Chronic β2 -adrenoceptor agonist treatment alters muscle proteome and functional adaptations induced by high intensity training in young men

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Chronic β2 -adrenoceptor agonist treatment alters muscle proteome and functional adaptations induced by high intensity training in young men. / Hostrup, Morten; Onslev, Johan; Jacobson, Glenn; Wilson, Richard; Bangsbo, Jens.

I: Journal of Physiology, Bind 596, Nr. 2, 2018, s. 231-252.

Publikation: Bidrag til tidsskriftTidsskriftartikelfagfællebedømt

Harvard

Hostrup, M, Onslev, J, Jacobson, G, Wilson, R & Bangsbo, J 2018, 'Chronic β2 -adrenoceptor agonist treatment alters muscle proteome and functional adaptations induced by high intensity training in young men', Journal of Physiology, bind 596, nr. 2, s. 231-252. https://doi.org/10.1113/JP274970

APA

Hostrup, M., Onslev, J., Jacobson, G., Wilson, R., & Bangsbo, J. (2018). Chronic β2 -adrenoceptor agonist treatment alters muscle proteome and functional adaptations induced by high intensity training in young men. Journal of Physiology, 596(2), 231-252. https://doi.org/10.1113/JP274970

Vancouver

Hostrup M, Onslev J, Jacobson G, Wilson R, Bangsbo J. Chronic β2 -adrenoceptor agonist treatment alters muscle proteome and functional adaptations induced by high intensity training in young men. Journal of Physiology. 2018;596(2):231-252. https://doi.org/10.1113/JP274970

Author

Hostrup, Morten ; Onslev, Johan ; Jacobson, Glenn ; Wilson, Richard ; Bangsbo, Jens. / Chronic β2 -adrenoceptor agonist treatment alters muscle proteome and functional adaptations induced by high intensity training in young men. I: Journal of Physiology. 2018 ; Bind 596, Nr. 2. s. 231-252.

Bibtex

@article{fc134c29f03d4ba29ca5757a3bdbcd57,
title = "Chronic β2 -adrenoceptor agonist treatment alters muscle proteome and functional adaptations induced by high intensity training in young men",
abstract = "Although the effects of training have been studied for decades, data on muscle proteome signature remodelling induced by high intensity training in relation to functional changes in humans remains incomplete. Likewise, β2 -agonists are frequently used to counteract exercise-induced bronchoconstriction, but the effects β2 -agonist treatment on muscle remodelling and adaptations to training are unknown. In a placebo-controlled parallel study, we randomized 21 trained men to four weeks of high intensity training with (HIT + β2 A) or without (HIT) daily inhalation of β2 -agonist (terbutaline, 4 mg d(-1) ). Of 486 proteins identified by mass-spectrometry proteomics of muscle biopsies sampled before and after the intervention, 32 and 85 were changing (FDR ≤ 5%) with the intervention in HIT and HIT + β2 A. Proteome signature changes were different in HIT and HIT + β2 A (P = 0.005), wherein β2 -agonist caused a repression of 25 proteins in HIT + β2 A compared to HIT, and an upregulation of 7 proteins compared to HIT. β2 -agonist repressed or even downregulated training-induced enrichment of pathways related to oxidative phosphorylation and glycogen metabolism, but upregulated pathways related to histone trimethylation and the nucleosome. Muscle contractile phenotype changed differently in HIT and HIT + β2 A (P ≤ 0.001), with a fast-to-slow twitch transition in HIT and a slow-to-fast twitch transition in HIT + β2 A. β2 -agonist attenuated training-induced enhancements in maximal oxygen consumption (P ≤ 0.01) and exercise performance (11.6 vs. 6.1%, P ≤ 0.05) in HIT + β2 A compared to HIT. These findings indicate that daily β2 -agonist treatment attenuates the beneficial effects of high intensity training on exercise performance and oxidative capacity, and causes remodelling of muscle proteome signature towards a fast-twitch phenotype. This article is protected by copyright. All rights reserved.",
keywords = "Physical activity, Proteomics, Metabolism, Beta-agonists, Adrenoceptors, Adrenergic, VO2max, Terbutaline, HIT, Athletes",
author = "Morten Hostrup and Johan Onslev and Glenn Jacobson and Richard Wilson and Jens Bangsbo",
note = "CURIS 2018 NEXS 031",
year = "2018",
doi = "10.1113/JP274970",
language = "English",
volume = "596",
pages = "231--252",
journal = "The Journal of Physiology",
issn = "0022-3751",
publisher = "Wiley-Blackwell",
number = "2",

