Do we “drive” dyspnoea?

Electromyography (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]. Changes between neural drive and dyspnoea were determined during exercise in severe COPD patients by measuring EMGdi <http://ow.ly/FCAs3>