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 < or = 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 synthasekinase-3beta (GSK-3beta) phosphorylation nor were there differences between trials. Immediately post-RE, eukaryotic initiation factor (eIF) 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.
RCT Entities:
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 < or = 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-3beta (GSK-3beta) phosphorylation nor were there differences between trials. Immediately post-RE, eukaryotic initiation factor (eIF) 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 S6KThr 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 S6KThr 389 phosphorylation.
Authors: Jenna M Apicella; Elaine C Lee; Brooke L Bailey; Catherine Saenz; Jeffrey M Anderson; Stuart A S Craig; William J Kraemer; Jeff S Volek; Carl M Maresh Journal: Eur J Appl Physiol Date: 2012-09-14 Impact factor: 3.078
Authors: Stephen M Cornish; Eric M Bugera; Todd A Duhamel; Jason D Peeler; Judy E Anderson Journal: Eur J Appl Physiol Date: 2020-03-06 Impact factor: 3.078
Authors: Adam M Gonzalez; Jay R Hoffman; Jeremy R Townsend; Adam R Jajtner; Carleigh H Boone; Kyle S Beyer; Kayla M Baker; Adam J Wells; Gerald T Mangine; Edward H Robinson; David D Church; Leonardo P Oliveira; Darryn S Willoughby; David H Fukuda; Jeffrey R Stout Journal: Physiol Rep Date: 2015-07
Authors: Gerald T Mangine; Jay R Hoffman; Adam M Gonzalez; Jeremy R Townsend; Adam J Wells; Adam R Jajtner; Kyle S Beyer; Carleigh H Boone; Amelia A Miramonti; Ran Wang; Michael B LaMonica; David H Fukuda; Nicholas A Ratamess; Jeffrey R Stout Journal: Physiol Rep Date: 2015-08