169-OR: Differential Effects of Amount, Intensity, and Mode of Exercise Training on the Diabetes Risk Index

Objective: Examine the effects of amount, intensity, and mode of exercise training on type 2 diabetes (T2D) risk. Methods: A total of 531 men and women with dyslipidemia [STRRIDE I (n=222), STRRIDE AT/RT (n=142) or prediabetes [STRRIDE-PD (n=167)] were randomized to control group or one of 10 exercise interventions, ranging from doses of 8-22 kcal/kg/week; intensities of 50-75% V?O2peak; and duration of 6-9 months. Two groups included resistance training and one included dietary intervention (weight loss goal of 7%). Fasting plasma samples were obtained at baseline and 16-24 h after last exercise bout. The Diabetes Risk Index (DRI) and its components—Lipoprotein Insulin Resistance Index (LP-IR) and branched chain amino acids (BCAA) valine and leucine—were determined by NMR spectroscopy. DRI scores range from 1-100, the latter representing those at greatest T2D risk. Paired t-tests determined significance within groups (p<0.05). Study-specific ANCOVA determined differences among groups. Results: The inactive control group did not significantly change DRI score. After training, four of ten exercise groups significantly improved DRI scores, ranging from -2.8 ± 8.2 to -8.3 ± 10.4. In STRRIDE AT/RT, only the aerobic-plus-resistance group significantly improved DRI. In STRRIDE-PD, the moderate-intensity-plus-diet group had a greater DRI change than the other exercise-only moderate intensity groups. Reductions in DRI appeared to be driven largely by decreases in insulin resistance (LP-IR) but not dysmetabolism (BCAA), except for the moderate-intensity-plus-diet group, which exhibited a reduction in both. Conclusions: Multiple exercise interventions led to improvements in DRI scores. Results provide compelling evidence that adding resistance to aerobic training elicits a synergistic effect on insulin resistance and T2D risk. In individuals with prediabetes, incorporating dietary intervention with aerobic training results in the most robust improvement in T2D risk. Disclosure L.M. Ross: None. C.A. Slentz: None. I.Y. Shalaurova: None. J.D. Otvos: Employee; Self; LabCorp. M.A. Connelly: Employee; Self; LabCorp. C.W. Bales: None. J.A. Houmard: None. W.E. Kraus: None. Funding National Institutes of Health (R01HL057354, R01DK081559, T32HL007101)