Jonathan Cunha, Antoinette Domingo, Fred W Kolkhorst, Harry B Rossiter, Daniel T Cannon
{"title":"Imposed expiratory resistance, dynamic hyperinflation and locomotor power and fatigue.","authors":"Jonathan Cunha, Antoinette Domingo, Fred W Kolkhorst, Harry B Rossiter, Daniel T Cannon","doi":"10.1113/EP092818","DOIUrl":null,"url":null,"abstract":"<p><p>Expiratory flow limitation results in dynamic hyperinflation, dyspnoea and premature exercise intolerance. We aimed to measure whether expiratory resistance reduces locomotor power via limiting maximal voluntary motor activity, exacerbating muscle fatigue, or both. Healthy volunteers (n = 14; 23 (3) years) performed a series of very heavy-domain constant power cycling exercise tests with and without an imposed expiratory flow resistance (7 cmH<sub>2</sub>O/L/s). The decline in maximal evocable isokinetic power at intolerance during each experimental condition was apportioned to: (1) the power equivalent from a reduction in maximum voluntary muscle activation (termed 'activation fatigue'); and (2) the deficit in expected power at a given isokinetic muscle activity (muscle fatigue). Imposed expiratory resistance reduced exercise tolerance (487 (145) vs. 575 (137) s; 95% confidence interval of the difference (CI<sub>diff</sub>) 52, 125 s; P = 0.0002). At isotime-control, imposed expiratory resistance resulted in a greater decline in inspiratory reserve volume (CI<sub>diff</sub> 0.20, 0.94 L; P = 0.007), and increased dyspnoea (Borg CR-10; CI<sub>diff</sub> 0.7, 3.0; P = 0.006) than without. Muscle fatigue was unaffected (CI<sub>diff</sub> -20, 17 W; P = 0.873), but activation fatigue was greater with expiratory resistance (CI<sub>diff</sub> 1, 49 W; P = 0.044) and related to the reduction in inspiratory reserve volume (r<sup>2 </sup>= 0.53; P = 0.028). As a result, locomotor power reserve was reduced with expiratory resistance (253 (83) vs. 201 (92) W; CI<sub>diff</sub> -10, 113; P = 0.09). Imposed expiratory resistive loading initiated a cascade of abnormal lung mechanics and symptoms. These abnormalities conflate to reduce exercise tolerance through limiting maximal voluntary motor activity.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.8000,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Experimental Physiology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1113/EP092818","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"PHYSIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Expiratory flow limitation results in dynamic hyperinflation, dyspnoea and premature exercise intolerance. We aimed to measure whether expiratory resistance reduces locomotor power via limiting maximal voluntary motor activity, exacerbating muscle fatigue, or both. Healthy volunteers (n = 14; 23 (3) years) performed a series of very heavy-domain constant power cycling exercise tests with and without an imposed expiratory flow resistance (7 cmH2O/L/s). The decline in maximal evocable isokinetic power at intolerance during each experimental condition was apportioned to: (1) the power equivalent from a reduction in maximum voluntary muscle activation (termed 'activation fatigue'); and (2) the deficit in expected power at a given isokinetic muscle activity (muscle fatigue). Imposed expiratory resistance reduced exercise tolerance (487 (145) vs. 575 (137) s; 95% confidence interval of the difference (CIdiff) 52, 125 s; P = 0.0002). At isotime-control, imposed expiratory resistance resulted in a greater decline in inspiratory reserve volume (CIdiff 0.20, 0.94 L; P = 0.007), and increased dyspnoea (Borg CR-10; CIdiff 0.7, 3.0; P = 0.006) than without. Muscle fatigue was unaffected (CIdiff -20, 17 W; P = 0.873), but activation fatigue was greater with expiratory resistance (CIdiff 1, 49 W; P = 0.044) and related to the reduction in inspiratory reserve volume (r2 = 0.53; P = 0.028). As a result, locomotor power reserve was reduced with expiratory resistance (253 (83) vs. 201 (92) W; CIdiff -10, 113; P = 0.09). Imposed expiratory resistive loading initiated a cascade of abnormal lung mechanics and symptoms. These abnormalities conflate to reduce exercise tolerance through limiting maximal voluntary motor activity.
期刊介绍:
Experimental Physiology publishes research papers that report novel insights into homeostatic and adaptive responses in health, as well as those that further our understanding of pathophysiological mechanisms in disease. We encourage papers that embrace the journal’s orientation of translation and integration, including studies of the adaptive responses to exercise, acute and chronic environmental stressors, growth and aging, and diseases where integrative homeostatic mechanisms play a key role in the response to and evolution of the disease process. Examples of such diseases include hypertension, heart failure, hypoxic lung disease, endocrine and neurological disorders. We are also keen to publish research that has a translational aspect or clinical application. Comparative physiology work that can be applied to aid the understanding human physiology is also encouraged.
Manuscripts that report the use of bioinformatic, genomic, molecular, proteomic and cellular techniques to provide novel insights into integrative physiological and pathophysiological mechanisms are welcomed.