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Endurance et hypertrophie font-ils bon ménage!

22/07/2014 | Etudes Musculation


Is muscle hypertrophy following resistance exercise regulated by truncated splice variants of PGC-1α?
Christopher G.R. Perry   Acta Physiologica 2014 Accepted Article (Accepted, unedited articles published online and citable. The final edited and typeset version of record will appear in future.)

In this issue, the investigation by Lundberg et al revisited a classic question of how muscle hypertrophy occurs following resistance exercise but not endurance exercise in human skeletal muscle. A recent study suggested the master transcriptional co-activator PGC-1α, known for regulating multiple transcriptional programs encoding mitochondrial and other metabolic proteins following endurance exercise, may also regulate muscle hypertrophy after resistance exercise through a truncated variant termed PGC-1α4 (Ruas et al 2012). Based on these findings, Lundberg and colleagues reasoned this model would predict a greater expression of this splice variant following resistance exercise vs endurance exercise in human skeletal muscle

A PGC-1α isoform induced by resistance training regulates skeletal muscle hypertrophy.

Cell. 2012 Dec 7;151(6):1319-31.  Ruas JL

PGC-1α is a transcriptional coactivator induced by exercise that gives muscle many of the best known adaptations to endurance-type exercise but has no effects on muscle strength or hypertrophy. We have identified a form of PGC-1α (PGC-1α4) that results from alternative promoter usage and splicing of the primary transcript. PGC-1α4 is highly expressed in exercised muscle but does not regulate most known PGC-1α targets such as the mitochondrial OXPHOS genes. Rather, it specifically induces IGF1 and represses myostatin, and expression of PGC-1α4 in vitro and in vivo induces robust skeletal muscle hypertrophy. Importantly, mice with skeletal muscle-specific transgenic expression of PGC-1α4 show increased muscle mass and strength and dramatic resistance to the muscle wasting of cancer cachexia. Expression of PGC-1α4 is preferentially induced in mouse and human muscle during resistance exercise. These studies identify a PGC-1α protein that regulates and coordinates factors involved in skeletal muscle hypertrophy.

Truncated splice variant PGC-1α4 is not associated with exercise-induced human muscle hypertrophy.
Lundberg TR           Acta Physiol (Oxf). 2014 May 6.

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.
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).
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.
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).
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.

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