Rob Wüst

🧵 THREAD: Skeletal Muscle Alterations in Long COVID and ME/CFS 1/ 💡 Study Overview We studied whether skeletal muscle changes in Long COVID and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) patients are due to inactivity or distinct pathological processes.

@mackinprof Sorry to hear you have to continue to defend publishing these big summary papers🥴. This paper is extremely helpful with providing an in-depth overview of resistance training for practical and academic use 🤩

It's a huge summary that now allows folks to say this is the case with evidence and it goes well beyond RWE.

@davidjglassMD Great study! Congratulations

Humans with function-disrupting variants in the myostatin gene (MSTN) have increased skeletal muscle mass and strength, and less adiposity nature.com/articles/s4146…

Congrats @ThibauxV & @TeamDerave on this well deserved award! 🥇 Super cool work on histamine signaling in skeletal muscle!

Heb jij #postCOVID en PEM? Doe mee met de #PEM #Pacing #studie! Onze studie onderzoekt hoe PEM beter meetbaar kan worden gemaakt, met als doel pacing-strategieën verder te verbeteren en mensen te helpen om veiliger binnen hun grenzen te bewegen. Kijk op pempacingstudie.nl

@MichelleBull4 @MEResearchUK Great I am picking my nose in public 😵‍💫😱

@MEResearchUK @RobWust

Pictured at yesterday's 'M.E. & Long COVID research' symposium' in Winchester is Prof Rob Wüst one of the 3 ME Research UK-funded researchers presenting. Read more of Professor Wüst's reseach funded by our supporters - tinyurl.com/49v22p9u

@HornbergerLab Coolio, I emailed earlier this week:).

@RobWust Take a look at the details in the manuscript and then let me know if you think a collaboration is still viable with the samples you have. Feel free to email me.

1/ Why do muscles atrophy with aging and disuse? Is it because each tiny little myofibril gets smaller… or is it because we lose myofibrils? In our new study, we addressed this in humans and mice. biorxiv.org/cgi/content/sh… Full breakdown of the findings in this thread 👇

@HarrySpoelstra @MarionKoopmans Remember that people can develop other diseases too, and a WHO definition is not applicable to people who do not test. You will never be able to causally prove your argument unfortunately. I look to your scientific paper addressing these issues,and surviving peer review scrutiny

Sorry, with all due respect for your excellent PCC contributions, I think you're biased and not fully in contact with our daily experiences. A further major problem with this study is their "self constructed PCC definition." The VASCO study’s conclusion of near-zero excess risk of post-COVID-19 condition after mild Omicron JN.1 infections is also misleading because the authors deliberately chose a narrow, self-constructed, high-threshold definition of “incident PCC-related symptoms” that is much stricter than the official WHO definition, thereby capturing only pronounced new or worsened moderate-to-severe symptoms while systematically excluding milder, fluctuating, borderline, or patient-perceived complaints that still qualify as PCC under WHO criteria and are reported at significantly higher rates in the study’s own self-attribution data and in today's broader Omicron-era research.🤔

thelancet.com/journals/lanep… risk of post covid condition no longer detectable in new infections

@HarrySpoelstra @MarionKoopmans Nou, dat er dus dagelijks veel nieuwe patienten bijkomen na reinfectie valt dus wel mee, dat laat deze wetenschappelijke studie zien. Ik ken de groep, en heb geen reden om te twijfelen aan deze data

@RobWust @MarionKoopmans Sorry Rob, natuurlijk willen we van C19 en LC verlost worden, wie niet? De werkelijkheid is helaas anders, met dagelijks nog nieuwe patiënten o.a. na reinfecties. Struisvogel politiek gebaseerd op slechte science helpt niemand. Study needs a major overhaul!😷

@HarrySpoelstra @MarionKoopmans Hoi Harry, dit is toch goed nieuws? of probeer je juist deze resultaten extra negatief te interpreteren? Had je liever gezien dat er nu nog steeds veel mensen long COVID ontwikkelen?

A further majoer problem is their limited Power and Wide Confidence Intervals: With 5621 matched pairs, the study is large, but the low event rates lead to wide 95% CIs around excess prevalence estimates (e.g, 0.2% at 90 days: -1.9% to 2.3%; p=0.84). These intervals include small positive effects (up to ~2–3%), meaning the true excess could be much higher but undetected due to insufficient power for rare/severe outcomes. The study notes no significant XBB.1.5 booster effect on PCC, but this subgroup analysis (unmatched, adjusted models) had even less power!!!

@HornbergerLab Hi Troy, great work! We have some human bed rest muscle biopsies, including plenty of electron microscopy images of Z-disk lengths which might be interesting for this too. Happy to chat about collaboration! R

8/ Take Home: Across species and conditions, the loss of myofibrils is a central and conserved mechanism of muscle fiber atrophy. Changes in myofibril CSA play a smaller, context-dependent role. Treatments for sarcopenia and disuse atrophy should target myofibril turnover.

Now recruiting an experienced Post‑Doc in Skeletal Muscle Molecular Physiology @nih_sognsvann Oslo, Norway Join our multi‑omics EMMA project on mitochondrial epigenetic memory in human muscle aging. 4‑year position Start May 2026 Apply via Jobbnorge: jobbnorge.no/en/available-j…

Thrilled to share our new @ScienceAdvances paper where we provide evidence that mechanical stimuli drive skeletal muscle growth through TWO distinct mechanisms—and use BONCAT to visualize where the growth occurs. Take a look: science.org/doi/10.1126/sc…

@PutrinoLab @KasperJanssen - Long COVID is not a uniform condition. - Training may be valuable, but not for everyone, and not in the same way. - Careful phenotyping and more biomedical research remain crucial. Scientific dialogue is how we move the field forward!

@PutrinoLab @KasperJanssen We wrote this response because we believe nuance is essential in the current debate. The AHA statement suggests that exercise intolerance in Long COVID may partly be explained by deconditioning, and that exercise training can be beneficial.

Today our response was published in British Journal of Sports Medicine, addressing the recent scientific statement by the American Heart Association in Circulation on exercise intolerance in Long COVID. 🔗 bjsm.bmj.com/content/early/… with @PutrinoLab @KasperJanssen

@PutrinoLab @KasperJanssen This has important implications. If symptoms are driven (at least in part) by dysregulated physiology rather than simple deconditioning, exercise prescriptions must be cautious and individualized.

@PutrinoLab @KasperJanssen In our view, that explanation is incomplete. For a subgroup of patients, additional mechanisms are likely involved, including autonomic dysfunction and post-exertional malaise (PEM).

@mecfsskeptic I feel that I have to respond to this. The letter is a response to the AHA statement about cardiovascular alterations in long covid (reference in the letter), being mainly driven by deconditioning. We focus therefore on long covid and not on ME.

3) One issue is that post-exertional malaise (PEM) is described as "a defining feature of Long Covid." PEM is the defining feature of ME/CFS, not of Long Covid. If PEM is common in Long Covid, it's likely because a substantial subgroup of Long Covid patients has ME/CFS.

1) "Incorporating PEM into a new conceptual model of long covid cardiac rehabilitation programmes is essential to clinically distinguish it from cardiovascular deconditioning and to safeguard patients from unintended harm"

Mr Beast lined up one person from each age 1-100 and had them race to a finish line, and the overhead camera is an oddly beautiful data visualization of speed by age.