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.
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.
Authors: Tommy R Lundberg; Rodrigo Fernandez-Gonzalo; Per A Tesch; Eric Rullman; Thomas Gustafsson Journal: Am J Physiol Regul Integr Comp Physiol Date: 2016-04-13 Impact factor: 3.619
Authors: Gilles Gouspillou; Nicolas Sgarioto; Brandon Norris; Sébastien Barbat-Artigas; Mylène Aubertin-Leheudre; Jose A Morais; Yan Burelle; Tanja Taivassalo; Russell T Hepple Journal: PLoS One Date: 2014-08-14 Impact factor: 3.240
Authors: Mika Silvennoinen; Juha P Ahtiainen; Juha J Hulmi; Satu Pekkala; Ritva S Taipale; Bradley C Nindl; Tanja Laine; Keijo Häkkinen; Harri Selänne; Heikki Kyröläinen; Heikki Kainulainen Journal: Physiol Rep Date: 2015-10