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1.
Eur Respir Rev ; 30(161)2021 Sep 30.
Artigo em Inglês | MEDLINE | ID: mdl-34289980

RESUMO

During submaximal exercise, minute ventilation (V' E) increases in proportion to metabolic rate (i.e. carbon dioxide production (V' CO2 )) to maintain arterial blood gas homeostasis. The ratio V' E/V' CO2 , commonly termed ventilatory efficiency, is a useful tool to evaluate exercise responses in healthy individuals and patients with chronic disease. Emerging research has shown abnormal ventilatory responses to exercise (either elevated or blunted V' E/V' CO2 ) in some chronic respiratory and cardiovascular conditions. This review will briefly provide an overview of the physiology of ventilatory efficiency, before describing the ventilatory responses to exercise in healthy trained endurance athletes, patients with asthma, and patients with obesity. During submaximal exercise, the V' E/V' CO2 response is generally normal in endurance-trained individuals, patients with asthma and patients with obesity. However, in endurance-trained individuals, asthmatics who demonstrate exercise induced-bronchoconstriction, and morbidly obese individuals, the V' E/V' CO2 can be blunted at maximal exercise, likely because of mechanical ventilatory constraint.

2.
J Physiol ; 599(5): 1665-1683, 2021 03.
Artigo em Inglês | MEDLINE | ID: mdl-33428233

RESUMO

KEY POINTS: Patients with mild chronic obstructive pulmonary disease (COPD) have an elevated ventilatory equivalent to CO2 production ( V ̇ E / V ̇ C O 2 ) during exercise, secondary to increased dead space ventilation. The reason for the increased dead space is unclear, although pulmonary microvascular dysfunction and the corresponding capillary hypoperfusion is a potential mechanism. Despite emerging evidence that mild COPD is associated with pulmonary microvascular dysfunction, limited research has focused on experimentally modulating the pulmonary microvasculature during exercise in mild COPD. The present study sought to examine the effect of inhaled nitric oxide (iNO), a selective pulmonary vasodilator, on V ̇ E / V ̇ C O 2 , dyspnoea and exercise capacity in patients with mild COPD. Experimental iNO increased peak oxygen uptake in mild COPD, secondary to reduced V ̇ E / V ̇ C O 2 and dyspnoea. This is the first study to demonstrate that experimental manipulation of the pulmonary circulation alone, can positively impact dyspnoea and exercise capacity in mild COPD. ABSTRACT: Patients with mild chronic obstructive pulmonary disease (COPD) have an exaggerated ventilatory response to exercise, contributing to dyspnoea and exercise intolerance. Previous research in mild COPD has demonstrated an elevated ventilatory equivalent to CO2 production ( V ̇ E / V ̇ C O 2 ) during exercise, secondary to increased dead space ventilation. The reason for the increased dead space is unclear, although pulmonary microvascular dysfunction and the corresponding capillary hypoperfusion is a potential mechanism. The present study tested the hypothesis that inhaled nitric oxide (iNO), a selective pulmonary vasodilator, would lower V ̇ E / V ̇ C O 2 and dyspnoea, and improve exercise capacity in patients with mild COPD. In this multigroup randomized-control cross-over study, 15 patients with mild COPD (FEV1  =  89 ± 11% predicted) and 15 healthy controls completed symptom-limited cardiopulmonary exercise tests while breathing normoxic gas or 40 ppm iNO. Compared with placebo, iNO significantly increased peak oxygen uptake (1.80 ± 0.14 vs. 1.53 ± 0.10 L·min-1 , P < 0.001) in COPD, whereas no effect was observed in controls. At an equivalent work rate of 60 W, iNO reduced V ̇ E / V ̇ C O 2 by 3.8 ± 4.2 units (P = 0.002) and dyspnoea by 1.1 ± 1.2 Borg units (P < 0.001) in COPD, whereas no effect was observed in controls. Operating lung volumes and oxygen saturation were unaffected by iNO in both groups. iNO increased peak oxygen uptake in COPD, secondary to reduced V ̇ E / V ̇ C O 2 and dyspnoea. These data suggest that mild COPD patients demonstrate pulmonary microvascular dysfunction that contributes to increased V ̇ E / V ̇ C O 2 , dyspnoea and exercise intolerance. This is the first study to demonstrate that experimental manipulation of the pulmonary circulation alone, can positively impact dyspnoea and exercise capacity in mild COPD.


Assuntos
Óxido Nítrico , Doença Pulmonar Obstrutiva Crônica , Estudos Cross-Over , Dispneia , Teste de Esforço , Tolerância ao Exercício , Humanos , Doença Pulmonar Obstrutiva Crônica/tratamento farmacológico
3.
J Appl Physiol (1985) ; 128(4): 925-933, 2020 04 01.
Artigo em Inglês | MEDLINE | ID: mdl-32163328

