Todos os pacientes do grupo CMCH concluíram o tempo previsto do ExAMI, mas relataram intenso cansaço ao final do exercício. Quando comparamos o basal vs. exercício (valor ) para ambos os grupos (CMHAS e CMCH), encontramos aumentos significativos da: PA sistólica ( = 9 ± 2 e = 7,6 ± 3 mmHg), diastólica ( = 4,8 ± 1 e = 4,2 ± 1 mmHg), FC ( = 5,5 ± 1,2 e = 6,6 ± 3 bpm) e DP ( = 1327 ± 208 e = 1319 ± 373 mmHg.bpm); o grupo CMHAS também apresentou aumento significativo do DC ( = 0,36 ± 0,1 l/min), Ic ( = 0,2 ± 0,1 l/min/m2), dp/dt ( = 118 ± 35 mmHg/s) e SPTI ( = 1,98 ± 0,6 mmHg.s). A modulação autonômica foi semelhante em ambos os grupos no momento basal e durante o exercício ocorreu um aumento da modulação vagal no grupo CMHAS ( = 258 ± 115 ms2). Os nossos resultados demonstraram que o ExAMI provocou alterações hemodinâmicas significativas nos pacientes dos dois grupos estudados, mas sem repercussão clínica na maioria deles. Um quarto (26%) dos pacientes com CMHAS apresentaram resposta exacerbada da PAS, referiram exaustão e portanto, não conseguiram realizar o tempo pré-determinado (10 min) do ExAMI. Sendo assim, concluímos que antes da indicação do TMI (3 séries de 10 min/dia) faz-se necessário a realização de uma sessão do exercício com monitorização cardíaca e respiratória, para avaliar se há ou não segurança da indicação deste modelo de exercício para pacientes com IC de diferentes etiologias
Patients with heart failure (HF) may show weakness of respiratory muscles. The inspiratory muscle training (IMT) has been used in this population to improve cardiorespiratory fitness, however, does not know the safety and hemodynamic changes that may occur during a session of exercise model. Therefore, our objective was to evaluate the cardiovascular response during acute inspiratory muscle exercise (AIME) in patients with HF associated with hypertensive cardiomyopathy (HCM) or Chagas (CCM). Initially, the patients responded to the questionnaire of quality of life of Minnesota and the test sequence performed by respiratory muscle strength equipment MVD300 digital manometer. Those patients who had inspiratory muscle weakness (values 70% predicted maximal inspiratory pressure - MIP) were AIME. During the basal (resting) and AIME recorded indirectly and non-invasive blood pressure curves (BP) beat to beat with the equipment Finometer. We also monitor the heart rate by electrocardiogram and respiration using the respiratory belt. The protocol was performed with patients sitting and lasted 25 minutes (10 min baseline, 10 min AIME and 5 min recovery). The exercise was carried out with the equipment inspiratory threshold load of 30% of MIP. The protocol of the AIME was performed for 27 patients with HCM and 9 patients with CCM (LVEF <45%), however, seven patients (26%) in group HCM not finalized the protocol for having elevated systolic BP 20mmHg and refer exhaustion. All patients in CCM group completed the scheduled time of the AIME, but reported heavy fatigue at the end of the exercise. When comparing the basal. vs. exercise (value ) for both groups (HCM and CCM), we found significant increases in: Systolic BP ( = 9 ± 2 e = 7,6 ± 3 mmHg), diastolic BP ( = 4,8 ± 1 e = 4,2 ± 1 mmHg), HR ( = 5,5 ± 1,2 e = 6,6 ± 3 bpm) e PD ( = 1327 ± 208 e = 1319 ± 373 mmHg.bpm); the HCM group also showed a significant increase in CO ( = 0,36 ± 0,1 l/min), CI ( = 0,2 ± 0,1 l/min/m2), dp/dt ( = 118 ± 35 mmHg/s) e SPTI ( = 1,98 ± 0,6 mmHg.s). The autonomic modulation was similar in both groups at baseline and during exercise there was an increase in vagal modulation in the group HCM ( = 258 ± 115 ms2). Our results demonstrate that the AIME caused significant hemodynamic changes in patients of both groups, but no clinical significance in most areas. A quarter (26%) patients with HCM showed exacerbated response of SBP, reported exhaustion and therefore could not perform the predetermined time (10 min) of the AIME. Thus, we conclude that before the indications of IMT (3 x 10 min / day) is necessary to carry out an exercise session with cardiac and respiratory monitoring, to evaluate whether or not the security alert to this type of exercise patients with HF of different etiologies
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Roquejani, Augusto Cesar. "Influencia da posição corporal na medida da pressão inspiratoria maxima (PImax) e da pressão expiratoria maxima (PEmax) em voluntarios adultos sadios". [s.n.], 2006. http://repositorio.unicamp.br/jspui/handle/REPOSIP/312005.

