The effect of work-matched exercise intensity on beta-cell function is unknown in people with prediabetes before clinical weight loss. We determined if short-term moderate continuous (CONT) versus high-intensity interval (INT) exercise increased beta-cell function. Thirty-one subjects (age 61.4 +/- 2.5 yr; body mass index 32.1 +/- 1.0 kg/m2) with prediabetes (American Diabetes Association criteria, 75-g oral glucose tolerance test (OGTT)) were randomized to work-matched CONT (70% HRpeak) or INT (3 min 90% HRpeak and 3 min 50% HRpeak) exercise for 60 min/day over 2 wk. A 75-g 2-h OGTT was conducted after an overnight fast, and plasma glucose, insulin, C-peptide, and free fatty acids were determined for calculations of skeletal muscle (oral minimal model (OMM)), hepatic (homeostatic model of insulin resistance), and adipose (Adipose-IR) insulin sensitivity. Beta-Cell function was defined from glucose-stimulated insulin secretion (GSIS, deconvolution modeling) and the disposition index (DI). Glucagon-like polypeptide-1 (GLP-1(active)) and glucose-dependent insulinotropic polypeptide (GIP) were also measured during the OGTT, along with peak oxygen consumption and body composition. CONT and INT increased skeletal muscle- but not hepatic- or adipose-derived DI (p < 0.05). Although both treatments tended to reduce fasting GLP-1-active (p = 0.08), early phase GLP-1(active) increased post-CONT and INT training (p < 0.001). Interestingly, CONT exercise increased fasting GIP compared with decreases in INT (p = 0.02). Early and total-phase skeletal muscle DI correlated with decreased total glucose area under the curve (r = -0.52, p = 0.002 and r = -0.50, p = 0.003, respectively). Independent of intensity, short-term training increased pancreatic function adjusted to skeletal muscle in relation to improved glucose tolerance in adults with prediabetes. Exercise also uniquely affected GIP and GLP-1-active. Further work is needed to elucidate the dose-dependent mechanism(s) by which exercise impacts glycemia.

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