Neural respiratory drive measured during inspiratory threshold loading and acute hypercapnia in healthy individuals

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Abstract

Understanding the effects of respiratory load on neural respiratory drive (NRD) and respiratory pattern are key to understanding the regulation of load compensation in respiratory disease. The aim of the study was to examine and compare the recruitment pattern of the diaphragm and parasternal intercostal muscles when the respiratory system was loaded using two methods. Twelve subjects performed incremental inspiratory threshold loading up to 50% of their maximum inspiratory pressure and ten subjects underwent incremental, steady state hypercapnia to a maximum inspired CO2 of 5%. The diaphragm electromyogram (EMGdi) was measured using a multipair oesophageal catheter and the parasternal intercostal muscle EMG (sEMGpara) was recorded from bipolar surface electrodes positioned in the second intercostal space. EMGdi and sEMGpara were analysed over the last minute of each increment of both protocols and normalised using the peak EMG recorded during maximum respiratory manoeuvres and expressed as EMG%max. EMGdi%max and sEMGpara%max increased in parallel during the two loading methods, although EMGdi%max was consistently greater than sEMGpara%max under both conditions; ITL (Bias (SD) 9 (3) %, 95% limits of agreement 4 to 15) and hypercapnia (Bias (SD) 6 (3) %, 95% limits of agreement -0.05 to 12 %) . ILT resulted in more pronounced increases in mean (SD) EMGdi%max (10 (7) % - 45 (28) %) and sEMGpara%max (5.3 (3.1)% -40 (28) %)from baseline compared to EMGdi%max (7 (4) % - 21(8) %) and sEMGpara%max (4.7 (2.3 )% - 10 (4) %)during hypercapnia, despite comparable levels of ventilation. These data support the use of sEMGpara%max as a non-invasive alternative to EMGdi%max recorded with an invasive oesophageal electrode catheter, for the quantification of NRD. This technique should make evaluation of respiratory muscle function both easier to undertake and hence more readily acceptable in patients with respiratory disease in whom transduction of NRD to pressure generation can be compromised.
Original languageEnglish
JournalExperimental Physiology,
DOIs
Publication statusE-pub ahead of print - 15 Mar 2013

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