Inspiratory muscle training reduces diaphragm activation and dyspnea during exercise in COPD

• Main Authors: Daniel Langer, Casey Ciavaglia, Azmy Faisal, Katherine A. Webb, J. Alberto Neder, Rik Gosselink, Sauwaluk Dacha, Marko Topalovic, Anna Ivanova, Denis E. O’Donnell
• Format: Journal
• Published: 2018
• Subjects: Biochemistry, Genetics and Molecular Biology; Medicine
• Online Access: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85052865304&origin=inward; http://cmuir.cmu.ac.th/jspui/handle/6653943832/62582
• Institution: Chiang Mai University

Copyright © 2018 the American Physiological Society. Among patients with chronic obstructive pulmonary disease (COPD), those with the lowest maximal inspiratory pressures experience greater breathing discomfort (dyspnea) during exercise. In such individuals, inspiratory muscle training (IMT) may be associated with improvement of dyspnea, but the mechanisms for this are poorly understood. Therefore, we aimed to identify physiological mechanisms of improvement in dyspnea and exercise endurance following inspiratory muscle training (IMT) in patients with COPD and low maximal inspiratory pressure (Pimax). The effects of 8 wk of controlled IMT on respiratory muscle function, dyspnea, respiratory mechanics, and diaphragm electromyography (EMGdi) during constant work rate cycle exercise were evaluated in patients with activity-related dyspnea (baseline dyspnea index 9). Subjects were randomized to either IMT or a sham training control group (n 10 each). Twenty subjects (FEV1 47 19% predicted; Pimax 59 14 cmH2O; cycle ergometer peak work rate 47 21% predicted) completed the study; groups had comparable baseline lung function, respiratory muscle strength, activity-related dyspnea, and exercise capacity. IMT, compared with control, was associated with greater increases in inspiratory muscle strength and endurance, with attendant improvements in exertional dyspnea and exercise endurance time (all P 0.05). After IMT, EMGdi expressed relative to its maximum (EMGdi/EMGdimax) decreased (P 0.05) with no significant change in ventilation, tidal inspiratory pressures, breathing pattern, or operating lung volumes during exercise. In conclusion, IMT improved inspiratory muscle strength and endurance in mechanically compromised patients with COPD and low Pimax. The attendant reduction in EMGdi/EMGdimax helped explain the decrease in perceived respiratory discomfort despite sustained high ventilation and intrinsic mechanical loading over a longer exercise duration. NEW & NOTEWORTHY In patients with COPD and low maximal inspiratory pressures, inspiratory muscle training (IMT) may be associated with improvement of dyspnea, but the mechanisms for this are poorly understood. This study showed that 8 wk of home-based, partially supervised IMT improved respiratory muscle strength and endurance, dyspnea, and exercise endurance. Dyspnea relief occurred in conjunction with a reduced activation of the diaphragm relative to maximum in the absence of significant changes in ventilation, breathing pattern, and operating lung volumes.