Key result
Previously hospitalized COVID-19 patients with exercise intolerance had lower peak workload (79W vs 104W; P=0.01) and peak indexed cardiac output than controls, suggesting failure to augment stroke volume.
Why the study?
Ongoing exercise intolerance of unclear cause following COVID-19 infection is well recognized but poorly understood.
What is the physiological mechanism of exercise intolerance in previously hospitalized patients with COVID-19 as assessed by magnetic resonance-augmented cardiopulmonary exercise testing?
Case-Control (n=60)
No
What is the physiological mechanism of exercise intolerance in previously hospitalized patients with COVID-19 as assessed by magnetic resonance-augmented cardiopulmonary exercise testing?
Exercise intolerance following COVID-19 hospitalization is associated with a failure to augment stroke volume during exercise, which appears to improve over time.
Impaired stroke volume augmentation may explain post-COVID intolerance; hypothesis-generating for mechanism-targeted trials before any practice change.
Background Ongoing exercise intolerance of unclear cause following COVID‐19 infection is well recognized but poorly understood. We investigated exercise capacity in patients previously hospitalized with COVID‐19 with and without self‐reported exercise intolerance using magnetic resonance–augmented cardiopulmonary exercise testing. Methods and Results Sixty subjects were enrolled in this single‐center prospective observational case‐control study, split into 3 equally sized groups: 2 groups of age‐, sex‐, and comorbidity‐matched previously hospitalized patients following COVID‐19 without clearly identifiable postviral complications and with either self‐reported reduced (COVID reduced ) or fully recovered (COVID normal ) exercise capacity; a group of age‐ and sex‐matched healthy controls. The COVID reduced group had the lowest peak workload (79W [Interquartile range (IQR), 65–100] versus controls 104W [IQR, 86–148]; P =0.01) and shortest exercise duration (13.3±2.8 minutes versus controls 16.6±3.5 minutes; P =0.008), with no differences in these parameters between COVID normal patients and controls. The COVID reduced group had: (1) the lowest peak indexed oxygen uptake (14.9 mL/minper kg [IQR, 13.1–16.2]) versus controls (22.3 mL/min per kg [IQR, 16.9–27.6]; P =0.003) and COVID normal patients (19.1 mL/min per kg [IQR, 15.4–23.7]; P =0.04); (2) the lowest peak indexed cardiac output (4.7±1.2 L/min per m 2 ) versus controls (6.0±1.2 L/min per m 2 ; P =0.004) and COVID normal patients (5.7±1.5 L/min per m 2 ; P =0.02), associated with lower indexed stroke volume (SVi:COVID reduced 39±10 mL/min per m 2 versus COVID normal 43±7 mL/min per m 2 versus controls 48±10 mL/min per m 2 ; P =0.02). There were no differences in peak tissue oxygen extraction or biventricular ejection fractions between groups. There were no associations between COVID‐19 illness severity and peak magnetic resonance–augmented cardiopulmonary exercise testing metrics. Peak indexed oxygen uptake, indexed cardiac output, and indexed stroke volume all correlated with duration from discharge to magnetic resonance–augmented cardiopulmonary exercise testing ( P <0.05). Conclusions Magnetic resonance–augmented cardiopulmonary exercise testing suggests failure to augment stroke volume as a potential mechanism of exercise intolerance in previously hospitalized patients with COVID‐19. This is unrelated to disease severity and, reassuringly, improves with time from acute illness.
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A 2022 study conducted a case-control in Ongoing exercise intolerance following COVID-19 (n=60). COVID-19 with self-reported reduced exercise capacity vs. Healthy controls and COVID-19 patients with fully recovered exercise capacity was evaluated on Peak workload (p=0.01). Previously hospitalized COVID-19 patients with exercise intolerance had lower peak workload (79W vs 104W; P=0.01) and peak indexed cardiac output than controls, suggesting failure to augment stroke volume.
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