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Review
. 2016 Aug 1;473(15):2295-314.
doi: 10.1042/BCJ20160009.

Unravelling the mechanisms regulating muscle mitochondrial biogenesis

David A Hood  1 , Liam D Tryon  2 , Heather N Carter  2 , Yuho Kim  2 , Chris C W Chen  2
Affiliations
Review

Unravelling the mechanisms regulating muscle mitochondrial biogenesis

David A Hood et al. Biochem J. .

Abstract

Skeletal muscle is a tissue with a low mitochondrial content under basal conditions, but it is responsive to acute increases in contractile activity patterns (i.e. exercise) which initiate the signalling of a compensatory response, leading to the biogenesis of mitochondria and improved organelle function. Exercise also promotes the degradation of poorly functioning mitochondria (i.e. mitophagy), thereby accelerating mitochondrial turnover, and preserving a pool of healthy organelles. In contrast, muscle disuse, as well as the aging process, are associated with reduced mitochondrial quality and quantity in muscle. This has strong negative implications for whole-body metabolic health and the preservation of muscle mass. A number of traditional, as well as novel regulatory pathways exist in muscle that control both biogenesis and mitophagy. Interestingly, although the ablation of single regulatory transcription factors within these pathways often leads to a reduction in the basal mitochondrial content of muscle, this can invariably be overcome with exercise, signifying that exercise activates a multitude of pathways which can respond to restore mitochondrial health. This knowledge, along with growing realization that pharmacological agents can also promote mitochondrial health independently of exercise, leads to an optimistic outlook in which the maintenance of mitochondrial and whole-body metabolic health can be achieved by taking advantage of the broad benefits of exercise, along with the potential specificity of drug action.

Keywords: PPARγ co-activator-1α (PGC-1α); Tfam; Tfeb; aging; calcium signalling; exercise; exercise training; mitochondrial protein import; mitochondrial reticulum; mitophagy; mtDNA; muscle disuse; p53; reactive oxygen species.

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