Forskning
Udskriv Udskriv
Switch language
Region Hovedstaden - en del af Københavns Universitetshospital
Udgivet

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

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

DOI

  1. Changes in metabolism but not myocellular signaling by training with CHO-restriction in endurance athletes

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. Four days of bed rest increases intrinsic mitochondrial respiratory capacity in young healthy males

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  3. Acute administration of interleukin-6 does not increase secretion of glucagon-like peptide-1 in mice

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  4. Resistance exercise stimulates mixed muscle protein synthesis in lean and obese young adults

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  5. Modulation of the sympathetic nervous system in youngsters by vitamin-D supplementation

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  • Tine L Dohlmann
  • Morten Hindsø
  • Flemming Dela
  • Jørn W Helge
  • Steen Larsen
Vis graf over relationer

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 (VO2max )). Mitochondrial respiration was measured in permeabilized muscle fibers and in abdominal SAT. Mitochondrial ADP sensitivity was determined using Michaelis Menten enzyme kinetics. VO2max , body composition and citrate synthase (CS) activity (skeletal muscle) and mtDNA (SAT) were measured before and after training. VO2max increased from 2.6 ± 0.2 to 2.8 ± 0.2 L O2 /min (P = 0.011) accompanied by a decreased mitochondrial ADP sensitivity in skeletal muscle (Km : 0.14 ± 0.02 to 0.29 ± 0.03 mmol/L ADP (P = 0.002)), with no changes in SAT (Km : 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 O2 ·mg-1 ·sec-1 (P < 0.001), but decreased with training in SAT from 1.3 ± 0.1 to 1.0 ± 0.1 pmol O2 ·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
TidsskriftPhysiological Reports
Vol/bind6
Udgave nummer18
Sider (fra-til)e13857
ISSN2051-817X
DOI
StatusUdgivet - sep. 2018

ID: 55467250