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 β-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 (VO2max), 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 VO2max 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 β-cell function may be a key determinant of training-induced improvements in glycemic control.
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 β-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 (VO2max), 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 VO2max 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 β-cell function may be a key determinant of training-induced improvements in glycemic control.
Authors: Normand G Boulé; S John Weisnagel; Timo A Lakka; Angelo Tremblay; Richard N Bergman; Tuomo Rankinen; Arthur S Leon; James S Skinner; Jack H Wilmore; D C Rao; Claude Bouchard Journal: Diabetes Care Date: 2005-01 Impact factor: 19.112
Authors: S E Kahn; R L Prigeon; D K McCulloch; E J Boyko; R N Bergman; M W Schwartz; J L Neifing; W K Ward; J C Beard; J P Palmer Journal: Diabetes Date: 1993-11 Impact factor: 9.461
Authors: X R Pan; G W Li; Y H Hu; J X Wang; W Y Yang; Z X An; Z X Hu; J Lin; J Z Xiao; H B Cao; P A Liu; X G Jiang; Y Y Jiang; J P Wang; H Zheng; H Zhang; P H Bennett; B V Howard Journal: Diabetes Care Date: 1997-04 Impact factor: 19.112
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