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

Gibala, Martin J., McGee, Sean L, Garnham, Andrew P., Howlett, Kirsten F., Snow, Rodney J. and Hargreaves, Mark 2009, Brief intense interval exercise activates AMPK and p38 MAPK signaling and increases the expression of PGC-1α in human skeletal muscle, Journal of applied physiology, vol. 106, pp. 929-934.

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Title Brief intense interval exercise activates AMPK and p38 MAPK signaling and increases the expression of PGC-1α in human skeletal muscle
Author(s) Gibala, Martin J.
McGee, Sean L
Garnham, Andrew P.
Howlett, Kirsten F.
Snow, Rodney J.
Hargreaves, Mark
Journal name Journal of applied physiology
Volume number 106
Start page 929
End page 934
Total pages 6
Publisher American Physiological Society
Place of publication Bethesda, Md.
Publication date 2009-03
ISSN 8750-7587
1522-1601
Keyword(s) metabolism
mitochondrial biogenesis
signal transduction
peroxisome proliferator-activated receptor- coactivator-1
Summary 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 {alpha}1 and {alpha}2) and the p38 mitogen-activated protein kinase (MAPK) was higher (P ≤ 0.05) immediately after bout 4 vs. preexercise. Peroxisome proliferator-activated receptor-{gamma} coactivator-1{alpha}(PGC-1{alpha}) mRNA was increased approximately twofold above rest after 3 h of recovery (P ≤ 0.05); however, PGC-1{alpha}protein 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{alpha} 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.
Language eng
Field of Research 110602 Exercise Physiology
Socio Economic Objective 929999 Health not elsewhere classified
HERDC Research category C1 Refereed article in a scholarly journal
HERDC collection year 2009
Copyright notice ©2009, American Physiological Society
Persistent URL http://hdl.handle.net/10536/DRO/DU:30019663

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