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Orientadores: Sebastião Araujo, Desanka Dragosavac
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
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Resumo: As medidas da PImáx e PEmáx são utilizadas para avaliar a força da musculatura respiratória. Porém, o efeito da posição corporal sobre essas medidas não se encontra bem estabelecido na literatura. O objetivo deste estudo foi avaliar a influência de diversas posições corporais nos valores da PImáx e PEmáx. MÉTODO: Foi realizado um estudo prospectivo e aberto, em que foram avaliados 50 indivíduos saudáveis (25 homens e 25 mulheres), com idade entre 18 e 55 anos, em sete diferentes decúbitos [sentado (PRE), Trendelenburg (TREND), prona, 0°, decúbitos lateral direito (DLD) e esquerdo (DLE) e 45°]. Foram também analisadas as influências do sexo sobre essas variáveis. RESULTADOS: O maior valor da PImáx (média ± DP) foi de -79,4 ± 21,7 cmH2O em 45° nas mulheres e de -82,8 ± 21,3 cmH2O em DLD no homem (p = NS) e o menor em TREND (-64,3 ± 21,6 cmH2O versus -79,1 ± 22,3 cmH2O; p < 0,05). Com relação à PEmáx todos os valores no sexo masculino foram maiores que no feminino (p < 0,0001), sem influência da posição corporal. CONCLUSÕES: Determinadas posições corporais e o sexo influenciaram nas medidas de PImáx. Com relação às medidas da PEmáx, apenas a influência do sexo foi significativa
Abstract: Measurements of PImax and PEmax are useful to evaluate respiratory muscle strength. However, the effects of body position on these variables are not well established in the literature. The objective if this study was to evaluate the influence of different body positions on PImax and PEmax values. METHODS: Prospective, open label study, in which 50 adult healthy volunteers (25 males e 25 females), aging 18-55 years, were evaluated in seven different positions: sitting (PRE), Trendelenburg (TREND), prone, 0°, right lateral (RLD) and left lateral (LLD) decubitus and 45°. The influence of gender on these variables was also analyzed. RESULTS: The greatest Plmax value (mean ± SD) was -79.4 ± 21.7 cmH2O at 45° in females and -82.8 ± 21.3 cmH2O at RDL in males (p=NS) and the smallest at TREND (-64,3 ± 21.6 cmH2O versus -79.1 ± 22,3 cmH2O; p<0.05). PEmax values were ever greater in males than in females (p < 0.0001), without influence of body position. CONCLUSIONS: In adult healthy volunteers, some body positions and gender have had significant influence on PImax values. Otherwise, PEmax values have been influenced only by gender.
Mestrado
Pesquisa Experimental
Mestre em Cirurgia
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Sabapathy, Surendran, i n/a. "Acute and Chronic Adaptations To Intermittent and Continuous Exercise in Chronic Obstructive Pulmonary Disease Patients". Griffith University. School of Physiotherapy and Exercise Science, 2006. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20070115.170236.

