Tidal volume inflection and its sensory consequences during exercise in patients with stable asthma

Do we “drive” dyspnoea?

“…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].…”

“…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].…”

“…This increasing dissociation between increased central neural drive (indirectly estimated as measure of effort: the ratio of tidal swings of oesophageal pressure (Poes)) relative to maximum inspiratory pressure and a blunted VT displacement (measured as the VT response expressed relative to the predicted vital capacity) induced by dynamic hyperinflation has been proposed to reflect, at least in part, the neurophysiological basis of dyspnoea perceived as unsatisfied inspiration [10][11][12]. In support of this contention, bronchodilator therapy in moderate-to-severe COPD has been associated with a significant reduction in lung hyperinflation, significant increase in VT expansion and significant improvement in the effort/displacement ratio [8,14].…”

Mechanisms, measurement and management of exertional dyspnoea in asthma

“…In asthma, DH occurs during bronchoconstriction provoked by methacholine, but DH only occurs in 36-65% of subjects during exercise and, therefore, is not the dominant mechanism of exertional dyspnoea in many individuals [20,21,43]. Those individuals with asthma who develop EIB more frequently develop DH during exercise than asthmatics without EIB [44].…”

“…with methacholine) may not reflect the experience of dyspnoea during exercise or activities in daily life. Recent evidence suggests that exertional dyspnoea in asthma is qualitatively different from that during methacholine testing [20] and results from bronchoconstriction, mechanical limitations due to dynamic lung hyperinflation [21], ventilatory effort [20] and psychological factors [22]. Importantly, resting measures of lung function, such as forced expiratory volume in 1 s (FEV1), and results of direct bronchoprovocation testing do not predict exertional symptoms or physiological adaptations during exercise in asthma.…”