RESUMO
Sarcopenia is the involuntary loss of skeletal muscle mass and strength that occurs with aging, resulting in physical frailty. One potential explanation for sarcopenia is the failure of muscle to regenerate after damage, some of which may be due to changes in the function of satellite cells. Recent studies have identified novel populations of adult stem cells in skeletal muscle, such as hematopoietic stem cells. To understand the cellular mechanisms of sarcopenia, we examined the expression of satellite cells and hematopoietic stem cells in old regenerating muscles based on the expression profiles of several markers related to those cells.
Assuntos
Células-Tronco Hematopoéticas/fisiologia , Músculo Esquelético/citologia , Músculo Esquelético/fisiopatologia , Regeneração/fisiologia , Células Satélites de Músculo Esquelético/fisiologia , Animais , Senescência Celular/fisiologia , Células-Tronco Hematopoéticas/citologia , Músculo Esquelético/lesões , Ratos , Células Satélites de Músculo Esquelético/patologia , Fatores de TempoRESUMO
We examined the effect of running training on age-related changes in cardiac myosin isozyme composition in rats. Female Fischer 344 rats (6, 12, 20, and 27 months old) were divided into two groups: sedentary control and trained. The trained group rats were trained by treadmill running for up to 60 minutes per day, 5 days per week for 8 weeks at up to 30 m per minute. In sedentary control rats, the proportion of V1 myosin, that is, alpha-myosin heavy chain (MyHC) isoform, decreased progressively from 6 to 27 months of age. In the younger age groups (6 or 12 months old), there was a shift from V1 myosin to V3 myosin (beta-MyHC isoform) in trained hearts. However, the training program did not induce a cardiac myosin isozyme transition in older rats (20 or 27 months old). These results suggest that the mechanisms mediating the responses of cardiac muscle to running training alter during aging.