Endurance training in obese humans improves glucose tolerance and mitochondrial fatty acid oxidation and alters muscle lipid content.

@article{Bruce2006EnduranceTI,
  title={Endurance training in obese humans improves glucose tolerance and mitochondrial fatty acid oxidation and alters muscle lipid content.},
  author={Clinton R. Bruce and A. Brianne Thrush and Valerie A Mertz and Véronic Bézaire and Adrian Chabowski and George J. F. Heigenhauser and David J. Dyck},
  journal={American journal of physiology. Endocrinology and metabolism},
  year={2006},
  volume={291 1},
  pages={
          E99-E107
        }
}
Muscle fatty acid (FA) metabolism is impaired in obesity and insulin resistance, reflected by reduced rates of FA oxidation and accumulation of lipids. It has been suggested that interventions that increase FA oxidation may enhance insulin action by reducing these lipid pools. Here, we examined the effect of endurance training on rates of mitochondrial FA oxidation, the activity of carnitine palmitoyltransferase I (CPT I), and the lipid content in muscle of obese individuals and related these… 
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Enhanced mitochondrial performance with exercise is related to better metabolic flexibility and insulin sensitivity in response to lipid overload, and Mitochondrial performance was positively associated with better NOGD and insulinensitivity in both conditions.

Training-induced improvement in lipid oxidation in type 2 diabetes mellitus is related to alterations in muscle mitochondrial activity. Effect of endurance training in type 2 diabetes.

Adiponectin resistance precedes the accumulation of skeletal muscle lipids and insulin resistance in high-fat-fed rats.

It is demonstrated that an early loss of Ad's stimulatory effect on FA oxidation precedes an increase in plasmalemmal FA transporters and the accumulation of intramuscular DAG and ceramide, blunted insulin signaling, and ultimately impaired maximal insulin-stimulated glucose transport in skeletal muscle induced by HF diets.

Skeletal muscle mitochondrial FAT/CD36 content and palmitate oxidation are not decreased in obese women.

The reduction in fatty acid oxidation in obese individuals is attributable to a decrease in mitochondrial content, not to an intrinsic defect in the mitochondria obtained from skeletal muscle of obese individuals, and it appears that mitochondrial FAT/CD36 may be involved in regulating fatty acids oxidation in human skeletal muscle.

Increased intramuscular lipid synthesis and low saturation relate to insulin sensitivity in endurance-trained athletes.

The data indicate endurance-trained athletes have increased synthesis rates of skeletal muscle IMTG and decreased saturation of skeletal Muscle triglyceride diacylglycerol, likely adaptations to chronic endurance exercise training.

Excess Lipid Availability Increases Mitochondrial Fatty Acid Oxidative Capacity in Muscle

It is suggested that high lipid availability does not lead to intramuscular lipid accumulation and insulin resistance in rodents by decreasing muscle mitochondrial fatty acid oxidative capacity.

Metabolic flexibility in the development of insulin resistance and type 2 diabetes: effects of lifestyle

Lifestyle changes in dietary fat intake, physical activity and weight loss may improve metabolic flexibility in skeletal muscle, and thereby contribute to the prevention of type 2 diabetes.

Restoration of skeletal muscle leptin response does not precede the exercise-induced recovery of insulin-stimulated glucose uptake in high-fat-fed rats.

In conclusion, endurance exercise training is able to restore leptin response, but this does not appear to be a necessary precursor for the restoration of insulin response.

Metformin and exercise reduce muscle FAT/CD36 and lipid accumulation and blunt the progression of high-fat diet-induced hyperglycemia.

Reduction of skeletal muscle FAT/CD36 and content of ceramide and DAG may be important mechanisms by which exercise training blunts the progression of diet-induced insulin resistance in skeletal muscle.

SKELETAL MUSCLE METABOLIC FLEXIBILITY IMPAIRMENTS IN RESPONSE TO LIPID WITH OBESITY : EFFECT OF EXERCISE TRAINING

Exercise training combined with a HFD produced a similar increase in FAO and citrate synthase activity in lean and obese individuals indicating that HFD-induce metabolic flexibility was restored with exercise training regardless of obesity status.
...

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