[Frontiers in Bioscience 6, d26-44, January 1, 2001]

SKELETAL MUSCLE AND AGING

Ana Navarro 1, José M ª López-Cepero 2 and María Jesús Sánchez del Pino 3

1 Department of Biochemistry and Molecular Biology, 2 Department of Cell Biology and 3 Department of Biochemistry and Molecular Biology, Faculty of Medicine. University of Cádiz. Plaza Fragela nº 9. 11003-Cádiz. Spain

TABLE OF CONTENTS

1. Abstract
2. Introduction
3. Sarcopenia of aging
4. Energy intake pattern and muscular aging
5. Hormonal factors that influence skeletal muscle
5.1. Growth hormone and insulin-like growth factor I
5.2. Glucocorticoids and muscle protein synthesis
5.3. Testosterone and muscular mass and strength
5.4. Thyroid hormone and phenotypic muscle effects
5.5. Insulin and muscle glucose uptake
6. Exercise, structural maintenance of skeletal muscle, and aging
7. Skeletal muscle cell changes associated with aging
7.1. Postsinaptic changes, sarcolemmal channel alterations and depolarisation properties
7.2. Altered excitation-contraction coupling and calcium homeostasis
7.3. Age-related mitochondrial changes
7.3.1. Mitochondrial changes and production of oxygen free radicals
7.3.2. Energetic effects of muscle mitochondrial alterations in aging
7.3.3. Secondary effects of mitochondrial free radical production
7.4. Nitric oxide, peroxynitrite and aging
8. Skeletal muscle aging modulation by caloric restriction and exercise
9. Perspective
10. Acknowledgments
11. References

1. ABSTRACT

Age-related changes in muscle mass (sarcopenia) and functional properties are the result of a very complex hierarchical system of basic cell aging processes and cell adaptive responses. A basic aging mechanism pertains to mitochondrial production of free radicals and their associated secondary effects. From this basic aging mechanism many other cellular changes can be explained as direct effects or compensatory changes. Altered skeletal muscle cell biochemical and functional properties during aging resulting from intrinsic mechanisms and from changes in hormonal or local signals that influence phenotype maintenance, are reviewed. The effect of skeletal muscle cell senescence on the cellular response to exercise, and the effect of dietary restriction on muscle cell senescence can also be explored from this perspective.