Article Title



Peyton C. Thompson1, Natalie E. Bonvie-Hill2, Igor A. Fernandes2, Brian P. Shapiro2, Bryan J. Taylor, FACSM2. 1Duke University, Durham, NC. 2Mayo Clinic, Jacksonville, FL.

BACKGROUND: Up to 40% of people infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) develop long COVID, defined as COVID-19 sequalae (e.g., fatigue, dyspnea, chest tightness, exertional intolerance) persisting >12 weeks. Cardiopulmonary exercise testing (CPET) is often used as first-line assessment when investigating the possible causes of dyspnea and exertional intolerance. PURPOSE: To investigate the potential causes of exercise limitation in people with long COVID by characterizing the pulmonary and cardiometabolic responses to CPET. METHODS: Twenty adults (13 females; 40±11 y) with a diagnosis of long COVID participated. Following comprehensive pulmonary function assessment, a maximal CPET was performed on a motorized treadmill. Peak oxygen uptake (V̇O2peak) was measured as exercise capacity. Heart rate (HR), carbon dioxide production (V̇CO2), and minute ventilation (V̇E), and derived variables including O2 pulse (V̇O2/HR), chronotropic index (CI), respiratory exchange ratio (RER), and ventilatory efficiency (V̇E/V̇CO2) were measured during each CPET. Anaerobic threshold (AT) was inferred from gas exchange threshold (GET). RESULTS: There was inter-individual heterogeneity in V̇O2peak (103±25% predicted [%p], range 76 to 188%p). We subdivided our population into group groups: 1) ‘low’ V̇O2peak (<85% predicted, 80±3%p; n=6) and 2) ‘normal’ V̇O2peak (≥85% predicted, 113±24%p; n=14). Indices of lung function tended to be lower in the low V̇O2peak group, but there was no relationship between forced expiratory volume in 1 s, forced vital capacity, or total lung capacity and V̇O2peak across the entire cohort (all r≤0.35, P≥0.41). Peak HR (95±10 vs 96±7%p), O2pulse (13±4 vs. 14±5%p), and RER (1.15±0.11 vs. 1.16±0.08), and CI (0.91±0.20 vs. 0.94±0.11) were not different between the ‘low’ vs. ‘normal’ V̇O2peak groups (all P≥0.59). Neither V̇E/V̇CO2 nadir (27±2 vs. 27±3, P=0.83) nor GET were different between the two groups. CONCLUSIONS: Some but not all people with long COVID have decreased exercise capacity (V̇O2peak <85% predicted). The pulmonary and cardiometabolic responses to CPET were not different in people with a ‘low’ vs. ‘normal’ V̇O2peak. In general, the cardiopulmonary responses to CPET were normal across our cohort. We suggest that decreased exercise capacity in people with long COVID may occur due to residual physical deconditioning, which may improve with regular exercise.

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