Metabolic stress-dependent regulation of the mitochondrial biogenic molecular response to high-intensity exercise in human skeletal muscle

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Standard

Metabolic stress-dependent regulation of the mitochondrial biogenic molecular response to high-intensity exercise in human skeletal muscle. / Fiorenza, Matteo; Gunnarsson, Thomas Pettursson; Hostrup, Morten; Iaia, F M; Schena, F; Pilegaard, Henriette; Bangsbo, Jens.

I: Journal of Physiology, Bind 596, Nr. 14, 2018, s. 2823-2840.

Publikation: Bidrag til tidsskriftTidsskriftartikelfagfællebedømt

Harvard

Fiorenza, M, Gunnarsson, TP, Hostrup, M, Iaia, FM, Schena, F, Pilegaard, H & Bangsbo, J 2018, 'Metabolic stress-dependent regulation of the mitochondrial biogenic molecular response to high-intensity exercise in human skeletal muscle', Journal of Physiology, bind 596, nr. 14, s. 2823-2840. https://doi.org/10.1113/JP275972

APA

Fiorenza, M., Gunnarsson, T. P., Hostrup, M., Iaia, F. M., Schena, F., Pilegaard, H., & Bangsbo, J. (2018). Metabolic stress-dependent regulation of the mitochondrial biogenic molecular response to high-intensity exercise in human skeletal muscle. Journal of Physiology, 596(14), 2823-2840. https://doi.org/10.1113/JP275972

Vancouver

Fiorenza M, Gunnarsson TP, Hostrup M, Iaia FM, Schena F, Pilegaard H o.a. Metabolic stress-dependent regulation of the mitochondrial biogenic molecular response to high-intensity exercise in human skeletal muscle. Journal of Physiology. 2018;596(14):2823-2840. https://doi.org/10.1113/JP275972

Author

Fiorenza, Matteo ; Gunnarsson, Thomas Pettursson ; Hostrup, Morten ; Iaia, F M ; Schena, F ; Pilegaard, Henriette ; Bangsbo, Jens. / Metabolic stress-dependent regulation of the mitochondrial biogenic molecular response to high-intensity exercise in human skeletal muscle. I: Journal of Physiology. 2018 ; Bind 596, Nr. 14. s. 2823-2840.

Bibtex

@article{d494c266971b4ed3b9c1151bab4beee7,
title = "Metabolic stress-dependent regulation of the mitochondrial biogenic molecular response to high-intensity exercise in human skeletal muscle",
abstract = "The aim of the present study was to examine the impact of exercise-induced metabolic stress on regulation of the molecular responses promoting skeletal muscle mitochondrial biogenesis. Twelve endurance-trained men performed three cycling-exercise protocols characterized by different metabolic profiles in a randomized, counter-balanced order. Specifically, two work-matched low-volume supramaximal-intensity intermittent regimes, consisting of repeated-sprint (RS) and speed endurance (SE) exercise, were employed and compared with a high-volume continuous moderate-intensity exercise (CM) protocol. Vastus lateralis muscle samples were obtained before, immediately after, and 3h after exercise. SE produced the most marked metabolic perturbations as evidenced by the greatest changes in muscle lactate and pH, concomitantly with higher post-exercise plasma adrenaline levels in comparison with RS and CM (P < 0.05). Exercise-induced phosphorylation of CaMKII and p38 MAPK was greater in SE than in RS and CM. The exercise-induced PGC-1α mRNA response was higher in SE and CM than in RS, with no difference between SE and CM. Muscle NRF-2, TFAM, MFN2, DRP1 and SOD2 mRNA content was elevated to the same extent by SE and CM, while RS had no effect on these mRNAs. The exercise-induced HSP72 mRNA response was larger in SE than in RS and CM. Thus, the present results suggest that, for a given exercise volume, the initial events associated with mitochondrial biogenesis are modulated by metabolic stress. In addition, high-intensity exercise seems to compensate for reduced exercise volume in the induction of mitochondrial biogenic molecular responses only when the intense exercise elicits marked metabolic perturbations.",
keywords = "Faculty of Science, Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) mRNA, Mitochondrial biogenesis and dynamics, Intracellular signaling, Sprint interval training",
author = "Matteo Fiorenza and Gunnarsson, {Thomas Pettursson} and Morten Hostrup and Iaia, {F M} and F Schena and Henriette Pilegaard and Jens Bangsbo",
note = "CURIS 2018 NEXS 234",
year = "2018",
doi = "10.1113/JP275972",
language = "English",
volume = "596",
pages = "2823--2840",
journal = "The Journal of Physiology",
issn = "0022-3751",
publisher = "Wiley-Blackwell",
number = "14",

