High-fat feeding inhibits exercise-induced increase in mitochondrial respiratory flux in skeletal muscle

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Standard

High-fat feeding inhibits exercise-induced increase in mitochondrial respiratory flux in skeletal muscle. / Skovbro, Mette; Boushel, Robert Christopher; Hansen, Christina Neigaard; Helge, Jørn Wulff; Dela, Flemming.

I: Journal of Applied Physiology, Bind 110, Nr. 6, 2011, s. 1607-14.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Skovbro, M, Boushel, RC, Hansen, CN, Helge, JW & Dela, F 2011, 'High-fat feeding inhibits exercise-induced increase in mitochondrial respiratory flux in skeletal muscle', Journal of Applied Physiology, bind 110, nr. 6, s. 1607-14. https://doi.org/10.1152/japplphysiol.01341.2010

APA

Skovbro, M., Boushel, R. C., Hansen, C. N., Helge, J. W., & Dela, F. (2011). High-fat feeding inhibits exercise-induced increase in mitochondrial respiratory flux in skeletal muscle. Journal of Applied Physiology, 110(6), 1607-14. https://doi.org/10.1152/japplphysiol.01341.2010

Vancouver

Skovbro M, Boushel RC, Hansen CN, Helge JW, Dela F. High-fat feeding inhibits exercise-induced increase in mitochondrial respiratory flux in skeletal muscle. Journal of Applied Physiology. 2011;110(6):1607-14. https://doi.org/10.1152/japplphysiol.01341.2010

Author

Skovbro, Mette ; Boushel, Robert Christopher ; Hansen, Christina Neigaard ; Helge, Jørn Wulff ; Dela, Flemming. / High-fat feeding inhibits exercise-induced increase in mitochondrial respiratory flux in skeletal muscle. I: Journal of Applied Physiology. 2011 ; Bind 110, Nr. 6. s. 1607-14.

Bibtex

@article{a1e3c8e43e2a4b9eaf1ce4193dc05491,
title = "High-fat feeding inhibits exercise-induced increase in mitochondrial respiratory flux in skeletal muscle",
abstract = "Twenty one healthy untrained male subjects were randomized to follow a high-fat diet (HFD; 55-60E{\%} fat, 25-30E{\%} carbohydrate, and 15E{\%} protein) or a normal diet (ND; 25-35E{\%} fat, 55-60E{\%} carbohydrate, and 10-15E{\%} protein) for 2(1/2) wk. Diets were isocaloric and tailored individually to match energy expenditure. At 2(1/2) wk of diet, one 60-min bout of bicycle exercise (70{\%} of maximal oxygen uptake) was performed. Muscle biopsies were obtained before and after the diet, immediately after exercise, and after 3-h recovery. Insulin sensitivity (hyperinsulinemic-euglycemic clamp) and intramyocellular triacylglycerol content did not change with the intervention in either group. Indexes of mitochondrial density were similar across the groups and intervention. Mitochondrial respiratory rates, measured in permeabilized muscle fibers, showed a 31 ± 11 and 26 ± 9{\%} exercise-induced increase (P <0.05) in state 3 (glycolytic substrates) and uncoupled respiration, respectively. However, in HFD this increase was abolished. At recovery, no change from resting respiration was seen in either group. With a lipid substrate (octanoyl-carnitine with or without ADP), similar exercise-induced increases (31-62{\%}) were seen in HFD and ND, but only in HFD was an elevated (P <0.05) respiratory rate seen at recovery. With HFD complex I and IV protein expression decreased (P <0.05 and P = 0.06, respectively). A fat-rich diet induces marked changes in the mitochondrial electron transport system protein content and in exercise-induced mitochondrial substrate oxidation rates, with the effects being present hours after the exercise. The effect of HFD is present even without effects on insulin sensitivity and intramyocellular lipid accumulation. An isocaloric high-fat diet does not cause insulin resistance.",
author = "Mette Skovbro and Boushel, {Robert Christopher} and Hansen, {Christina Neigaard} and Helge, {J{\o}rn Wulff} and Flemming Dela",
year = "2011",
doi = "10.1152/japplphysiol.01341.2010",
language = "English",
volume = "110",
pages = "1607--14",
journal = "Journal of Applied Physiology",
issn = "8750-7587",
publisher = "American Physiological Society",
number = "6",