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The primary aim of this thesis was to develop a better understanding of the physiology and perceptual responses associated with the performance of continuous (CE) and intermittent exercise (IE) in patients with moderate chronic obstructive pulmonary disease (COPD). A secondary aim was to examine factors that could potentially limit exercise tolerance in COPD patients, particularly in relation to the dynamics of the cardiovascular system and muscle metabolism. The results of the four studies conducted to achieve these aims are presented in this thesis. In Study 1, the physiological, metabolic and perceptual responses to an acute bout of IE and CE were examined in 10 individuals with moderate COPD. Each subject completed an incremental exercise test to exhaustion on a cycle ergometer. Subjects then performed IE (1 min exercise: 1 min rest ratio) and CE tests at 70% of peak power in random order on separate days. Gas exchange, heart rate, plasma lactate concentration, ratings of breathlessness, inspiratory capacity and the total amount of work completed were measured during each exercise test. Subjects were able to complete a significantly greater amount of work during IE (71 ± 32 kJ) compared with CE (31 ± 24 kJ). Intermittent exercise was associated with significantly lower values for oxygen uptake, expired ventilation and plasma lactate concentration when compared with CE. Subjects also reported a significantly lower rating of breathlessness during IE compared to CE. The degree of dynamic lung hyperinflation (change in end-expiratory lung volume) was lower during IE (0.23 ± 0.07 L) than during CE (0.52 ± 0.13 L). The results suggest that IE may be superior to CE as a mode of training for patients with COPD. The greater amount of total work performed and the lower measured physiological responses attained with intermittent exercise could potentially allow greater training adaptations to be achieved in individuals with more limited lung function. The purpose of Study 2 was to compare the adaptations to 8 wk of supervised intermittent and continuous cycle ergometry training, performed at the same relative intensity and matched for total work completed, in patients with COPD. Nineteen subjects with moderate COPD were stratified according to age, gender, and pulmonary function, and then randomly assigned to either an IE (1 min exercise: 1 min rest ratio) or CE training group. Subjects trained 3 d per week for 8 wk and completed 30 min of exercise. Initial training intensity, i.e., the power output applied during the CE bouts and during the exercise interval of the IE bouts, was determined as 50% of the peak power output achieved during incremental exercise and was increased by 5% each week after 2 wk of training. The total amount of work performed was not significantly different (P=0.74) between the CE (750 ± 90 kJ) and IE (707 ± 92 kJ) groups. The subjects who performed IE (N=9) experienced significantly lower levels of perceived breathlessness and lower limb fatigue during the exercise-training bouts than the group who performed CE (N=10). However, exercise capacity (peak oxygen uptake) and exercise tolerance (peak power output and 6-min walk distance) improved to a similar extent in both training groups. During submaximal constant-load exercise, the improved (faster) phase II oxygen uptake kinetic response with training was independent of exercise mode. Furthermore, training-induced reductions in submaximal exercise heart rate, carbon dioxide output, expired ventilation and blood lactate concentrations were not different between the two training modes. Exercise training also resulted in an equivalent reduction for both training modes in the degree of dynamic hyperinflation observed during incremental exercise. Thus, when total work performed and relative intensity were the same for both training modes, 8 wk of CE or IE training resulted in similar functional improvements and physiological adaptations in patients with moderate COPD. Study 3 examined the relationship between exercise capacity (peak oxygen uptake) and lower limb vasodilatory capacity in 9 patients with moderate COPD and 9 healthy age-matched control subjects. While peak oxygen uptake was significantly lower in the COPD patients (15.8 ± 3.5 mL·min-1·kg-1) compared to the control subjects (25.2 ± 3.5 mL·kg-1·min-1), there were no significant differences between groups in peak calf blood flow or peak calf conductance measured 7 s post-ischemia. Peak oxygen uptake was significantly correlated with peak calf blood flow and peak conductance in the control group, whereas there was no significant relationship found between these variables in the COPD group. However, the rate of decay in blood flow following ischemia was significantly slower (p less than 0.05) for the COPD group (-0.036 ± 0.005 mL·100 mL-1·min-1·s-1) when compared to the control group (-0.048 ± 0.015 mL·100 mL-1·min-1·s-1). The results of this study suggest that the lower peak exercise capacity in patients with moderate COPD is not related to a loss in leg vasodilatory capacity. Study 4 examined the dynamics of oxygen uptake kinetics during high-intensity constant-load cycling performed at 70% of the peak power attained during an incremental exercise test in 7 patients with moderate COPD and 7 healthy age-matched controls. The time constant of the primary component (phase II) of oxygen uptake was significantly slower in the COPD patients (82 ± 8 s) when compared to healthy control subjects (44 ± 4 s). Moreover, the oxygen cost per unit increment in power output for the primary component and the overall response were significantly higher in patients with COPD than in healthy control subjects. A slow component was observed in 5 of the 7 patients with COPD (49 ± 11 mL·min-1), whereas all of the control subjects demonstrated a slow component of oxygen uptake (213 ± 35 mL·min-1). The slow component comprised a significantly greater proportion of the total oxygen uptake response in the healthy control group (18 ± 2%) than in the COPD group (10 ± 2%). In the COPD patients, the slow component amplitude was significantly correlated with the decrease in inspiratory capacity (r = -0.88, P less than 0.05; N=5), indicating that the magnitude of the slow component was larger in individuals who experienced a greater degree of dynamic hyperinflation. This study demonstrated that most patients with moderate COPD are able to exercise at intensities high enough to elicit a slow component of oxygen uptake during constant-load exercise. The significant correlation observed between the slow component amplitude and the degree of dynamic hyperinflation suggests that the work of breathing may contribute to the slow component in patients with COPD.
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Oliveira, Flávia Roberta Rocha de. "Influência da reserva ventilatória na mobilidade diafragmática em pacientes com doença pulmonar obstrutiva crônica". Universidade do Estado de Santa Catarina, 2015. http://tede.udesc.br/handle/handle/1841.

