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Resistance exercise-induced S6K1 kinase activity is not inhibited in human skeletal muscle despite prior activation of AMPK by high-intensity interval cycling
Swedish Sch Sport & Hlth Sci, Astrand Lab, SE-11486 Stockholm, Sweden.
Swedish Sch Sport & Hlth Sci, Astrand Lab, SE-11486 Stockholm, Sweden.
Univ Stirling, Hlth & Exercise Sci Res Grp, Stirling FK9 4LA, Scotland.
Swedish Sch Sport & Hlth Sci, Astrand Lab, SE-11486 Stockholm, Sweden.
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2015 (English)In: American Journal of Physiology. Endocrinology and Metabolism, ISSN 0193-1849, E-ISSN 1522-1555, Vol. 308, no 6, E470-E481 p.Article in journal (Refereed) Published
Abstract [en]

Combining endurance and strength training in the same session has been reported to reduce the anabolic response to the latter form of exercise. The underlying mechanism, based primarily on results from rodent muscle, is proposed to involve AMPK-dependent inhibition of mTORC1 signaling. This hypothesis was tested in eight trained male subjects who in randomized order performed either resistance exercise only (R) or interval cycling followed by resistance exercise (ER). Biopsies taken from the vastus lateralis before and after endurance exercise and repeatedly after resistance exercise were assessed for glycogen content, kinase activity, protein phosphorylation, and gene expression. Mixed muscle fractional synthetic rate was measured at rest and during 3 h of recovery using the stable isotope technique. In ER, AMPK activity was elevated immediately after both endurance and resistance exercise (similar to 90%, P < 0.05) but was unchanged in R. Thr(389) phosphorylation of S6K1 was increased severalfold immediately after exercise (P < 0.05) in both trials and increased further throughout recovery. After 90 and 180 min recovery, S6K1 activity was elevated (similar to 55 and similar to 110%, respectively, P < 0.05) and eukaryotic elongation factor 2 phosphorylation was reduced (similar to 55%, P < 0.05) with no difference between trials. In contrast, markers for protein catabolism were differently influenced by the two modes of exercise; ER induced a significant increase in gene and protein expression of MuRF1 (P < 0.05), which was not observed following R exercise only. In conclusion, cycling-induced elevation in AMPK activity does not inhibit mTOR complex 1 signaling after subsequent resistance exercise but may instead interfere with the hypertrophic response by influencing key components in protein breakdown.

Place, publisher, year, edition, pages
2015. Vol. 308, no 6, E470-E481 p.
Keyword [en]
AMPK, concurrent exercise, S6K1, mTORC1
National Category
Sport and Fitness Sciences
Identifiers
URN: urn:nbn:se:miun:diva-25653DOI: 10.1152/ajpendo.00486.2014ISI: 000351062500004PubMedID: 25605643Scopus ID: 2-s2.0-84930905029OAI: oai:DiVA.org:miun-25653DiVA: diva2:849411
Available from: 2015-08-28 Created: 2015-08-18 Last updated: 2015-08-28Bibliographically approved

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