Does expiratory muscle activity influence dynamic hyperinflation and exertional dyspnea in COPD?
Introduction
Activity-related dyspnea occurs in the majority of patients with moderate-to-severe chronic obstructive pulmonary disease (COPD) and current treatments are only partially effective in providing relief (Parshall et al., 2012). Previous studies on mechanisms of dyspnea during exercise in COPD have largely focused on the role of the inspiratory muscles and the mechanical constraints imposed by resting and dynamic lung hyperinflation (Guenette et al., 2012, Kyroussis et al., 2000, Laveneziana et al., 2011, Leblanc et al., 1986, O’Donnell et al., 1997, O’Donnell et al., 2012, O’Donnell et al., 2006, Puente-Maestu et al., 2005). The influence of increased expiratory muscle activity on the intensity and quality of dyspnea is unknown and is the primary focus of the current study.
Expiratory muscle activity in more advanced COPD has been shown to be variable and, in the majority of mechanical studies, peak tidal expiratory esophageal pressure rose smoothly to ∼20–25% of maximal expiratory pressure at end-exercise (Kyroussis et al., 2000, Marin et al., 1999, Montes de Oca and Celli, 2000). It has been proposed that increased expiratory muscle activity may convey a mechanical advantage in COPD by optimizing the length-tension characteristics of the diaphragm (Dodd et al., 1984), with possible attendant salutary effects on perceived dyspnea (Younes, 1991). A contrasting view is that excessive abdominal and internal intercostal muscle activation at higher levels of ventilation (V′E) may contribute to the overall sense of dyspnea (Aliverti et al., 2004, Aliverti et al., 2008). Thus, the inability of patients with expiratory flow limitation to increase tidal expiratory flow rates and reduce end-expiratory lung volume (EELV) below the resting value, by increasing expiratory muscle activity, places the diaphragm under a mechanical disadvantage and excessive intra-thoracic expiratory pressures may also have negative cardio-circulatory consequences (Kyroussis et al., 2000, Potter et al., 1971). Moreover, it has recently been proposed based on optoelectronic plethysmography that a subset of patients with COPD may avoid dynamic lung hyperinflation during exercise (“euvolumics”) by increasing expiratory muscle recruitment (Aliverti et al., 2004). However, the paucity of esophageal and gastric pressure measurements in that study precluded any definitive conclusion about the interaction between expiratory muscle activity and dynamic hyperinflation.
The purpose of the current study was therefore to examine the relationships between expiratory muscle activity, dynamic end-inspiratory and end-expiratory lung volumes, diaphragmatic function and perceived dyspnea during exercise in COPD. Accordingly, we compared detailed dynamic respiratory mechanics (including measurements of expiratory and inspiratory muscle function) and the intensity and quality of dyspnea in COPD and age-matched healthy controls during incremental cycle exercise.
Section snippets
Subjects
Twelve clinically stable patients with COPD (FEV1/FVC < 0.7), a FEV1 ≤ 80%predicted (Rabe et al., 2007), and a smoking history ≥10 pack-years were included. Twelve age- and sex-matched healthy controls with normal spirometry and a smoking history <10 pack-years were included for comparison. Exclusion criteria were as follows: a disease other than COPD that could contribute to dyspnea or exercise limitation; important contraindications to clinical exercise testing; or use of supplemental oxygen or
Results
Subject characteristics and pulmonary function measurements are summarized in Table 1. There were 6 subjects with GOLD stage II COPD (2 men, 4 women) and 6 with GOLD stage III COPD (4 men, 2 women). In the COPD group, 5 subjects (2 men, 3 woman) were current smokers and the remaining 7 subjects (4 men, 3 women) were ex-smokers. In the control group, 9 subjects (4 men, 5 women) had never smoked and 3 ex-smokers (2 men, 1 woman) had less than a 10 pack-year history and had stopped smoking for at
Discussion
The main findings of this study are as follows: (1) patients with moderate-to-severe COPD showed increased expiratory muscle activity at any given during exercise compared with healthy controls; (2) significant dynamic lung hyperinflation occurred despite increased expiratory muscle activity in COPD; (3) dynamic diaphragmatic function was not different in health and in COPD throughout exercise; and (4) qualitative descriptor choices alluding to perceived expiratory difficulty were selected
Contributions
All authors played a role in the content and writing of the manuscript. In addition: DEO was the principal investigator and contributed the original idea for the study; DEO, PL and KAW had input into the study design and conduct of study; PL and KW collected the data; KAW and PL performed data analysis and prepared it for presentation.
Sources of support
William Spear/Richard Start Endowment Fund, Queen's University (2005–2006); Pierantonio Laveneziana received a John Alexander Stuart Fellowship, Department of Medicine, Queen's University (2007–2008).
Acknowledgements
This study was supported by the William Spear/Richard Start Endowment Fund, Queen's University. Pierantonio Laveneziana received a John Alexander Stuart Fellowship, Department of Medicine, Queen's University.
References (53)
- et al.
Effects of various respiratory stimuli on the depth and frequency of breathing in man
Respir. Physiol.
(1966) - et al.
The measurement of dyspnea. Contents, interobserver agreement, and physiologic correlates of two new clinical indexes
Chest
(1984) - et al.