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Patients with Chronic Obstructive Pulmonary Disease (COPD) have reduced diaphragmatic mobility (DM) and ventilatory reserve (VR). DM has demonstrated relationship with lung function, air trapping, lung hyperinflation, distance covered on the six-minute walk test (6MWT), mortality and dyspnea in patients with COPD. Similarly, VR is correlated with exercise capacity, disease severity and dyspnea. However, there are no studies investigating whether static hyperinflation and VR influence DM in patients with COPD. Objective: To investigate the influence of static hyperinflation and VR on DM in patients with COPD, as well as to compare the anthropometric characteristics, spirometric data, DM, dyspnea and submaximal exercise capacity among VR> 11l / minute (l / min) and VR <11l / min groups. Methods: This is a cross-sectional study that evaluated 42 patients with COPD. On the first day, patients underwent the following assessments: anthropometry, vital signs, spirometry and dyspnea. On the second day, patients performed the six-minute walk test and after one week, DM was evaluated by radiographic method considering the distance between maximal inspiration and expiration (DMdist). The sample was divided into VR > 11l / min and VR <11l / min groups for the comparison of anthropometric characteristics, spirometric data, DM, dyspnea and submaximal exercise capacity. Statistical analysis: Data normality was tested by Shapiro Wilk. According to data distribution, parametric or nonparametric test was used. Simple linear regression found the influence of lung hyperinflation and VR on DM. The Pearson s linear correlation coefficient correlated DM with static hyperinflation and VR. The t test for independent samples or the Mann Whitney U test was used to compare VR> 11l / min and VR <11l / min groups. Significance level of 5% (p <0.05). Results: Static hyperinflation influenced DM by 46%, i.e., to increase 1 liter in inspiratory capacity (IC), DM increased 1.56 cm (p 0.001, F = 34.55), while VR influenced only 25%, and for every increase of 1 l / min of VR, DM increased by 0.38 mm (p = 0.001, F =13.78). By comparing VR >11l / min and VR < 11l / min groups, it was found that in the VR <11l / min group, patients were older (69 ± 5 versus 61 ± 8 years) and showed reduction in the following variables: IC, forced expiratory volume in the first second (FEV1), DM, worse submaximal exercise capacity and increased dyspnea. Conclusions: Static hyperinflation and VR influence DM. However, hyperinflation exerts greater influence on DM compared to VR. In addition, patients with COPD who have VR <11l / min are more committed both in the lung function and DM as in submaximal exercise capacity and dyspnea when compared to patients with COPD with who have VR> 11l / min.
Pacientes com doença pulmonar obstrutiva crônica (DPOC) apresentam redução da mobilidade diafragmática (MD) e da reserva ventilatória (RV). A MD tem demonstrado relação com a função pulmonar, aprisionamento de ar, hiperinsuflação pulmonar, distância percorrida no teste da caminhada de seis minutos (TC6min), mortalidade e dispneia em pacientes com DPOC. Da mesma forma, a RV apresenta relação com a capacidade de exercício, gravidade da doença e dispneia. Contudo não há estudos que investiguem se a RV influencia a MD em pacientes com DPOC. Objetivo: Investigar a influência da RV na MD em pacientes com DPOC, bem como comparar as características antropométricas, função pulmonar, MD, dispneia e capacidade de exercício entre os grupos RV >11litros/minuto (l/min) e RV <11l/min. Métodos: Tratou-se de um estudo com delineamento transversal, no qual foram avaliados 42 pacientes com DPOC de ambos os sexos e idade média de 64±8 anos. No primeiro dia, os pacientes foram submetidos às seguintes avaliações: antropometria, sinais vitais, espirometria e dispneia. No segundo dia foram submetidos ao TC6min, e após uma semana foi avaliada a MD pelo método radiográfico da distância entre a inspiração e expiração máxima (MDdist). A amostra foi subdividida nos grupos RV >11l/min e RV <11l/min para comparação das características antropométricas, dados espirométricos, MD, dispneia e capacidade submáxima de exercício. Análise estatística: A normalidade dos dados foi testada pelo teste de Shapiro Wilk. Conforme a distribuição dos dados utilizou-se um teste paramétrico ou não paramétrico. O coeficiente de correlação linear de Pearson correlacionou a RV com a MD. O teste de regressão linear simples verificou a influência da RV na MD. O teste t de Student para amostras independentes ou o teste U de Mann Whitney foi usado para comparação dos grupos RV >11l/min e RV <11l/min. Adotou-se nível de significância de 5% (p < 0,05). Resultados: A RV influenciou em 25% a MD, sendo que para cada aumento de 1 l/min da RV, a MD aumentou em 0,38 mm (p=0,001, F=13,78). Ao comparar os grupos RV ˃ 11l/min e RV ˂ 11l/min, constatou-se que no grupo RV ˂11l/min os pacientes eram mais idosos (69±5 versus 61±8 anos) e apresentaram menores valores das variáveis: CI, volume expiratório forçado no primeiro segundo (VEF1), MD, pior capacidade submáxima de exercício e maior dispneia. Conclusões: A RV influencia a MD. Além disso, pacientes com DPOC que apresentaram RV <11l/min são mais comprometidos tanto na função pulmonar e MD quanto na capacidade submáxima de exercício e dispneia, em comparação a pacientes com DPOC que apresentam RV >11l/min.
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Gass, Ricardo. "Investigação dos efeitos de dois níveis de pressão expiratória positiva nas vias aéreas sobre a dispneia, hiperinsuflação pulmonar dinâmica e tolerância ao exercício em portadores de Doença Pulmonar Obstrutiva Crônica". reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2017. http://hdl.handle.net/10183/159082.