}

RIS

TY - JOUR

T1 - High-fat feeding inhibits exercise-induced increase in mitochondrial respiratory flux in skeletal muscle

AU - Skovbro, Mette

AU - Boushel, Robert Christopher

AU - Hansen, Christina Neigaard

AU - Helge, Jørn Wulff

AU - Dela, Flemming

PY - 2011

Y1 - 2011

N2 - Twenty one healthy untrained male subjects were randomized to follow a high-fat diet (HFD; 55-60E% fat, 25-30E% carbohydrate, and 15E% protein) or a normal diet (ND; 25-35E% fat, 55-60E% carbohydrate, and 10-15E% protein) for 2(1/2) wk. Diets were isocaloric and tailored individually to match energy expenditure. At 2(1/2) wk of diet, one 60-min bout of bicycle exercise (70% of maximal oxygen uptake) was performed. Muscle biopsies were obtained before and after the diet, immediately after exercise, and after 3-h recovery. Insulin sensitivity (hyperinsulinemic-euglycemic clamp) and intramyocellular triacylglycerol content did not change with the intervention in either group. Indexes of mitochondrial density were similar across the groups and intervention. Mitochondrial respiratory rates, measured in permeabilized muscle fibers, showed a 31 ± 11 and 26 ± 9% exercise-induced increase (P <0.05) in state 3 (glycolytic substrates) and uncoupled respiration, respectively. However, in HFD this increase was abolished. At recovery, no change from resting respiration was seen in either group. With a lipid substrate (octanoyl-carnitine with or without ADP), similar exercise-induced increases (31-62%) were seen in HFD and ND, but only in HFD was an elevated (P <0.05) respiratory rate seen at recovery. With HFD complex I and IV protein expression decreased (P <0.05 and P = 0.06, respectively). A fat-rich diet induces marked changes in the mitochondrial electron transport system protein content and in exercise-induced mitochondrial substrate oxidation rates, with the effects being present hours after the exercise. The effect of HFD is present even without effects on insulin sensitivity and intramyocellular lipid accumulation. An isocaloric high-fat diet does not cause insulin resistance.

AB - Twenty one healthy untrained male subjects were randomized to follow a high-fat diet (HFD; 55-60E% fat, 25-30E% carbohydrate, and 15E% protein) or a normal diet (ND; 25-35E% fat, 55-60E% carbohydrate, and 10-15E% protein) for 2(1/2) wk. Diets were isocaloric and tailored individually to match energy expenditure. At 2(1/2) wk of diet, one 60-min bout of bicycle exercise (70% of maximal oxygen uptake) was performed. Muscle biopsies were obtained before and after the diet, immediately after exercise, and after 3-h recovery. Insulin sensitivity (hyperinsulinemic-euglycemic clamp) and intramyocellular triacylglycerol content did not change with the intervention in either group. Indexes of mitochondrial density were similar across the groups and intervention. Mitochondrial respiratory rates, measured in permeabilized muscle fibers, showed a 31 ± 11 and 26 ± 9% exercise-induced increase (P <0.05) in state 3 (glycolytic substrates) and uncoupled respiration, respectively. However, in HFD this increase was abolished. At recovery, no change from resting respiration was seen in either group. With a lipid substrate (octanoyl-carnitine with or without ADP), similar exercise-induced increases (31-62%) were seen in HFD and ND, but only in HFD was an elevated (P <0.05) respiratory rate seen at recovery. With HFD complex I and IV protein expression decreased (P <0.05 and P = 0.06, respectively). A fat-rich diet induces marked changes in the mitochondrial electron transport system protein content and in exercise-induced mitochondrial substrate oxidation rates, with the effects being present hours after the exercise. The effect of HFD is present even without effects on insulin sensitivity and intramyocellular lipid accumulation. An isocaloric high-fat diet does not cause insulin resistance.

U2 - 10.1152/japplphysiol.01341.2010

DO - 10.1152/japplphysiol.01341.2010

M3 - Journal article

C2 - 21415171

VL - 110

SP - 1607

EP - 1614

JO - Journal of Applied Physiology

JF - Journal of Applied Physiology

SN - 8750-7587

IS - 6

ER -

ID: 33815592