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Truncated splice variant PGC-1 alpha 4 is not associated with exercise-induced human muscle hypertrophy
Mid Sweden University, Faculty of Human Sciences, Department of Health Sciences.
Karolinska Inst, Dept Physiol & Pharmacol, S-17177 Stockholm, Sweden.
Karolinska Inst, Dept Physiol & Pharmacol, S-17177 Stockholm, Sweden.
Karolinska Inst, Dept Lab Med, Sect Clin Physiol, Karolinska Univ Hosp, S-17177 Stockholm, Sweden.
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2014 (English)In: Acta Physiologica, ISSN 1748-1708, E-ISSN 1748-1716, Vol. 212, no 2, p. 142-151Article in journal (Refereed) Published
Abstract [en]

Introduction: A truncated PGC-1 alpha splice variant (PGC-1 alpha 4) has been implicated in the regulation of resistance exercise (RE)-induced muscle hypertrophy, and basal expression levels said to be augmented in response to concurrent aerobic (AE) and RE training.Aim: The current study investigated human muscle truncated and non-truncated PGC-1a transcripts in response to both acute and chronic RE, and with or without preceding AE (AE+RE).Methods: Ten men performed 5 weeks of unilateral AE+RE and RE training.Before (untrained) and after (trained) this intervention, PGC-1a transcripts were assessed in vastus lateralis muscle biopsies obtained before and 3 h after acute RE, with or without preceding AE.Additionally, samples were collected 72 h after the last exercise bout of the training programme.Results: The truncated splice variant increased (P < 0.05) its expression after acute exercise regardless of mode. However, the expression was greater (P < 0.05) after AE+RE than RE. Other PGC-1a transcripts showed similar response. Truncated transcripts originated from both the alternative and proximal promoter, and AE+RE increasedPGC-1 alpha expression from both promoter sites. RE induced transcripts from the alternative promoter only. PGC-1 alpha expressions after acute exercise were comparable across isoforms in both untrained and trained muscle. Steady-state levels of isoforms were unchanged after 5-week training (P > 0.05). Exercise-induced expression of PGC-1a variants did not correlate with changes in muscle size or strength (P > 0.05).Conclusion: Our results do not support the view that truncated PGC-1a coordinates exercise-induced hypertrophy in human skeletal muscle.Rather, all PGC-1 alpha isoforms appear to be regulated transiently in response to acute exercise and regardless of mode.

Place, publisher, year, edition, pages
2014. Vol. 212, no 2, p. 142-151
Keywords [en]
aerobic exercise, concurrent exercise, endurance, gene expression, muscle strength, resistance exercise
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:miun:diva-21916DOI: 10.1111/apha.12310ISI: 000341828700006Scopus ID: 2-s2.0-84912530292OAI: oai:DiVA.org:miun-21916DiVA, id: diva2:716114
Available from: 2014-05-08 Created: 2014-05-08 Last updated: 2017-12-05Bibliographically approved

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