Influence of CO2 on upper airway muscles and chest wall/diaphragm corticomotor responses assessed by transcranial magnetic stimulation in awake healthy subjects

Borel J-C, Melo-Silva CA, Gakwaya S, Sériès F. Influence of CO2 on upper airway muscles and chest wall/diaphragm corticomotor responses assessed by transcranial magnetic stimulation in awake healthy subjects. J Appl Physiol 112: 798–805, 2012. First published December 8, 2011; doi:10.1152/japplphysiol.00713.2011.—Rationale: functional interaction between upper airway (UA) dilator muscles and the diaphragm is crucial in the maintenance of UA patency. This interaction could be altered by increasing respiratory drive. The aim of our study was to compare the effects of hypercapnic stimulation on diaphragm and genioglossus corticomotor responses to transcranial magnetic stimulation (TMS). Methods: 10 self-reported healthy men (32 9 yr; body mass index 24 3 kg/m ) breathed, in random order, room air or 5% and then 7% FICO2, both balanced with pure O2. Assessments included ventilatory variables, isoflow UA resistance (at 300 ml/s), measurement of lower chest wall/diaphragm (LCW/diaphragm), and genioglossus motor threshold (MT) and motor-evoked potential (MEP) characteristics. TMS twitches were applied during early inspiration and end expiration at stimulation intensity 30% above LCW/diaphragm and genioglossus MT. Results: compared with room air, CO2 inhalation significantly augmented minute ventilation, maximal inspiratory flow, tidal volume, and tidal volume/respiratory time ratio. UA resistance was unchanged with CO2 inhalation. During 7% CO2 breathing, LCW/ diaphragm MT decreased by 9.6 10.1% whereas genioglossus MT increased by 7.2 9%. CO2-induced ventilatory stimulation led to elevation of LCW/diaphragm MEP amplitudes during inspiration but not during expiration. LCW/diaphragm MEP latencies remained unaltered both during inspiration and expiration. Genioglossus MEP latencies and amplitudes were unchanged with CO2. Conclusion: in awake, healthy subjects, CO2-induced hyperventilation is associated with heightened LCW/diaphragm corticomotor activation without modulating genioglossus MEP responses. This imbalance may promote UA instability during increased respiratory drive.