Abstract
Every time a bout of exercise is performed, a change in gene expression occurs
within the contracting muscle. Over the course of many repeated bouts of
exercise (i.e. training), the cumulative effects of these alterations lead to a
change in muscle phenotype. One of the most prominent of these adaptations
is an increase in mitochondrial content, which confers a greater resistance to
muscle fatigue. This essay reviews current knowledge on the regulation of
exercise-induced mitochondrial biogenesis at the molecular level. The major
steps involved include, (i) transcriptional regulation of nuclear-encoded genes
encoding mitochondrial proteins by the coactivator peroxisome-proliferatoractivated
receptor coactivator-1, (ii) control of mitochondrial DNA gene
1To whom correspondence should be addressed (email [email protected]).
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© 2006 The Biochemical Society
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© 2006 The Biochemical Society
14 Essays in Biochemistry volume 42 2006
expression by the transcription factor Tfam, (iii) mitochondrial fi ssion and
fusion mechanisms, and (iv) import of nuclear-derived gene products into
the mitochondrion via the protein import machinery. It is now known that
exercise can modify the rates of several of these steps, leading to mitochondrial
biogenesis. An understanding of how exercise can produce this effect could
help us decide whether exercise is beneficial for patients suffering from
mitochondrial disorders, as well as a variety of metabolic diseases.
Originalsprog | Engelsk |
---|---|
Tidsskrift | Essays in Biochemistry |
Vol/bind | 42 |
Sider (fra-til) | 13-29 |
ISSN | 0071-1365 |
Status | Udgivet - 2006 |