Muscle abnormalities worsen after post-exertional malaise in long COVID

The study “Muscle abnormalities worsen after post-exertional malaise in long COVID” provides crucial insights into the pathophysiology of long COVID, particularly focusing on post-exertional malaise (PEM) and its effects on skeletal muscle.

Here’s a detailed summary:

Background: Long COVID, characterized by symptoms persisting for months after acute SARS-CoV-2 infection, commonly includes limited exercise tolerance and PEM. This study aimed to understand the underlying biology of these symptoms, especially the role of skeletal muscle structure and metabolic function​​.

Methodology: The study involved 25 long COVID patients and 21 control participants who had recovered from a mild SARS-CoV-2 infection. Participants underwent cardiopulmonary exercise tests, and the researchers collected blood and skeletal muscle biopsies before and after these tests to analyze changes related to PEM induction​​.

Findings on Exercise Capacity: Long COVID patients exhibited significantly lower exercise capacity, evidenced by reduced maximal oxygen uptake and peak power output. This limitation was not due to compromised cardiovascular or ventilatory function but appeared related to peripheral skeletal muscle impairments. The study noted a higher proportion of fatigable glycolytic fibers and signs of mitochondrial dysfunction in long COVID patients​​.

Metabolic Dysfunction and Post-Exertional Malaise: Post-exercise, all long COVID patients experienced PEM, with symptoms like muscle pain, increased fatigue, and cognitive issues. The study found a correlation between these symptoms and metabolic and mitochondrial dysfunction in the skeletal muscle​​.

Amyloid-Containing Deposits: Researchers observed a higher concentration of amyloid-containing deposits in the skeletal muscle of long COVID patients, both at baseline and post-exercise. These deposits were not located in capillaries or lymphatic vessels, challenging the hypothesis that they contribute to tissue hypoxia by blocking vessel perfusion​​.

Exercise-Induced Myopathy: Long COVID patients showed signs of exercise-induced myopathy, including small atrophic fibers and focal necrosis, which worsened after exercise. This suggests exacerbated muscle tissue damage in these patients, contributing to PEM symptoms like muscle pain and fatigue​​.

Conclusion: The study concluded that long COVID is associated with a shift in skeletal muscle towards a less oxidative, more glycolytic phenotype, which contributes to reduced exercise capacity. However, this shift does not fully explain the rapid onset of PEM following exercise. The findings suggest that long COVID’s impact on skeletal muscle might lead to a vicious cycle of reduced exercise capacity and exacerbated muscle metabolism and damage following PEM. The study calls for further research into the role of chronic endotheliitis, reduced blood flow, and amyloid deposits in long COVID’s pathophysiology​​.

Overall, this study sheds light on the complex interplay of skeletal muscle alterations and metabolic changes in long COVID, contributing to our understanding of its debilitating impact on patients’ exercise capacity and quality of life.

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