Changes in Aerobic Capacity and Visceral Fat but not Myocyte Lipid Levels Predict increased Insulin Action After Exercise in Overweight and Obese Men

To examine the effect of moderate intensity physical activity on the interactions between central abdominal adiposity, myocyte lipid content, and insulin action in overweight and obese, sedentary men. Myocyte lipid (biochemical triglyceride and long-chain acyl CoA [LCAC] from vastus lateralis biopsy and soleus and tibialis anterior intramyocellular lipid by 1H-magnetic resonance spectroscopy), regional body and abdominal fat (dual-energy X-ray absorptiometry and magnetic resonance imaging), serum lipids, insulin action (hyperinsulinemic-euglycemic clamp), and substrate oxidation were measured in 18 nondiabetic, sedentary, and overweight to obese men (aged 37.4 ± 1.3 years and BMI 30.9 ± 0.7 kg/m2, range 26.4–37.6) at baseline, after the first two to four bouts of aerobic exercise (55–70% of VO2max for 40 min/session), and at completion of 4.1 ± 0.2 exercise sessions/week for 9.7 ± 0.5 weeks (postexercise measurements performed 24–36 h after the last exercise bout). Mean whole body insulin-stimulated glucose uptake and basal fat oxidation rate increased 16 and 41%, respectively, after two to four bouts of exercise, without further increase at program end. Mean aerobic capacity increased 11%, and central abdominal fat decreased 5% at program end, but myocyte lipid levels were not significantly changed. Posttraining increases in insulin-stimulated glucose uptake were predicted by increase in aerobic capacity (r = 0.726, P = 0.001) and magnitude of reduction in visceral fat (r = −0.544, P = 0.02) and not by changes in myocyte lipid or LCAC levels. These results suggest that in overweight and obese sedentary men, increase in insulin sensitivity with moderate intensity exercise is predicted by improvement in aerobic capacity and reduction in visceral fat but is independent of myocyte triglyceride or LCAC levels.