The output from brainstem respiratory centres, neural respiratory drive (NRD), is directly proportional to the ventilation required to maintain blood gas homeostasis. Increases in the load imposed upon the respiratory muscles or a reduction in force-generating capacity, as occurs in respiratory disease, results in higher levels of NRD. The neural output of the brainstem respiratory centres cannot be measured directly in humans, but it can be assessed indirectly by quantifying the electromyogram (EMG) of the respiratory muscles, which provides a method of assessing the level and pattern of their activation. The EMG of the diaphragm (EMGdi), the major inspiratory muscle during resting tidal breathing in healthy individuals, can be recorded using multipair oesophageal electrodes positioned at the diaphragm crus. In chronic obstructive pulmonary disease (COPD), mechanical abnormalities including airflow obstruction, static and dynamic hyperinflation and intrinsic positive end expiratory pressure increase the load on the respiratory muscles. This results in high NRD in COPD, and disproportionate increases whenever airway obstruction worsens (and hyperinflation increases) or ventilatory requirements increase. EMGdi activity is significantly higher in COPD than in healthy controls, and is closely related to COPD disease severity as defined by spirometry and hyperinflation (1). Work by our group, and others, has also demonstrated that exertional breathlessness intensity in health (2, 3), obstructive lung disease (COPD (4), cystic fibrosis (2)), and interstitial lung disease (5) is closely related to levels of EMGdi activity. In severe respiratory disease, breathlessness intensity is better related to EMGdi activity than respiratory muscle pressure generation and ventilation (2, 4), reflecting the impaired translation of NRD to mechanical output and respiratory airflow as a consequence of impaired ventilatory mechanics. These findings support the “corollary discharge” theory of breathlessness, that perception of breathlessness intensity involves conscious appraisal of increased motor drive to the principal respiratory muscles. This emphasises the importance of accurate recordings of NRD to advancing our understanding of the physiological basis of breathlessness in health and disease. These observations also have clear clinical implications. If breathlessness intensity is closely related to levels of NRD, simply asking the patient to rate breathlessness intensity could provide insights into the load on the respiratory system, disease severity and response to treatment that are not always evident from conventional measures of pulmonary function (6, 7).