Skeletal Muscle Reloading After Disuse Acutely Elevates Autophagy and Myogenesis Markers

Muscle atrophy from disuse, such as prolonged bed rest or microgravity, leads to significant loss of muscle mass and function. Understanding the molecular mechanisms governing muscle recovery upon reloading is crucial for developing effective rehabilitation strategies. Autophagy, a cellular recycling process, and myogenesis, muscle regeneration, are critical pathways involved in muscle adaptation and repair. This study investigates their acute response during recovery.

Initially, after 14 days of hind limb suspension, no significant changes were observed in the expression of autophagy or myogenesis markers compared to baseline. However, upon acute reloading (at day 1), a notable increase occurred in both inhibitory and activating phosphorylation of ULK1. This acute reloading also led to an increase in LC3B mRNA expression, a key marker for autophagosome formation. Furthermore, P62 mRNA and protein expression, indicative of autophagy flux and substrate accumulation, were also elevated. These findings suggest a rapid activation of both autophagy and myogenesis pathways during the initial phase of muscle recovery.