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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Patients with chronic kidney disease (CKD) often show a decline in skeletal muscle mass and function, recognized as uremic sarcopenia, impairing physical function. Physical training and exercise are highly recommended for the prevention and treatment of sarcopenia, but are poorly tolerated by elderly and frail patients with CKD. Electrical stimulation of skeletal muscles has been studied as a substitute method, which is unfortunately not optimized or practical in terms of effectiveness and safety concerns. Magnetic stimulation (MS) has recently attracted attention as an alternative ergogenic strategy to provoke skeletal muscle contraction by inducing an electric field non-contact and non-invasively based on Faraday's law of induction. Our study therefore aimed to investigate the effect of MS application on rat skeletal muscle atrophy model.
Muscle atrophy was induced in rats by spiral wire immobilization (SWI) of the hindlimbs. Rats were divided into the control, spiral wire immobilization (SWI), and SWI+ MS groups. MS was applied using a magnetic stimulator (Cool-40 Rat coil, MagVenture, Denmark), and the stimulation parameters were set at 30 Hz, intensity 25%, 800 trains, 12,000 pulses/day for 5 days. Then, rats were sacrificed to harvest soleus (SOL) and gastrocnemius (GC) muscles for pathological evaluation and unbiased comprehensive molecular analysis, RNA-seq analysis and metabolomics.
The total body weight and the wet weight of the SOL and GC muscles decreased in the SWI group. Intriguingly, in the SWI+MS group compared to the SWI group, the weight of GC muscle (SWI+MS 0.654 ± 0.024 g vs SWI 0.599 ± 0.01 g, p<0.05) and maximal knee extension twitch torque (SWI+MS 110.49 ± 8.57 mNm versus SWI 84.57 ± 6.61 mNm, p<0.05) were greater. Cross sectional areas of GC muscles of the SWI+MS group were also larger than that of the SWI group (p<0.0001). RNA-seq identified 469 genes that were down-regulated by SWI, 190 genes that were up-regulated by MS, and 15 overlapping genes, which were suggested to have been restored by MS. Notably, Gda (guanine deaminase), a regulator of purine metabolism, was reactivated by MS, suggesting a role in muscle recovery. Metabolome profiling indicated altered glutathione metabolism in SWI muscles, whereas MS influenced purine metabolism.
MS improved the weight and function of atrophied GC muscles of the rat model with immobilization-induced muscle atrophy. RNA-seq analysis and metabolome analysis pinpointed purine metabolism as a central mechanism by which MS affects skeletal muscle. MS has the potential to be a safe therapeutic option to prevent or treat uremic sarcopenia.
