Is Long Covid a Real Disease?

Surprisingly, Long Covid has divided the scientific community in a way that could not have been anticipated. What is the recent science showing us?

Note the weekly working hours are significantly reduced for the long covid cohort.

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SDH activity was not reduced in healthy controls one day after exercise, but was reduced in the long COVID patients, suggesting that the combination of a reduced maximal mitochondrial respiration and decreased mitochondrial content are part of the pathophysiology of post-exertional malaise.

Maximal pulmonary oxygen uptake (V̇O2max, A, n =23 long COVID, n = 21 healthy control), peak power output (B, n = 25 long COVID, n = 21 healthy control) and gas exchange threshold (C, n = 23 long COVID, n = 21 healthy control) were all lower (p<0.0001, p=0.001 and p = 0.014, respectively)in patients with long COVID compared to healthy controls.

It has been hypothesized that amyloid-containing deposits in the circulation can block local perfusion in long COVID, causing ischemia reperfusion injury.

We demonstrate that the concentration of amyloid containing deposits was greater in the skeletal muscle of long COVID patients at baseline, and increased similarly in both groups after the induction of post-exertional malaise.

Appelman, Brent, et al. "Muscle abnormalities worsen after post-exertional malaise in long COVID." Nature communications 15.1 (2024): 1-15.