Exercise-induced molecular mechanisms promoting glycogen supercompensation in human skeletal muscle

Research output: Contribution to journalJournal articleResearchpeer-review

Standard

Exercise-induced molecular mechanisms promoting glycogen supercompensation in human skeletal muscle. / Hingst, Janne Rasmuss; Bruhn, Lea; Hansen, Mads B; Rosschou, Marie F; Birk, Jesper Bratz; Fentz, Joachim; Foretz, Marc; Viollet, Benoit; Sakamoto, Kei; Færgeman, Nils J; Havelund, Jesper F; Parker, Benjamin L; James, David E; Kiens, Bente; Richter, Erik A.; Jensen, Jørgen; Wojtaszewski, Jørgen.

In: Molecular Metabolism, Vol. 16, 2018, p. 24-34.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Hingst, JR, Bruhn, L, Hansen, MB, Rosschou, MF, Birk, JB, Fentz, J, Foretz, M, Viollet, B, Sakamoto, K, Færgeman, NJ, Havelund, JF, Parker, BL, James, DE, Kiens, B, Richter, EA, Jensen, J & Wojtaszewski, J 2018, 'Exercise-induced molecular mechanisms promoting glycogen supercompensation in human skeletal muscle', Molecular Metabolism, vol. 16, pp. 24-34. https://doi.org/10.1016/j.molmet.2018.07.001

APA

Hingst, J. R., Bruhn, L., Hansen, M. B., Rosschou, M. F., Birk, J. B., Fentz, J., ... Wojtaszewski, J. (2018). Exercise-induced molecular mechanisms promoting glycogen supercompensation in human skeletal muscle. Molecular Metabolism, 16, 24-34. https://doi.org/10.1016/j.molmet.2018.07.001

Vancouver

Hingst JR, Bruhn L, Hansen MB, Rosschou MF, Birk JB, Fentz J et al. Exercise-induced molecular mechanisms promoting glycogen supercompensation in human skeletal muscle. Molecular Metabolism. 2018;16:24-34. https://doi.org/10.1016/j.molmet.2018.07.001

Author

Hingst, Janne Rasmuss ; Bruhn, Lea ; Hansen, Mads B ; Rosschou, Marie F ; Birk, Jesper Bratz ; Fentz, Joachim ; Foretz, Marc ; Viollet, Benoit ; Sakamoto, Kei ; Færgeman, Nils J ; Havelund, Jesper F ; Parker, Benjamin L ; James, David E ; Kiens, Bente ; Richter, Erik A. ; Jensen, Jørgen ; Wojtaszewski, Jørgen. / Exercise-induced molecular mechanisms promoting glycogen supercompensation in human skeletal muscle. In: Molecular Metabolism. 2018 ; Vol. 16. pp. 24-34.

Bibtex

@article{c168c1d31dd54a39992314059b8b8a0d,
title = "Exercise-induced molecular mechanisms promoting glycogen supercompensation in human skeletal muscle",
abstract = "Objective: A single bout of exercise followed by intake of carbohydrates leads to glycogen supercompensation in prior exercised muscle. Our objective was to illuminate molecular mechanisms underlying this phenomenon in skeletal muscle of man. Methods: We studied the temporal regulation of glycogen supercompensation in human skeletal muscle during a 5 day recovery period following a single bout of exercise. Nine healthy men depleted (day 1), normalized (day 2) and supercompensated (day 5) muscle glycogen in one leg while the contralateral leg served as a resting control. Euglycemic hyperinsulinemic clamps in combination with leg balance technique allowed for investigating insulin-stimulated leg glucose uptake under these 3 experimental conditions. Cellular signaling in muscle biopsies was investigated by global proteomic analyses and immunoblotting. We strengthened the validity of proposed molecular effectors by follow-up studies in muscle of transgenic mice. Results: Sustained activation of glycogen synthase (GS) and AMPK in combination with elevated expression of proteins determining glucose uptake capacity were evident in the prior exercised muscle. We hypothesize that these alterations offset the otherwise tight feedback inhibition of glycogen synthesis and glucose uptake by glycogen. In line with key roles of AMPK and GS seen in the human experiments we observed abrogated ability for glycogen supercompensation in muscle with inducible AMPK deletion and in muscle carrying a G6P-insensitive form of GS in muscle. Conclusion: Our study demonstrates that both AMPK and GS are key regulators of glycogen supercompensation following a single bout of glycogen-depleting exercise in skeletal muscle of both man and mouse.",
keywords = "AMP-activated protein kinase (AMPK), Exercise, Glucose uptake, Glycogen synthase (GS), Insulin action, TBC1 domain family member 4 (TBC1D4)",
author = "Hingst, {Janne Rasmuss} and Lea Bruhn and Hansen, {Mads B} and Rosschou, {Marie F} and Birk, {Jesper Bratz} and Joachim Fentz and Marc Foretz and Benoit Viollet and Kei Sakamoto and F{\ae}rgeman, {Nils J} and Havelund, {Jesper F} and Parker, {Benjamin L} and James, {David E} and Bente Kiens and Richter, {Erik A.} and J{\o}rgen Jensen and J{\o}rgen Wojtaszewski",
note = "CURIS 2018 NEXS 269",
year = "2018",
doi = "10.1016/j.molmet.2018.07.001",
language = "English",
volume = "16",
pages = "24--34",
journal = "Molecular Metabolism",
issn = "2212-8778",
publisher = "Elsevier",