Ventilatory drive at rest and perception of exertional dyspnea in severe COPD
Chest
(1999) - et al.
Fifteen-year interval spirometric evaluation of the Oregon predictive equations
Chest
(1988) - et al.
Decline of resting inspiratory capacity in COPD: the impact on breathing pattern, dyspnea, and ventilatory capacity during exercise
Chest
(2012) - et al.
Dyspnea, ventilatory pattern, and changes in dynamic hyperinflation related to the intensity of constant work rate exercise in COPD
Chest
(2005) - et al.
Regional chest wall volumes during exercise in chronic obstructive pulmonary disease
Thorax
(2004) - et al.
Point: counterpoint – the major limitations to exercise performance in COPD
J. Appl. Physiol.
(2008) ATS/ERS Statement on respiratory muscle testing
Am. J. Respir. Crit. Care Med.
(2002)- et al.
Quadriceps and respiratory muscle fatigue following high-intensity cycling in COPD patients
PLoS ONE
(2013)
Maximal respiratory pressures: normal values and relationship to age and sex
Am. Rev. Respir. Dis.
Psychophysical bases of perceived exertion
Med. Sci. Sports Exerc.
The relationship between airway resistance, airway conductance and lung volume in subjects of different age and body size
J. Clin. Invest.
Clinical usefulness of the single-breath pulmonucy diffusing capacity test
Am. Rev. Respir. Dis.
Lung volumes in healthy nonsmoking adults
Bull. Eur. Physiopathol. Respir.
Chest wall mechanics during exercise in patients with severe chronic air-flow obstruction
Am. Rev. Respir. Dis.
The significance of respiratory symptoms and the diagnosis of chronic bronchitis in a working population
Br. Med. J.
Relative contribution of rib cage and abdomen to ventilation during exercise
J. Appl. Physiol.
Does dynamic hyperinflation contribute to dyspnoea during exercise in patients with COPD?
Eur. Respir. J.
Muscle strength, symptom intensity, and exercise capacity in patients with cardiorespiratory disorders
Am. J. Respir. Crit. Care Med.
Abdominal muscle fatigue following exercise in chronic obstructive pulmonary disease
Respir. Res.
Forced expiration
Clinical Exercise Testing
Respiratory muscle activity in patients with COPD walking to exhaustion with and without pressure support
Eur. Respir. J.
Evolution of dyspnea during exercise in chronic obstructive pulmonary disease: impact of critical volume constraints
Am. J. Respir. Crit. Care Med.
Flow-volume curves and expiratory pressures during exercise in patients with chronic airways obstruction. Scandinavian journal of respiratory diseases
Supplementum
Cited by (52)
Relevance of Respiratory Muscle Function Assessment in Respiratory Disease
2020, Archivos de BronconeumologiaThe Pathophysiology of Dyspnea and Exercise Intolerance in Chronic Obstructive Pulmonary Disease
2019, Clinics in Chest MedicineCitation Excerpt :Reduced VE after training was likely explained by altered central and peripheral chemoreflex activation as a result of increased oxidative capacity and reduced hydrogen ion generation in the reconditioned peripheral muscles. Improved breathing pattern (manifested as reduced Bf) improves ventilatory efficiency and reduces pulmonary gas trapping, with consequent delay of intolerable dyspnea.128–131 It is now clear from recent studies that important improvement in activity-related and anticipatory dyspnea, quality of life, and perceived self-efficacy can occur in the absence of consistent physiologic training effects.48
Sensory-mechanical effects of a dual bronchodilator and its anticholinergic component in COPD
2018, Respiratory Physiology and NeurobiologyCitation Excerpt :Expiratory muscle activity, assessed by increased Pga and expiratory pleural pressures, was increased in our patients compared with historic controls (Faisal et al., 2016; Guenette et al., 2014). In the setting of expiratory flow limitation, excess expiratory activity fails to further increase expiratory flow rates or reduce end-expiratory lung volume during exercise below its resting value (Laveneziana et al., 2014; O’Donnell et al., 2015; Pride and Milic-Emili, 1995). Moreover, it is suggested that altered afferent information from dynamically compressed airways in expiration and from abundant mechanoreceptors in overactive abdominal and rib-cage expiratory muscles, conveyed directly to the somato-sensory cortex, can contribute to perceived breathing discomfort in COPD (O’Donnell et al., 1987, 1988a, 1988b).
The effect of carotid chemoreceptor inhibition on exercise tolerance in chronic obstructive pulmonary disease: A randomized-controlled crossover trial
2019, Respiratory MedicineCitation Excerpt :Previous work has suggested that the observed dyspnea during incremental exercise in COPD is the result of increased work of breathing and diaphragmatic activity [2]. It has been shown that the increased work of breathing and thus dyspnea in COPD comes from 1) expiratory flow limitation and resulting dynamic hyperinflation [3,5–11], and 2) an exaggerated ventilatory response to exercise (i.e. increased minute ventilation relative to carbon dioxide production, V̇E/V̇CO2) [1,3,12,13]. A great deal of work has focused on improving airflow limitation in COPD; however, very little has been done to understand and treat the exaggerated ventilatory response to exercise in COPD [14].