Role of Myofibrillar Protein Catabolism in Development of Glucocorticoid Myopathy: Aging and Functional Activity Aspects

Abstract

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 MyHC in myopathic muscle, shows that these changes of contractile and elastic proteins are the result of increased catabolism of the abovementioned 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 AMP-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 are leading to the qualitative remodeling of muscle fibers. As a result of these changes, possible maximal muscle strength is increasing. 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 exercise 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 oxidative capacity. The aim of the present short review is to assess the role of myofibrillar protein catabolism in the development of glucocorticoid-caused myopathy from aging and physical activity aspects.

Changes in Body Composition of Old Rats at Different Time Points After Dexamethasone Administration

“…The present study shows that in old rats ST muscle mass has a tendency to decrease after hormone treatment. The catabolic action of both aging and glucocorticoids depend on the activity of muscles [27]. Soleus muscle remained unchanged throughout 10 days of dexamethasone treatment, which is in agreement with previous publications showing that glucocorticoids have different catabolic effects among slow and fast fiber type muscles [28-30].…”

Precocious glucocorticoid exposure reduces skeletal muscle satellite cells in the fetal rat

“…Although secondary fibers mostly mature into fast fibers, a small proportion, transition from embryonic to neonatal to slow MyHC. In adult muscle, pharmacological doses of GLC produce a fast-to-slow fiber-type transformation and selective atrophy of fast fibers (Polla et al 1994; Seene & Kaasik 2016). Hind limb muscles of DEX fetuses contained a relatively greater abundance of MyHC-slow than CON muscles with proportionately lower MHC-neo and, importantly, no difference in MHC-emb.…”

Improvement in muscular strength and aerobic capacities in elderly people occurs independently of physical training type or exercise model

“…This combination seems important because each of these exercise types has different effects on the organs. Adaptations to strength training promote improvements in muscle strength and hypertrophy, neural adaptations, increases in motor unit recruitment, increases in maximum motor unit firing rate, and increases in neuronal excitability 14,15. On the other hand, aerobic resistance training induces central and peripheral adaptations that increase VO 2 max and the ability of skeletal muscle to generate energy through oxidative metabolism without a concurrent increase in muscle strength or hypertrophy 16.…”