Professor Adam P. Sharples

Proteomic profiling of skeletal muscle ribosomes from higher versus lower responders to 10 weeks of resistance training Ribosome biogenesis is a key driver of resistance training (RT)-induced skeletal muscle hypertrophy in humans. However, high resolution insight into RT-induced compositional alterations in ribosomes r...

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...

Exercise training improves sarcopenic muscle function via restoration of mitochondrial quality control Mitophagy is an essential component of the mitochondrial quality control program, maintaining mitochondrial homeostasis in metabolic tissues such as skeletal muscle. With age, it is thought that mitoc...

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.

First post on Blue Sky

New pre-print!

Does muscle remember disuse muscle wasting?

Our new study shows skeletal muscle retains a molecular memory of disuse!

Young muscle shows transcriptional resilience to repeated atrophy.

Aged muscle shows exaggerated susceptibility.

doi.org/10.1101/2025...

A heavy lift from a literal strongman, PhD candidate PJ Koopmans “The Age-Dependent Resident Myonuclear Multi-Omic Response to a Skeletal Muscle Hypertrophic Stimulus” 💪🏻 www.biorxiv.org/content/10.1...

Played a small part in this project, but there some really interesting and cool findings from the Sharples Lab here. Focus on the memory of repeat muscle atrophy in human skeletal muscle 💪