Functional and Morphological Differences of Muscle Mitochondria in Chronic Fatigue Syndrome and Post-COVID Syndrome, 2024, Bizjak et al.

[SNT Gatchaman]

Functional and Morphological Differences of Muscle Mitochondria in Chronic Fatigue Syndrome and Post-COVID Syndrome
Bizjak, Daniel Alexander; Ohmayer, Birgit; Buhl, Jasmine Leonike; Schneider, Elisabeth Marion; Walther, Paul; Calzia, Enrico; Jerg, Achim; Matits, Lynn; Steinacker, Jürgen Michael

Patients suffering from chronic fatigue syndrome (CFS) or post-COVID syndrome (PCS) exhibit a reduced physiological performance capability. Impaired mitochondrial function and morphology may play a pivotal role. Thus, we aimed to measure the muscle mitochondrial oxidative phosphorylation (OXPHOS) capacity and assess mitochondrial morphology in CFS and PCS patients in comparison to healthy controls (HCs).

Mitochondrial OXPHOS capacity was measured in permeabilized muscle fibers using high-resolution respirometry. Mitochondrial morphology (subsarcolemmal / intermyofibrillar mitochondrial form / cristae / diameter / circumference / area) and content (number and proportion/cell) were assessed via electron microscopy. Analyses included differences in OXPHOS between HC, CFS, and PCS, whereas comparisons in morphology/content were made for CFS vs. PCS.

OXPHOS capacity of complex I, which was reduced in PCS compared to HC. While the subsarcolemmal area, volume/cell, diameter, and perimeter were higher in PCS vs. CFS, no difference was observed for these variables in intermyofibrillar mitochondria. Both the intermyofibrillar and subsarcolemmal cristae integrity was higher in PCS compared to CFS. Both CFS and PCS exhibit increased fatigue and impaired mitochondrial function, but the progressed pathological morphological changes in CFS suggest structural changes due to prolonged inactivity or unknown molecular causes. Instead, the significantly lower complex I activity in PCS suggests probably direct virus-induced alterations.

Link | PDF (International Journal of Molecular Sciences)

 

[poetinsf]

Sick people have difficulty generating energy, duh. I don't understand why they keep comparing with HC when they should compare it with similarly sick people and deconditioned people. How about comparing with other chronically sick people like sinus infection or Lymes?

Can other conditions cause mitochondrial diseases?
Yes. Mitochondrial dysfunction occurs when mitochondria don’t work as well as they should due to another disease or condition. Many conditions can lead to secondary mitochondrial dysfunction,

 

[Andy]

CCC criteria for the ME/CFS cohort. Frustratingly, as far as I could see, they don't report if they recorded length of illness, even though they use (unspecified) length of illness as a possible explanation for the difference between PCC and ME/CFS cohorts.

 

[SNT Gatchaman]

they should compare it with similarly sick people and deconditioned people

The controls were healthy, sedentary.

Healthy age-matched unfit individuals (N = 13, 7f/6m; age 36.2 ± 13.2 years; BMI 25.1 ± 4.5 kg/m 2) were used as control group.

as far as I could see, they don't report if they recorded length of illness

They do give time since diagnosis in table 1. Possibly some CFS were > 7 years from diagnosis. (Presumably PCS were not sub-grouped if diagnosed prior to the pandemic (so ≤4 yrs), whereas CFS might have been during the pandemic.)

"CFS" 35.2 ± 44.06 months
"PCS" 20.47 ± 15.56 months

The sex ratios are quite unbalanced —

HC 7F/6M
CFS 10F/5M
PCS 13F/2M

 

[ME/CFS Skeptic]

As far as I can see Mitochondrial oxidative phosphorylation (OXPHOS) capacity was not significantly different in the 15 ME/CFS patients compared to controls (figure 1).

The interesting part of this study is that they took muscle biopsies but I don't really understand the results. Anyone who can make a comparison to the study by Appelman et al.?

 

[EndME]

As far as I can see Mitochondrial oxidative phosphorylation (OXPHOS) capacity was not significantly different in the 15 ME/CFS patients compared to controls (figure 1).

The interesting part of this study is that they took muscle biopsies but I don't really understand the results. Anyone who can make a comparison to the study by Appelman et al.?

Rob Wüst (Appelman et al) has said on Twitter that he can neither meaningfully interpret the study results (including the earlier ones of Scheibenbogen) nor that he is able to compare them to the results to his study.

www.twitter.com/RobWust/status/1755111198096245100