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Resistance exercise induced mTORC1 signaling is not impaired by subsequent endurance exercise in human skeletal muscle.
Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Eva Blomstrand's research group.ORCID iD: 0000-0003-1942-2919
Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Research group for Mitokondriell funktion och metabolisk kontroll.
Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Research group for Mitokondriell funktion och metabolisk kontroll.
Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Eva Blomstrand's research group.ORCID iD: 0000-0002-6537-042X
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2013 (English)In: American Journal of Physiology. Endocrinology and Metabolism, ISSN 0193-1849, E-ISSN 1522-1555, Vol. 305, no 1, E22-32 p.Article in journal (Refereed) Published
Abstract [en]

The current dogma is that the muscle adaptation to resistance exercise is blunted when combined with endurance exercise. The suggested mechanism (based on rodent experiments) is that activation of adenosine monophosphate-activated protein kinase (AMPK) during endurance exercise impairs muscle growth through inhibition of the mechanistic target of rapamycin complex 1 (mTORC1). The purpose of this study was to investigate potential interference of endurance training on the signaling pathway of resistance training [mTORC1 phosphorylation of ribosomal protein S6 kinase 1 (S6K1)] in human muscle. Ten healthy and moderately trained male subjects performed on two separate occasions either acute high-intensity and high-volume resistance exercise (leg press, R) or R followed by 30 min of cycling (RE). Muscle biopsies were collected before and 1 and 3 h post resistance exercise. Phosphorylation of mTOR (Ser(2448)) increased 2-fold (P < 0.05) and that of S6K1 (Thr(389)) 14-fold (P < 0.05), with no difference between R and RE. Phosphorylation of eukaryotic elongation factor 2 (eEF2, Thr(56)) was reduced ∼70% during recovery in both trials (P < 0.05). An interesting finding was that phosphorylation of AMPK (Thr(172)) and acetyl-CoA carboxylase (ACC, Ser(79)) decreased ∼30% and ∼50%, respectively, 3 h postexercise (P < 0.05). Proliferator-activated receptor-γ coactivator-1 (PGC-1α) mRNA increased more after RE (6.5-fold) than after R (4-fold) (RE vs. R: P < 0.01) and was the only gene expressed differently between trials. These data show that the signaling of muscle growth through the mTORC1-S6K1 axis after heavy resistance exercise is not inhibited by subsequent endurance exercise. It is also suggested that prior activation of mTORC1 signaling may repress subsequent phosphorylation of AMPK.

Place, publisher, year, edition, pages
2013. Vol. 305, no 1, E22-32 p.
National Category
Physiology
Research subject
Medicine/Technology
Identifiers
URN: urn:nbn:se:gih:diva-2851DOI: 10.1152/ajpendo.00091.2013PubMedID: 23632629OAI: oai:DiVA.org:gih-2851DiVA: diva2:639012
Funder
Swedish National Centre for Research in Sports, P2011-0026
Available from: 2013-08-05 Created: 2013-08-05 Last updated: 2016-06-20Bibliographically approved
In thesis
1. Regulation of protein synthesis in human skeletal muscle: separate and combined effects of exercise and amino acids
Open this publication in new window or tab >>Regulation of protein synthesis in human skeletal muscle: separate and combined effects of exercise and amino acids
2014 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Skeletal muscle is a highly plastic tissue which has the ability to adapt to various forms of external stimuli such as diverse modes of contractile activity. Thus, performance of endurance exercise over several of weeks results in increased oxidative capacity. In contrast, prolonged performance of resistance exercise ultimately results in increased muscle mass. These adaptations are brought about by transient alterations in gene expression and mRNA translation which result in altered protein turnover, i.e. the balance between protein synthesis and protein breakdown. Protein synthesis is the major determinant of muscle growth, which at the molecular level, is regulated by the mTORC1 pathway. This pathway is potently activated by resistance exercise and amino acids, but the stimulatory role of individual amino acids in human skeletal muscle is unclear. Muscle adaptations in response to endurance exercise are largely dependent on the PGC-1 α pathway, which regulates mitochondrial biogenesis. Given the different training adaptations after resistance and endurance exercise, it has been suggested that these exercise modalities may be incompatible when combined. Such potential interference could be exerted at the molecular level between the pathways responsible for each adaptive response. AMPK, an enzyme usually activated by endurance exercise and, when pharmacologically activated in cell culture and rodent models, has been shown to inhibit mTORC1 and protein synthesis. However, it is not known if activation of AMPK by endurance exercise inhibits resistance exercise induced signaling through the mTORC1 pathway in human skeletal muscle.

Thus, the main objective of this thesis was to examine the molecular mechanisms regulating protein synthesis in response to amino acids and various modes of exercise in human skeletal muscle.

In study I, the role of BCAAs in stimulating the mTORC1 pathway was examined in both resting and exercising muscle. BCAA increased mTORC1 activity, as assessed by S6K1 phosphorylation, in both resting and exercising muscle, but more so when exercise and BCAA were combined. In study II, the effect of leucine was compared to that of essential amino acids with or without leucine. It was found that when leucine was combined with the remaining essential amino acids, S6K1 phosphorylation was more pronounced than when leucine was provided alone. Furthermore, when leucine was removed from the essential amino acids, the effect was equal to that of placebo. In study III, the impact of endurance exercise on resistance exercise induced mTORC1 signaling was examined. When performed after resistance exercise, endurance exercise did not inhibit S6K1 phosphorylation compared to when single mode resistance exercise was performed. In study IV, performance of high intensity endurance exercise prior to resistance exercise did not inhibit S6K1 phosphorylation compared to single mode resistance exercise, despite prior activation of AMPK.

In conclusion, amino acids and resistance exercise activate mTORC1 signaling, as assessed by S6K1 phosphorylation, in a synergistic manner. Leucine is crucial in mediating the amino acid response, however, additional amino acids appear to be required to induce a maximal response downstream of mTORC1. Activation of the mTORC1 pathway in response to heavy resistance exercise is robust and this activation does not appear to be inhibited by prior or by subsequent endurance exercise. As such, these results do not lend support to the existence of molecular interference when resistance and endurance exercise are combined acutely.

Place, publisher, year, edition, pages
Karolinska Institutet, 2014
National Category
Medical and Health Sciences
Research subject
Medicine/Technology
Identifiers
urn:nbn:se:gih:diva-3323 (URN)978-91-7549-513-2 (ISBN)
Public defence
2014-06-13, Aulan, Gymnastik- och idrottshögskolan, Lidingövägen 1, Stockholm, 10:00 (English)
Opponent
Supervisors
Available from: 2014-05-28 Created: 2014-05-28 Last updated: 2016-06-20Bibliographically approved

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