Mechanisms of exercise intolerance in Global Initiative for Chronic Obstructive Lung Disease grade 1 COPD

Guenette, Jordan A.; Chin, Roberto C.; Cheng, Sicheng; Dominelli, Paolo B.; Raghavan, Natya; Webb, Katherine A.; Neder, J. Alberto; O’Donnell, Denis E.

doi:10.1183/09031936.00034714

Cited by 120 publications

(161 citation statements)

References 36 publications

Supporting

Mentioning

152

Contrasting

Unclassified

Order By: Relevance

“…This latter contention is supported by previous findings that bronchodilators, by decreasing lung hyperinflation, allow greater VT expansion during exercise even in mild COPD [20,21]. GUENETTE et al [19] reported that EMGdi was markedly higher at rest and throughout cycle exercise in mild COPD compared with healthy controls. The ratio of EMGdi to diaphragmatic pressure (Pdi) was also significantly higher relative to controls, indicating some degree of neuromuscular dissociation of the diaphragm.…”

supporting

confidence: 56%

“…Patients with moderate-to-severe COPD have been shown to present with an EMGdi of 70% of maximum at peak incremental exercise [23], which corresponds to a V´E of around 32±10 L·min −1 using the same catheter as used in the study by JOLLEY et al [18]. At a similar absolute V´E, GUENETTE et al [19] found that patients with mild COPD have an EMGdi of 37% of maximum, suggesting that respiratory neural drive increases dramatically with advancing COPD severity. This is supported by data from patients with severe COPD who showed a reduction in the inspiratory discharge rate of single motor units recorded from the costal diaphragm following lung volume reduction surgery [24].…”

mentioning

confidence: 88%

“…Nonetheless, the O'Donnell group [19] has recently pointed out that increases in EMGdi%max and Poes expressed as a percentage of maximal pressure were closely correlated throughout exercise in health and mild COPD, thus supporting the contention that Poes measures are reasonable surrogates of respiratory neural drive, at least in mild COPD. Remarkably, even in the setting of mild spirometric abnormalities, VT expansion and V´E were significantly reduced for a given EMGdi (and respiratory muscle effort) compared with controls [19]. In both groups, dyspnoea increased as a function of increasing EMGdi, Poes and V´E, all relative to maximum.…”

mentioning

confidence: 98%

See 2 more Smart Citations

Do we “drive” dyspnoea?

Hudson

Laveneziana

2015

Eur Respir J

View full text Add to dashboard Cite

@ERSpublicationsChanges between neural drive and dyspnoea were determined during exercise in severe COPD patients by measuring EMGdi http://ow.ly/FCAs3Electromyography (EMG) measures neural drive, and is routinely used to investigate movement control and pathophysiology in human subjects. The electrical signals recorded from a muscle indicate the recruitment and discharge of spinal motor neurones by voluntary and reflex activation. EMG recordings are typically made with surface electrodes placed on the skin over the muscle of interest, or intramuscular needle or wire electrodes inserted into the muscle of interest. There are advantages and disadvantages of both techniques [1] but the disadvantages are somewhat amplified for EMG recordings from the respiratory muscles. As many respiratory muscles are small and located close to one other, often in layers of muscle with different functions (e.g. the external and internal intercostal muscles), surface recordings are easily contaminated by activity from neighbouring muscles. Intramuscular recordings are more selective but the risks associated with needle use are more serious for the respiratory muscles because of the underlying lung. In saying that, inspiratory muscle surface EMG recordings are possible [2,3] and electrode position can be optimised for the diaphragm [4] for some protocols. With intramuscular electrodes, the risk of pneumothorax can be minimised by using ultrasound to visualise the muscle and lung and estimate maximal insertion depth prior to recordings [5], and on-line audio and visual feedback of EMG activity during recordings [6]. Intramuscular recordings have been used to assess diaphragm activity with three-fold increases in minute ventilation (V´E) associated with hypercapnia [7] but have not been used in exercise protocols, potentially due to the high risk of pneumothorax with large changes in lung volume. As surface and intramuscular EMG recordings from the respiratory muscles are complicated by their anatomy, alternative measures, such as V´E and intrathoracic pressures, have been used as surrogates to assess respiratory neural drive, particularly in clinical populations.Much of the insight into the pathophysiology of exertional dyspnoea in respiratory disease, including chronic obstructive pulmonary disease (COPD), asthma and pulmonary arterial hypertension, has come from studies using pressure measurements, V´E and lung volumes to assess respiratory mechanics [8][9][10][11][12][13]. Neurophysiologically, increased perceived breathing effort is believed to reflect the awareness of increased motor command output to the respiratory muscles ("neural respiratory drive") and increased central corollary discharge from the respiratory motor centres to the somatosensory cortex [8]. It cannot be neglected that when the spontaneous increase in tidal volume (VT) is constrained (either volitionally or by external imposition) in the face of increased chemostimulation, respiratory discomfort (specifically, air hunger or unsatisfied inspiration) arises [8]...

