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Brief intense interval exercise activates AMPK and p38 MAPK signaling and increases the expression of PGC-1α in human skeletal muscle

journal contribution
posted on 2009-03-01, 00:00 authored by M Gibala, Sean McgeeSean Mcgee, Andrew GarnhamAndrew Garnham, Kirsten HowlettKirsten Howlett, Rod SnowRod Snow, Mark Hargreaves
From a cell signaling perspective, short-duration intense muscular work is typically associated with resistance training and linked to pathways that stimulate growth. However, brief repeated sessions of sprint or high-intensity interval exercise induce rapid phenotypic changes that resemble traditional endurance training. We tested the hypothesis that an acute session of intense intermittent cycle exercise would activate signaling cascades linked to mitochondrialbiogenesis in human skeletal muscle. Biopsies (vastus lateralis) were obtained from six young men who performed four 30-s "all out" exercise bouts interspersed with 4 min of rest (<80 kJ total work). Phosphorylation of AMP-activated protein kinase (AMPK; subunits 1 and 2) and the p38 mitogen-activated protein kinase (MAPK) was higher (P  0.05) immediately after bout 4 vs. preexercise. Peroxisome proliferator-activated receptor- coactivator-1(PGC-1) mRNA was increased approximately twofold above rest after 3 h of recovery (P  0.05); however, PGC-1protein content was unchanged. In contrast, phosphorylation of protein kinase B/Akt (Thr308 and Ser473) tended to decrease, and downstream targets linked to hypertrophy (p70 ribosomal S6 kinase and 4E binding protein 1) were unchanged after exercise and recovery. We conclude that signaling through AMPK and p38 MAPK to PGC-1 may explain in part the metabolic remodeling induced by low-volume intense interval exercise, including mitochondrial biogenesis and an increased capacity for glucose and fatty acid oxidation.



Journal of applied physiology




929 - 934


American Physiological Society


Bethesda, Md.







Publication classification

C1 Refereed article in a scholarly journal

Copyright notice

2009, American Physiological Society