Ebbing Strength, Fading Power: Unveiling the Impact of Persistent Fatigue on Muscle Performance in COVID-19 Survivors, 2024, Kowal et al.

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Ebbing Strength, Fading Power: Unveiling the Impact of Persistent Fatigue on Muscle Performance in COVID-19 Survivors
Kowal, Mateusz; Morgiel, Ewa; Winiarski, Sławomir; Dymarek, Robert; Bajer, Weronika; Madej, Marta; Sebastian, Agata; Madziarski, Marcin; Wedel, Nicole; Proc, Krzysztof; Madziarska, Katarzyna; Wiland, Piotr; Paprocka-Borowicz, Małgorzata

The total number of confirmed cases of COVID-19 caused by SARS-CoV-2 virus infection is over 621 million. Post-COVID-19 syndrome, also known as long COVID or long-haul COVID, refers to a persistent condition where individuals experience symptoms and health issues after the acute phase of COVID-19. The aim of this study was to assess the strength and fatigue of skeletal muscles in people recovered from COVID-19.

A total of 94 individuals took part in this cross-sectional study, with 45 participants (referred to as the Post-COVID Cohort, PCC) and 49 healthy age-matched volunteers (Healthy Control Cohort, HCC). This research article uses the direct dynamometry method to provide a detailed analysis of post-COVID survivors’ strength and power characteristics. The Biodex System 4 Pro was utilized to evaluate muscle strength characteristics during the fatigue test.

The fatigue work in extensors and flexors was significantly higher in the PCC. The PCC also showed significantly less power in both extensors and flexors compared to the HCC.

In conclusion, this study provides compelling evidence of the impact of post-COVID-19 fatigue on muscle performance, highlighting the importance of considering these effects in the rehabilitation and care of individuals recovering from the virus. PCC achieved lower muscle strength values than HCC.

Link | PDF (Sensors) [Open Access]
 
It contradicts.

However, this group was hospitalised, some on O2, others needing drugs including antibiotics, steroids or baricitinib, but none requiring invasive mechanical ventilation or other ICU support. But they do say —

Both study groups met WHO recommendations for physical activity.

They ask "what are the mechanisms causing this?"

Investigating the potential role of factors such as inflammation, metabolic changes, and neurological effects in contributing to these muscle performance disparities would be valuable.

Those mechanisms may well relate to findings we've previously seen of —

1) More type IIx glycolytic fibres, evidence of atrophy and regeneration, increased necrosis as part of PEM, plus whatever the "amyloid"-staining deposits are.
Muscle abnormalities worsen after post-exertional malaise in long COVID (2024, Nature Communications)

2) Type-2b-fiber atrophy and increased numbers of tissue macrophages, increased capillary basement membrane thickness.
Post-COVID exercise intolerance is associated with capillary alterations and immune dysregulations in skeletal muscles (2023, Acta Neuropathologica Communications)

This paper summarised with —

these results suggest that individuals in the PCC experience greater work fatigue and reduced power in the knee extensors and flexors compared to those in the HCC. In contrast, no significant difference was observed in the agonist/antagonist ratio. The results suggest that post-COVID patients may exhibit lower muscle strength and work capacity and greater fatigue compared to healthy controls. The effect sizes for these differences, as measured by Cohen’s d, were significant for most variables.

The most noteworthy finding was the lower relative peak torque to body weight in the PCC compared to the HCC, with large effect sizes. This suggests that individuals in the PCC had significantly weaker knee extensors and flexors, which might directly affect their overall physical performance, mobility, and quality of life.

work fatigue (or strength loss) is seldom reported in the literature. Generally, it is recognised in the literature that work fatigue can significantly affect the performance of knee flexors and extensors. Fatigue can result in a decrease in muscle power output, which could potentially affect the work produced by these muscles.

In conclusion, this study provides compelling evidence of the impact of post-COVID-19 fatigue on muscle performance

Screenshot 2024-02-25 at 5.09.07 PM copy.jpg
 
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(a late cross-post with SNT - apologies for any repetition)

Polish study

Hospitalised Covid-19 patients, but not severe disease or significant comorbidities. All had had Covid-19 pneumonia.
Patient cohort: 23 female, 22 male; healthy cohort similar
Young cohort - Patient cohort mean 38 years; healthy cohort similar - 20 to 50 year age range
35 of the 45 patients reported fatigue

Time between hospital discharge and study commencement - 8 to 26 weeks (that's quite a range, including relatively soon after discharge)

Biodex system (electrically adjustable dynamometer) used to assess knee flexor and extensor strength and power.
Four trials of 30 flex repetitions.


Looks to have been well done. 11 parameters measured e.g. PEAK TORQUE normalised by body weight;
WORK FATIGUE—the ratio of work in the last third to work in the first third (reduced by 100%) and expressed as a percentage.

Results
In comparing the Post-COVID Cohort (PCC) and the Healthy Control Cohort (HCC), there were significant differences in numerous knee extensor and flexor performance measures, with large effect sizes evident in most parameters
The results suggest that post-COVID patients may exhibit lower muscle strength and work capacity and greater fatigue compared to healthy controls. The effect sizes for these differences, as measured by Cohen’s d, were significant for most variables.
The most noteworthy finding was the lower relative peak torque to body weight in the PCC compared to the HCC, with large effect sizes. This suggests that individuals in the PCC had significantly weaker knee extensors and flexors, which might directly affect their overall physical performance, mobility, and quality of life.
The finding that the PCC took longer to reach peak torque for extensors might imply that their muscles cannot generate force rapidly, which could indicate impaired muscle power.

They noted another study that also found reduced muscle performance, but also reduced muscle mass, I guess implying that deconditioning might be a cause. This group however call for more research to understand the mechanism. The referenced studies might be interesting.
A pivotal study by Chandra et al. [39], outlined the direct and indirect mechanisms through which SARS-CoV-2 affects skeletal muscle cells and the inflammatory responses triggered by the virus. This aligns with our observation of strength loss in COVID-19 survivors, suggesting a potential link between these molecular mechanisms and the clinical manifestations of muscle weakness and fatigue. Furthermore, our findings contribute to the broader discourse on COVID-19′s musculoskeletal impact, as reported by Awosanya et al. [40], which emphasizes the multifaceted nature of the virus’s effects on musculoskeletal health, including bone loss and altered osteoclastogenesis. These insights collectively underscore the need for a comprehensive evaluation of COVID-19 survivors, considering both molecular and functional aspects.


Longitudinal data would be great - ideally from as early as possible after the triggering disease.
In terms of methodology, the study’s cross-sectional design provides a snapshot of the condition but lacks longitudinal data, which would be crucial in understanding the progression and potential recovery of muscle strength post-COVID-19.

I like these researchers - clear write-up, they don't over claim and seem ready to investigate further.
In light of these considerations, the authors suggest caution in interpreting the study’s findings, acknowledging that they represent a specific subset of COVID-19 survivors. This study lays the groundwork for further research, emphasising the need for more comprehensive investigations to fully understand the long-term musculoskeletal impacts of COVID-19.

Edit - they noted their sample size as a limitation :). 45 in the patient cohort? Luxury. The NIH can make conclusions with 15, or even 8....
 
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