{"id":{"repo_id":"uic","oai_identifier":"oai:figshare.com:article/31451182"},"canonical_url":"https://search.dev.ndltd.org/etd/uic/oai:figshare.com:article/31451182","repository":{"repo_id":"uic","name":"University of Illinois - Chicago","base_url":"https://api.figshare.com/v2/oai"},"display":{"title":"Unexplained Exercise Intolerance and Dyspnea in Long COVID","abstract":"Long COVID is characterized by persistent dyspnea, fatigue, and exercise intolerance despite normal cardiopulmonary findings. This study examined whether peripheral impairments—specifically respiratory muscle dysfunction and endothelial impairment—contribute to these symptoms. Thirty COVID-19 convalescent adults (20 with long COVID, 10 controls) underwent respiratory muscle testing, flow-mediated dilation (FMD), heart-rate variability (HRV), and cardiopulmonary exercise testing (CPET). Participants with long COVID exhibited marked reductions in inspiratory muscle performance—MIP (−52%), SMIP (−71%), and FIT (−79%)—and lower aerobic capacity (VO₂ peak = 21.1 ± 7.2 vs. 30.2 ± 11.0 mL·kg⁻¹·min⁻¹; p = 0.01). FMD was significantly reduced (5.3% vs 8.4%; p < 0.001), whereas ventilatory efficiency and autonomic indices were preserved. VO₂ peak correlated strongly with SMIP (r = 0.79) and MIP (r = 0.73), while FMD correlated only with MIP (r = 0.65, p < 0.001). A prediction model that included MIP accounted for 79% of the variance in VO₂ peak (VO₂ peak = 57.6 + 0.168 [MIP] − 0.271 [HR] − 0.520 [BMI] − 0.225 [Age] − 1.956 [Sex]), showing that inspiratory muscle strength is a good predictor of functional aerobic performance. MIP < 63 cmH₂O distinguished long COVID with 90% sensitivity and 93% specificity (AUC = 0.93). These findings highlight that exercise intolerance in long COVID arises primarily from peripheral mechanisms involving respiratory muscle and endothelial dysfunction rather than central cardiopulmonary limitation.","abstract_html":"Long COVID is characterized by persistent dyspnea, fatigue, and exercise intolerance despite normal cardiopulmonary findings. This study examined whether peripheral impairments—specifically respiratory muscle dysfunction and endothelial impairment—contribute to these symptoms. Thirty COVID-19 convalescent adults (20 with long COVID, 10 controls) underwent respiratory muscle testing, flow-mediated dilation (FMD), heart-rate variability (HRV), and cardiopulmonary exercise testing (CPET). Participants with long COVID exhibited marked reductions in inspiratory muscle performance—MIP (−52%), SMIP (−71%), and FIT (−79%)—and lower aerobic capacity (VO₂ peak = 21.1 ± 7.2 vs. 30.2 ± 11.0 mL·kg⁻¹·min⁻¹; p = 0.01). FMD was significantly reduced (5.3% vs 8.4%; p &lt; 0.001), whereas ventilatory efficiency and autonomic indices were preserved. VO₂ peak correlated strongly with SMIP (r = 0.79) and MIP (r = 0.73), while FMD correlated only with MIP (r = 0.65, p &lt; 0.001). A prediction model that included MIP accounted for 79% of the variance in VO₂ peak (VO₂ peak = 57.6 + 0.168 [MIP] − 0.271 [HR] − 0.520 [BMI] − 0.225 [Age] − 1.956 [Sex]), showing that inspiratory muscle strength is a good predictor of functional aerobic performance. MIP &lt; 63 cmH₂O distinguished long COVID with 90% sensitivity and 93% specificity (AUC = 0.93). These findings highlight that exercise intolerance in long COVID arises primarily from peripheral mechanisms involving respiratory muscle and endothelial dysfunction rather than central cardiopulmonary limitation.","abstract_has_math":false,"creators":["Firas Hudaib (23291407)"],"institution":null,"degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2025,"date_issued":"2025-12-01T00:00:00Z","date_published":"2025-12-01T00:00:00Z","updated_at":"2026-07-27T21:34:23Z","subjects":["Long COVID"],"languages":[],"rights":["In Copyright"],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://doi.org/10.25417/uic.31451182.v1","outbound_label":"DOI","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["Firas Hudaib (23291407)"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2025-12-01T00:00:00Z"]},{"key":"dc:relation","label":"Dc