Truncated splice variant PGC‐1α4 is not associated with exercise‐induced human muscle hypertrophy
Published online on May 21, 2014
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.