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Matched work high-intensity interval and continuous running induce similar increases in PGC-1α mRNA, AMPK, p38, and p53 phosphorylation in human skeletal muscle.
- Source :
-
Journal of applied physiology (Bethesda, Md. : 1985) [J Appl Physiol (1985)] 2012 Apr; Vol. 112 (7), pp. 1135-43. Date of Electronic Publication: 2012 Jan 19. - Publication Year :
- 2012
-
Abstract
- The aim of the present study was to test the hypothesis that acute high-intensity interval (HIT) running induces greater activation of signaling pathways associated with mitochondrial biogenesis compared with moderate-intensity continuous (CONT) running matched for work done. In a repeated-measures design, 10 active men performed two running protocols consisting of HIT [6 × 3-min at 90% maximal oxygen consumption (Vo(2max)) interspersed with 3-min recovery periods at 50% Vo(2max) with a 7-min warm-up and cool-down period at 70% Vo(2max)] or CONT (50-min continuous running at 70% Vo(2max)). Both protocols were matched, therefore, for average intensity, duration, and distance run. Muscle biopsies (vastus lateralis) were obtained preexercise, postexercise, and 3 h postexercise. Muscle glycogen decreased (P < 0.05) similarly in HIT and CONT (116 ± 11 vs. 111 ± 17 mmol/kg dry wt, respectively). Phosphorylation (P-) of p38MAPK(Thr180/Tyr182) (1.9 ± 0.1- vs. 1.5 ± 0.2-fold) and AMPK(Thr172) (1.5 ± 0.3- vs. 1.5 ± 0.1-fold) increased immediately postexercise (P < 0.05) in HIT and CONT, respectively, and returned to basal levels at 3 h postexercise. P-p53(Ser15) (HIT, 2.7 ± 0.8-fold; CONT, 2.1 ± 0.8-fold), PGC-1α mRNA (HIT, 4.2 ± 1.7-fold; CONT, 4.5 ± 0.9-fold) and HSP72 mRNA (HIT, 4.4 ± 2-fold; CONT, 3.5 ± 1-fold) all increased 3 h postexercise (P < 0.05) although neither parameter increased (P > 0.05) immediately postexercise. There was no difference between trials for any of the above signaling or gene expression responses (P > 0.05). We provide novel data by demonstrating that acute HIT and CONT running (when matched for average intensity, duration, and work done) induces similar activation of molecular signaling pathways associated with regulation of mitochondrial biogenesis. Furthermore, this is the first report of contraction-induced p53 phosphorylation in human skeletal muscle, thus highlighting an additional pathway by which exercise may initiate mitochondrial biogenesis.
- Subjects :
- Anaerobic Threshold physiology
Biopsy
Blood Chemical Analysis
Blotting, Western
Calcium Signaling physiology
Cross-Over Studies
HSP72 Heat-Shock Proteins biosynthesis
Heart Rate physiology
Humans
Lactic Acid metabolism
Male
Muscle, Skeletal chemistry
Oxygen Consumption physiology
Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
Phosphorylation
Real-Time Polymerase Chain Reaction
Superoxide Dismutase biosynthesis
Young Adult
AMP-Activated Protein Kinases biosynthesis
Heat-Shock Proteins biosynthesis
Muscle, Skeletal metabolism
Muscle, Skeletal physiology
RNA, Messenger biosynthesis
Running physiology
Transcription Factors biosynthesis
Tumor Suppressor Protein p53 biosynthesis
p38 Mitogen-Activated Protein Kinases biosynthesis
Subjects
Details
- Language :
- English
- ISSN :
- 1522-1601
- Volume :
- 112
- Issue :
- 7
- Database :
- MEDLINE
- Journal :
- Journal of applied physiology (Bethesda, Md. : 1985)
- Publication Type :
- Academic Journal
- Accession number :
- 22267390
- Full Text :
- https://doi.org/10.1152/japplphysiol.01040.2011