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Exercise‐induced metabolic fluctuations influence AMPK, p38‐MAPK and CaMKII phosphorylation in human skeletal muscle
During transition from rest to exercise, metabolic reaction rates increase substantially to sustain intracellular ATP use. These metabolic demands activate several kinases that initiate signal transduction pathways which modulate transcriptional regulation of mitochondrial biogenesis. The purpose of...
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Published in: | Physiological reports 2015-09, Vol.3 (9), p.e12462-n/a |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | During transition from rest to exercise, metabolic reaction rates increase substantially to sustain intracellular ATP use. These metabolic demands activate several kinases that initiate signal transduction pathways which modulate transcriptional regulation of mitochondrial biogenesis. The purpose of this study was to determine whether metabolic fluctuations per se affect the signaling cascades known to regulate peroxisome proliferator‐activated receptor γ coactivator‐1α (PGC‐1α). On two separate occasions, nine men performed a continuous (30‐min) and an intermittent exercise (30 × 1‐min intervals separated by 1‐min of recovery) at 70% of V˙O2peak. Skeletal muscle biopsies from the vastus lateralis were taken at rest and at +0 h and +3 h after each exercise. Metabolic fluctuations that correspond to exercise‐induced variation in metabolic rates were determined by analysis of VO2 responses. During intermittent exercise metabolic fluctuations were 2.8‐fold higher despite identical total work done to continuous exercise (317 ± 41 vs. 312 ± 56 kJ after intermittent and continuous exercise, respectively). Increased phosphorylation of AMP‐activated protein kinase (AMPK) (~2.9‐fold, P |
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ISSN: | 2051-817X 2051-817X |
DOI: | 10.14814/phy2.12462 |