Exercise and exercise training-induced increase in autophagy markers in human skeletal muscle

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Exercise and exercise training-induced increase in autophagy markers in human skeletal muscle. / Brandt, Nina; Gunnarsson, Thomas Gunnar Petursson; Bangsbo, Jens; Pilegaard, Henriette.

I: Physiological Reports, Bind 6, Nr. 7, e13651, 2018.

Publikation: Bidrag til tidsskriftTidsskriftartikelfagfællebedømt

Harvard

Brandt, N, Gunnarsson, TGP, Bangsbo, J & Pilegaard, H 2018, 'Exercise and exercise training-induced increase in autophagy markers in human skeletal muscle', Physiological Reports, bind 6, nr. 7, e13651. https://doi.org/10.14814/phy2.13651

APA

Brandt, N., Gunnarsson, T. G. P., Bangsbo, J., & Pilegaard, H. (2018). Exercise and exercise training-induced increase in autophagy markers in human skeletal muscle. Physiological Reports, 6(7), [e13651]. https://doi.org/10.14814/phy2.13651

Vancouver

Brandt N, Gunnarsson TGP, Bangsbo J, Pilegaard H. Exercise and exercise training-induced increase in autophagy markers in human skeletal muscle. Physiological Reports. 2018;6(7). e13651. https://doi.org/10.14814/phy2.13651

Author

Brandt, Nina ; Gunnarsson, Thomas Gunnar Petursson ; Bangsbo, Jens ; Pilegaard, Henriette. / Exercise and exercise training-induced increase in autophagy markers in human skeletal muscle. I: Physiological Reports. 2018 ; Bind 6, Nr. 7.

Bibtex

@article{1515250779ce4bca9352d4b492c6ebd0,
title = "Exercise and exercise training-induced increase in autophagy markers in human skeletal muscle",
abstract = "Moderately trained male subjects (mean age 25 years; range 19-33 years) completed an 8-week exercise training intervention consisting of continuous moderate cycling at 157 ± 20 W for 60 min (MOD; n = 6) or continuous moderate cycling (157 ± 20 W) interspersed by 30-sec sprints (473 ± 79 W) every 10 min (SPRINT; n = 6) 3 days per week. Sprints were followed by 3:24 min at 102 ± 17 W to match the total work between protocols. A muscle biopsy was obtained before, immediately and 2 h after the first training session as well as at rest after the training session. In both MOD and SPRINT, skeletal muscle AMPKThr172 and ULKSer317 phosphorylation was elevated immediately after exercise, whereas mTORSer2448 and ULKSer757 phosphorylation was unchanged. Two hours after exercise LC3I, LC3II and BNIP3 protein content was overall higher than before exercise with no change in p62 protein. In MOD, Beclin1 protein content was higher immediately and 2 h after exercise than before exercise, while there were no differences within SPRINT. Oxphos complex I, LC3I, BNIP3 and Parkin protein content was higher after the training intervention than before in both groups, while there was no difference in LC3II and p62 protein. Beclin1 protein content was higher after the exercise training intervention only in MOD. Together this suggests that exercise increases markers of autophagy in human skeletal muscle within the first 2 h of recovery and 8 weeks of exercise training increases the capacity for autophagy and mitophagy regulation. Hence, the present findings provide evidence that exercise and exercise training regulate autophagy in human skeletal muscle and that this in general was unaffected by interspersed sprint bouts.",
keywords = "Faculty of Science, Autophagy, High-intensity exercise training, Skeletal muscle",
author = "Nina Brandt and Gunnarsson, {Thomas Gunnar Petursson} and Jens Bangsbo and Henriette Pilegaard",
note = "CURIS 2018 NEXS 130",
year = "2018",
doi = "10.14814/phy2.13651",
language = "English",
volume = "6",
journal = "Physiological Reports",
issn = "2051-817X",
publisher = "Wiley Periodicals, Inc.",
number = "7",

