Exertional dyspnoea and cortical oxygenation in patients with COPD

Abstract

This study was designed to investigate the association of perceived dyspnoea intensity with cortical oxygenation and cortical activation during exercise in patients with chronic obstructive pulmonary disease (COPD) and exertional hypoxaemia.Low-intensity exercise was performed at a constant work rate by patients with COPD and exertional hypoxaemia (n=11) or no hypoxaemia (n=16), and in control participants (n=11). Cortical oxyhaemoglobin (oxy-Hb) and deoxyhaemoglobin (deoxy-Hb) concentrations were measured by multichannel near-infrared spectroscopy. Increased deoxy-Hb is assumed to reflect impaired oxygenation, whereas decreased deoxy-Hb signifies cortical activation.Exercise decreased cortical deoxy-Hb in control and nonhypoxaemic patients. Deoxy-Hb was increased in hypoxaemic patients and oxygen supplementation improved cortical oxygenation. Decreased deoxy-Hb in the pre-motor cortex (PMA) was significantly correlated with exertional dyspnoea in control participants and patients with COPD without hypoxaemia. In contrast, increased cortical deoxy-Hb concentration was correlated with dyspnoea in patients with COPD and hypoxaemia. With the administration of oxygen supplementation, exertional dyspnoea was correlated with decreased deoxy-Hb in the PMA of COPD patients with hypoxaemia.During exercise, cortical oxygenation was impaired in patients with COPD and hypoxaemia compared with control and nonhypoxaemic patients; this difference was ameliorated with oxygen supplementation. Exertional dyspnoea was related to activation of the pre-motor cortex in COPD patients. @ERSpublications Exertional dyspnoea was related to activation of the pre-motor cortex in COPD patients

Measuring the breathless brain: is real life too noisy?

“…I'd argue that because a lower intensity of exercise is needed to induce dyspnoea in COPD patients, the problem of exercise related head-movement would be less in patients than it was in the healthy individuals used in these studies. However, in the report by HIGASHIMOTO et al [10], the pre-motor cortex (PMA) activation is consistent with laboratory dyspnoea induced by tidal volume reduction [7] and resistance-loaded breathing [14]. But, none of these studies can determine whether the PMA activation is integral to dyspnoea itself, or part of the downstream response to it.…”

“…The study by HIGASHIMOTO et al [10] provides a very limited comparison with previous lab-based models and the restricted view is the ironic cost of generating "real-life" dyspnoea. The exercise-based protocol led the authors to reject more comprehensive brain imaging techniques, such as functional magnetic resonance imaging (fMRI) and positron emission tomography (PET).…”

“…The second issue with the HIGASHIMOTO et al [10] "real-life" dyspnoea is that exercise is a very noisy stimulus that not only involves dyspnoea-related activity, but also numerous central activations [15] and afferent signals generated by the exercise itself. As exercise becomes more intense the exercise-related neural activity increases, as does that associated with dyspnoea.…”

“…For the long term we need to unravel the sensory, emotional and behavioural components [11] of "real-life" dyspnoea to focus the development and assessment of therapies. So have HIGASHIMOTO et al [10] taken us closer to achieving these goals?…”

“…Published in this issue, HIGASHIMOTO et al [10] have been the first to investigate the neural activity of "real-life" dyspnoea in chronic obstructive pulmonary disease (COPD) patients with the "real-life" stimulus of exercise. But as much as marking a new era of study, the paper led me to re-assess what we should be looking for as the investigation of dyspnoea's central mechanisms moves forward.…”