Disuse-induced muscle-type specific alterations and adiponectin pathway response in male mice.

Disuse-mediated Muscle Atrophy (DMA) causes persistent muscle weakness, limiting exercise training as a treatment. Adiponectin (ApN) emerged as a therapeutic candidate for muscle disorders. However, the effect of DMA on the ApN pathway remains poorly studied. Given ApN's metabolic effects, examining the ApN pathway response to disuse in relation with muscle type is essential. To mimic DMA while avoiding confounding factors, we combined HindLimb Unloading with Immobilization (HLUI) through a device allowing mouse displacements. The effects of disuse on DMA severity were studied in the slow-twitch Soleus and the fast-twitch Tibialis anterior (TA) muscles, together with the ApN pathway. The Soleus muscle presents a moderate atrophy of type IIa myofibers, whereas the TA muscle is more severely affected and exhibits a type I to IIa switch. HLUI increased the hybrid I/IIa myofiber proportion in both muscles, suggesting an ongoing myofiber switch that is delayed in the Soleus muscle. Concomitantly, HLUI enhances ApN plasma level, modifies oligomeric form proportions, and downregulates Adiporeceptors in the Soleus but not in the TA muscle. In conclusion, HLUI is associated with a higher ApN plasma level and disturbances in oligomeric form proportions. DMA severity, myofiber switch kinetics, and adiporeceptor regulation are muscle-type dependent.