Lack of muscle recovery after immobilization in old rats does not result from a defect in normalization of the ubiquitin-proteasome and the caspase-dependent apoptotic pathways.

摘要

Immobilization periods increase with age because of decreased mobility and/or because of increased pathological episodes that require bed-rest. Then, sarcopaenia might be partially explained by an impaired recovery of skeletal muscle mass after a catabolic state due to an imbalance of muscle protein metabolism, apoptosis and cellular regeneration. Mechanisms involved during muscle recovery have been little studied and in elderly they remain almost unknown. We show, in rats, that a short immobilization period during ageing initiated muscle atrophy that was indeed not recovered after 40 days. Immobilization was associated with an activation of both the ubiquitin-proteasome and the mitochondria-associated apoptotic pathways and the inflammatory and redox processes, and a decrease of cellular regeneration. We show that the lack of muscle recovery during ageing is not due to a defect in proteolysis or apoptosis down-regulation. These observations lead us to hypothesize that muscle protein synthesis activation after immobilization was altered during ageing.