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;a2gasg;a2gasgJ Appl Physiol. 2012 Jan 19. [Epub ahead of print]
Matched work high-intensity interval and continuous running induce similar increases in PGC-1α mRNA, AMPK, p38 and p53 phosphorylation in human skeletal muscle.
Bartlett JD, Hwa-Joo C, Jeong TS, Louhelainen J, Cochran AJ, Gibala MJ, Gregson W, Close GL, Drust B, Morton JP.
Source
1Liverpool John Moores University.
Abstract
The aim of the present study was to test the hypothesis that acute high-intensity interval (HIT) running induces greater activation of signalling pathways associated with mitochondrial biogenesis compared with moderate-intensity continuous (CONT) running matched for work done. In a repeated measures design, ten active men performed two running protocols consisting of HIT (6 x 3-min at 90% 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 ran. Muscle biopsies (vastus lateralis) were obtained pre-exercise, post-exercise and 3 h post-exercise. Muscle glycogen decreased (P < 0.05) similarly in HIT and CONT (116 ± 11 v 111 ± 17 mmol.kg(-1) dw, respectively). Phosphorylation (P-) of p38MAPK(Thr180/Tyr182) (1.9 ± 0.1 v 1.5 ± 0.2-fold) and AMPK(Thr172) (1.5 ± 0.3 v 1.5 ± 0.1-fold) increased immediately post-exercise (P < 0.05) in HIT and CONT, respectively, and returned to basal levels at 3 h post-exercise. 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: v 4.5 ± 0.9-fold) and HSP72 mRNA (HIT: 4.4 ± 2-fold; CONT: 3.5 ± 1-fold) all increased 3 h post-exercise (P < 0.05) though neither parameter increased (P > 0.05) immediately post-exercise. There was no difference between trials for any of the above signalling 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 signalling 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.