Frailty and muscle metabolism dysregulation in the elderly.

Published

Journal Article

The frailty syndrome is increasingly recognized by geriatricians to identify elders at an extreme risk of adverse health outcomes. The physiological changes that result in frailty are complex and up to now have been extremely difficult to characterize due to the frequent coexistence of acute and chronic illness. Frailty is characterized by an decline in the functional reserve with several alterations in diverse physiological systems, including lower energy metabolism, decreased skeletal muscle mass and quality, altered hormonal and inflammatory functions. This altered network leads to an extreme vulnerability for disease, functional dependency, hospitalization and death. One of the most important core components of the frailty syndrome is a decreased reserve in skeletal muscle functioning which is clinically characterized by a loss in muscle mass and strength (sarcopenia), in walking performance and in endurance associated with a perception of exhaustion and fatigue. There are a number of physiological changes that occur in senescent muscle tissues that have a critical effect on body metabolism. The causes of sarcopenia are multi-factorial and can include disuse, changing hormonal function, chronic diseases, inflammation, insulin resistance, and nutritional deficiencies. In this review, we will explore the dysregulation of some biological mechanisms that may contribute to the pathophysiology of the frailty syndrome through age-related changes in skeletal muscle mass and function.

Full Text

Duke Authors

Cited Authors

  • Evans, WJ; Paolisso, G; Abbatecola, AM; Corsonello, A; Bustacchini, S; Strollo, F; Lattanzio, F

Published Date

  • October 2010

Published In

Volume / Issue

  • 11 / 5

Start / End Page

  • 527 - 536

PubMed ID

  • 20683658

Pubmed Central ID

  • 20683658

Electronic International Standard Serial Number (EISSN)

  • 1573-6768

International Standard Serial Number (ISSN)

  • 1389-5729

Digital Object Identifier (DOI)

  • 10.1007/s10522-010-9297-0

Language

  • eng