High-intensity interval training changes mitochondrial respiratory capacity differently in adipose tissue and skeletal muscle

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Standard

High-intensity interval training changes mitochondrial respiratory capacity differently in adipose tissue and skeletal muscle. / Dohlmann, Tine L.; Hindsø, Morten; Dela, Flemming; Helge, Jørn W.; Larsen, Steen.

I: Physiological Reports, Bind 6, Nr. 18, e13857, 01.09.2018, s. 1-11.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Dohlmann, TL, Hindsø, M, Dela, F, Helge, JW & Larsen, S 2018, 'High-intensity interval training changes mitochondrial respiratory capacity differently in adipose tissue and skeletal muscle', Physiological Reports, bind 6, nr. 18, e13857, s. 1-11. https://doi.org/10.14814/phy2.13857

APA

Dohlmann, T. L., Hindsø, M., Dela, F., Helge, J. W., & Larsen, S. (2018). High-intensity interval training changes mitochondrial respiratory capacity differently in adipose tissue and skeletal muscle. Physiological Reports, 6(18), 1-11. [e13857]. https://doi.org/10.14814/phy2.13857

Vancouver

Dohlmann TL, Hindsø M, Dela F, Helge JW, Larsen S. High-intensity interval training changes mitochondrial respiratory capacity differently in adipose tissue and skeletal muscle. Physiological Reports. 2018 sep 1;6(18):1-11. e13857. https://doi.org/10.14814/phy2.13857

Author

Dohlmann, Tine L. ; Hindsø, Morten ; Dela, Flemming ; Helge, Jørn W. ; Larsen, Steen. / High-intensity interval training changes mitochondrial respiratory capacity differently in adipose tissue and skeletal muscle. I: Physiological Reports. 2018 ; Bind 6, Nr. 18. s. 1-11.

Bibtex

@article{47d582dc72dd4069a0fde48612ef9014,
title = "High-intensity interval training changes mitochondrial respiratory capacity differently in adipose tissue and skeletal muscle",
abstract = "The effect of high-intensity training (HIT) on mitochondrial ADP sensitivity and respiratory capacity was investigated in human skeletal muscle and subcutaneous adipose tissue (SAT). Twelve men and women underwent 6 weeks of HIT (7 × 1 min at app. 100{\%} of maximal oxygen uptake (VO 2max )). Mitochondrial respiration was measured in permeabilized muscle fibers and in abdominal SAT. Mitochondrial ADP sensitivity was determined using Michaelis Menten enzyme kinetics. VO 2max , body composition and citrate synthase (CS) activity (skeletal muscle) and mtDNA (SAT) were measured before and after training. VO 2max increased from 2.6 ± 0.2 to 2.8 ± 0.2 L O 2 /min (P = 0.011) accompanied by a decreased mitochondrial ADP sensitivity in skeletal muscle (K m : 0.14 ± 0.02 to 0.29 ± 0.03 mmol/L ADP (P = 0.002)), with no changes in SAT (K m : 0.12 ± 0.02 to 0.16 ± 0.05 mmol/L ADP; P = 0.186), following training. Mitochondrial respiratory capacity increased in skeletal muscle from 57 ± 4 to 67 ± 4 pmol O 2 ·mg -1 ·sec -1 (P < 0.001), but decreased with training in SAT from 1.3 ± 0.1 to 1.0 ± 0.1 pmol O 2 ·mg -1 ·sec -1 (P < 0.001). CS activity increased (P = 0.027) and mtDNA was unchanged following training. Intrinsic mitochondrial respiratory capacity was unchanged in skeletal muscle, but increased in SAT after HIT. In summary, our results demonstrate that mitochondrial adaptations to HIT in skeletal muscle are comparable to adaptations to endurance training, with an increased mitochondrial respiratory capacity and CS activity. However, mitochondria in SAT adapts differently compared to skeletal muscle mitochondria, where mitochondrial respiratory capacity decreased and mtDNA remained unchanged after HIT.",
keywords = "Adipose tissue, ADP sensitivity, high-intensity training, mitochondria, mitochondrial respiratory capacity, skeletal muscle",
author = "Dohlmann, {Tine L.} and Morten Hinds{\o} and Flemming Dela and Helge, {J{\o}rn W.} and Steen Larsen",
year = "2018",
month = "9",
day = "1",
doi = "10.14814/phy2.13857",
language = "English",
volume = "6",
pages = "1--11",
journal = "Physiological Reports",
issn = "2051-817X",
publisher = "Wiley Periodicals, Inc.",
number = "18",

}

RIS

TY - JOUR

T1 - High-intensity interval training changes mitochondrial respiratory capacity differently in adipose tissue and skeletal muscle

AU - Dohlmann, Tine L.

