Adithya Hari1,2, Ciaràn Fealy3, Thomas P J Solomon4, Jacob M Haus5, Karen R Kelly6, Hope Barkoukis2, John P Kirwan7,8,9. 1. Department of Pathobiology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA. 2. Case Western Reserve University, Cleveland, OH, USA. 3. Maastricht University, Maastricht, The Netherlands. 4. University of Birmingham, Birmingham, UK. 5. University of Michigan, Ann Arbor, MI, USA. 6. Warfighter Performance Department, Naval Health Research Center, 140 Sylvester Road, San Diego, CA, USA. 7. Department of Pathobiology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA. John.Kirwan@pbrc.edu. 8. Case Western Reserve University, Cleveland, OH, USA. John.Kirwan@pbrc.edu. 9. Pennington Biomedical Research Center, 6400 Perkins Road, Baton Rouge, LA, 70808, USA. John.Kirwan@pbrc.edu.
Abstract
AIMS: Glucose effectiveness (GE) refers to the ability of glucose to influence its own metabolism through insulin-independent mechanisms. Diminished GE is a predictor of progression to type 2 diabetes. Exercise training improves GE, however, little is known about how dietary interventions, such as manipulating the glycemic index of diets, interact with exercise-induced improvements in GE in at-risk populations. METHODS: We enrolled 33 adults with obesity and pre-diabetes (17 males, 65.7 ± 4.3 years, 34.9 ± 4.2 kg m-2) into a 12-week exercise training program (1 h day-1 and 5 day week-1 at ~ 85% of maximum heart rate) while being randomized to concurrently receive either a low (EX-LOG: 40 ± 0.3 au) or high (EX-HIG: 80 ± 0.6 au) glycemic index diet. A 75-g oral-glucose-tolerance test (OGTT) was performed before and after the intervention and GE was calculated using the Nagasaka equation. Insulin resistance was estimated using a hyperinsulinemic-euglycemic clamp and cardiorespiratory fitness using a VO2max test. RESULTS: Both EX-LOG and EX-HIG groups had similar improvements in weight (8.6 ± 5.1 kg, P < 0.001), VO2max (6 ± 3.5 mL kg-1 min-1, P < 0.001) and clamp-measured peripheral insulin resistance (1.7 ± 0.9 mg kg-1 min-1, P < 0.001), relative to baseline data. GE in EX-LOG and EX-HIG was similar at baseline (1.9 ± 0.38 vs. 1.85 ± 0.3 mg dL-1 min-1, respectively; P > 0.05) and increased by ~ 20% post-intervention in the EX-LOG arm (∆GE: 0.07-0.57 mg dL-1 min-1, P < 0.05). Plasma free fatty acid (FFA) concentrations also decreased only in the EX-LOG arm (∆FFA: 0.13 ± 0.23 mmol L-1, P < 0.05). CONCLUSIONS: Our data suggest that a high glycemic index diet may suppress exercise-induced enhancement of GE, and this may be mediated through plasma FFAs.
RCT Entities:
AIMS: Glucose effectiveness (GE) refers to the ability of glucose to influence its own metabolism through insulin-independent mechanisms. Diminished GE is a predictor of progression to type 2 diabetes. Exercise training improves GE, however, little is known about how dietary interventions, such as manipulating the glycemic index of diets, interact with exercise-induced improvements in GE in at-risk populations. METHODS: We enrolled 33 adults with obesity and pre-diabetes (17 males, 65.7 ± 4.3 years, 34.9 ± 4.2 kg m-2) into a 12-week exercise training program (1 h day-1 and 5 day week-1 at ~ 85% of maximum heart rate) while being randomized to concurrently receive either a low (EX-LOG: 40 ± 0.3 au) or high (EX-HIG: 80 ± 0.6 au) glycemic index diet. A 75-g oral-glucose-tolerance test (OGTT) was performed before and after the intervention and GE was calculated using the Nagasaka equation. Insulin resistance was estimated using a hyperinsulinemic-euglycemic clamp and cardiorespiratory fitness using a VO2max test. RESULTS: Both EX-LOG and EX-HIG groups had similar improvements in weight (8.6 ± 5.1 kg, P < 0.001), VO2max (6 ± 3.5 mL kg-1 min-1, P < 0.001) and clamp-measured peripheral insulin resistance (1.7 ± 0.9 mg kg-1 min-1, P < 0.001), relative to baseline data. GE in EX-LOG and EX-HIG was similar at baseline (1.9 ± 0.38 vs. 1.85 ± 0.3 mg dL-1 min-1, respectively; P > 0.05) and increased by ~ 20% post-intervention in the EX-LOG arm (∆GE: 0.07-0.57 mg dL-1 min-1, P < 0.05). Plasma free fatty acid (FFA) concentrations also decreased only in the EX-LOG arm (∆FFA: 0.13 ± 0.23 mmol L-1, P < 0.05). CONCLUSIONS: Our data suggest that a high glycemic index diet may suppress exercise-induced enhancement of GE, and this may be mediated through plasma FFAs.