Age-related changes - Essay Example

p53: may induce apoptosis by the induction of oxidative stress caused by an inappropriate up regulation of Mn superoxide dismutase and glutathione peroxidase; may play a role in apoptosis mediated muscle wasting; and, is increased in quail muscles after 7 or 14 days of unloading. p53 has been reported to be unaltered during atrophy induced by nerve injury as an example. Immobilisation at shortened length induces atrophy, while in a lengthened position it produces hypertrophy attributable to addition of sarcomeres in the longitudinal direction.

In the shortened position it induces fast isoforms. These differences may be due to the elevated expression of Insulin-like Growth Factor-| (check symbol) | in stretched muscle which are not altered in shortened length. Atrophy and loss of strength are not prevented by regular unloaded contractions due to electrical stimulation but are attenuated or followed by hypertrophy by the application of intermittent weight bearing or strength training in human and animal studies. Neurotrophic factors are important determinants of the skeletal muscle contractile properties.

During chronic electrical stimulation via the nerve the effect of the neurotrophic factors cannot be totally excluded. The disuse and denervation may not have the same effect on skeletal muscle. During CORP and C (cutoff in the document), muscle wasting is a serious complication and it contributes to exercise intolerance and reduced survivability in many cases. Atrophy is not always evident. The lower muscles seem to lose more strength than the upper muscles. This may be due to muscle disuse.

Inactivity is not necessary the main account for the skeletal muscle alteration during CORP and CHF. It may be due to hypoxaemia. There is a strong predictor that the systematic inflammation is the primary cause of muscle wasting. This may be seen by elevated plasma levels of TNFa. It has been reported TNFa to reduce titanic force in single muscle fibres within an hour