AU - Hindsø, Morten

AU - Dela, Flemming

AU - Helge, Jørn W.

AU - Larsen, Steen

PY - 2018/9/1

Y1 - 2018/9/1

N2 - The effect of high-intensity training (HIT) on mitochondrial ADP sensitivity and respiratory capacity was investigated in human skeletal muscle and subcutaneous adipose tissue (SAT). Twelve men and women underwent 6 weeks of HIT (7 × 1 min at app. 100% of maximal oxygen uptake (VO 2max )). Mitochondrial respiration was measured in permeabilized muscle fibers and in abdominal SAT. Mitochondrial ADP sensitivity was determined using Michaelis Menten enzyme kinetics. VO 2max , body composition and citrate synthase (CS) activity (skeletal muscle) and mtDNA (SAT) were measured before and after training. VO 2max increased from 2.6 ± 0.2 to 2.8 ± 0.2 L O 2 /min (P = 0.011) accompanied by a decreased mitochondrial ADP sensitivity in skeletal muscle (K m : 0.14 ± 0.02 to 0.29 ± 0.03 mmol/L ADP (P = 0.002)), with no changes in SAT (K m : 0.12 ± 0.02 to 0.16 ± 0.05 mmol/L ADP; P = 0.186), following training. Mitochondrial respiratory capacity increased in skeletal muscle from 57 ± 4 to 67 ± 4 pmol O 2 ·mg -1 ·sec -1 (P < 0.001), but decreased with training in SAT from 1.3 ± 0.1 to 1.0 ± 0.1 pmol O 2 ·mg -1 ·sec -1 (P < 0.001). CS activity increased (P = 0.027) and mtDNA was unchanged following training. Intrinsic mitochondrial respiratory capacity was unchanged in skeletal muscle, but increased in SAT after HIT. In summary, our results demonstrate that mitochondrial adaptations to HIT in skeletal muscle are comparable to adaptations to endurance training, with an increased mitochondrial respiratory capacity and CS activity. However, mitochondria in SAT adapts differently compared to skeletal muscle mitochondria, where mitochondrial respiratory capacity decreased and mtDNA remained unchanged after HIT.

AB - The effect of high-intensity training (HIT) on mitochondrial ADP sensitivity and respiratory capacity was investigated in human skeletal muscle and subcutaneous adipose tissue (SAT). Twelve men and women underwent 6 weeks of HIT (7 × 1 min at app. 100% of maximal oxygen uptake (VO 2max )). Mitochondrial respiration was measured in permeabilized muscle fibers and in abdominal SAT. Mitochondrial ADP sensitivity was determined using Michaelis Menten enzyme kinetics. VO 2max , body composition and citrate synthase (CS) activity (skeletal muscle) and mtDNA (SAT) were measured before and after training. VO 2max increased from 2.6 ± 0.2 to 2.8 ± 0.2 L O 2 /min (P = 0.011) accompanied by a decreased mitochondrial ADP sensitivity in skeletal muscle (K m : 0.14 ± 0.02 to 0.29 ± 0.03 mmol/L ADP (P = 0.002)), with no changes in SAT (K m : 0.12 ± 0.02 to 0.16 ± 0.05 mmol/L ADP; P = 0.186), following training. Mitochondrial respiratory capacity increased in skeletal muscle from 57 ± 4 to 67 ± 4 pmol O 2 ·mg -1 ·sec -1 (P < 0.001), but decreased with training in SAT from 1.3 ± 0.1 to 1.0 ± 0.1 pmol O 2 ·mg -1 ·sec -1 (P < 0.001). CS activity increased (P = 0.027) and mtDNA was unchanged following training. Intrinsic mitochondrial respiratory capacity was unchanged in skeletal muscle, but increased in SAT after HIT. In summary, our results demonstrate that mitochondrial adaptations to HIT in skeletal muscle are comparable to adaptations to endurance training, with an increased mitochondrial respiratory capacity and CS activity. However, mitochondria in SAT adapts differently compared to skeletal muscle mitochondria, where mitochondrial respiratory capacity decreased and mtDNA remained unchanged after HIT.

KW - Adipose tissue

KW - ADP sensitivity

KW - high-intensity training

KW - mitochondria

KW - mitochondrial respiratory capacity

KW - skeletal muscle

U2 - 10.14814/phy2.13857

DO - 10.14814/phy2.13857

M3 - Journal article

C2 - 30221839

AN - SCOPUS:85053873106

VL - 6

SP - 1

EP - 11

JO - Physiological Reports

JF - Physiological Reports

SN - 2051-817X

IS - 18

M1 - e13857

ER -

ID: 203979006