show abstract

supporting

confidence: 56%

mentioning

confidence: 88%

mentioning

confidence: 98%

See 1 more Smart Citation

Do we “drive” dyspnoea?

Hudson

Laveneziana

2015

Eur Respir J

View full text Add to dashboard Cite

show abstract

“…Accumulating evidence suggests that neural respiratory drive (and 'central corollary discharge') is the proximate source of dyspnea during exercise in health [74,75,81] and in patients with COPD [63,82,83]. It follows that preservation of the EMGdi,rms%max-work rate relationship during incremental treadmill vs. cycle exercise testing in our study was primarily responsible for preservation of the dyspnea intensity (and unpleasantness)-work rate relationship, despite significant differences in V E and contractile respiratory muscle effort (pressure) requirements.…”

Section: Resultsmentioning

confidence: 99%

Physiological and perceptual responses to incremental exercise testing in healthy men: effect of exercise test modality

Muscat

Kotrach

Wilkinson-Maitland

et al. 2015

Appl. Physiol. Nutr. Metab.

View full text Add to dashboard Cite

In a randomized cross-over study of 15 healthy men aged 20–30 years, we compared physiological and perceptual responses during treadmill and cycle exercise test protocols matched for increments in work rate — the source of increased locomotor muscle metabolic and contractile demands. The rates of O2 consumption and CO2 production were higher at the peak of treadmill versus cycle testing (p ≤ 0.05). Nevertheless, work rate, minute ventilation, tidal volume (VT), breathing frequency (fR), inspiratory capacity (IC), inspiratory reserve volume (IRV), tidal esophageal (Pes,tidal) and transdiaphragmatic pressure swings (Pdi,tidal), peak expiratory gastric pressures (Pga,peak), the root mean square of the diaphragm electromyogram (EMGdi,rms) expressed as a percentage of maximum EMGdi,rms (EMGdi,rms%max), and dyspnea ratings were similar at the peak of treadmill versus cycle testing (p > 0.05). Ratings of leg discomfort were higher at the peak of cycle versus treadmill exercise (p ≤ 0.05), even though peak O2 consumption was lower during cycling. Oxygen consumption, CO2 production, minute ventilation, fR, Pes,tidal, Pdi,tidal and Pga,peak were higher (p ≤ 0.05), while VT, IC, IRV, EMGdi,rms%max, and ratings of dyspnea and leg discomfort were similar (p > 0.05) at all or most submaximal work rates during treadmill versus cycle exercise. Our findings highlight important differences (and similarities) in physiological and perceptual responses at maximal and submaximal work rates during incremental treadmill and cycle exercise testing protocols. The lack of effect of exercise test modality on peak work rate advocates for the use of this readily available parameter to optimize training intensity determination, regardless of exercise training mode.

show abstract

“…In their small but elegant physiological study, the authors compared the trajectory of dyspnoea rating, dynamic lung mechanics and the response of respiratory muscles to the inspiratory neural drive, as obtained during a standard incremental symptom-limited cycle ergometry in smokers and healthy age-matched nonsmokers. They concluded that the increased dyspnoea perception and associated reduced exercise capacity (25% lower maximal oxygen consumption reached in the incremental test), as recorded in smokers who do not meet the criteria for COPD, are explained by the increased mechanical load of the respiratory system: these patients have a preserved and appropriate ventilatory response, which is not usually the case in individuals developing COPD even at a mild stage [8]. In particular, the difference in dyspnoea intensity between smokers and healthy control subjects, as assessed by the Borg scale at a comparable workload (80 W), is close to 2.0 Borg units, which is likely to be sensitive from a clinical point of view.…”

Section: @Erspublicationsmentioning

confidence: 99%