Abstract
Aging is associated with a progressive decline of muscle mass, strength, and quality, a condition described as sarcopenia of aging. Despite the significance of skeletal muscle atrophy, the mechanisms responsible for the deterioration of muscle performance are only partially understood. The purpose of this chapter is to highlight cellular, molecular, and biochemical changes that contribute to age-related muscle dysfunction, particularly the molecular basis of contraction, changes in muscle protein structure assessed by electron paramagnetic resonance spectroscopy, oxidative damage from reactive oxygen species, and post-translational modifications in key contractile proteins. Age-related changes in the interaction between the contractile proteins, actin and myosin, provide insights into potential molecular mechanisms responsible for changes in muscle contractility with advancing age.
Original language | English (US) |
---|---|
Title of host publication | Sarcopenia - Age-Related Muscle Wasting and Weakness |
Subtitle of host publication | Mechanisms and Treatments |
Publisher | Springer Netherlands |
Pages | 75-111 |
Number of pages | 37 |
ISBN (Electronic) | 9789048197132 |
ISBN (Print) | 9789048197125 |
DOIs | |
State | Published - 2011 |
Bibliographical note
Funding Information:We thank Dawn Lowe, Deborah Ferrington, and Daniel Spakowicz for many useful discussions. This work was supported by NIH Grants to DDT (AR27906 and AG26160) and LT (AG17768 and AG21626).
Keywords
- Actin
- Cabonylation
- Glycation
- In vitro motility assay
- Myosin
- Nitrotyrosine
- Oxidative stress
- Post-translation modifications
- Proteome
- Reactive oxygen species
- Single permeabilized muscle fibers