Dyspnea and Ventilatory Muscle Function During Exercise on Air and Oxygen Breathing in Patients with Chronic Obstructive Pulmonary Disease (COPD)

Abstract

Exercise performance and dyspnea in COPD patients have been shown to be improved with supplemental oxygen, although the exact mechanisms resulting in the improvement are still unclear. The purpose of the present study was to investigate a possible relationship between ventilatory muscle function and sensation of dyspnea (modified Borg Scale) during exercise on 20% O₂ and 30% O₂. Eight patients with COPD (FEV₁ 1.06L±0.30L) exercised on a treadmill two times breathing compressed air or 30% oxygen with a one hour rest in between. The electrical activity of the diaphragm (EMGdi) was recorded with esophageal electrodes, and that of the sternomastoid muscle (EMGsm) was recorded from the fine wire electrodes. The ratio of high frequency (150 to 350Hz) to low frequency (20 to 47Hz) power (H/L) of EMGdi was analyzed to assess diaphragmatic fatigue, which was defined as a 20% fall of H/L ratio from the control value. Flow, volume, O₂ Saturation (SaO₂), esophageal pressure (Pes) and transdiaphragmatic pressure (Pdi) were measured. Tension time index (TTdi) was calculated from Pdi and the ratio of inspiratory time to total time for one cycle (Ti/Ttot). At rest, we measured maximal esophageal pressure (Pesmax), maximal transdiaphragmatic pressure (Pdimax), maximal integrated EMGdi (EMGdimax) and EMGsm (EMGsmmax). Incremental exercise was discontinued by dyspnea. The walking distance achieved was increased in all patients on 30% O₂. Dyspnea and desaturation were significantly improved on 30% O₂ breathing, and the onset of diaphragmatic fatigue was delayed. Integrated EMGdi activity, integrated EMGsm activity, Pes/Pesmax and minute ventilation were also significantly decreased at isotime on 30% O₂, but Pdi/Pdimax and TTdi did not change.
These findings suggest that oxygen supplementation diminishes the activity of inspiratory muscles except the diaphragm. We conclude that in COPD patients, oxygen supplementation may decrease the central drive to inspiratory muscles and may alter inspiratory muscle recruitment, which are strongly related to the decrease of the sensation of dyspnea.