Exercise Intensity Modulates Glucose-Stimulated Insulin Secretion when Adjusted for Adipose, Liver and Skeletal Muscle Insulin Resistance

<div><p>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 HbA_1c) 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; SM_IR), hepatic (HOMA_IR), and adipose (ADIPOSE_IR) IR. Insulin secretion rates were determined by deconvolution modeling for GSIS, and disposition index (DI; GSIS/IR; DI_SMIR, DI_HOMAIR, DI_ADIPOSEIR) calculations. Compared to Control, exercise lowered SM_IR independent of intensity (<i>P</i><0.05), with HIE raising HOMA_IR and ADIPOSE_IR compared with Control (<i>P</i><0.05). GSIS was not reduced following exercise, but DI_HOMAIR and DI_ADIPOSEIR were lowered more following HIE compared with Control (<i>P</i><0.05). However, DI_SMIR increased in an intensity based manner relative to Control (<i>P</i><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.</p></div

Effect of exercise intensity on multi-organ insulin resistance.

<p>Data are expressed as mean ± SEM. OMM = oral minimal model was calculated from plasma glucose and insulin to measure skeletal muscle insulin resistance. Homeostatic model of insulin resistance (HOMR-IR) was calculated as fasting PG x fasting PI to depict hepatic insulin resistance. Adipose-IR was calculated as fasting FFA x fasting PI to determine adipose insulin resistance. *Compared to Control, P<0.05. ^Compared to MIE, P<0.05.</p

Effect of exercise intensity on β-cell function.

<p>Data are expressed as mean ± SEM. DI = disposition index and was used to characterize pancreatic β-cell function. Skeletal muscle DI was calculated as AUC of ISR/Glucose x oral glucose minimal model. Hepatic DI was estimated as AUC of ISR/Glucose x HOMA-IR. Adipose DI was determined as AUC of ISR/Glucose x Adipose-IR. *Compared to Control, <i>P</i><0.05. ^Compared to MIE, <i>P</i><0.05.</p

Subject Characteristics.

<p>Subject Characteristics.</p

Effect of exercise intensity on glucose-stimulated insulin secretion.

<p>Data are expressed as mean ± SEM. ISR = insulin secretion rate derived from deconvolution of plasma C-peptide. GSIS = glucose-stimulated insulin secretion rate (ISR; total AUC C-peptide divided by total AUC Glucose). *Compared to Control, P<0.05.</p

sj-docx-1-jbr-10.1177_07487304221123455 – Supplemental material for A Naturalistic Actigraphic Assessment of Changes in Adolescent Sleep, Light Exposure, and Activity Before and During COVID-19

Supplemental material, sj-docx-1-jbr-10.1177_07487304221123455 for A Naturalistic Actigraphic Assessment of Changes in Adolescent Sleep, Light Exposure, and Activity Before and During COVID-19 by Corey A. Rynders, Anne E. Bowen, Emily Cooper, John T. Brinton, Janine Higgins, Kristen J. Nadeau, Kenneth P. Wright Jr. and Stacey L. Simon in Journal of Biological Rhythms</p