}

RIS

TY - JOUR

T1 - Metabolic stress-dependent regulation of the mitochondrial biogenic molecular response to high-intensity exercise in human skeletal muscle

AU - Fiorenza, Matteo

AU - Gunnarsson, Thomas Pettursson

AU - Hostrup, Morten

AU - Iaia, F M

AU - Schena, F

AU - Pilegaard, Henriette

AU - Bangsbo, Jens

N1 - CURIS 2018 NEXS 234

PY - 2018

Y1 - 2018

N2 - The aim of the present study was to examine the impact of exercise-induced metabolic stress on regulation of the molecular responses promoting skeletal muscle mitochondrial biogenesis. Twelve endurance-trained men performed three cycling-exercise protocols characterized by different metabolic profiles in a randomized, counter-balanced order. Specifically, two work-matched low-volume supramaximal-intensity intermittent regimes, consisting of repeated-sprint (RS) and speed endurance (SE) exercise, were employed and compared with a high-volume continuous moderate-intensity exercise (CM) protocol. Vastus lateralis muscle samples were obtained before, immediately after, and 3h after exercise. SE produced the most marked metabolic perturbations as evidenced by the greatest changes in muscle lactate and pH, concomitantly with higher post-exercise plasma adrenaline levels in comparison with RS and CM (P < 0.05). Exercise-induced phosphorylation of CaMKII and p38 MAPK was greater in SE than in RS and CM. The exercise-induced PGC-1α mRNA response was higher in SE and CM than in RS, with no difference between SE and CM. Muscle NRF-2, TFAM, MFN2, DRP1 and SOD2 mRNA content was elevated to the same extent by SE and CM, while RS had no effect on these mRNAs. The exercise-induced HSP72 mRNA response was larger in SE than in RS and CM. Thus, the present results suggest that, for a given exercise volume, the initial events associated with mitochondrial biogenesis are modulated by metabolic stress. In addition, high-intensity exercise seems to compensate for reduced exercise volume in the induction of mitochondrial biogenic molecular responses only when the intense exercise elicits marked metabolic perturbations.

AB - The aim of the present study was to examine the impact of exercise-induced metabolic stress on regulation of the molecular responses promoting skeletal muscle mitochondrial biogenesis. Twelve endurance-trained men performed three cycling-exercise protocols characterized by different metabolic profiles in a randomized, counter-balanced order. Specifically, two work-matched low-volume supramaximal-intensity intermittent regimes, consisting of repeated-sprint (RS) and speed endurance (SE) exercise, were employed and compared with a high-volume continuous moderate-intensity exercise (CM) protocol. Vastus lateralis muscle samples were obtained before, immediately after, and 3h after exercise. SE produced the most marked metabolic perturbations as evidenced by the greatest changes in muscle lactate and pH, concomitantly with higher post-exercise plasma adrenaline levels in comparison with RS and CM (P < 0.05). Exercise-induced phosphorylation of CaMKII and p38 MAPK was greater in SE than in RS and CM. The exercise-induced PGC-1α mRNA response was higher in SE and CM than in RS, with no difference between SE and CM. Muscle NRF-2, TFAM, MFN2, DRP1 and SOD2 mRNA content was elevated to the same extent by SE and CM, while RS had no effect on these mRNAs. The exercise-induced HSP72 mRNA response was larger in SE than in RS and CM. Thus, the present results suggest that, for a given exercise volume, the initial events associated with mitochondrial biogenesis are modulated by metabolic stress. In addition, high-intensity exercise seems to compensate for reduced exercise volume in the induction of mitochondrial biogenic molecular responses only when the intense exercise elicits marked metabolic perturbations.

KW - Faculty of Science

KW - Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) mRNA

KW - Mitochondrial biogenesis and dynamics

KW - Intracellular signaling

KW - Sprint interval training

U2 - 10.1113/JP275972

DO - 10.1113/JP275972

M3 - Journal article

C2 - 29727016

VL - 596

SP - 2823

EP - 2840

JO - The Journal of Physiology

JF - The Journal of Physiology

SN - 0022-3751

IS - 14

ER -

ID: 196203046