Low Cardiorespiratory Fitness Post-COVID-19: A Narrative Review, 2022, Schwendinger et al

[Sly Saint]

Abstract


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—VO2peak), VO2peak was < 90% of predicted value in patients. VO2peak was notably below normal even in the long-term.

Given the available evidence, the contribution of respiratory function to low VO2peak 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 VO2peak 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 VO2peak. More data are required, however. The findings of this review do not support deconditioning as the primary mechanism of low VO2peak post-COVID-19. Post-COVID-19 sequelae are multifaceted and require individual diagnosis and treatment.


FormalPara Key Points
Exercise intolerance post-COVID-19 may likely have several causes and is not solely explained by deconditioning.
Peripheral followed by cardiovascular factors as well as lung diffusion limitations are central for long-term sequelae.
This work will improve the understanding of possible underlying mechanisms of low cardiorespiratory fitness post-COVID-19 and at the same time promote cardiopulmonary exercise testing as a valuable diagnostic tool in patients post-COVID-19. Based on this, more targeted rehabilitation programmes could be developed in the future.

https://link.springer.com/article/10.1007/s40279-022-01751-7

 

[rvallee]

Exercise intolerance post-COVID-19 may likely have several causes and is not solely explained by deconditioning.

They only need to pay attention to the many, many, many people who were in peak physical conditions mere days or weeks before they developed the condition to know that it plays no role at all. In the end weeks or months of inability to exert will obviously lower that conditioning but if the symptoms are present at the start it's absurd to attribute them to time since it began. It's very important to differentiate the factors that are relevant before, during and after.

That's really the most disappointing part of how medical research works, it's not at all like investigative work, they ignore most of the leads and evidence to focus on a small subset, but never bother checking whether it's consistent with the rest of the evidence. Like trying to solve a puzzle by arbitrarily taking a few pieces and extrapolating from that. It would prevent so much waste and obsession over dead-ends if there was a real investigative process. If this was the approach law enforcement took in criminal investigations it would be disastrous, completely ineffective. With these standards white collar crimes would be rampant as they would simply never get caught.

 

[SNT Gatchaman]

Generally reasonable literature review (covid-related) and overview of the physiology of the levels that may ultimately impact VO2(peak). They divide these into: respiratory, cardiovascular and peripheral muscle/mitochondria. Generally argues against deconditioning, as above.

However, there's an absolute howler at the end —

In addition, psychological factors may contribute substantially to the prolonged symptoms fostering exercise intolerance. Schaeffer et al. for instance, found lower V̇O2peak in patients with post-COVID-19 fatigue than in those without fatigue. This was accompanied by greater dyspnoea during exercise. Psychological factors should thus not be disregarded in research, diagnosis or therapy/treatment.

Are they really suggesting that fatigue by necessity == psychological? The paper they reference in this section is Cardiorespiratory physiology, exertional symptoms, and psychological burden in post-COVID-19 fatigue (2022). The relevant passage from that paper is —

Participants with fatigue reported higher dyspnoea intensity ratings during CPET despite no differences in cardiovascular or ventilatory measures compared to those without fatigue. Additionally, those with fatigue reported higher anxiety, depression, distress, and functional disability attributable to dyspnoea. These observations are in the context of normal resting cardiopulmonary function and similar infection severity across groups, which is consistent with previous findings. A higher psychological impact of COVID-19 could be associated with enhanced perception of symptoms, such as persistent fatigue, and the higher dyspnoea ratings for a given ventilation and VO2 we observed during exercise. Accordingly, the roles of extra-cardiopulmonary factors, such as mental health, warrant further consideration.

— concluding —

Our study also highlights the psychological burden faced by individuals with post-COVID-19 fatigue, which may amplify symptom perception such as dyspnoea during exercise.

I don't understand how the authors of this thread's paper could spend pages discussing around a framework of (1) respiratory (2) cardiovascular and (3) peripheral muscular/mitochondrial causes, and then take this other paper that does not mention (3) at all — instead proposing normal (1) and normal (2) therefore must be (x) psychological.