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

Research output: Contribution to journalArticlepeer-review

37 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)1039-1048
Number of pages10
JournalMedicine and Science in Sports and Exercise
Issue number6
Publication statusPublished - 2008
Externally publishedYes


  • Endocrine
  • MTOR
  • Muscle signaling
  • PKB

ASJC Scopus subject areas

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


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