Insulin-stimulated GLUT4 translocation is impaired in people with type 2 diabetes. In contrast, exercise results in a normal increase in GLUT4 translocation and glucose uptake in these patients. Several groups have recently hypothesized that exercise increases glucose uptake via an insulin-independent mechanism mediated by the activation of AMP-activated protein kinase (AMPK). If this hypothesis is correct, people with type 2 diabetes should have normal AMPK activation in response to exercise. Seven subjects with type 2 diabetes and eight matched control subjects exercised on a cycle ergometer for 45 min at 70% of maximum workload. Biopsies of vastus lateralis muscle were taken before exercise, after 20 and 45 min of exercise, and at 30 min postexercise. Blood glucose concentrations decreased from 7.6 to 4.77 mmol/l with 45 min of exercise in the diabetic group and did not change in the control group. Exercise significantly increased AMPK ␣2 activity 2.7-fold over basal at 20 min in both groups and remained elevated throughout the protocol, but there was no effect of exercise on AMPK ␣1 activity. Subjects with type 2 diabetes had similar protein expression of AMPK ␣1, ␣2, and ␤1 in muscle compared with control subjects. AMPK ␣2 was shown to represent approximately two-thirds of the total ␣ mRNA in the muscle from both groups. In conclusion, people with type 2 diabetes have normal exercise-induced AMPK ␣2 activity and normal expression of the ␣1, ␣2 and ␤1 isoforms. Pharmacological activation of AMPK may be an attractive target for the treatment of type 2 diabetes. Diabetes 50:921-927, 2001

Twenty‐four fasting male subjects exercised until exhaustion on a bicycle at a relative workload of about 70% of the workload at heart rate 170 per min. Muscle tissue was obtained by needle biopsy from the lateral femoral muscle before and after exercise.—The average work time was 99 min. The muscle triglyceride concentration decreased during the exercise from 10.4 to 7.8 μmoles per gram and that of glycogen from 10.4 to 3.4 mg per gram. The concentration of phospholipids in the muscle remained unchanged.‐The amount of fatty acids and of glucose which were oxidized during the exercise was calculated from the oxygen uptake and the respiratory quotient and found to be 39 % and 61 % respectively of the caloric output. It was estimated that the muscle triglyceride and plasma free fatty acids (FFA) contributed about 2/3 and 1/3 respectively of the fatty acids oxidized. Similar calculations showed that muscle glycogen covered about 2/3 of the amount of glucose oxidized.—A number of correlation coefficients were calculated between the various parameters studied. There was no correlation between the triglyceride and glycogen content of the muscle. The amount of work performed was correlated to the glycogen (r = 0.60) and to the triglyceride (r = − 0.53) content of the muscle. These two muscle substrates could be used to predict the work performance by multiple linear regression analysis with an error of only 17 % and with a multiple correlation coefficient of 0.774.—The work performance was positively correlated to the amount of fatty acids oxidized but negatively correlated to the decrease in muscle triglycerides which suggests that the capacity to perform aerobic work is related to the utilization and mobilization of fatty acids from extramuscular sources.The obvious importance of local tissue stores of substrate such as glycogen and triglycerides for the energy metabolism was discussed.

Muscle tissue from the lateral vastus of the femoral muscle was taken by needle biopsy technique in 7 male subjects before and after strenuous exercise by skiing for about 7 hrs. The mean muscle triglyceride concentration decreased from 17 to 8 μmoles/g wet weight during the exercise. No change was observed in the phospholipid concentration. The mean glycogen concentration in the muscle decreased from 16 to 7 mg/g sswet weight during the exercise. The results indicate that not only muscle glycogen but also muscle triglycerides are of importance for the energy metabolism in man during exercise.

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