Journal
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
Volume 98, Issue 10, Pages 4176-4186Publisher
ENDOCRINE SOC
DOI: 10.1210/jc.2013-2232
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Funding
- European Foundation for the Study of Diabetes
- National Institutes of Health (NIH) [RO1 AG12834, T32 DK007319]
- Danish National Research Foundation
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Context: Understanding intersubject variability in glycemic control following exercise training will help individualize treatment. Objective: Our aim was to determine whether this variability is related to training-induced changes in insulin sensitivity or pancreatic beta-cell function. Design, Setting, and Participants: We conducted an observational clinical study of 105 subjects with impaired glucose tolerance or type 2 diabetes. Interventions and Main Outcome Measures: Individual subject changes in fitness (VO(2)max), glycemia (glycosylated hemoglobin, fasting glucose, oral glucose tolerance test), insulin sensitivity (hyperinsulinemic-euglycemic clamp), oral glucose-stimulated insulin secretion (GSIS), and disposition index (DI) were measured following 12 to 16 weeks of aerobic exercise training. Regression analyses were used to identify relationships between variables. Results: After training, 86% of subjects increased VO(2)max and lost weight. Glycosylated hemoglobin, fasting glucose, and 2-hour oral glucose tolerance test were reduced in 69%, 62%, and 68% of subjects, respectively, while insulin sensitivity improved in 90% of the participants. Changes in glycemic control were congruent with changes in GSIS such that 66% of subjects had a reduction in first-phase GSIS, and 46% had reduced second-phase GSIS. Training increased first-and second-phase DI in 83% and 74% of subjects. Training-induced changes in glycemic control were related to changes in GSIS (P < .05), but not insulin sensitivity or DI, and training-induced improvements in glycemic control were largest in subjects with greater pretraining GSIS. Conclusions: Intersubject variability in restoring glycemic control following exercise is explained primarily by changes in insulin secretion. Thus, baseline and training-induced changes in beta-cell function may be a key determinant of training-induced improvements in glycemic control.
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