| First Author | Brandt N | Year | 2017 |
| Journal | PLoS One | Volume | 12 |
| Issue | 10 | Pages | e0185993 |
| PubMed ID | 29049322 | Mgi Jnum | J:246114 |
| Mgi Id | MGI:5916541 | Doi | 10.1371/journal.pone.0185993 |
| Citation | Brandt N, et al. (2017) PGC-1alpha and exercise intensity dependent adaptations in mouse skeletal muscle. PLoS One 12(10):e0185993 |
| abstractText | The aim of the present study was to examine the role of PGC-1alpha in intensity dependent exercise and exercise training-induced metabolic adaptations in mouse skeletal muscle. Whole body PGC-1alpha knockout (KO) and littermate wildtype (WT) mice performed a single treadmill running bout at either low intensity (LI) for 40 min or moderate intensity (MI) for 20 min. Blood and quadriceps muscles were removed either immediately after exercise or at 3h or 6h into recovery from exercise and from resting controls. In addition PGC-1alpha KO and littermate WT mice were exercise trained at either low intensity (LIT) for 40 min or at moderate intensity (MIT) for 20 min 2 times pr. day for 5 weeks. In the first and the last week of the intervention period, mice performed a graded running endurance test. Quadriceps muscles were removed before and after the training period for analyses. The acute exercise bout elicited intensity dependent increases in LC3I and LC3II protein and intensity independent decrease in p62 protein in skeletal muscle late in recovery and increased LC3II with exercise training independent of exercise intensity and volume in WT mice. Furthermore, acute exercise and exercise training did not increase LC3I and LC3II protein in PGC-1alpha KO. In addition, exercise-induced mRNA responses of PGC-1alpha isoforms were intensity dependent. In conclusion, these findings indicate that exercise intensity affected autophagy markers differently in skeletal muscle and suggest that PGC-1alpha regulates both acute and exercise training-induced autophagy in skeletal muscle potentially in a PGC-1alpha isoform specific manner. |