}

RIS

TY - JOUR

T1 - Exercise and exercise training-induced increase in autophagy markers in human skeletal muscle

AU - Brandt, Nina

AU - Gunnarsson, Thomas Gunnar Petursson

AU - Bangsbo, Jens

AU - Pilegaard, Henriette

N1 - CURIS 2018 NEXS 130

PY - 2018

Y1 - 2018

N2 - Moderately trained male subjects (mean age 25 years; range 19-33 years) completed an 8-week exercise training intervention consisting of continuous moderate cycling at 157 ± 20 W for 60 min (MOD; n = 6) or continuous moderate cycling (157 ± 20 W) interspersed by 30-sec sprints (473 ± 79 W) every 10 min (SPRINT; n = 6) 3 days per week. Sprints were followed by 3:24 min at 102 ± 17 W to match the total work between protocols. A muscle biopsy was obtained before, immediately and 2 h after the first training session as well as at rest after the training session. In both MOD and SPRINT, skeletal muscle AMPKThr172 and ULKSer317 phosphorylation was elevated immediately after exercise, whereas mTORSer2448 and ULKSer757 phosphorylation was unchanged. Two hours after exercise LC3I, LC3II and BNIP3 protein content was overall higher than before exercise with no change in p62 protein. In MOD, Beclin1 protein content was higher immediately and 2 h after exercise than before exercise, while there were no differences within SPRINT. Oxphos complex I, LC3I, BNIP3 and Parkin protein content was higher after the training intervention than before in both groups, while there was no difference in LC3II and p62 protein. Beclin1 protein content was higher after the exercise training intervention only in MOD. Together this suggests that exercise increases markers of autophagy in human skeletal muscle within the first 2 h of recovery and 8 weeks of exercise training increases the capacity for autophagy and mitophagy regulation. Hence, the present findings provide evidence that exercise and exercise training regulate autophagy in human skeletal muscle and that this in general was unaffected by interspersed sprint bouts.

AB - Moderately trained male subjects (mean age 25 years; range 19-33 years) completed an 8-week exercise training intervention consisting of continuous moderate cycling at 157 ± 20 W for 60 min (MOD; n = 6) or continuous moderate cycling (157 ± 20 W) interspersed by 30-sec sprints (473 ± 79 W) every 10 min (SPRINT; n = 6) 3 days per week. Sprints were followed by 3:24 min at 102 ± 17 W to match the total work between protocols. A muscle biopsy was obtained before, immediately and 2 h after the first training session as well as at rest after the training session. In both MOD and SPRINT, skeletal muscle AMPKThr172 and ULKSer317 phosphorylation was elevated immediately after exercise, whereas mTORSer2448 and ULKSer757 phosphorylation was unchanged. Two hours after exercise LC3I, LC3II and BNIP3 protein content was overall higher than before exercise with no change in p62 protein. In MOD, Beclin1 protein content was higher immediately and 2 h after exercise than before exercise, while there were no differences within SPRINT. Oxphos complex I, LC3I, BNIP3 and Parkin protein content was higher after the training intervention than before in both groups, while there was no difference in LC3II and p62 protein. Beclin1 protein content was higher after the exercise training intervention only in MOD. Together this suggests that exercise increases markers of autophagy in human skeletal muscle within the first 2 h of recovery and 8 weeks of exercise training increases the capacity for autophagy and mitophagy regulation. Hence, the present findings provide evidence that exercise and exercise training regulate autophagy in human skeletal muscle and that this in general was unaffected by interspersed sprint bouts.

KW - Faculty of Science

KW - Autophagy

KW - High-intensity exercise training

KW - Skeletal muscle

U2 - 10.14814/phy2.13651

DO - 10.14814/phy2.13651

M3 - Journal article

C2 - 29626392

VL - 6

JO - Physiological Reports

JF - Physiological Reports

SN - 2051-817X

IS - 7

M1 - e13651

ER -

ID: 195154372