Gattoni C; The Lundquist Institute at Harbor-UCLA Medical Center, Torrance, CA, USA.
Abbasi A; Ferguson C; Lanks CW; Decato TW; Rossiter HB; Casaburi R; Stringer WW;
Respiratory physiology & neurobiology [Respir Physiol Neurobiol] 2024 Oct 28; Vol. 331, pp. 104362. Date of Electronic Publication: 2024 Oct 28.
Background: Long COVID patients present with a myriad of symptoms that can include fatigue, exercise intolerance and post exertional malaise (PEM). Long COVID has been compared to other post viral syndromes, including myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), where a reduction in day 2 cardiopulmonary exercise test (CPET) performance of a two-day CPET protocol is suggested to be a result of PEM. We investigated cardiopulmonary and perceptual responses to a two-day CPET protocol in Long COVID patients.
Methods: 15 Long COVID patients [n=7 females; mean (SD) age: 53(11) yr; BMI = 32.2(8.5) kg/m 2 ] performed a pulmonary function test and two ramp-incremental CPETs separated by 24 hr. CPET variables included gas exchange threshold (GET), peak oxygen uptake (V̇O 2peak ) and peak work rate (WR peak ). Ratings of perceived dyspnoea and leg effort were recorded at peak exercise using the modified 0-10 Borg Scale. PEM (past six months) was assessed using the modified DePaul Symptom Questionnaire (mDSQ). One-sample t-tests were used to test significance of mean difference between days (p<0.05).
Results: mDSQ revealed PEM in 80 % of patients. Lung function was normal. Responses to day 1 CPET were consistent with the presence of aerobic deconditioning in 40 % of patients (V̇O 2peak <80 % predicted, in the absence of evidence of cardiovascular and pulmonary limitations). There were no differences between day-1 and day-2 CPET responses (all p>0.05).
Conclusion: PEM symptoms in Long COVID patients, in the absence of differences in two-day CPET responses separated by 24 hours, suggests that PEM is not due to impaired recovery of exercise capacity between days.
Competing Interests: Declaration of Competing Interest Chiara Gattoni has no conflict of interest to declare. Asghar Abbasi is supported by awards from Johnny Carson Foundation and NIH (1R43 HL167289–01). Carrie Ferguson is supported by grants from NIH (R01HL166850). She reports consulting fees from Respira Therapeutics. She is involved in contracted clinical research with United Therapeutics, Genentech, Regeneron and Respira Therapeutics. She has received honoraria for teaching on the ACCP CPET live-learning course. She is a visiting Associate Professor at the University of Leeds, UK. Charles W. Lanks has no conflict of interest to declare. Thomas DeCato is supported by a grant from the NIH (R01HL166850). He reports consulting fees from MannKind Corporation and has received honoraria for teaching on the ACCP CPET live-learning course. Harry Rossiter is supported by grants from NIH (R01HL151452, R01HL166850, R01HL153460, P50HD098593, R01DK122767) and the Tobacco Related Disease Research Program (T31IP1666). He reports consulting fees from the NIH RECOVER-ENERGIZE working group (1OT2HL156812) and is involved in contracted clinical research with United Therapeutics, Genentech, Regeneron, Respira and Intervene Immune. He is a visiting Professor at the University of Leeds, UK. Richard Casaburi is involved in contracted research and is a consultant with Regeneron. He is an advisory board member for Inogen and a speaker bureau member for GlaxoSmithKline. William Stringer is involved in contracted clinical research with Genentech, Regeneron, Roche, AstraZeneca and the NIH Recover-Vital and Recover-Neuro clinical trials. He performs CPET Data Center activities for the NIH funded PETRACT study (UG3HL155798–01A1). He is a co-investigator on an NIH Small Business Innovation Award (1R43HL167289–01) and has been a site PI for the NIH RETHINC (5U01HL128954-04) and BLOCK-COPD (W81XWH-15–1–0705) studies. He performs Data Safety Monitoring Board activities for SYNEOS and CAPRICOR. He receives royalty payments from a CPET book from Wolters Kluwer. He is a paid consultant for Genentech, Verona and Regeneron. He owns stock in HIA. The current study was funded by the Pulmonary Education and Research Foundation.