Inspiratory muscle training (IMT) has consistently been shown to reduce exertional dyspnea in health and disease; however, the physiological mechanisms remain poorly understood. A growing body of literature suggests that dyspnea intensity can largely be explained by an awareness of increased neural respiratory drive, as indirectly measured using diaphragmatic electromyography (EMGdi). Accordingly, we sought to determine if improvements in dyspnea following IMT can be explained by decreases in inspiratory muscle EMG activity. Twenty-five healthy recreationally-active men completed a detailed familiarization visit followed by two maximal incremental cycle exercise tests separated by 5 weeks of randomly assigned pressure threshold IMT or sham control training (SC). The IMT group (n=12) performed 30 inspiratory efforts twice daily against a 30 repetition maximum intensity. The SC group (n=13) performed a daily bout of 60 inspiratory efforts against 10% maximal inspiratory pressure (MIP), with no weekly adjustments. Dyspnea intensity was measured throughout exercise using the modified 0-10 Borg scale. Sternocleidomastoid and scalene EMG were measured using surface electrodes whereas EMGdi was measured using a multi-pair esophageal electrode catheter. IMT significantly improved MIP (pre:-138±45 vs. post:-160±43cmH2O, p<0.01) whereas the SC intervention did not. Dyspnea was significantly reduced at the highest equivalent work rate (pre:7.6±2.5 vs. post:6.8±2.9Borg units, p<0.05), but not in the SC group, with no between-group interaction effects. There were no significant differences in respiratory muscle EMG during exercise in either group. Improvements in dyspnea intensity ratings following IMT in healthy humans cannot be explained by changes in the electrical activity of the inspiratory muscles.
- inspiratory muscle training
- neural respiratory drive
- Copyright © 2017, Journal of Applied Physiology