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Aging muscle.

K Sreekumaran Nair1

  • 1Mayo Clinic College of Medicine, Division of Endocrinology and Endocrine Research, Rochester, MN 55905, USA. nair.sree@mayo.edu

The American Journal of Clinical Nutrition
|May 11, 2005
PubMed
Summary

Aging skeletal muscles experience reduced protein synthesis and mitochondrial function, leading to frailty and metabolic disorders. Exercise and nutrition can counteract these age-related declines in muscle health.

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Area of Science:

  • Gerontology
  • Skeletal Muscle Physiology
  • Mitochondrial Biology

Background:

  • Aging leads to significant structural and functional changes in skeletal muscle, beginning in the fourth decade of life.
  • These muscle changes contribute to frailty, disabilities, and metabolic disorders like insulin resistance, type 2 diabetes, hypertension, and hyperlipidemia.
  • Age-related decreases in muscle protein synthesis, particularly myosin heavy chain and mitochondrial proteins, are linked to reduced mitochondrial DNA and messenger RNA, impacting ATP production.

Purpose of the Study:

  • To explore the age-related decline in skeletal muscle function and its connection to metabolic disorders.
  • To investigate the role of mitochondrial dysfunction in aging muscle and its relationship with insulin resistance.
  • To examine the impact of exercise, insulin, and amino acids on muscle protein synthesis and mitochondrial biogenesis in the context of aging.

Main Methods:

  • Review of existing literature on age-related muscle changes, mitochondrial function, and metabolic health.
  • Analysis of studies investigating the effects of exercise (aerobic and resistance) on muscle protein synthesis and mitochondrial biogenesis.
  • Examination of research on the influence of insulin and amino acids on mitochondrial function and the implications for insulin resistance.

Main Results:

  • Aging is associated with decreased muscle protein synthesis and mitochondrial ATP production due to reduced mitochondrial DNA and messenger RNA.
  • Both aerobic and resistance exercise can enhance muscle protein synthesis and mitochondrial biogenesis.
  • Insulin's effect on muscle mitochondrial ATP production is impaired in type 2 diabetes, and a dissociation exists between mitochondrial biogenesis and insulin sensitivity post-exercise in older adults.

Conclusions:

  • Age-related mitochondrial dysfunction may contribute to or result from insulin resistance, though the causal relationship requires further investigation.
  • Exercise interventions show promise in enhancing muscle mitochondrial efficiency and potentially attenuating age-related decline.
  • Reduced physical activity might be a consequence of decreased mitochondrial ATP production, suggesting a feedback loop impacting overall physical activity levels with age.

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