See discussions, stats, and author profiles for this publication at: https://www.researchgate.

net/publication/313793184

Integrating Exercise and Meal Type into a Novel Glucoregulation Model: Diabetic
Implications

Conference Paper · October 2015

CITATIONS READS

0 19

2 authors, including:

Jack Winters
Marquette University
162 PUBLICATIONS   3,858 CITATIONS   

SEE PROFILE

Some of the authors of this publication are also working on these related projects:

Novel Artificial Muscle Design: Development and Testing View project

All content following this page was uploaded by Jack Winters on 02 March 2017.

The user has requested enhancement of the downloaded file.

 Integrating Exercise and Meal Type into a Novel Glucoregulation Model: Diabetic Implications
Sofie Schunk, Jack Winters
Marquette University, Milwaukee, Wisconsin, Department of Biomedical Engineering

Introduction: Factors of glucoregulation include exercise variants, daily movement activities, tissue
compartment metabolism and meal type distinction, challenging to model in a robust and comprehensive manner.
A nonlinear 9-state lumped compartmental model is presented addressing these challenges, and providing
flexibility for variable body mass, muscle ratio, and types of diabetes (T1D, T2D) informing drug delivery design.

Materials and Methods: Model compartments are shown in Figure 1. Workload (aerobic vs. anaerobic) includes
immediate and longer-term effects on blood glucose (BG) levels based on muscle fuel consumption demand,
nonlinear flux modulation for stored glucose (glycogen) breakdown, insulin sensitivity, and (for aerobic)
addressing fat-carbohydrate oxidative fuel mix as a function of intensity and duration. Exercise induces other non-
insulin mediated glucose uptake into skeletal muscle via GLUT4 and hepatic glycogenolysis (key for non-muscle
compartment), especially in athletes. Foodstuff enters a slow or fast absorption path based on glycemic index.
The model’s non-linear phenomena utilize saturating Hill kinetic equations, applied for strategic signals and rates.
Figure 1. Compartmental model with 7-state core model in
solid [3-state glucose compartmental model (lower right,
thick lines representing material flow) receiving signal from
a 2-state digested glucose from meals (top left), modulated
via insulin and glucagon control action (bottom left), and
consuming glucose through exercise and daily activity (top
right)]. 8th and 9th states (dashed block) relate to exogenous
control. Implemented in Matlab, signal variables are
separated into 4 distinct sub-models including mass flow
(thick arrows, metab=metabolism) and storage and control
action (unidirectional signals). Nonlinear relations include
both flux terms and heuristics that change fitting equations
based on different state or input (u) signal ranges.
Results and Discussion: BG is sensitive to meal type and to muscle tissue glucose consumption with exercise
(also resulting in up-regulation via non-muscle glycogenolysis). In non-diabetic simulations (not shown), BG
remains in a healthy range (80 to 120 mg/dl), due primarily to glucagon/insulin control action, except for
temporary fluxes due to meals (e.g., high glycemic index) or exercise. Figure 2 is a T1D example, where GLUT4
mechanisms allow glycolytic influx based on energy demands during exercise despite suppressed insulin.
Tissue (g/Kgm ,t) Gluc Bl (mg/dl) G-Flow (Kcal/hr)

1000 High GI
Figure 2: Four 24-hour T1D simulations: 1)
Exercise
500 No insulin injection, 2) Meal rapid-acting
Activity meal injections, 3) long-acting injection and
0
300 4) reaching ‘unhealthy’ T1D with higher
No exercise; larger meal
200
caloric intake, no exercise and missed
Low GI snack OK for T1D
breakfast injection. Inputs (top plot) include
100
3 meals/3 snacks (black solid, red digestive
15
BG lowers due to GLUT4 outflux to muscle state), 600 kcal/hr exercise and 70 kg
Non-Muscle increases in BG too high, muscle depletes
10 normal adult parameters (30 kg muscle). A
5
Healthy (large exercise, ~2000 kcal/day and
'Unhealthy' Diabetic lifestyle causes accumulation; esp. in muscle mainly low GI meals) T1D shows natural
5
regulation (good steady-state BG range) vs.
Glucagon (pg/dL)
Insulin (mU/dl)

4 1
0.8
3
0.6 an ‘unhealthy’ lifestyle. With non-muscle
2
1
0.4
0.2
accumulation, muscle glucose-glycogen
0
0 5 10 15 20
0 energy stores become depleted.

Conclusions: Adding the aforementioned practical everyday features could help current real-time innovative
technology controllers (i.e. artificial pancreas and/or pumps and continuous glucose monitors) take advantage of a
modeled framework enabling personalized adaptive tuning for drug delivery. Simulation results here focus on a
Type 1 athletic version, recognizing the importance of non-insulin mediated glucose flux as well.

Acknowledgements: The first author is living with T1D. Thanks to 70 students who used our models in projects.

View publication stats