Clinical Trial Details
— Status: Completed
Administrative data
| NCT number |
NCT06468722 |
| Other study ID # |
PCS_Fettoxidation |
| Secondary ID |
|
| Status |
Completed |
| Phase |
|
| First received |
|
| Last updated |
|
| Start date |
April 1, 2021 |
| Est. completion date |
May 21, 2024 |
Study information
| Verified date |
June 2024 |
| Source |
University of Witten/Herdecke |
| Contact |
n/a |
| Is FDA regulated |
No |
| Health authority |
|
| Study type |
Observational
|
Clinical Trial Summary
Post-COVID-19 Syndrome (PCS) is characterized by symptoms, including fatigue, reduced
physical performance, dyspnea, cognitive impairment, and psychological distress. The
mechanisms underlying the onset and severity of PCS point to mitochondrial dysfunction as
significant contributor. This study examined fat oxidation as a function of mitochondrial
capacity during exercise.
Description:
Post-COVID-19 Syndrome (PCS), also known as post-acute sequelae of COVID-19, manifests
following an acute infection with the SARS-CoV-2 virus (COVID-19 infection). PCS is
characterized by the persistence of symptoms beyond 12 weeks from the onset of infection
and/or the emergence of new symptoms within this time. Although recent guidelines offer
specific criteria to diagnose PCS, ambiguity persists due to the complex nature of its
symptomatology and the lack of definitive diagnostic tools. PCS is a multisystemic disorder
characterized by symptoms such as (chronic) fatigue, diminished physical performance,
muscular weakness and pain, dyspnea, cognitive impairments and alterations of the autonomous
nervous system, as well as mental and psychological distress. The severity of symptoms varies
widely among patients, from mild impairment to significant restrictions in daily activities,
potentially leading to partial or complete incapacity to work. Of note, the severity of the
acute infection does not predict the onset or severity of PCS. Even though many patients
experience gradual recovery without specific treatment, there is a substantial need for
effective medical rehabilitation, especially for those with persistent PCS. To this respect,
exercise-based programs have been shown to induce significantly exercise capacity as well as
higher quality of life, reduced fatigue, and less depression. Despite ongoing investigations,
the mechanisms contributing to the onset and severity of PCS remain largely unknown. Factors
may include endothelial dysfunction and detrimental effects on the microvasculature, as well
as a "cytokine storm" associated with excessive oxidative stress and subsequent mitochondrial
dysfunction which has emerged as a significant potential contributor.
Notably, detrimental effects on mitochondrial function have been described as a result of
severe acute infections triggering an excessive immune response, systemic inflammation and
oxidative stress. Recent studies suggested that impaired mitochondrial function in PCS may be
associated with impaired fatty acid oxidation (FatOx) which can be identified using
cardiopulmonary exercise testing (CPET). Currently, the number of PCS patients characterized
for changes in FatOx using CPET is low and associations with signs and symptoms of PCS such
as fatigue have not been reported in detail. Moreover, reports on the potential of
exercise-based rehabilitation to restore FatOx capacity in PCS are not available. Thus, the
current study aimed to investigate if analysis of breath-by-breath spirometric data followed
by an estimation of individual FatOx capacity can be used for the stratification of PCS
patients. We hypothesized that a lower FatOx potential would be associated with PCS-specific
signs and symptoms such as mental and physical fatigue. In addition, we sought to analyze if
exercise-based rehabilitation would be effective in restoring PCS patients' FatOx capacity as
a sign of improved mitochondrial function.
