Abstract
Little is known about the effects of exercise intensity on compensatory changes in glucose-stimulated insulin secretion (GSIS) when adjusted for adipose, liver and skeletal muscle insulin resistance (IR). Fifteen participants (8F, Age: 49.9±3.6yr; BMI: 31.0±1.5kg/m2; VO2peak: 23.2±1.2mg/kg/min) with prediabetes (ADA criteria, 75g OGTT and/or HbA1c) underwent a time-course matched Control, and isocaloric (200kcal) exercise at moderate (MIE; at lactate threshold (LT)), and high-intensity (HIE; 75% of difference between LT and VO2peak). A 75g OGTT was conducted 1 hour post-exercise/Control, and plasma glucose, insulin, C-peptide and free fatty acids were determined for calculations of skeletal muscle (1/Oral Minimal Model; SMIR), hepatic (HOMAIR), and adipose (ADIPOSEIR) IR. Insulin secretion rates were determined by deconvolution modeling for GSIS, and disposition index (DI; GSIS/IR; DISMIR, DIHOMAIR, DIADIPOSEIR) calculations. Compared to Control, exercise lowered SMIR independent of intensity (P<0.05), with HIE raising HOMAIR and ADIPOSEIR compared with Control (P<0.05). GSIS was not reduced following exercise, but DIHOMAIR and DIADIPOSEIR were lowered more following HIE compared with Control (P<0.05). However, DISMIR increased in an intensity based manner relative to Control (P<0.05), which corresponded with lower post-prandial blood glucose levels. Taken together, pancreatic insulin secretion adjusts in an exercise intensity dependent manner to match the level of insulin resistance in skeletal muscle, liver and adipose tissue. Further work is warranted to understand the mechanism by which exercise influences the cross-talk between tissues that regulate blood glucose in people with prediabetes.
Highlights
470 million worldwide have prediabetes [1], with approximately 86 million individuals in the U.S population being diagnosed [2,3]
We recently demonstrated that acute high intensity exercise lowered post-prandial blood glucose more than an isocaloric bout of moderate intensity exercise in men and women with prediabetes, but the role of pancreatic function was not assessed [19]
Given that high intensity exercise in our prior work [19] improved postprandial blood glucose more than moderate intensity exercise, we hypothesized that changes in glucose-stimulated insulin secretion (GSIS) adjusted for skeletal muscle, liver and/or adipose insulin resistance may in part explain this improved glycemic control response in men and women
Summary
470 million worldwide have prediabetes [1], with approximately 86 million individuals in the U.S population being diagnosed [2,3]. Maintaining the capacity of β-cells to secrete adequate amounts of insulin in response to multi-organ insulin resistance is paramount to preventing progression from prediabetes to type 2 diabetes [5]. The purpose this study was to test the effect of exercise intensity on β-cell function to determine if this change in insulin secretion would correspond with favorable changes in blood glucose. Given that high intensity exercise in our prior work [19] improved postprandial blood glucose more than moderate intensity exercise, we hypothesized that changes in GSIS adjusted for skeletal muscle, liver and/or adipose insulin resistance may in part explain this improved glycemic control response in men and women
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