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Prog Mol Biol Transl Sci. 2015;135:99-127. doi: 10.1016/bs.pmbts.2015.07.007. Epub 2015 Aug 5.

Exercise and the Regulation of Mitochondrial Turnover.

Author information

1
Muscle Health Research Centre, School of Kinesiology and Health Science, York University, Toronto, Ontario, Canada. Electronic address: dhood@yorku.ca.
2
Muscle Health Research Centre, School of Kinesiology and Health Science, York University, Toronto, Ontario, Canada.

Abstract

Exercise is a well-known stimulus for the expansion of the mitochondrial pool within skeletal muscle. Mitochondria have a remarkable ability to remodel their networks and can respond to an array of signaling stimuli following contractile activity to adapt to the metabolic demands of the tissue, synthesizing proteins to expand the mitochondrial reticulum. In addition, when they become dysfunctional, these organelles can be recycled by a specialized intracellular system. The signals regulating this mitochondrial life cycle of synthesis and degradation during exercise are still an area of great research interest. As mitochondrial turnover has valuable consequences in physical performance, in addition to metabolic health, disease, and aging, consideration of the signals which control this cycle is vital. This review focuses on the regulation of mitochondrial turnover in skeletal muscle and summarizes our current understanding of the impact that exercise has in modulating this process.

KEYWORDS:

Aging; Apoptosis; Autophagy; Exercise; High-intensity interval training; Mitochondria; Mitochondrial DNA; Mitochondrial morphology; Protein import; Skeletal muscle

PMID:
26477912
DOI:
10.1016/bs.pmbts.2015.07.007
[Indexed for MEDLINE]

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