There are multiple theories proposed to explain the mechanisms of muscle changes of<unk>  including changes in satellite cell recruitment, changes in anabolic signalling, protein oxidation, inflammation, and developmental factors. The pathologic changes of<unk>  include a reduction in muscle tissue quality as reflected in the replacement of muscle fibers with fat, an increase in fibrosis, changes in muscle metabolism, oxidative stress, and degeneration of the neuromuscular junction. The distribution of muscle fibers types also changes in<unk>  muscle causing a decrease in type II muscle fibers, or "fast twitch," with little to no decrease in type I muscle fibers, or "slow-twitch" muscle fibers. Deinervated type II fibers are often converted to type I fibers by reinnervation by slow type I fiber motor nerves. The failure to activate satellite cells upon injury or exercise is also thought to contribute to the pathophysiology of<unk> . Additionally, oxidized proteins can lead to a buildup of lipofuscin and cross-linked proteins causing an accumulation of non-contractile material in the skeletal muscle and contribute to<unk>  muscle. An apparent protective factor is sufficient levels of the protein BNIP3, which prevents cells' buildup of damaged mitochondria. Deficiency of BNIP3 leads to muscle inflammation and atrophy.
Sarcopenia
Urinary incontinence
Orthostatic intolerance
Hyperesthesia
Gastroparesis
Arachnophobia
Dynapenia
Dyscopia