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Introdução: A aplicação da pressão positiva expiratória (EPAP) em pacientes com DPOC durante o exercício pode reduzir a hiperinflação dinâmica (HD) e consequentemente a dispneia, enquanto, por outro lado, pode aumentar o trabalho resistivo da respiração. O objetivo do presente estudo foi avaliar os efeitos de duas intensidades de EPAP sobre a capacidade inspiratória, dispneia e tolerância ao exercício em pacientes com DPOC moderada a muito grave. Métodos: Estudo transversal, experimental, de 4 visitas. Na visita 1, os participantes realizaram um teste de exercício cardiopulmonar incremental limitados por sintomas (TECP). Nas visitas 2-4, com pelo menos 48 horas de intervalo, em ordem aleatória, eles realizaram TECP com carga constante (TECPct; 75% da carga de pico) sem EPAP, EPAP com 5cmH2O (EPAP5), ou EPAP com 10cmH2O (EPAP10). Resultados: O estudo incluiu 15 participantes não hipoxêmicos com DPOC moderada a muito grave (média de VEF1= 35,3 ± 10,9% do previsto). As intensidades sucessivas de EPAP durante o TECPct tenderam a causar uma redução progressiva da tolerância ao exercício (p=0,11). Destaca-se que 10 dos 15 pacientes apresentaram menor duração de exercício quando o EPAP10 foi comparado ao teste sem EPAP (-151 ± 105s, p <0,01 ou -41 ± 26%). Além disso, observou-se com EPAP (p <0,05) uma redução significativa da ventilação minuto, as custas de uma restrição na expansão do volume corrente. Por fim, a sensação de dispneia e medidas seriadas da capacidade inspiratória durante o exercício não foram diferentes entre as três intervenções. Conclusão: Níveis progressivos de EPAP durante o exercício tendem a causar uma redução progressiva na tolerância ao exercício em pacientes com DPOC sem melhora na dispneia e HD.
Introduction: The application of expiratory positive aiway pressure (EPAP) in COPD patients during exercise may reduce dynamic hyperinflation (DH), and consequently dyspnea, while, on the other hand, can increase the resistive work of breathing. Therefore, the objective of the current study was to evaluate the effects of two intensities of EPAP on inspiratory capacity, dyspnea and exercise tolerance in patients with moderate to very-severe COPD. Methods: Cross-sectional, experimental, 4-visit study. In the Visit 1, participants performed symptom-limited cycling incremental cardiopulmonary exercise test (CPET). In Visits 2-4, at least 48hrs apart, in a randomized order, they performed constant CPET (ctCPET) without EPAP, EPAP with 5cmH2O (EPAP5), or EPAP with 10cmH2O (EPAP10). Results: The study included 15 non-hypoxemic subjects ranging from moderate-to-very-severe COPD (mean FEV1=35.3 ± 10.9% of predicted). Successive intensities of EPAP during ctCPET tended to cause a progressive reduction in exercise tolerance (p=0.11). Of note, 10 of 15 presented shorter exercise duration when EPAP10 was compared to the test without EPAP (-151±105s, p<0.01 or -41±26%). Moreover, significant constraint to minute-ventilation, at expenses of limited tidal volume expansion, was observed with EPAP (p<0.05). Finally, dyspnea sensation and IC measurements were similar during exercise among the interventions. Conclusion: Progressive levels of EPAP during exercise tented to cause a progressive reduction in exercise tolerance in COPD patients without improvement in exercise dyspnea and DH.
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Sabapathy, Surendran. "Acute and Chronic Adaptations To Intermittent and Continuous Exercise in Chronic Obstructive Pulmonary Disease Patients". Thesis, Griffith University, 2006. http://hdl.handle.net/10072/366117.

