Maximal lipid oxidation in patients with type 2 diabetes is normal and shows an adequate increase in response to aerobic training.
OBJECTIVE
Insulin resistance in subjects with type 2 diabetes (T2D) and obesity is associated with an imbalance between the availability and the oxidation of lipids. We hypothesized that maximal whole-body lipid oxidation during exercise (FATmax) is reduced and that training-induced metabolic adaptation is attenuated in T2D.


METHODS
Obese T2D (n = 12) and control (n = 11) subjects matched for age, sex, physical activity and body mass index completed 10 weeks of aerobic training. Subjects were investigated before and after training with maximal and submaximal exercise tests and euglycaemic-hyperinsulinaemic clamps combined with muscle biopsies.


RESULTS
Training increased maximal oxygen consumption (VO(2max)) and muscle citrate synthase activity and decreased blood lactate concentrations during submaximal exercise in both groups (all p < 0.01). FATmax increased markedly (40-50%) in both T2D and control subjects after training (all p < 0.001). There were no significant differences in these variables and lactate threshold (%VO(2max)) between groups before or after training. Insulin-stimulated glucose disappearance rate (Rd) was lower in T2D vs. control subjects both before and after training. Rd increased in response to training in both groups (all p < 0.01). There was no correlation between Rd and measures of oxidative capacity or lipid oxidation during exercise or the training-induced changes in these parameters.


CONCLUSIONS
FATmax was not reduced in T2D, and muscle oxidative capacity increased adequately in response to aerobic training in obese subjects with and without T2D. These metabolic adaptations to training seem to be unrelated to changes in insulin sensitivity and indicate that an impaired capacity for lipid oxidation is not a major cause of insulin resistance in T2D.
Mogensen
M
M
Institute of Sports Science and Clinical Biomechanics, University of Southern Denmark, Odense, Denmark. mmogensen@mfi.ku.dk
Vind
B F
BF
Højlund
K
K
Beck-Nielsen
H
H
Sahlin
K
K
D002950:Citrate (si)-Synthase / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism / Q000503:physiopathology*; D004734:Energy Metabolism / Q000502:physiology; D015444:Exercise / Q000502:physiology*; D005260:Female; D005947:Glucose / Q000378:metabolism; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology; D019344:Lactic Acid / Q000097:blood; D050356:Lipid Metabolism / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000378:metabolism; D009765:Obesity / Q000503:physiopathology; D010084:Oxidation-Reduction; D010101:Oxygen Consumption / Q000502:physiology
D019344:Lactic Acid; D002950:Citrate (si)-Synthase; D005947:Glucose