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We are recruiting a Post‑Doc in Skeletal Muscle Molecular Physiology, Oslo, Norway
Join our EMMA multi‑omics project on mitochondrial epigenetic memory in human muscle ageing.
4‑year position. Start May 2026.
Apply: www.jobbnorge.no/en/available...
Grateful to the full team and collaborators: Raastad, Jarvis, Bodine, @hughesdc-muscle.bsky.social, Owens, Treebak, Dalbram, Ullrich, Christiansen, Sutherland, Boot, Wozniak, Mein, Seynnes, Hallen, Dalen and Ødemark
Special thanks to amazing researcher Daniel Turner!
Thanks to the Research Council of Norway (RCN 314157) for funding this work
Huge thanks to all participants who volunteered to lose muscle (twice!) so we could understand how muscle responds to repeated disuse
Young muscle = full recovery and transcriptional resilience to repeated atrophy
Aged muscle = impaired recovery, exaggerated molecular suppression to repeated atrophy
Muscle remembers disuse, and age may determine whether that memory protects or harms
In aged rats, repeated atrophy caused the strongest reductions in mitochondrial gene expression and mtDNA content
Even when physical activity was restored, aged muscle could not recover mtDNA content
In young adults, mitochondrial genes recovered during reloading, but repeated atrophy still reduced citrate synthase and mtDNA content
Young muscle is resilient, but repeated disuse may still increase mitochondrial vulnerability over time
NAD+metabolism was highly affected
NMRK2 was consistently downregulated across atrophy periods
Aged muscle showed the largest NAD+ losses
Human muscle stem cells responded to supplementation of nicotinamide riboside with larger myotubes after atrophy
NR4A3 was the most downregulated gene & remained suppressed after initial disuse
AChR subunit genes CHRNA1 & CHRND were epigenetically primed after atrophy, showing amplified hypomethylation in humans and stronger expression in both humans & rats after repeated atrophy
Integrated DNA methylome & transcriptome data showed that aerobic metabolism & mitochondrial genes undergo coordinated hypermethylation & downregulation after disuse across species & age
In humans, NR4A1 gained recovery‑phase hypermethylation that sustains its repression
Comparing very old rats with previously published young rats found age was the key factor
Young rats recover mass after atrophy; aged rats continue to lose it
Only young muscle converts recovery into regrowth after loss
Aged muscle showed the opposite pattern
Repeated atrophy led to far more altered genes, with greater suppression of aerobic metabolism, mitochondrial & NAD‑related genes
With activation of ECM, proteasomal & DNA‑damage pathways
A detrimental molecular memory emerged with age
Young human muscle showed strong transcriptional changes after the first atrophy, but these responses were attenuated after repeated disuse
This suggests a protective molecular memory, especially in aerobic metabolism and mitochondrial genes
In aged animals, repeated disuse caused a greater loss of muscle mass and fibre size
Unlike young muscle, aged muscle did not recover during the return to habitual activity during the recovery period, and demonstrated susceptibility to repeated atrophy
In young adults, two periods of leg immobilisation caused similar losses in muscle size and strength, and full recovery
Physiologically, the repeated atrophy was not worse (except muscle quality), but the molecular responses told a different story….
Our new study is now published in Advanced Science
We show that skeletal muscle retains a molecular memory of disuse
Young muscle shows transcriptional resilience
Aged muscle shows exaggerated vulnerability
advanced.onlinelibrary.wiley.com/doi/10.1002/...
Now recruiting an experienced Post‑Doc in Skeletal Muscle Molecular Physiology @nih-sport-sciences.bsky.social Oslo, Norway
Join our multi‑omics EMMA project on mitochondrial epigenetic memory in human muscle aging
4‑year position
Start May
Apply at Jobbnorge: www.jobbnorge.no/en/available...
Excited to share our Nordic project EMMA has been awarded ≈17M DKK from The Novo Nordisk Foundation
We will study how aging reshapes epigenetic “memory” of mitochondrial function in muscle
With Tinna Stevnsner & Kristian Vissing
Proud to lead key aspects @NIH Norway
Position announcement soon!
Nice feature in @theatlantic.com by @bonnietsui.bsky.social
Our lab’s latest study reveals that skeletal muscle doesn’t just remember growth- it also remembers inactivity. Repeated disuse leaves a molecular imprint that shapes future responses.
www.theatlantic.com/health/2026/...
Nice new data from @DrMikeRoberts team!
Proteomic profiling of skeletal muscle ribosomes from higher versus lower responders to 10 weeks of resistance training
doi.org/10.1101/2025...
New @biorxivpreprint.bsky.social
Exercise training improves sarcopenic muscle function via restoration of mitochondrial quality control
doi.org/10.1101/2025...
Special thanks to collaborators Jonathan Jarvis, Sue Bodine, @hughesdc-muscle.bsky.social, Daniel Owens, Truls Raastad, Jonas Treebek, Emilie Dalbram, Max Ullrich,
Stian Christiansen, Hazel Sutherland, James Boot, Eva Wozniak and Charles Mein. As well as Olivier Seynnes, Jostein Hallen, Siri & Hege!
So thankful to have been able to work closely with the incredible Daniel C. Turner who spearheaded all the experiments!
This work was supported by the Research Council of Norway (RCN - 314157).
So grateful to all the participants who agreed to lose their muscle (twice!) and made this possible!
Key takeaway:
Muscle “remembers” disuse at the molecular level.
Young muscle = transcriptional protection.
Aged muscle = exaggerated transcriptional vulnerability.
Epigenetic marks may in-part encode this memory.
Nicotinamide riboside (NR) supplementation in human MuSCs post-atrophy improved myotube size
Suggests NAD⁺ salvage may support recovery from atrophy (with more in-vivo work required to confirm!)
NAD⁺ biosynthesis gene NMRK2 was among the most downregulated genes after both atrophy periods.
Reduced NAD⁺ levels and mtDNA loss was observed to be greatest after repeated atrophy in aged muscle.
NR4A1 stayed suppressed during recovery with hypermethylation in young muscle.
AChR genes (CHRNA1, CHRND) were epigenetically primed & upregulated after repeated disuse - suggesting a memory of atrophy in these genes.
DNA methylome analyses revealed conserved hypermethylation of mitochondrial and aerobic metabolism genes across species after disuse atrophy.
Some epigenetic marks were retained or exaggerated with repeated disuse.
In aged rats, repeated disuse led to greater muscle loss.
Despite transcriptional recovery after initial atrophy, aged muscle showed an exaggerated transcriptional suppression after repeated disuse suggesting a detrimental molecular memory.
In young adults, repeated immobilization caused similar muscle loss as initial disuse.
However, the transcriptional response was blunted-especially in aerobic metabolism & mitochondrial genes.
Suggests a protective molecular memory characterised by transcriptional attenuation.