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Published on: July 5, 2017
Mitochondrial theory of aging in human age-related sarcopenia
Gianni Parise1, Michael De Lisio
1Department of Kinesiology, McMaster University, Hamilton, Ont., Canada. pariseg@mcmaster.ca
Abstract:
Understanding age-related sarcopenia and, more importantly, devising counterstrategies require an intimate knowledge of the underlying mechanism(s) of sarcopenia. The mitochondrial theory of aging (MTA) has been a leading theory on aging for the last decade; however, there is relatively little information from human tissue to support or rebut the involvement of the MTA in aging skeletal muscle. It is believed that mitochondria may contribute to sarcopenia in a stochastic fashion where regions of fibers containing dysfunctional mitochondria are forced to atrophy. Resistance exercise, a known hypertrophic stimulus, has been shown to improve the mitochondrial phenotype of aged skeletal muscle. Furthermore, activation of skeletal muscle stem cells by resistance exercise may attenuate sarcopenia in two ways. First by inducing nuclear addition to postmitotic fibers, and, second, by increasing the proportion of functional mitochondria donated by muscle stem cells in a process termed 'gene shifting'. In this chapter we review the evidence supporting the MTA, the potential to attenuate the MTA with a known hypertrophic stimuli and explore the role of muscle stem cells in gene shifting to determine the connection between mitochondrial dysfunction and age-related sarcopenia.
Insights
Age-related sarcopenia may stem from mitochondrial dysfunction. Resistance exercise may counteract this by improving muscle mitochondria and activating stem cells for
Area of Science:
- Gerontology
- Skeletal Muscle Physiology
- Mitochondrial Biology
Background:
- Age-related sarcopenia is a significant health concern, yet its underlying mechanisms, particularly the role of mitochondrial dysfunction, remain incompletely understood in human skeletal muscle.
- The mitochondrial theory of aging (MTA) posits that accumulating mitochondrial damage contributes to cellular aging, but direct evidence in aging muscle is limited.
- Dysfunctional mitochondria are hypothesized to cause localized fiber atrophy, leading to sarcopenia.
Purpose of the Study:
- To review evidence supporting the mitochondrial theory of aging (MTA) in skeletal muscle.
- To explore the potential of resistance exercise to attenuate age-related mitochondrial dysfunction.
- To investigate the role of muscle stem cells and 'gene shifting' in mitigating sarcopenia.
Main Methods:
- Review of existing literature on the mitochondrial theory of aging and sarcopenia.
- Analysis of studies investigating the effects of resistance exercise on mitochondrial function in aged skeletal muscle.
- Examination of research on muscle stem cell activation and their potential contribution to mitochondrial health.
Main Results:
- Resistance exercise demonstrates a positive effect on the mitochondrial phenotype in aged skeletal muscle.
- Activation of skeletal muscle stem cells via resistance exercise may offer a dual benefit.
- Muscle stem cells might contribute to sarcopenia attenuation through nuclear addition and mitochondrial 'gene shifting'.
Conclusions:
- Mitochondrial dysfunction is a plausible contributor to age-related sarcopenia.
- Resistance exercise presents a viable strategy to counteract sarcopenia by improving mitochondrial health.
- Muscle stem cell-mediated 'gene shifting' offers a novel mechanism to combat age-related muscle decline.
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