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.

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.

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

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.

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.

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.

Made available in DSpace on 2016-12-12T17:32:55Z (GMT). No. of bitstreams: 1 Cintia Laura Pereira de Araujo.pdf: 891905 bytes, checksum: 68d6cdcc41dfe7c353a29f0ca21b680c (MD5) Previous issue date: 2013-07-04 / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior / Evidence has shown that dynamic hyperinflation (DH) is an important factor leading to dyspnea and consequent limitations in functional capacity of COPD patients. It is not been completely elucidated whether the pursed-lips breathing (PLB) is able to minimize DH and its effects on exercise tolerance in these patients. The aim of this study was to evaluate the acute effect of PLB on DH and functional capacity in patients with COPD. Twenty-five patients with COPD (16 men, mean age 64±7 years, FEV1=41.7±14.7% predicted, BMI=27.6±5.13kg/m2) randomly performed two six-minute walk tests with and without PLB (6MWTPLB and 6MWTNon-PLB) and two Glittre-ADL tests with and without PLB (TGlittrePLB e TGlittreNon-PLB). At baseline and immediately after the tests, the inspiratory capacity (IC) was assessed by the slow vital capacity (SVC) maneuver. The 6MWTNon-PLB and TGlittreNon-PLB induced similar DH magnitude (0.22±0.24L and. 0.31±0.23L respectively; p>0.05). PLB did not improve DH induced by the 6MWT (0.24±0.20L PLB and 0.22±0,24L non-PLB, respectively; p>0.05). DH in the TGlittrePLB was significantly lower than TGlittreNon-PLB (0.19±0.20L and 0.31±0.23L, respectively; p=0.02). PLB did not improve exercise tolerance neither on the 6MWT (457±63m PLB and 466±71m Non-PLB, respctively; p>0.05) or on the TGlittre (4.38min PLB and 4.23min Non-PLB, respectively; p>0.05). In conclusion, PLB reduced DH only on TGlittre and did not improve functional capacity. / Evidências têm demonstrado que a hiperinsuflação dinâmica é um dos fatores que levam a dispneia e consequente limitação na capacidade funcional de indivíduos com DPOC. Não está completamente elucidado se o freno labial (FL) é capaz de minimizar a hiperinsuflação dinâmica e seus efeitos na tolerância ao exercício nesses pacientes. O objetivo desse estudo foi avaliar os efeitos agudos do freno labial na hiperinsuflação dinâmica e na tolerância ao exercício em pacientes com DPOC moderada a muito grave. Vinte e cinco pacientes com DPOC (16 homens, 64±7 anos, VEF1=41,7±14,7% do previsto, IMC=27,6±5,13kg/m2) realizaram em dois dias, de forma aleatória dois testes de caminhada de seis minutos com e sem freno labial (TC6MFL e TC6MSem-FL) e dois testes de AVD-Glittre com e sem freno labial (TGlittreFL e TGlittreSem-FL). Antes e após cada teste foi avaliada a capacidade inspiratória (CI), por meio de espirometria simples com manobra de capacidade vital lenta (CVL) para avaliar a hiperinsuflação dinâmica (HD). O TC6MSem- FL e TGlittreSem-FL induziram similar magnitude de HD (0.22±0.24L vs. 0.31±0.23L; p>0.05). HD induzida pelo TGlittreFL foi significativamente menor que a induzida pelo TGlittreSem-FL (0.19±0.20L vs. 0.31±0.23L; p=0.02). FL não melhorou a HD induzida pelo TC6M (0.24±0.20L FL vs. 0.22±0,24L Sem-FL; p>0.05). FL não melhorou o desempenho no TC6M (457±63m FL vs. 466±71m Sem-FL; p>0.05); nem no TGlittre (4.38min FL vs. 4.23min Sem-FL; p>0.05). Conclui-se que o FL reduziu apenas a HD induzida pelo TGlittre e não melhorou o desempenho nos testes.

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.

With the rapid somatic growth and development in infants, simultaneous accurate measurements of lung volume and airway function are essential. Raised volume rapid thoracoabdominal compression (RTC) is widely used to generate forced expiration from an airway opening pressure of 30 cmH2O (V30). The (dynamic) functional residual capacity (FRCdyn) remains the lung volume most routinely measured. The aim of this study was to develop comprehensive integrated spirometry that included all subdivisions of lung volume at V30 or total lung capacity (TLC30). Measurements were performed on 17 healthy infants aged 8.6-119.7 weeks. A commercial system for multiple-breath nitrogen washout (MBNW) to measure lung volumes and a custom made system to perform RTC were used in unison. A refined automated raised volume RTC and the following two novel single maneuvers with dual volume measurements were performed from V30 during a brief post-hyperventilation apneic pause: (1) the passive expiratory flow was integrated to produce the inspiratory capacity (IC) and the static (passive) FRC (FRCst) was estimated by initiating MBNW after end-passive expiration; (2) RTC was initiated late during passive expiration, flow was integrated to produce the slow vital capacity (jSVC) and the residual volume (RV) was measured by initiating MBNW after end-expiration while the jacket (j) was inflated. Intrasubject FRCdyn and FRCst measurements overlapped (p = 0.6420) but neither did with the RV (p < 0.0001). Means (95% confidence interval) of FRCdyn, IC, FRCst, jSVC, RV, forced vital capacity and tidal volume were 21.2 (19.7-22.7), 36.7 (33.0-40.4), 21.2 (19.6-22.8), 40.7 (37.2-44.2), 18.1 (16.6-19.7), 40.7 (37.1-44.2) and 10.2 (9.6-10.7) ml/kg, respectively. Static lung volumes and capacities at V30 and variables from the best forced expiratory flow-volume curve were dependent on age, body length and weight. In conclusion, we developed a comprehensive physiologically integrated approach for in-depth investigation of lung function at V30 in infants.