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The primary aim of this thesis was to develop a better understanding of the physiology and perceptual responses associated with the performance of continuous (CE) and intermittent exercise (IE) in patients with moderate chronic obstructive pulmonary disease (COPD). A secondary aim was to examine factors that could potentially limit exercise tolerance in COPD patients, particularly in relation to the dynamics of the cardiovascular system and muscle metabolism. The results of the four studies conducted to achieve these aims are presented in this thesis. In Study 1, the physiological, metabolic and perceptual responses to an acute bout of IE and CE were examined in 10 individuals with moderate COPD. Each subject completed an incremental exercise test to exhaustion on a cycle ergometer. Subjects then performed IE (1 min exercise: 1 min rest ratio) and CE tests at 70% of peak power in random order on separate days. Gas exchange, heart rate, plasma lactate concentration, ratings of breathlessness, inspiratory capacity and the total amount of work completed were measured during each exercise test. Subjects were able to complete a significantly greater amount of work during IE (71 ± 32 kJ) compared with CE (31 ± 24 kJ). Intermittent exercise was associated with significantly lower values for oxygen uptake, expired ventilation and plasma lactate concentration when compared with CE. Subjects also reported a significantly lower rating of breathlessness during IE compared to CE. The degree of dynamic lung hyperinflation (change in end-expiratory lung volume) was lower during IE (0.23 ± 0.07 L) than during CE (0.52 ± 0.13 L). The results suggest that IE may be superior to CE as a mode of training for patients with COPD. The greater amount of total work performed and the lower measured physiological responses attained with intermittent exercise could potentially allow greater training adaptations to be achieved in individuals with more limited lung function. The purpose of Study 2 was to compare the adaptations to 8 wk of supervised intermittent and continuous cycle ergometry training, performed at the same relative intensity and matched for total work completed, in patients with COPD. Nineteen subjects with moderate COPD were stratified according to age, gender, and pulmonary function, and then randomly assigned to either an IE (1 min exercise: 1 min rest ratio) or CE training group. Subjects trained 3 d per week for 8 wk and completed 30 min of exercise. Initial training intensity, i.e., the power output applied during the CE bouts and during the exercise interval of the IE bouts, was determined as 50% of the peak power output achieved during incremental exercise and was increased by 5% each week after 2 wk of training. The total amount of work performed was not significantly different (P=0.74) between the CE (750 ± 90 kJ) and IE (707 ± 92 kJ) groups. The subjects who performed IE (N=9) experienced significantly lower levels of perceived breathlessness and lower limb fatigue during the exercise-training bouts than the group who performed CE (N=10). However, exercise capacity (peak oxygen uptake) and exercise tolerance (peak power output and 6-min walk distance) improved to a similar extent in both training groups. During submaximal constant-load exercise, the improved (faster) phase II oxygen uptake kinetic response with training was independent of exercise mode. Furthermore, training-induced reductions in submaximal exercise heart rate, carbon dioxide output, expired ventilation and blood lactate concentrations were not different between the two training modes. Exercise training also resulted in an equivalent reduction for both training modes in the degree of dynamic hyperinflation observed during incremental exercise. Thus, when total work performed and relative intensity were the same for both training modes, 8 wk of CE or IE training resulted in similar functional improvements and physiological adaptations in patients with moderate COPD. Study 3 examined the relationship between exercise capacity (peak oxygen uptake) and lower limb vasodilatory capacity in 9 patients with moderate COPD and 9 healthy age-matched control subjects. While peak oxygen uptake was significantly lower in the COPD patients (15.8 ± 3.5 mL·min-1·kg-1) compared to the control subjects (25.2 ± 3.5 mL·kg-1·min-1), there were no significant differences between groups in peak calf blood flow or peak calf conductance measured 7 s post-ischemia. Peak oxygen uptake was significantly correlated with peak calf blood flow and peak conductance in the control group, whereas there was no significant relationship found between these variables in the COPD group. However, the rate of decay in blood flow following ischemia was significantly slower (p less than 0.05) for the COPD group (-0.036 ± 0.005 mL·100 mL-1·min-1·s-1) when compared to the control group (-0.048 ± 0.015 mL·100 mL-1·min-1·s-1). The results of this study suggest that the lower peak exercise capacity in patients with moderate COPD is not related to a loss in leg vasodilatory capacity. Study 4 examined the dynamics of oxygen uptake kinetics during high-intensity constant-load cycling performed at 70% of the peak power attained during an incremental exercise test in 7 patients with moderate COPD and 7 healthy age-matched controls. The time constant of the primary component (phase II) of oxygen uptake was significantly slower in the COPD patients (82 ± 8 s) when compared to healthy control subjects (44 ± 4 s). Moreover, the oxygen cost per unit increment in power output for the primary component and the overall response were significantly higher in patients with COPD than in healthy control subjects. A slow component was observed in 5 of the 7 patients with COPD (49 ± 11 mL·min-1), whereas all of the control subjects demonstrated a slow component of oxygen uptake (213 ± 35 mL·min-1). The slow component comprised a significantly greater proportion of the total oxygen uptake response in the healthy control group (18 ± 2%) than in the COPD group (10 ± 2%). In the COPD patients, the slow component amplitude was significantly correlated with the decrease in inspiratory capacity (r = -0.88, P less than 0.05; N=5), indicating that the magnitude of the slow component was larger in individuals who experienced a greater degree of dynamic hyperinflation. This study demonstrated that most patients with moderate COPD are able to exercise at intensities high enough to elicit a slow component of oxygen uptake during constant-load exercise. The significant correlation observed between the slow component amplitude and the degree of dynamic hyperinflation suggests that the work of breathing may contribute to the slow component in patients with COPD.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Physiotherapy and Exercise Science
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Książki na temat "Inspiratory capacity"

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Chegwidden, Lynn. The effect of shoulder girdle fixation on maximal inspiratory pressure and vital capacity in normal subjects. 1999.

