PGC-1α and exercise intensity dependent adaptations in mouse skeletal muscle

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PGC-1α and exercise intensity dependent adaptations in mouse skeletal muscle. / Brandt, Nina; Dethlefsen, Maja Munk; Bangsbo, Jens; Pilegaard, Henriette.

I: P L o S One, Bind 12, Nr. 10, e0185993, 2017.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Brandt, N, Dethlefsen, MM, Bangsbo, J & Pilegaard, H 2017, 'PGC-1α and exercise intensity dependent adaptations in mouse skeletal muscle', P L o S One, bind 12, nr. 10, e0185993. https://doi.org/10.1371/journal.pone.0185993

APA

Brandt, N., Dethlefsen, M. M., Bangsbo, J., & Pilegaard, H. (2017). PGC-1α and exercise intensity dependent adaptations in mouse skeletal muscle. P L o S One, 12(10), [e0185993]. https://doi.org/10.1371/journal.pone.0185993

Vancouver

Brandt N, Dethlefsen MM, Bangsbo J, Pilegaard H. PGC-1α and exercise intensity dependent adaptations in mouse skeletal muscle. P L o S One. 2017;12(10). e0185993. https://doi.org/10.1371/journal.pone.0185993

Author

Brandt, Nina ; Dethlefsen, Maja Munk ; Bangsbo, Jens ; Pilegaard, Henriette. / PGC-1α and exercise intensity dependent adaptations in mouse skeletal muscle. I: P L o S One. 2017 ; Bind 12, Nr. 10.

Bibtex

@article{dfc2189a5a5e47518c265bde170c8ee2,
title = "PGC-1α and exercise intensity dependent adaptations in mouse skeletal muscle",
abstract = "The aim of the present study was to examine the role of PGC-1α in intensity dependent exercise and exercise training-induced metabolic adaptations in mouse skeletal muscle. Whole body PGC-1α knockout (KO) and littermate wildtype (WT) mice performed a single treadmill running bout at either low intensity (LI) for 40 min or moderate intensity (MI) for 20 min. Blood and quadriceps muscles were removed either immediately after exercise or at 3h or 6h into recovery from exercise and from resting controls. In addition PGC-1α KO and littermate WT mice were exercise trained at either low intensity (LIT) for 40 min or at moderate intensity (MIT) for 20 min 2 times pr. day for 5 weeks. In the first and the last week of the intervention period, mice performed a graded running endurance test. Quadriceps muscles were removed before and after the training period for analyses. The acute exercise bout elicited intensity dependent increases in LC3I and LC3II protein and intensity independent decrease in p62 protein in skeletal muscle late in recovery and increased LC3II with exercise training independent of exercise intensity and volume in WT mice. Furthermore, acute exercise and exercise training did not increase LC3I and LC3II protein in PGC-1α KO. In addition, exercise-induced mRNA responses of PGC-1α isoforms were intensity dependent. In conclusion, these findings indicate that exercise intensity affected autophagy markers differently in skeletal muscle and suggest that PGC-1α regulates both acute and exercise training-induced autophagy in skeletal muscle potentially in a PGC-1α isoform specific manner.",
keywords = "Journal Article",
author = "Nina Brandt and Dethlefsen, {Maja Munk} and Jens Bangsbo and Henriette Pilegaard",
note = "CURIS 2017 NEXS 279",
year = "2017",
doi = "10.1371/journal.pone.0185993",
language = "English",
volume = "12",
journal = "P L o S One",
issn = "1932-6203",
publisher = "Public Library of Science",
number = "10",

}

RIS

TY - JOUR

T1 - PGC-1α and exercise intensity dependent adaptations in mouse skeletal muscle

AU - Brandt, Nina

AU - Dethlefsen, Maja Munk

AU - Bangsbo, Jens

AU - Pilegaard, Henriette

N1 - CURIS 2017 NEXS 279

PY - 2017

Y1 - 2017

N2 - The aim of the present study was to examine the role of PGC-1α in intensity dependent exercise and exercise training-induced metabolic adaptations in mouse skeletal muscle. Whole body PGC-1α knockout (KO) and littermate wildtype (WT) mice performed a single treadmill running bout at either low intensity (LI) for 40 min or moderate intensity (MI) for 20 min. Blood and quadriceps muscles were removed either immediately after exercise or at 3h or 6h into recovery from exercise and from resting controls. In addition PGC-1α KO and littermate WT mice were exercise trained at either low intensity (LIT) for 40 min or at moderate intensity (MIT) for 20 min 2 times pr. day for 5 weeks. In the first and the last week of the intervention period, mice performed a graded running endurance test. Quadriceps muscles were removed before and after the training period for analyses. The acute exercise bout elicited intensity dependent increases in LC3I and LC3II protein and intensity independent decrease in p62 protein in skeletal muscle late in recovery and increased LC3II with exercise training independent of exercise intensity and volume in WT mice. Furthermore, acute exercise and exercise training did not increase LC3I and LC3II protein in PGC-1α KO. In addition, exercise-induced mRNA responses of PGC-1α isoforms were intensity dependent. In conclusion, these findings indicate that exercise intensity affected autophagy markers differently in skeletal muscle and suggest that PGC-1α regulates both acute and exercise training-induced autophagy in skeletal muscle potentially in a PGC-1α isoform specific manner.

AB - The aim of the present study was to examine the role of PGC-1α in intensity dependent exercise and exercise training-induced metabolic adaptations in mouse skeletal muscle. Whole body PGC-1α knockout (KO) and littermate wildtype (WT) mice performed a single treadmill running bout at either low intensity (LI) for 40 min or moderate intensity (MI) for 20 min. Blood and quadriceps muscles were removed either immediately after exercise or at 3h or 6h into recovery from exercise and from resting controls. In addition PGC-1α KO and littermate WT mice were exercise trained at either low intensity (LIT) for 40 min or at moderate intensity (MIT) for 20 min 2 times pr. day for 5 weeks. In the first and the last week of the intervention period, mice performed a graded running endurance test. Quadriceps muscles were removed before and after the training period for analyses. The acute exercise bout elicited intensity dependent increases in LC3I and LC3II protein and intensity independent decrease in p62 protein in skeletal muscle late in recovery and increased LC3II with exercise training independent of exercise intensity and volume in WT mice. Furthermore, acute exercise and exercise training did not increase LC3I and LC3II protein in PGC-1α KO. In addition, exercise-induced mRNA responses of PGC-1α isoforms were intensity dependent. In conclusion, these findings indicate that exercise intensity affected autophagy markers differently in skeletal muscle and suggest that PGC-1α regulates both acute and exercise training-induced autophagy in skeletal muscle potentially in a PGC-1α isoform specific manner.

KW - Journal Article

U2 - 10.1371/journal.pone.0185993

DO - 10.1371/journal.pone.0185993

M3 - Journal article

C2 - 29049322

VL - 12

JO - P L o S One

JF - P L o S One

SN - 1932-6203

IS - 10

M1 - e0185993

ER -

ID: 184877678