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

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Tine L. Dohlmann, Morten Hindsø, Flemming Dela, Jørn W. Helge, Steen Larsen

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.

OriginalsprogEngelsk
Artikelnummere13857
TidsskriftPhysiological Reports
Vol/bind6
Udgave nummer18
Sider (fra-til)1-11
ISSN2051-817X
DOI
StatusUdgivet - 1 sep. 2018

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