Effects of elevated circulating hormones on resistance exercise-induced Akt signaling

Barry A. Spiering, William J. Kraemer, Jeffrey M. Anderson, Lawrence E. Armstrong, Bradley C. Nindl, Jeff S. Volek, Daniel A. Judelson, Michael Joseph, Jakob L. Vingren, Disa L. Hatfield, Maren S. Fragala, Jen Yu Ho, Carl M. Maresh

研究成果: 雜誌貢獻文章同行評審

33 引文 斯高帕斯(Scopus)

摘要

Purpose: Hormones and muscle contraction alter protein kinase B (Akt) signaling via distinct mechanisms. Therefore, the purpose of this study was to determine whether physiologically elevated circulating hormones modulate resistance exercise (RE)-induced signaling of Akt and its downstream targets. We hypothesized that elevated circulating hormones would potentiate the signaling response. Methods: Seven healthy men (mean ± SD age, 27 ± 4 yr; body mass, 79.1 ± 13.6 kg; body fat, 16% ± 7%) performed two identical lower-body RE protocols (five sets of five maximal repetitions of knee extensions) in a randomized order and separated by 1-3 wk: one protocol was preceded by rest [low-circulating hormonal concentration (LHC) trial], and the other was preceded by a bout of high-volume upper-body RE using short rest periods designed to elicit a large increase in circulating hormones [high-circulating hormonal concentration (HHC) trial]. Results: The HHC trial invoked significantly (P ≤ 0.05) greater growth hormone (GH) and cortisol concentrations compared with the LHC trial. There were minimal differences between trials in insulin and insulin-like growth factor-I (IGF-I) concentrations. Contrary to our hypothesis, 70-kDa ribosomal protein S6 kinase (p70 S6K) threonine (Thr) 389 phosphorylation within the vastus lateralis was attenuated at 180 min post-RE during the HHC trial. RE did not affect Akt or glycogen synthase kinase-3β (GSK-3β) phosphorylation nor were there differences between trials. Immediately post-RE, eukaryotic initiation factor (elF) 4E binding protein-1 (4E-BP1) phosphorylation declined, and adenosine monophosphate-activated protein kinase (AMPK) phosphorylation increased; however, there were no differences between trials in these variables. Conclusion: p70 S6K Thr 389 phosphorylation was attenuated during the HHC trial despite dramatically greater (<2.5-fold) circulating GH concentrations; this was potentially due to cortisol-induced inhibition of p70 S6K Thr 389 phosphorylation.

原文英語
頁(從 - 到)1039-1048
頁數10
期刊Medicine and Science in Sports and Exercise
40
發行號6
DOIs
出版狀態已發佈 - 2008 十二月 1

ASJC Scopus subject areas

  • Orthopedics and Sports Medicine
  • Physical Therapy, Sports Therapy and Rehabilitation

指紋 深入研究「Effects of elevated circulating hormones on resistance exercise-induced Akt signaling」主題。共同形成了獨特的指紋。

引用此