}

RIS

TY - JOUR

T1 - Chronic β2 -adrenoceptor agonist treatment alters muscle proteome and functional adaptations induced by high intensity training in young men

AU - Hostrup, Morten

AU - Onslev, Johan

AU - Jacobson, Glenn

AU - Wilson, Richard

AU - Bangsbo, Jens

N1 - CURIS 2018 NEXS 031

PY - 2018

Y1 - 2018

N2 - Although the effects of training have been studied for decades, data on muscle proteome signature remodelling induced by high intensity training in relation to functional changes in humans remains incomplete. Likewise, β2 -agonists are frequently used to counteract exercise-induced bronchoconstriction, but the effects β2 -agonist treatment on muscle remodelling and adaptations to training are unknown. In a placebo-controlled parallel study, we randomized 21 trained men to four weeks of high intensity training with (HIT + β2 A) or without (HIT) daily inhalation of β2 -agonist (terbutaline, 4 mg d(-1) ). Of 486 proteins identified by mass-spectrometry proteomics of muscle biopsies sampled before and after the intervention, 32 and 85 were changing (FDR ≤ 5%) with the intervention in HIT and HIT + β2 A. Proteome signature changes were different in HIT and HIT + β2 A (P = 0.005), wherein β2 -agonist caused a repression of 25 proteins in HIT + β2 A compared to HIT, and an upregulation of 7 proteins compared to HIT. β2 -agonist repressed or even downregulated training-induced enrichment of pathways related to oxidative phosphorylation and glycogen metabolism, but upregulated pathways related to histone trimethylation and the nucleosome. Muscle contractile phenotype changed differently in HIT and HIT + β2 A (P ≤ 0.001), with a fast-to-slow twitch transition in HIT and a slow-to-fast twitch transition in HIT + β2 A. β2 -agonist attenuated training-induced enhancements in maximal oxygen consumption (P ≤ 0.01) and exercise performance (11.6 vs. 6.1%, P ≤ 0.05) in HIT + β2 A compared to HIT. These findings indicate that daily β2 -agonist treatment attenuates the beneficial effects of high intensity training on exercise performance and oxidative capacity, and causes remodelling of muscle proteome signature towards a fast-twitch phenotype. This article is protected by copyright. All rights reserved.

AB - Although the effects of training have been studied for decades, data on muscle proteome signature remodelling induced by high intensity training in relation to functional changes in humans remains incomplete. Likewise, β2 -agonists are frequently used to counteract exercise-induced bronchoconstriction, but the effects β2 -agonist treatment on muscle remodelling and adaptations to training are unknown. In a placebo-controlled parallel study, we randomized 21 trained men to four weeks of high intensity training with (HIT + β2 A) or without (HIT) daily inhalation of β2 -agonist (terbutaline, 4 mg d(-1) ). Of 486 proteins identified by mass-spectrometry proteomics of muscle biopsies sampled before and after the intervention, 32 and 85 were changing (FDR ≤ 5%) with the intervention in HIT and HIT + β2 A. Proteome signature changes were different in HIT and HIT + β2 A (P = 0.005), wherein β2 -agonist caused a repression of 25 proteins in HIT + β2 A compared to HIT, and an upregulation of 7 proteins compared to HIT. β2 -agonist repressed or even downregulated training-induced enrichment of pathways related to oxidative phosphorylation and glycogen metabolism, but upregulated pathways related to histone trimethylation and the nucleosome. Muscle contractile phenotype changed differently in HIT and HIT + β2 A (P ≤ 0.001), with a fast-to-slow twitch transition in HIT and a slow-to-fast twitch transition in HIT + β2 A. β2 -agonist attenuated training-induced enhancements in maximal oxygen consumption (P ≤ 0.01) and exercise performance (11.6 vs. 6.1%, P ≤ 0.05) in HIT + β2 A compared to HIT. These findings indicate that daily β2 -agonist treatment attenuates the beneficial effects of high intensity training on exercise performance and oxidative capacity, and causes remodelling of muscle proteome signature towards a fast-twitch phenotype. This article is protected by copyright. All rights reserved.

KW - Physical activity

KW - Proteomics

KW - Metabolism

KW - Beta-agonists

KW - Adrenoceptors

KW - Adrenergic

KW - VO2max

KW - Terbutaline

KW - HIT

KW - Athletes

U2 - 10.1113/JP274970

DO - 10.1113/JP274970

M3 - Journal article

C2 - 28983994

VL - 596

SP - 231

EP - 252

JO - The Journal of Physiology

JF - The Journal of Physiology

SN - 0022-3751

IS - 2

ER -

ID: 184391087