}

RIS

TY - JOUR

T1 - Exercise-induced molecular mechanisms promoting glycogen supercompensation in human skeletal muscle

AU - Hingst, Janne Rasmuss

AU - Bruhn, Lea

AU - Hansen, Mads B

AU - Rosschou, Marie F

AU - Birk, Jesper Bratz

AU - Fentz, Joachim

AU - Foretz, Marc

AU - Viollet, Benoit

AU - Sakamoto, Kei

AU - Færgeman, Nils J

AU - Havelund, Jesper F

AU - Parker, Benjamin L

AU - James, David E

AU - Kiens, Bente

AU - Richter, Erik A.

AU - Jensen, Jørgen

AU - Wojtaszewski, Jørgen

N1 - CURIS 2018 NEXS 269

PY - 2018

Y1 - 2018

N2 - Objective: A single bout of exercise followed by intake of carbohydrates leads to glycogen supercompensation in prior exercised muscle. Our objective was to illuminate molecular mechanisms underlying this phenomenon in skeletal muscle of man. Methods: We studied the temporal regulation of glycogen supercompensation in human skeletal muscle during a 5 day recovery period following a single bout of exercise. Nine healthy men depleted (day 1), normalized (day 2) and supercompensated (day 5) muscle glycogen in one leg while the contralateral leg served as a resting control. Euglycemic hyperinsulinemic clamps in combination with leg balance technique allowed for investigating insulin-stimulated leg glucose uptake under these 3 experimental conditions. Cellular signaling in muscle biopsies was investigated by global proteomic analyses and immunoblotting. We strengthened the validity of proposed molecular effectors by follow-up studies in muscle of transgenic mice. Results: Sustained activation of glycogen synthase (GS) and AMPK in combination with elevated expression of proteins determining glucose uptake capacity were evident in the prior exercised muscle. We hypothesize that these alterations offset the otherwise tight feedback inhibition of glycogen synthesis and glucose uptake by glycogen. In line with key roles of AMPK and GS seen in the human experiments we observed abrogated ability for glycogen supercompensation in muscle with inducible AMPK deletion and in muscle carrying a G6P-insensitive form of GS in muscle. Conclusion: Our study demonstrates that both AMPK and GS are key regulators of glycogen supercompensation following a single bout of glycogen-depleting exercise in skeletal muscle of both man and mouse.

AB - Objective: A single bout of exercise followed by intake of carbohydrates leads to glycogen supercompensation in prior exercised muscle. Our objective was to illuminate molecular mechanisms underlying this phenomenon in skeletal muscle of man. Methods: We studied the temporal regulation of glycogen supercompensation in human skeletal muscle during a 5 day recovery period following a single bout of exercise. Nine healthy men depleted (day 1), normalized (day 2) and supercompensated (day 5) muscle glycogen in one leg while the contralateral leg served as a resting control. Euglycemic hyperinsulinemic clamps in combination with leg balance technique allowed for investigating insulin-stimulated leg glucose uptake under these 3 experimental conditions. Cellular signaling in muscle biopsies was investigated by global proteomic analyses and immunoblotting. We strengthened the validity of proposed molecular effectors by follow-up studies in muscle of transgenic mice. Results: Sustained activation of glycogen synthase (GS) and AMPK in combination with elevated expression of proteins determining glucose uptake capacity were evident in the prior exercised muscle. We hypothesize that these alterations offset the otherwise tight feedback inhibition of glycogen synthesis and glucose uptake by glycogen. In line with key roles of AMPK and GS seen in the human experiments we observed abrogated ability for glycogen supercompensation in muscle with inducible AMPK deletion and in muscle carrying a G6P-insensitive form of GS in muscle. Conclusion: Our study demonstrates that both AMPK and GS are key regulators of glycogen supercompensation following a single bout of glycogen-depleting exercise in skeletal muscle of both man and mouse.

KW - AMP-activated protein kinase (AMPK)

KW - Exercise

KW - Glucose uptake

KW - Glycogen synthase (GS)

KW - Insulin action

KW - TBC1 domain family member 4 (TBC1D4)

U2 - 10.1016/j.molmet.2018.07.001

DO - 10.1016/j.molmet.2018.07.001

M3 - Journal article

C2 - 30093357

AN - SCOPUS:85050996496

VL - 16

SP - 24

EP - 34

JO - Molecular Metabolism

JF - Molecular Metabolism

SN - 2212-8778

ER -

ID: 200969099