Decreased Fatty Acid Oxidation and Altered Lactate Production during Exercise in Patients with Post-acute COVID-19 Syndrome, 2022, de Boer et al

To the Editor:

After acute infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), many individuals experience a range of symptoms including dyspnea, exercise intolerance, and chest pain commonly referred to as “post–COVID-19 syndrome” or as post-acute sequelae of SARS-CoV-2 infection (PASC) (1). Exertional dyspnea and physical activity intolerance in PASC can be debilitating despite mild acute coronavirus disease (COVID-19) and normal resting pulmonary physiology and cardiac function (2). There is an urgent need to understand the pathogenesis of PASC and find effective treatments. The cardiopulmonary exercise test (CPET) is commonly used to investigate unexplained exertional dyspnea; as such, it could provide insight into mechanisms of PASC. CPET data can be used to calculate rates of β-oxidation of fatty acids (FATox) and of lactate clearance, providing insight into mitochondrial function (3). Fit individuals have better mitochondrial function and a higher rate of FATox during exercise than less fit individuals (4). Our results suggest that patients with PASC have significant impairment in fat β-oxidation and increased blood lactate accumulation during exercise, regardless of previous comorbidities.

Open access, https://www.atsjournals.org/doi/full/10.1164/rccm.202108-1903LE

 

One of the authors of this study just posted on Twitter:

https://twitter.com/user/status/1696951922505429028


2 years ago we published this study suggesting significant mitochondrial dysfunction in Long-Covid patients. The idea was so crazy that we weren't able to include "mitochondrial dysfunction" in the article title. Instead, we had to used "decreased fat oxidation and altered lactate production" as surrogates for mitochondrial function through the methodology that I developed. It as also such a wild idea that the journal didn't want to publish it as an article and instead it was just as a "correspondence" to the Editor. Link here

https://atsjournals.org/doi/10.1164/rccm.202108-1903LE?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed…

2 years later, there are dozens of very well articulated and sophisticated studies showing mitochondrial dysfunction in long-covid patients. The evidence now is quite robust. While we don't have any medication to treat mitochondrial dysfunction, exercise is the only method we know that can work. With so much evidence, it is time for hospitals and healthcare systems to invest in supervised exercise programs for long-covid patients. In my previous post, I showed a pioneer exercise intervention study led by my colleagues
@alberenguel
and
@ManoloGallango
at the
@HospitalUnivTO
in Spain where they showed that 8 weeks of supervised exercise training improved multiple parameters in Long-Covid patients.

 

OK, but what if an abnormal response to exercise is the thing that causes or perpetuates mitochondrial dysfunction?