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 tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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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