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The truncated splic...
The truncated splice variants, NT-PGC-1alpha and PGC-1alpha4, increase with both endurance and resistance exercise in human skeletal muscle
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Ydfors, Mia (författare)
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Fischer, Helene (författare)
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Mascher, Henrik (författare)
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- Blomstrand, Eva (författare)
- Gymnastik- och idrottshögskolan,Eva Blomstrands forskningsgrupp
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Norrbom, Jessica (författare)
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Gustafsson, Thomas (författare)
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(creator_code:org_t)
- 2013-11-05
- 2013
- Engelska.
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Ingår i: Physiological Reports. - : Wiley. - 2051-817X. ; 1:6, s. e00140 Page 1-e00140 Page 9
- Relaterad länk:
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https://doi.org/10.1...
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https://gih.diva-por... (primary) (Raw object)
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https://physoc.onlin...
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https://urn.kb.se/re...
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https://doi.org/10.1...
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Abstract
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- Recently, a truncated peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α) splice variant, PGC-1α4, that originates from the alternative promoter was shown to be induced by resistance exercise and to elicit muscle hypertrophy without coactivation of “classical” PGC-1α targets involved in mitochondrial biogenesis and angiogenesis. In order to test if distinct physiological adaptations are characterized by divergent induction of PGC-1α splice variants, we investigated the expression of truncated and nontruncated PGC-1α splice variants and PGC-1α transcripts originating from the alternative and the proximal promoter, in human skeletal muscle in response to endurance and resistance exercise. Both total PGC-1α and truncated PGC-1α mRNA expression were increased 2 h after endurance (P < 0.01) and resistance exercise (P < 0.01), with greater increases after endurance exercise (P < 0.05). Expression of nontruncated PGC-1α increased significantly in both exercise groups (P < 0.01 for both groups) without any significant differences between the groups. Both endurance and resistance exercise induced truncated as well as nontruncated PGC-1α transcripts from both the alternative and the proximal promoter. Further challenging the hypothesis that induction of distinct PGC-1α splice variants controls exercise adaptation, both nontruncated and truncated PGC-1α transcripts were induced in AICAR-treated human myotubes (P < 0.05). Thus, contrary to our hypothesis, resistance exercise did not specifically induce the truncated forms of PGC-1α. Induction of truncated PGC-1α splice variants does not appear to underlie distinct adaptations to resistance versus endurance exercise. Further studies on the existence of numerous splice variants originating from different promoters are needed.
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