Premium
Truncated splice variant PGC ‐1 α 4 is not associated with exercise‐induced human muscle hypertrophy
Author(s) -
Lundberg T. R.,
FernandezGonzalo R.,
Norrbom J.,
Fischer H.,
Tesch P. A.,
Gustafsson T.
Publication year - 2014
Publication title -
acta physiologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.591
H-Index - 116
eISSN - 1748-1716
pISSN - 1748-1708
DOI - 10.1111/apha.12310
Subject(s) - splice , muscle hypertrophy , gene isoform , vastus lateralis muscle , medicine , endocrinology , aerobic exercise , alternative splicing , basal (medicine) , gene expression , biology , skeletal muscle , gene , genetics , insulin
A truncated PGC ‐1 α splice variant ( PGC ‐1 α 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 ‐1 α 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 ‐1 α 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 ‐1 α transcripts showed similar response. Truncated transcripts originated from both the alternative and proximal promoter, and AE + RE increased PGC ‐1 α expression from both promoter sites. RE induced transcripts from the alternative promoter only. PGC ‐1 α 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 ‐1 α 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 ‐1 α coordinates exercise‐induced hypertrophy in human skeletal muscle. Rather, all PGC ‐1 α isoforms appear to be regulated transiently in response to acute exercise and regardless of mode.