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Difference between revisions of "Skovbro 2011 J Appl Physiol"

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{{Publication
{{Publication
|title=Skovbro M, Boushel R, Hansen CN, Helge JW, Dela F (2011) High-fat feeding inhibits exercise-induced increase in mitochondrial respiratory flux in skeletal muscle. J. Appl. Physiol. 110: 1607-1614.
|title=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. J Appl Physiol 110:1607-14.
|info=[http://www.ncbi.nlm.nih.gov/pubmed/21415171 PMID:21415171]
|info=[http://www.ncbi.nlm.nih.gov/pubmed/21415171 PMID: 21415171 Open Access]
|authors=Skovbro M, Boushel R, Hansen CN, Helge JW, Dela F
|authors=Skovbro M, Boushel RC, Hansen CN, Helge JW, Dela F
|year=2011
|year=2011
|journal=J. Appl. Physiol.
|journal=J Appl Physiol
|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 Β± 11 and 26 Β± 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.
|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 Β± 11 and 26 Β± 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.
|keywords=high-fat diet, Complex IV
|keywords=High-fat diet, Complex IV
|mipnetlab=DK_Copenhagen_Dela F, DK Copenhagen Boushel R
|mipnetlab=CA Vancouver Boushel RC, DK Copenhagen Dela F, SE Stockholm Boushel RC, DK Copenhagen Larsen S
}}
}}
{{Labeling
{{Labeling
|organism=Human
|tissues=Skeletal muscle
|preparations=Permeabilized tissue
|instruments=Oxygraph-2k
|instruments=Oxygraph-2k
|organism=Human
|tissues=Skeletal Muscle
|preparations=Permeabilized Cell or Tissue; Homogenate
}}
}}

Latest revision as of 14:44, 5 March 2019

Publications in the MiPMap
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. J Appl Physiol 110:1607-14.

Β» PMID: 21415171 Open Access

Skovbro M, Boushel RC, Hansen CN, Helge JW, Dela F (2011) J Appl Physiol

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 Β± 11 and 26 Β± 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. β€’ Keywords: High-fat diet, Complex IV

β€’ O2k-Network Lab: CA Vancouver Boushel RC, DK Copenhagen Dela F, SE Stockholm Boushel RC, DK Copenhagen Larsen S


Labels:


Organism: Human  Tissue;cell: Skeletal muscle  Preparation: Permeabilized tissue 



HRR: Oxygraph-2k