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Differentiated mTOR but not AMPK signaling after strength vs endurance exercise in training‐accustomed individuals
Author(s) -
Vissing K.,
McGee S. L.,
Farup J.,
Kjølhede T.,
Vendelbo M. H.,
Jessen N.
Publication year - 2013
Publication title -
scandinavian journal of medicine and science in sports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.575
H-Index - 115
eISSN - 1600-0838
pISSN - 0905-7188
DOI - 10.1111/j.1600-0838.2011.01395.x
Subject(s) - mtorc1 , p70 s6 kinase 1 , endocrinology , ampk , endurance training , medicine , protein kinase b , protein kinase a , phosphorylation , pi3k/akt/mtor pathway , amp activated protein kinase , glycogen , chemistry , signal transduction , biology , microbiology and biotechnology
The influence of adenosine mono phosphate ( AMP )‐activated protein kinase ( AMPK ) vs Akt ‐mammalian target of rapamycin C 1 ( mTORC1 ) protein signaling mechanisms on converting differentiated exercise into training specific adaptations is not well‐established. To investigate this, human subjects were divided into endurance, strength, and non‐exercise control groups. Data were obtained before and during post‐exercise recovery from single‐bout exercise, conducted with an exercise mode to which the exercise subjects were accustomed through 10 weeks of prior training. Blood and muscle samples were analyzed for plasma substrates and hormones and for muscle markers of AMPK and Akt ‐ mTORC 1 protein signaling. Increases in plasma glucose, insulin, growth hormone ( GH ), and insulin‐like growth factor ( IGF )‐1, and in phosphorylated muscle phospho‐ Akt substrate ( PAS ) of 160 kDa, mTOR , 70 kDa ribosomal protein S 6 kinase, eukaryotic initiation factor 4 E , and glycogen synthase kinase 3α were observed after strength exercise. Increased phosphorylation of AMPK , histone deacetylase5 ( HDAC 5), cAMP response element‐binding protein, and acetyl‐ CoA carboxylase ( ACC ) was observed after endurance exercise, but not differently from after strength exercise. No changes in protein phosphorylation were observed in non‐exercise controls. Endurance training produced an increase in maximal oxygen uptake and a decrease in submaximal exercise heart rate, while strength training produced increases in muscle cross‐sectional area and strength. No changes in basal levels of signaling proteins were observed in response to training. The results support that in training‐accustomed individuals, mTORC 1 signaling is preferentially activated after hypertrophy‐inducing exercise, while AMPK signaling is less specific for differentiated exercise.