ABSTRACT
Aging is a multifactorial process leading to changes in skeletal muscle quantity and quality, which cause muscle weakness and disability in the aging population. Muscle weakness in corticosteroid myopathy is mainly the result of the destruction and atrophy of the myofibrillar compartment of fast-twitch muscle fibers. Decrease of titin and myosin, and the ratio of nebulin and myosin heavy chain (MyHC) in myopathic muscle, shows that these changes of contractile and elastic proteins are the result of increased catabolism of the above mentioned proteins in skeletal muscle. Slow regeneration of skeletal muscle is in good correlation with a decreased number of satellite cells under the basal lamina of muscle fibers.
Aging causes a reduction of adenosine monophosphate-activated protein kinase (AMPK) activity as the result of the reduced function of the mitochondrial compartment. AMPK activity increases as a result of increased functional activity. Resistance exercise causes anabolic and anticatabolic effects in skeletal muscle: muscle fibers experience hypertrophy while higher myofibrillar proteins turn over. These changes lead to the qualitative remodeling of muscle fibers. As a result of these changes, possible maximal muscle strength increases. Endurance exercise improves capillary blood supply, increases mitochondrial biogenesis and muscle oxidative capacity, and causes a faster turnover rate of sarcoplasmic proteins as well as qualitative remodeling of type I and IIA muscle fibers. The combination of resistance and endurance type of physical activity (concurrent activity) may be the fastest way to prevent or decelerate muscle atrophy due to the anabolic and anticatabolic effects of exercise combined with an increase in the oxidative capacity of skeletal muscle. Concurrent resistance and endurance type of physical activity is an effective measure in the elderly and corticosteroid myopathic patients which improve muscle metabolism and thereby muscle function and life quality.
