Please use this identifier to cite or link to this item: http://bura.brunel.ac.uk/handle/2438/14168
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dc.contributor.authorRomer, LM-
dc.contributor.authorRamsook, AH-
dc.contributor.authorMolgat-Seon, Y-
dc.contributor.authorSchaeffer, MR-
dc.contributor.authorWilkie, SS-
dc.contributor.authorCamp, PG-
dc.contributor.authorReid, WD-
dc.contributor.authorGuenette, JA-
dc.date.accessioned2017-03-02T11:25:01Z-
dc.date.available2017-03-02T11:25:01Z-
dc.date.issued2017-
dc.identifier.citationJournal of Applied Physiology,(2017)en_US
dc.identifier.issn1522-1601-
dc.identifier.urihttp://bura.brunel.ac.uk/handle/2438/14168-
dc.description.abstractInspiratory 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.en_US
dc.description.sponsorshipThis 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.en_US
dc.language.isoenen_US
dc.subjectDyspneaen_US
dc.subjectElectromyography,en_US
dc.subjectInspiratory muscle trainingen_US
dc.subjectNeural respiratory driveen_US
dc.titleEffects of inspiratory muscle training on respiratory muscle electromyography and dyspnea during exercise in healthy menen_US
dc.typeArticleen_US
dc.relation.isPartOfJournal of Applied Physiology-
pubs.publication-statusAccepted-
Appears in Collections:Dept of Life Sciences Research Papers

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