Figure 1.

Role of mitochondrial bioenergetics and proteostasis in mediating skeletal muscle quality in older adults. Left panel, Sarcopenia is associated with mitochondrial dysfunction, which encompasses impaired bioenergetics and turnover. The impairment results in increased reactive oxygen species (ROS) generation and chronic low-grade inflammation, leading to impaired muscle proteostasis. The derangement in proteostasis impedes mitochondrial turnover, resulting in an accumulation of dysfunctional mitochondria and further exacerbation of organelle and tissue dysfunction. Right panel, Targeting mitochondrial bioenergetics and turnover by therapeutics and exercise impedes the age-associated rise in ROS and systemic inflammation, which results in the maintenance of muscle proteostasis. The maintained protein turnover allows for the removal of damaged proteins, such as dysfunctional mitochondria and damaged contractile proteins, while also synthesizing new functional proteins. Collectively, this leads to preservation of mitochondrial quality, muscle mass, and strength.