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Effects of elevated circulating hormones on resistance exercise-induced Akt signaling.
Med Sci Sports Exerc. 2008 Jun; 40(6):1039-48.MS

Abstract

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 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.

Authors+Show Affiliations

Human Performance Laboratory, Department of Kinesiology, University of Connecticut, Storrs, CT 06269, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18461003

Citation

Spiering, Barry A., et al. "Effects of Elevated Circulating Hormones On Resistance Exercise-induced Akt Signaling." Medicine and Science in Sports and Exercise, vol. 40, no. 6, 2008, pp. 1039-48.
Spiering BA, Kraemer WJ, Anderson JM, et al. Effects of elevated circulating hormones on resistance exercise-induced Akt signaling. Med Sci Sports Exerc. 2008;40(6):1039-48.
Spiering, B. A., Kraemer, W. J., Anderson, J. M., Armstrong, L. E., Nindl, B. C., Volek, J. S., Judelson, D. A., Joseph, M., Vingren, J. L., Hatfield, D. L., Fragala, M. S., Ho, J. Y., & Maresh, C. M. (2008). Effects of elevated circulating hormones on resistance exercise-induced Akt signaling. Medicine and Science in Sports and Exercise, 40(6), 1039-48. https://doi.org/10.1249/MSS.0b013e31816722bd
Spiering BA, et al. Effects of Elevated Circulating Hormones On Resistance Exercise-induced Akt Signaling. Med Sci Sports Exerc. 2008;40(6):1039-48. PubMed PMID: 18461003.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effects of elevated circulating hormones on resistance exercise-induced Akt signaling. AU - Spiering,Barry A, AU - Kraemer,William J, AU - Anderson,Jeffrey M, AU - Armstrong,Lawrence E, AU - Nindl,Bradley C, AU - Volek,Jeff S, AU - Judelson,Daniel A, AU - Joseph,Michael, AU - Vingren,Jakob L, AU - Hatfield,Disa L, AU - Fragala,Maren S, AU - Ho,Jen-Yu, AU - Maresh,Carl M, PY - 2008/5/8/pubmed PY - 2008/10/22/medline PY - 2008/5/8/entrez SP - 1039 EP - 48 JF - Medicine and science in sports and exercise JO - Med Sci Sports Exerc VL - 40 IS - 6 N2 - 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 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. SN - 0195-9131 UR - https://www.unboundmedicine.com/medline/citation/18461003/Effects_of_elevated_circulating_hormones_on_resistance_exercise_induced_Akt_signaling_ L2 - https://doi.org/10.1249/MSS.0b013e31816722bd DB - PRIME DP - Unbound Medicine ER -