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Vassilakopoulos, Theodoros, i Charis Roussos. Respiratory muscle function in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0077.

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The inspiratory muscles are the diaphragm, external intercostals and parasternal internal intercostal muscles. The internal intercostals and abdominal muscles are expiratory. The ability of a subject to take one breath depends on the balance between the load faced by the inspiratory muscles and their neuromuscular competence. The ability of a subject to sustain the respiratory load over time (endurance) depends on the balance between energy supplied to the inspiratory muscles and their energy demands. Hyperinflation puts the diaphragm at a great mechanical disadvantage, decreasing its force-generating capacity. In response to acute increases in load the inspiratory muscles become fatigued and inflammed. In response to reduction in load by the use of mechanical ventilation they develop atrophy and dysfunction. Global respiratory muscle function can be tested using maximum static inspiratory and expiratory mouth pressures, and sniff pressure. Diaphragm function can be tested by measuring the transdiaphragmatic and twitch pressures developed upon electrical or magnetic stimulation of the phrenic nerve.
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Frew, Anthony. Air pollution. Redaktorzy Patrick Davey i David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0341.

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Any public debate about air pollution starts with the premise that air pollution cannot be good for you, so we should have less of it. However, it is much more difficult to determine how much is dangerous, and even more difficult to decide how much we are willing to pay for improvements in measured air pollution. Recent UK estimates suggest that fine particulate pollution causes about 6500 deaths per year, although it is not clear how many years of life are lost as a result. Some deaths may just be brought forward by a few days or weeks, while others may be truly premature. Globally, household pollution from cooking fuels may cause up to two million premature deaths per year in the developing world. The hazards of black smoke air pollution have been known since antiquity. The first descriptions of deaths caused by air pollution are those recorded after the eruption of Vesuvius in ad 79. In modern times, the infamous smogs of the early twentieth century in Belgium and London were clearly shown to trigger deaths in people with chronic bronchitis and heart disease. In mechanistic terms, black smoke and sulphur dioxide generated from industrial processes and domestic coal burning cause airway inflammation, exacerbation of chronic bronchitis, and consequent heart failure. Epidemiological analysis has confirmed that the deaths included both those who were likely to have died soon anyway and those who might well have survived for months or years if the pollution event had not occurred. Clean air legislation has dramatically reduced the levels of these traditional pollutants in the West, although these pollutants are still important in China, and smoke from solid cooking fuel continues to take a heavy toll amongst women in less developed parts of the world. New forms of air pollution have emerged, principally due to the increase in motor vehicle traffic since the 1950s. The combination of fine particulates and ground-level ozone causes ‘summer smogs’ which intensify over cities during summer periods of high barometric pressure. In Los Angeles and Mexico City, ozone concentrations commonly reach levels which are associated with adverse respiratory effects in normal and asthmatic subjects. Ozone directly affects the airways, causing reduced inspiratory capacity. This effect is more marked in patients with asthma and is clinically important, since epidemiological studies have found linear associations between ozone concentrations and admission rates for asthma and related respiratory diseases. Ozone induces an acute neutrophilic inflammatory response in both human and animal airways, together with release of chemokines (e.g. interleukin 8 and growth-related oncogene-alpha). Nitrogen oxides have less direct effect on human airways, but they increase the response to allergen challenge in patients with atopic asthma. Nitrogen oxide exposure also increases the risk of becoming ill after exposure to influenza. Alveolar macrophages are less able to inactivate influenza viruses and this leads to an increased probability of infection after experimental exposure to influenza. In the last two decades, major concerns have been raised about the effects of fine particulates. An association between fine particulate levels and cardiovascular and respiratory mortality and morbidity was first reported in 1993 and has since been confirmed in several other countries. Globally, about 90% of airborne particles are formed naturally, from sea spray, dust storms, volcanoes, and burning grass and forests. Human activity accounts for about 10% of aerosols (in terms of mass). This comes from transport, power stations, and various industrial processes. Diesel exhaust is the principal source of fine particulate pollution in Europe, while sea spray is the principal source in California, and agricultural activity is a major contributor in inland areas of the US. Dust storms are important sources in the Sahara, the Middle East, and parts of China. The mechanism of adverse health effects remains unclear but, unlike the case for ozone and nitrogen oxides, there is no safe threshold for the health effects of particulates. Since the 1990s, tax measures aimed at reducing greenhouse gas emissions have led to a rapid rise in the proportion of new cars with diesel engines. In the UK, this rose from 4% in 1990 to one-third of new cars in 2004 while, in France, over half of new vehicles have diesel engines. Diesel exhaust particles may increase the risk of sensitization to airborne allergens and cause airways inflammation both in vitro and in vivo. Extensive epidemiological work has confirmed that there is an association between increased exposure to environmental fine particulates and death from cardiovascular causes. Various mechanisms have been proposed: cardiac rhythm disturbance seems the most likely at present. It has also been proposed that high numbers of ultrafine particles may cause alveolar inflammation which then exacerbates preexisting cardiac and pulmonary disease. In support of this hypothesis, the metal content of ultrafine particles induces oxidative stress when alveolar macrophages are exposed to particles in vitro. While this is a plausible mechanism, in epidemiological studies it is difficult to separate the effects of ultrafine particles from those of other traffic-related pollutants.
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Części książek na temat "Inspiratory capacity"

