fibers over "fast twitch" or type II fibers. The rate of muscle loss is dependent on exercise level, co-morbidities, nutrition and other factors. There are many proposed mechanisms of sarcopenia and is considered to be the result of changes in muscle synthesis signalling pathways and gradual failure in the satellite cells which help to regenerate skeletal muscle fibers, but is incompletely understood. Sarcopenia can lead to reduction in functional status and cause significant disability but is a distinct condition from cachexia although they may co-exist. In 2016 an ICD code for sarcopenia was released, contributing to its acceptance as a disease entity. Intrinsic muscle diseases Muscle diseases, such as muscular dystrophy, amyotrophic lateral sclerosis (ALS), or myositis such as inclusion body myositis can cause muscle atrophy. Central nervous system damage Damage to neurons in the brain or spinal cord can cause prominent muscle atrophy. This can be localized muscle atrophy and weakness or paralysis such as in stroke or spinal cord injury. More widespread damage such as in traumatic brain injury or cerebral palsy can cause generalized muscle atrophy. Peripheral nervous system damage Injuries or diseases of peripheral nerves supplying specific muscles can also cause muscle atrophy. This is seen in nerve injury due to trauma or surgical complication, nerve entrapment, or inherited diseases such as Charcot-Marie-Tooth disease. Medications Some medications are known to cause muscle atrophy, usually due to direct effect on muscles. This includes glucocorticoids causing glucocorticoid myopathy or medications toxic to muscle such as doxorubicin. Endocrinopathies Disorders of the endocrine system such as Cushing's disease or hypothyroidism are known to cause muscle atrophy. Pathophysiology Muscle atrophy occurs due to an imbalance between the normal balance between protein synthesis and protein degradation. This involves complex cell signalling that is incompletely understood and muscle atrophy is likely the result of multiple contributing mechanisms. Mitochondrial function is crucial to skeletal muscle health and detrimental changes at the level of the mitochondria may contribute to muscle atrophy. A decline in mitochondrial density as well as quality is consistently seen in muscle atrophy due to disuse. The ATP-dependent ubiquitin/proteasome pathway is one mechanism by which proteins are degraded in muscle. This involves specific proteins being tagged for destruction by a small peptide called ubiquitin which allows recognition by the proteasome to degrade the protein. Diagnosis Screening for muscle atrophy is limited by a lack of established diagnostic criteria, although many have been