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Study · In vitro (cells) · 2013

2 results

The truncated splice variants, NT-PGC-1α and PGC-1α4, increase with both endurance and resistance exercise in human skeletal muscle.

Ydfors M, Fischer H, Mascher H, Blomstrand E, Norrbom J, Gustafsson T

Physiological reports5 Nov 2013Cited by 62 (Europe PMC)

Summary

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.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study2

2 results from studies that gave the peptide. No result from this study comes from people.

  1. 01LabIn vitro (cells)Mechanism

    In human myotubes, AICAR induced nontruncated PGC-1α transcripts (P < 0.05).

    In plain wordsIn cells, AICAR increased nontruncated PGC-1α transcripts.

    Outcome
    IncreaseNontruncated PGC-1α transcripts
    Study

    humann: not reported in source

    Human myotubes
    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    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).
  2. 02LabIn vitro (cells)Mechanism

    In human myotubes, AICAR induced truncated PGC-1α transcripts (P < 0.05).

    In plain wordsIn cells, AICAR increased truncated PGC-1α transcripts.

    Outcome
    IncreaseTruncated PGC-1α transcripts
    Study

    humann: not reported in source

    Human myotubes
    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    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).

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

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  1. Version 2Current

    21 Oct 2026, 15:58 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 12:50 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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