Larsen S 2013 Abstract MiP2013

From Bioblast
Larsen S, Dohlmann TL, HindsΓΈ M, Dela F, Helge JW (2013) High intensity training decreases mitochondrial ADP sensitivity in human adipose and skeletal muscle tissue. Mitochondr Physiol Network 18.08.



MiP2013, Book of Abstracts Open Access

Larsen S, Dohlmann TL, Hindsoe M, Dela F, Helge JW (2013)

Event: MiPNet18.08_MiP2013

It has previously been reported that mitochondrial ADP sensitivity decreases (higher Km’) with endurance training in human skeletal muscle [1]. This decrease was accompanied by an increased maximal ADP stimulated mt-respiration (Jmax) and an increased maximal oxygen uptake (VO2max). It is not known whether high intensity training (HIT) has the same effect on mitochondria and if these changes also occur in mitochondria from human adipose tissue. The aim of this project was to investigate mitochondrial ADP sensitivity and maximal ADP stimulated respiration in human adipose and skeletal muscle tissue after six weeks of HIT. Twelve healthy overweight subjects (7 F/5 M) (age: 40Β±2 yrs, BMI: 32Β±2, VO2max: 2612Β±166 ml/min) were included in the study. The subjects underwent six weeks (3 times a week) of HIT. VO2max was measured pre and post training. Mitochondrial ADP sensitivity (Km’) and Jmax was measured pre and post HIT in adipose tissue and permeabilized muscle fibers by high-resolution respirometry (Oxygraph-2k, Oroboros, Insbruck, Austria). The adipose tissue was permeabilized with digitonin and the skeletal muscle fibers with saponin. The protocol used for respirometry was as follows: Malate (2 mM), Glutamate (10 mM) and ADP titrated in the following steps (0.05 – 0.10 – 0.25 – 0.50 – 1.00 – 2.50 – 5.00 mM). SigmaPlot was used to determine Km’ for ADP and Jmax.

VO2max was significantly improved after HIT. Mitochondrial ADP sensitivity was significantly (P<0.05) decreased after HIT in permeabilized skeletal muscle (0.14Β±0.02 mM vs. 0.29Β±0.03 mM), and the same trend was seen in adipose tissue although not significant (P=0.056; 0.11Β±0.02 mM vs. 0.16Β±0.04 mM). Jmax was similar after HIT in permeabilized skeletal muscle (21Β±1 pmolβˆ™s-1βˆ™mg-1 vs. 22Β±1 pmolβˆ™s-1βˆ™mg-1) as well as in adipose tissue (0.36Β±0.03 pmolβˆ™s-1βˆ™mg-1 vs. 0.36Β±0.03 pmolβˆ™s1βˆ™mg-1), before vs. after, respectively.

ADP sensitivity decreased in permeabilized human skeletal muscle and the same trend was seen in adipose tissue. This was accompanied by a similar maximal ADP stimulated respiration pre and post training in both skeletal muscle and adipose tissue. This is the first time that ADP sensitivity has been investigated in adipose tissue. Interestingly the HIT training adaptation in mitochondria from adipose tissue is similar to that observed in skeletal muscle although not with the same magnitude.

β€’ O2k-Network Lab: DK Copenhagen Dela F, DK Copenhagen Larsen S

Labels: MiParea: Respiration, Exercise physiology;nutrition;life style 

Organism: Human  Tissue;cell: Skeletal muscle, Fat  Preparation: Intact organism, Permeabilized tissue 

Regulation: ADP  Coupling state: OXPHOS 

HRR: Oxygraph-2k 


Affiliations and author contributions

Center for Healthy Aging, Dept of Biomedical Sciences, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark. - Email: [email protected]


  1. Walsh B, Tonkonogi M, Sahlin K (2001) Effect of endurance training on oxidative and antioxidative function in human permeabilized muscle fibres. Eur J Physiol 442: 420-425.

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