title: Pancreatic β-cell function is a stronger predictor of changes in glycemic control after an aerobic exercise intervention than insulin sensitivity.
abstract: BACKGROUND
  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.
  
  
  METHODS
  We conducted an observational clinical study of 105 subjects with impaired glucose tolerance or type 2 diabetes.
  
  
  METHODS
  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: PhD, Department of Biomedical Sciences, Panum Institute 4.5.13, University of Copenhagen, Blegdamsvej 3B, Copenhagen 2200, Denmark. thomas.solomon@sund.ku.dk.
authors: Thomas P J
authors: TP
authors: Solomon
authors: Steven K
authors: SK
authors: Malin
authors: Kristian
authors: K
authors: Karstoft
authors: Sangeeta R
authors: SR
authors: Kashyap
authors: Jacob M
authors: JM
authors: Haus
authors: John P
authors: JP
authors: Kirwan
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000378:metabolism*; D015992:Body Mass Index; D003924:Diabetes Mellitus, Type 2 / Q000503:physiopathology / Q000628:therapy*; D015444:Exercise / Q000502:physiology*; D005081:Exercise Therapy; D005260:Female; D018149:Glucose Intolerance / Q000503:physiopathology / Q000628:therapy*; D005951:Glucose Tolerance Test; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology*; D050417:Insulin-Secreting Cells / Q000502:physiology*; D008297:Male; D009765:Obesity / Q000503:physiopathology / Q000628:therapy; D016896:Treatment Outcome; D015431:Weight Loss / Q000502:physiology
chemical_list: D001786:Blood Glucose
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