Dohlmann 2013 Abstract IOC75
|Dohlmann T (2013) Effects of high-intense interval training on mitochondrial respiratory capacity. Mitochondr Physiol Network 18.03.|
Link: IOC75 Open Access
Dohlmann T, Hindsoe M, Larsen S, Dela F, Helge JW (2013)
Alteration in mitochondrial respiratory capacity has been linked to several conditions that are associated with a sedentary lifestyle, such as obesity and insulin resistance. It is well known that endurance training can diminish these conditions, but some high intensity interval training (HIIT) protocols have shown similar improvements in insulin sensitivity, in spite of the reduced training volume. However it is sparse with literature regarding HIIT and the effect on mitochondrial respiratory capacity. The aim of this study was to investigate the effects of a low volume HIIT protocol on mitochondrial respiratory capacity and VO2max in sedentary overweight adults. 8 healthy sedentary men (n=2) and women (n=6) (age 40±3 yrs, BMI 32±2, VO2max 2383 ±115 ml•min-1) were recruited for this study. They underwent 6 weeks of supervised HIIT on a cycle ergometer (18 sessions of 7x1min exercise bouts interspersed with 1min rest periods). Muscle biopsies were taken from m. vastus lateralis before and after training. Mitochondrial respiratory capacity was measured ex vivo in permeabilized muscle fibers using high resolution respirometry (Oxygraph-2k, Oroboros, Innsbruck, Austria). The respiratory protocol investigated maximal coupled state 3 respiration (complex I + II linked substrates) with the following substrates (malate, glutamate, octanoyl carnitine, succinate and ADP; GMSO3), as well as state 4o (oligomycin; LEAK). Body composition was measured by DXA, and VO2max using an incremental cycle test to exhaustion. Mitochondrial respiratory capacity increased significantly following training; GMSO3 respiration increased by 13% (57± 4 to 64±5 pmol O2•mg-1•s-1) and LEAK respiration increased by 24% (21±2 to 25±2 pmol O2 •mg-1•s-1).The present training protocol didn’t elicit a significant improvement in VO2max (4%, P = 0.37), but time to fatigue during the VO2max test was significantly increased by 18% post training (P <0.001). BMI and body composition were not changed following training. Interestingly the present training protocol induced a significant improvement in mitochondrial respiratory capacity, but not in whole body VO2max, thus implying that the training stimulus was adequate to improve the respiratory capacity locally. The observed improvement in mitochondrial respiratory capacity and time to fatigue suggest that the HIIT training may induce positive metabolic effects that can attenuate the development of lifestyle diseases, independently of VO2max.
The project is funded by the EU FP7 program
• Keywords: Exercise, high intensity interval training, mitochondrial respiratory capacity
• O2k-Network Lab: DK Copenhagen Dela F, DK Copenhagen Larsen S
Organism: Human Tissue;cell: Skeletal muscle Preparation: Permeabilized cells
Pathway: NS HRR: Oxygraph-2k
Center for Healthy Aging, Department of Biomedical Sciences, University of Copenhagen, Denmark.