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Acta Physiol (Oxf). 2014 Oct;212(2):142-51. doi: 10.1111/apha.12310. Epub 2014 May 21.

Truncated splice variant PGC-1α4 is not associated with exercise-induced human muscle hypertrophy.

Author information

1
Department of Health Sciences, Mid Sweden University, Östersund, Sweden.

Abstract

INTRODUCTION:

A truncated PGC-1α splice variant (PGC-1α4) 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-1α 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-1α 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-1α transcripts showed similar response. Truncated transcripts originated from both the alternative and proximal promoter, and AE+RE increased PGC-1α expression from both promoter sites. RE induced transcripts from the alternative promoter only. PGC-1α 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-1α 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-1α coordinates exercise-induced hypertrophy in human skeletal muscle. Rather, all PGC-1α isoforms appear to be regulated transiently in response to acute exercise and regardless of mode.

KEYWORDS:

aerobic exercise; concurrent exercise; endurance; gene expression; muscle strength; resistance exercise

PMID:
24800995
DOI:
10.1111/apha.12310
[Indexed for MEDLINE]

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