Low Cardiorespiratory Fitness Post-COVID-19: A Narrative Review

Patients recovering from COVID-19 often report symptoms of exhaustion, fatigue and dyspnoea and present with exercise intolerance persisting for months post-infection. Numerous studies investigated these sequelae and their possible underlying mechanisms using cardiopulmonary exercise testing. We aimed to provide an in-depth discussion as well as an overview of the contribution of selected organ systems to exercise intolerance based on the Wasserman gears. The gears represent the pulmonary system, cardiovascular system, and periphery/musculature and mitochondria. Thirty-two studies that examined adult patients post-COVID-19 via cardiopulmonary exercise testing were included. In 22 of 26 studies reporting cardiorespiratory fitness (herein defined as peak oxygen uptake—VO(2peak)), VO(2peak) was < 90% of predicted value in patients. VO(2peak) was notably below normal even in the long-term. Given the available evidence, the contribution of respiratory function to low VO(2peak) seems to be only minor except for lung diffusion capacity. The prevalence of low lung diffusion capacity was high in the included studies. The cardiovascular system might contribute to low VO(2peak) via subnormal cardiac output due to chronotropic incompetence and reduced stroke volume, especially in the first months post-infection. Chronotropic incompetence was similarly present in the moderate- and long-term follow-up. However, contrary findings exist. Peripheral factors such as muscle mass, strength and perfusion, mitochondrial function, or arteriovenous oxygen difference may also contribute to low VO(2peak). More data are required, however. The findings of this review do not support deconditioning as the primary mechanism of low VO(2peak) post-COVID-19. Post-COVID-19 sequelae are multifaceted and require individual diagnosis and treatment. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s40279-022-01751-7.