Larsen 2014 Abstract MiP2014
|The effect of high intensity training on mitochondrial fat oxidation in skeletal muscle and subcutaneous adipose tissue.|
High intensity interval training (HIT) is known to increase mitochondrial content in a similar way as endurance training (60-90% of maximal oxygen uptake (VO2peak). Whether HIT increases mitochondria’s ability to oxidize lipids is currently debated. We investigated the effect of HIT on mitochondrial fat oxidation in skeletal muscle and adipose tissue. Mitochondrial oxidative phosphorylation (OXPHOS) capacity, mitochondrial substrate sensitivity (K’m) and mitochondrial content were measured in skeletal muscle and adipose tissue in healthy overweight subjects before and after six weeks of HIT (three times per week at 298±21 W).
HIT significantly increased VO2peak from 2.9±0.2 to 3.1±0.2 l•min-1. No differences were seen in maximal fat oxidation in either skeletal muscle or adipose tissue. K’m for octanoyl carnitine or palmitoyl carnitine were similar after training in skeletal muscle and adipose tissue. Maximal OXPHOS capacity with Complex I+II-linked substrates was increased after training in skeletal muscle but not in adipose tissue.
In conclusion, six weeks of HIT increased VO2peak. Mitochondrial content and mitochondrial OXPHOS capacity were increased in skeletal muscle but not in adipose tissue. Furthermore, mitochondrial fat oxidation was not improved in either skeletal muscle or adipose tissue.
Labels: MiParea: Respiration, mt-Biogenesis;mt-density, Exercise physiology;nutrition;life style Pathology: Obesity
Organism: Human Tissue;cell: Skeletal muscle, Fat Preparation: Permeabilized tissue
Regulation: Oxygen kinetics Coupling state: OXPHOS Pathway: F, N, S, NS HRR: Oxygraph-2k Event: A3, Oral MiP2014
Xlab, Center Healthy Aging, Dep Biomed Sc, Fac Health Sc, Univ Copenhagen, Denmark. - email@example.com