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Milic-Emili, J., i C. Tantucci. "Inspiratory Capacity and Exercise Tolerance in Chronic Obstructive Pulmonary Disease". W Mechanics of Breathing, 201–9. Milano: Springer Milan, 2002. http://dx.doi.org/10.1007/978-88-470-2916-3_17.

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Milic–Emili, J., i O. Diaz. "Inspiratory Capacity, Exercise Tolerance, and Respiratory Failure in Chronic Obstructive Pulmonary Disease". W Anaesthesia, Pain, Intensive Care and Emergency Medicine — A.P.I.C.E., 269–73. Milano: Springer Milan, 2001. http://dx.doi.org/10.1007/978-88-470-2903-3_24.

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Kinnear, William J. M., i James H. Hull. "Additional respiratory measurements". W A Practical Guide to the Interpretation of Cardiopulmonary Exercise Tests, redaktorzy William J. M. Kinnear i James H. Hull, 102–6. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198834397.003.0015.

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This chapter describes how additional information can be obtained during an exercise test to detect the airflow obstruction of exercise-induced asthma. The forced expiratory volume in one second (FEV1) may fall a few minutes after cessation of exercise, but this test is not particularly sensitive for detecting exercise-induced bronchoconstriction. The flow–volume loop during exercise can be compared with the pre-test maximal trace to detect expiratory airflow limitation. Addition of inspiratory capacity measurements can be helpful. The flow–volume loop may also suggest exercise-induced laryngeal obstruction, which can be confirmed by continuous fibreoptic laryngoscopy during exercise.
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Streszczenia konferencji na temat "Inspiratory capacity"

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Berens, Tjerk, Denise Mannee, Bram Van Den Borst i Hanneke Van Helvoort. "Reliability of inspiratory capacity assessment". W ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.2166.

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Dickson, J., E. Ferrufino Rivera, A. Sahadevan i S. J. Linnane. "Inspiratory muscle capacity in Long Covid". W ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.1599.

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Phillips, D., M. James, S. Vincent, J. P. De-Torres, J. A. Neder, D. Langer, D. O'Donnell i M. D. James. "Prognostic value of a low resting inspiratory capacity and reduced inspiratory muscle strength in COPD". W ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.3603.

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Buhr, Russell, Xioayan Wang, Mehrdad Arjomandi, Igor Barjaktarevic, R. Graham Barr, Eugene Bleecker, Russell Bowler i in. "Inspiratory capacity is associated with dyspnea, exercise capacity, and survival in COPD". W ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa351.

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Brandão Galotti Panico, Ana Luiza, Mayra Caleffi Pereira i André Albuquerque. "Inspiratory capacity during exercise in patients with diaphragmatic paralysis". W ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa2204.

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Thirion, Ireri, Silvia Cid-Juarez, Rogelio Perez-Padilla, Laura Gochicoa-Rangel, Selene Guerrero-ZuÑiga i Luis Torre-Bouscoulet. "Inspiratory capacity in healthy people living at moderate altitude". W ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.oa3441.

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Barros, Raquel, Liliana Raposo, Nuno Moreira, Margarida Rocha, Paula Calaça, Ana Sofia Oliveira, João Valença i Cristina Bárbara. "Slow vital capacity : differences between expiratory and inspiratory vital capacities". W ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa3912.

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Mokaddem Mohsen, Salma, Khadija Ayed, Asma Chaker, Soumaya Khaldi i Saloua Jameleddine. "Inspiratory-to-total lung capacity ratio in COPD: the missed information". W ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.167.

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Vesteng, Liv Karin, Ingunn Skjørten, Morten Melsom i Anne Edvardsen. "COPD and oxygen supplementation: Improvement in inspiratory capacity and dyspnea during exercise". W Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa4603.

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Nuryanti, Widy Dewi, Hena Hena i Angelia Angelia. "The Effects of Senam Perkasa Indonesia on the Elderly’s Lung Inspiratory Capacity". W 2nd International Conference on Sports Science, Health and Physical Education. SCITEPRESS - Science and Technology Publications, 2017. http://dx.doi.org/10.5220/0007071208180821.

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