Enhanced Peripheral and Splanchnic Insulin Sensitivity in NIDDM Men After Single Bout of Exercise

We studied glucose metabolism in non-insulin-dependent diabetic (NIDDM) men with and without glycogendepleting cycle exercise 12 h beforehand and have compared the results to our previous data in lean and obese subjects. Rates of total glucose utilization, glucose oxidation, nonoxidative glucose disposal (NOGD), glucose metabolic clearance rate (MCR), and endogenous glucose production (EGP) were determined with a “two-level” insulin-clamp technique (100-min infusions at 40 and 400 mU · m−2 · min−1) combined with indirect calorimetry and D-3-3Hglucose infusion. Muscle biopsy specimens from vastus lateralis were analyzed for glycogen content and glycogen synthase activity before and after insulin infusions. After exercise, NIDDM subjects had muscle glycogen concentrations comparable with those of lean and obese subjects. The activation of glycogen synthase both by prior exercise and insulin infusion was similar to lean controls. After exercise, total glucose disposal was significantly increased during the 40-mU · m−2 · min−1 infusion (P .05), but the increase observed during the 400-mU · m−2 · min−1 infusion was not significant. These increases after exercise were the result of significantly higher NOGD duringboth levels of insulin infusion. The MCR of glucose during both insulin infusions was reduced in NIDDM compared with lean subjects but was very similar to that in obese nondiabetics. Basal EGP was significantly reduced on the morning after exercise (4.03 ± 0.27 vs. 3.21 ± 0.21 mg · kg−1 fat-free mass · min−1) (P .05) and associated with significant reductions of fasting plasma glucose (197 ± 12 vs. 164 ± 9 mg/dl). Suppression of EGP by the 40-mU · m−2 · min−1 infusion was also greater on the morning after exercise (54 vs. 90% of basal) (P .05). This study demonstrates that a single bout of glycogen-depleting exercise significantly increases periph-eral and splanchnic insulin sensitivity 12–16 h later in NIDDM men. Increased peripheral glucose utilization after exercise is the result of increased NOGD, presumably reflecting increased glucose storage as glycogen. Insulin-stimulated rates of glucose oxidation are decreased after exercise. The lower fasting glucose concentration after exercise is due to decreased EGP rather than increased glucose utilization.