RESUMO

Patients with mild chronic obstructive pulmonary disease (COPD) demonstrate resting pulmonary vascular dysfunction as well as a blunted pulmonary diffusing capacity (DLCO) and pulmonary capillary blood volume (VC) response to exercise. The transition from the upright to supine position increases central blood volume and perfusion pressure, which may overcome microvascular dysfunction in an otherwise intact alveolar-capillary interface. The present study examined whether the supine position normalized DLCO and VC responses to exercise in mild COPD. Sixteen mild COPD participants and 13 age-, gender-, and height-matched controls completed DLCO maneuvers at rest and during exercise in the upright and supine position. The multiple FIO2-DLCO method was used to determine DLCO, VC, and membrane diffusion capacity (DM). All three variables were adjusted for alveolar volume (DLCOAdj, VCAdj, and DMAdj). The supine position reduced alveolar volume similarly in both groups, but oxygen consumption and cardiac output were unaffected. DLCOAdj, DMAdj, and VCAdj were all lower in COPD. These same variables all increased with upright and supine exercise in both groups. DLCOAdj was unaffected by the supine position. VCAdj increased in the supine position similarly in both groups. DMAdj was reduced in the supine position in both groups. While the supine position increased exercise VCAdj in COPD, the increase was of similar magnitude to healthy controls; therefore, exercise VC remained blunted in COPD. The persistent reduction in exercise DLCO and VC when supine suggests that pulmonary vascular destruction is a contributing factor to the blunted DLCO and VC response to exercise in mild COPD.NEW & NOTEWORTHY Patients with mild chronic obstructive pulmonary disease demonstrate a combination of reversible pulmonary microvascular dysfunction and irreversible pulmonary microvascular destruction.


Assuntos
Capacidade de Difusão Pulmonar , Doença Pulmonar Obstrutiva Crônica , Volume Sanguíneo , Capilares , Exercício Físico , Humanos , Decúbito Dorsal
4.
Respir Med ; 155: 133-140, 2019 08.
Artigo em Inglês | MEDLINE | ID: mdl-31349187

RESUMO

BACKGROUND: Asthmatics are at increased cardiovascular disease risk, which has been linked to beta2(ß2)-agonist use. Inhalation of ß2-agonists increases sympathetic nerve activity (SNA) in healthy individuals, however the systemic impact of salbutamol in asthmatics using ß2-agonists regularly is unknown. OBJECTIVES: This study compared the systemic vascular responses to a clinical dose of salbutamol (Phase I) and following an acute increase in SNA (Phase II) in asthmatics and controls. METHODS: Fourteen controls and 14 asthmatics were recruited for Phase I. On separate days, flow-mediated dilation (FMD) and peripheral arterial stiffness (pPWV) were evaluated at baseline and following either 400 µg inhaled salbutamol or a placebo inhaler. For Phase II, heart rate, blood pressure, vascular conductance, pPWV, and central (c)PWV were evaluated in response to a large increase in SNA brought on by cold-water hand immersion (i.e. cold-pressor test) or body-temperature water hand immersion (i.e. control) in 10 controls and 10 asthmatics. RESULTS: Following salbutamol, asthmatics demonstrated reduced FMD (-3.0%, p < 0.05) and increased pPWV (+0.7 m/s, p < 0.05); however, salbutamol had no effect in controls. The cold-pressor test resulted in similar increases in blood pressure, vascular flow rates and conductance, pPWV, and cPWV in both asthmatics and controls, suggesting similar neurovascular transduction in asthmatics and controls. CONCLUSION: Inhaled Salbutamol leads to increased arterial stiffness and reduced FMD in asthmatics. As asthmatics and controls had similar vascular responses to an increase in SNA, these findings suggest asthmatics have heightened sympathetic responses to ß2-agonists which may contribute to the increased cardiovascular risk in asthma.


Assuntos
Agonistas de Receptores Adrenérgicos beta 2/administração & dosagem , Albuterol/administração & dosagem , Asma/tratamento farmacológico , Asma/fisiopatologia , Administração por Inalação , Agonistas de Receptores Adrenérgicos beta 2/efeitos adversos , Adulto , Albuterol/efeitos adversos , Pressão Sanguínea , Doenças Cardiovasculares/etiologia , Feminino , Humanos , Masculino , Risco , Rigidez Vascular , Adulto Jovem
5.
J Appl Physiol (1985) ; 125(3): 870-877, 2018 09 01.
Artigo em Inglês | MEDLINE | ID: mdl-29878869

RESUMO

Dyspnea has been reported to be a main contributor to exercise avoidance in asthma. While traditional markers of ventilation do not explain the heightened dyspnea during exercise in patients with asthma, this study proposed that exertional dyspnea in asthma was due to high-operating lung volumes, which may be improved with a short-acting ß2-agonist. On two separate days, 16 patients with asthma and 16 controls completed a lung function test and incremental exercise tests to exhaustion. On one of the days (order randomized), 400 µg salbutamol was administered before exercise. Inspiratory capacity (IC), inspiratory reserve volume (IRV), and dyspnea (modified Borg scale) were evaluated throughout exercise. Compared with controls, patients with asthma reported greater dyspnea at the same absolute submaximal workloads. Furthermore, patients with asthma demonstrated altered breathing responses to exercise, characterized by reduced IC and IRV throughout exercise compared with controls. The reduced IRV was associated with increased dyspnea in patients with asthma. Salbutamol did not affect dyspnea or operating lung volumes in either group. The increased perception of dyspnea during incremental exercise in patients with asthma appears to be secondary to a reduction in IRV, which is unaffected by an inhaled ß2-agonist. NEW & NOTEWORTHY Increased exertional dyspnea in asthma appears to be due to high operating lung volumes and is not affected by salbutamol.


Assuntos
Asma/patologia , Dispneia/patologia , Pulmão/patologia , Agonistas Adrenérgicos beta/uso terapêutico , Adulto , Resistência das Vias Respiratórias , Albuterol/uso terapêutico , Antiasmáticos/uso terapêutico , Asma/tratamento farmacológico , Dispneia/tratamento farmacológico , Teste de Esforço , Tolerância ao Exercício , Feminino , Humanos , Volume de Reserva Inspiratória , Medidas de Volume Pulmonar , Masculino , Testes de Função Respiratória , Adulto Jovem
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