Relation","values":["https://figshare.com/articles/thesis/Unexplained_Exercise_Intolerance_and_Dyspnea_in_Long_COVID/31451182"]},{"key":"dc:type","label":"Dc Type","values":["Text","Thesis"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Long COVID"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:rights","label":"Dc Rights","values":["In Copyright"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["10.25417/uic.31451182.v1"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Long COVID is characterized by persistent dyspnea, fatigue, and exercise intolerance despite normal cardiopulmonary findings. This study examined whether peripheral impairments—specifically respiratory muscle dysfunction and endothelial impairment—contribute to these symptoms. Thirty COVID-19 convalescent adults (20 with long COVID, 10 controls) underwent respiratory muscle testing, flow-mediated dilation (FMD), heart-rate variability (HRV), and cardiopulmonary exercise testing (CPET). Participants with long COVID exhibited marked reductions in inspiratory muscle performance—MIP (−52%), SMIP (−71%), and FIT (−79%)—and lower aerobic capacity (VO₂ peak = 21.1 ± 7.2 vs. 30.2 ± 11.0 mL·kg⁻¹·min⁻¹; p = 0.01). FMD was significantly reduced (5.3% vs 8.4%; p < 0.001), whereas ventilatory efficiency and autonomic indices were preserved. VO₂ peak correlated strongly with SMIP (r = 0.79) and MIP (r = 0.73), while FMD correlated only with MIP (r = 0.65, p < 0.001). A prediction model that included MIP accounted for 79% of the variance in VO₂ peak (VO₂ peak = 57.6 + 0.168 [MIP] − 0.271 [HR] − 0.520 [BMI] − 0.225 [Age] − 1.956 [Sex]), showing that inspiratory muscle strength is a good predictor of functional aerobic performance. MIP < 63 cmH₂O distinguished long COVID with 90% sensitivity and 93% specificity (AUC = 0.93). These findings highlight that exercise intolerance in long COVID arises primarily from peripheral mechanisms involving respiratory muscle and endothelial dysfunction rather than central cardiopulmonary limitation."]},{"key":"dc:title","label":"Title","values":["Unexplained Exercise Intolerance and Dyspnea in Long COVID"]}]}],"canonical_facts":{"dc:creator":["Firas Hudaib (23291407)"],"dc:date":["2025-12-01T00:00:00Z"],"dc:description":["Long COVID is characterized by persistent dyspnea, fatigue, and exercise intolerance despite normal cardiopulmonary findings. This study examined whether peripheral impairments—specifically respiratory muscle dysfunction and endothelial impairment—contribute to these symptoms. Thirty COVID-19 convalescent adults (20 with long COVID, 10 controls) underwent respiratory muscle testing, flow-mediated dilation (FMD), heart-rate variability (HRV), and cardiopulmonary exercise testing (CPET). Participants with long COVID exhibited marked reductions in inspiratory muscle performance—MIP (−52%), SMIP (−71%), and FIT (−79%)—and lower aerobic capacity (VO₂ peak = 21.1 ± 7.2 vs. 30.2 ± 11.0 mL·kg⁻¹·min⁻¹; p = 0.01). FMD was significantly reduced (5.3% vs 8.4%; p < 0.001), whereas ventilatory efficiency and autonomic indices were preserved. VO₂ peak correlated strongly with SMIP (r = 0.79) and MIP (r = 0.73), while FMD correlated only with MIP (r = 0.65, p < 0.001). A prediction model that included MIP accounted for 79% of the variance in VO₂ peak (VO₂ peak = 57.6 + 0.168 [MIP] − 0.271 [HR] − 0.520 [BMI] − 0.225 [Age] − 1.956 [Sex]), showing that inspiratory muscle strength is a good predictor of functional aerobic performance. MIP < 63 cmH₂O distinguished long COVID with 90% sensitivity and 93% specificity (AUC = 0.93). These findings highlight that exercise intolerance in long COVID arises primarily from peripheral mechanisms involving respiratory muscle and endothelial dysfunction rather than central cardiopulmonary limitation."],"dc:identifier":["10.25417/uic.31451182.v1"],"dc:relation":["https://figshare.com/articles/thesis/Unexplained_Exercise_Intolerance_and_Dyspnea_in_Long_COVID/31451182"],"dc:rights":["In Copyright"],"dc:subject":["Long COVID"],"dc:title":["Unexplained Exercise Intolerance and Dyspnea in Long COVID"],"dc:type":["Text","Thesis"]},"updated_at":"2026-07-27T21:34:23Z"}