The effect of high-intensity training on mitochondrial fat oxidation in skeletal muscle and subcutaneous adipose tissue
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The effect of high-intensity training on mitochondrial fat oxidation in skeletal muscle and subcutaneous adipose tissue. / Larsen, Steen; Danielsen, J H; Søndergård, Stine Dam; Søgaard, D; Vigelsoe, A; Dybboe, R; Skaaby, S; Dela, F; Helge, J W.
I: Scandinavian Journal of Medicine & Science in Sports, Bind 25, Nr. 1, 02.2015, s. e59-e69.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › fagfællebedømt
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T1 - The effect of high-intensity training on mitochondrial fat oxidation in skeletal muscle and subcutaneous adipose tissue
AU - Larsen, Steen
AU - Danielsen, J H
AU - Søndergård, Stine Dam
AU - Søgaard, D
AU - Vigelsoe, A
AU - Dybboe, R
AU - Skaaby, S
AU - Dela, F
AU - Helge, J W
N1 - © 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
PY - 2015/2
Y1 - 2015/2
N2 - 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 the 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 (Km (app) ), and mitochondrial content were measured in skeletal muscle and adipose tissue in healthy overweight subjects before and after 6 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. No differences were seen in maximal fat oxidation in either skeletal muscle or adipose tissue. Km (app) for octanoyl carnitine or palmitoyl carnitine were similar after training in skeletal muscle and adipose tissue. Maximal OXPHOS capacity with complex I- and II-linked substrates was increased after training in skeletal muscle but not in adipose tissue. In conclusion, 6 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.
AB - 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 the 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 (Km (app) ), and mitochondrial content were measured in skeletal muscle and adipose tissue in healthy overweight subjects before and after 6 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. No differences were seen in maximal fat oxidation in either skeletal muscle or adipose tissue. Km (app) for octanoyl carnitine or palmitoyl carnitine were similar after training in skeletal muscle and adipose tissue. Maximal OXPHOS capacity with complex I- and II-linked substrates was increased after training in skeletal muscle but not in adipose tissue. In conclusion, 6 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.
U2 - 10.1111/sms.12252
DO - 10.1111/sms.12252
M3 - Journal article
C2 - 24845952
VL - 25
SP - e59-e69
JO - Scandinavian Journal of Medicine & Science in Sports
JF - Scandinavian Journal of Medicine & Science in Sports
SN - 0905-7188
IS - 1
ER -
ID: 113988370