5 research outputs found

    Influence of inspiratory resistive loading on expiratory muscle fatigue in healthy humans

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    Expiratory resistive loading elicits inspiratory as well as expiratory muscle fatigue, suggesting parallel co-activation of the inspiratory muscles during expiration. It is unknown whether the expiratorymuscles are similarly co-activated to the point of fatigue during inspiratory resistive loading (IRL).The purpose of this study was to determine whether IRL elicits expiratory as well as inspiratory muscle fatigue. Healthy male subjects (n=9) underwent isocapnic IRL (60% maximal inspiratory pressure, 15 breaths∙min-1, 0.7 inspiratory duty cycle) to task failure. Abdominal and diaphragm contractile function was assessed at baseline and at 3, 15 and 30 min post-IRL by measuring gastric twitch pressure (Pga,tw) and transdiaphragmatic twitch pressure (Pdi,tw) in response to potentiated magnetic stimulation of the thoracic and phrenic nerves, respectively. Fatigue was defined as a significant reduction from baseline in Pga,tw or Pdi,tw. Throughout IRL, there was a time-dependent increase in cardiac frequency and mean arterial blood pressure, suggesting activation of the respiratory muscle metaboreflex. Pdi,tw was significantly lower than baseline (34.3 9.6 cmH2O) at 3min (23.2 5.7 cmH2O, P<0.001), 15 min (24.2 5.1 cmH2O, P<0.001) and 30 min post-IRL (26.3 6.0 cmH2O, P<0.001). Pga,tw was not significantly different from baseline (37.6 17.1 cmH2O) at 3min (36.5 14.6 cmH2O), 15 min (33.7 12.4 cmH2O) and 30 min post-IRL (32.9 11.3 cmH2O). IRL elicits objective evidence of diaphragm, but not abdominal, muscle fatigue. Agonist-antagonist interactions for the respiratory muscles appear to be more important during expiratory versus inspiratory loading.The Natural Sciences and Engineering Research Council (NSERC) of Canada supported this study. C.M. Peters, P.B. Dominelli, and Y. Molgat-Seon were supported by NSERC postgraduate scholarships. J.F Welch was supported by a University of British Columbia graduate fellowship

    Effects of inspiratory muscle training on respiratory muscle electromyography and dyspnea during exercise in healthy men

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    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 young, 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. 66 Improvements in dyspnea intensity ratings following IMT in healthy humans cannot be explained by 67 changes in the electrical activity of the inspiratory muscles.This research was supported by a Discovery Grant from the Natural Sciences and Engineering Research Council (NSERC) of Canada and an Infrastructure Grant from the Canada Foundation for Innovation. AHR was supported by the University of British Columbia 4 Year Fellowship (4YF). YMS was supported by a 4YF and a Post Graduate Scholarship from the NSERC. MRS was supported by a 4YF and a fellowship from the British Columbia Lung Association. PGC was supported by a Scholar Award from the Michael Smith Foundation for Health Research (MSFHR). JAG was supported by a Scholar Award from the MSFHR, a Canadian Institutes of Health Research Clinical Rehabilitation New Investigator Award, and a New Investigator Award from the Providence Health Care Research Institute and St. Paul’s Hospital Foundation
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