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Improving Strength, Power, Muscle Aerobic Capacity, and Glucose Tolerance through Short-term Progressive Strength Training Among Elderly People
Published on: July 5, 2017
Resistance exercise reverses aging in human skeletal muscle
Simon Melov1, Mark A Tarnopolsky, Kenneth Beckman
1Buck Institute for Age Research, Novato, California, United States of America. smelov@buckinstitute.org
Plos One
|May 24, 2007
Summary
Healthy aging involves muscle weakness and mitochondrial issues. Resistance exercise partially reverses muscle strength and significantly improves the gene expression profile associated with aging in older adults.
Area of Science:
- Gerontology
- Molecular Biology
- Exercise Physiology
Background:
- Human aging is characterized by sarcopenia, a decline in skeletal muscle mass and function.
- Mitochondrial dysfunction is increasingly recognized as a key factor contributing to age-related sarcopenia.
Purpose of the Study:
- To investigate the transcriptional profile of healthy aging in skeletal muscle, focusing on mitochondrial function.
- To determine if resistance exercise training can reverse age-associated transcriptional changes and improve muscle strength.
Main Methods:
- Gene expression profiling of skeletal muscle biopsies from young and older adults.
- Comparison of transcriptional profiles before and after a six-month resistance exercise program in older adults.
- Correlation of gene expression changes with muscle strength measurements.
Main Results:
- Older adults exhibited significantly lower muscle strength compared to younger adults.
- Aging was associated with differential expression of 596 genes, with a notable enrichment of mitochondrial function genes.
- Resistance exercise training improved muscle strength in older adults and substantially reversed age-associated transcriptional changes.
Conclusions:
- Healthy aging is linked to skeletal muscle mitochondrial impairment and reduced strength.
- Resistance exercise training offers a viable strategy to partially restore muscle function and significantly ameliorate the molecular signature of aging in skeletal muscle.
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