One Bout of Exercise Alters Free-Living Postprandial Glycemia in Type 2 Diabetes

Douglas J. Oberlin; Catherine R. Mikus; Monica L. Kearney; Pamela S. Hinton; Camila Manrique; Heather J. Leidy; Jill A. Kanaley; R. Scott Rector; John P. Thyfault


Med Sci Sports Exerc. 2014;46(2):232-238. 

In This Article

Abstract and Introduction


Purpose: Elevated postprandial glycemic (PPG) excursions are significant risk factors for cardiovascular disease in type 2 diabetes patients. In this study, we tested if and for how many meals a single bout of exercise would reduce PPG responses to subsequent meals in type 2 diabetes (T2D) patients using a continuous glucose monitor system (CGMS).

Methods: We recruited nine sedentary (<30 min·wk−1 of exercise) individuals with T2D (mean ± SD; body mass index = 36.0 ± 1.1 kg·m−2, age = 60.3 ± 1.0 yr, HbA1c = 6.3% ± 0.2%). The subjects consumed a eucaloric diet (51% carbohydrate, 31% fat, and 18% protein) consisting of three meals, identical in composition, for a 2-d period while wearing a continuous glucose monitor system in two different conditions (exercise [EX], one 60-min bout at 60%–75% of heart rate reserve performed before breakfast), vs a sedentary [SED] condition). We quantified 24-h average glucose, PPG area under the curve (AUC; 4-h glucose AUC after meals), and PPG-2 h (2 h postprandial glucose).

Results: EX significantly reduced average [glucose] during the first 24-h period (P = 0.03). EX caused a reduction in PPG-AUC (P = 0.02) for all of the meals during the 2 d (main effect between conditions). A comparison between the EX and the SED conditions at each meal revealed that EX reduced PPG-AUC after the second meal of day 1 (lunch) (P = 0.04). PPG-2 h was not significantly different between EX and SED.

Conclusions: Although a single EX bout does lower 24-h average [glucose], it only significantly lowered PPG-AUC at the second meal after the bout, suggesting that daily exercise may be needed to most effectively improve PPG at the advent of exercise training in T2D patients.


Hyperglycemia is linked to increased risk for cardiovascular disease (CVD) as well as all-cause mortality; thus, improved glycemic control is a critical target for diabetes management.[6,33] Individuals with type 2 diabetes (T2D) are therefore given the goal of maintaining glycated hemoglobin (HbA1c), a measure of long-term glycemic control, less than 7%.[2,31,39] However, although HbA1c is a good indicator of average blood glucose levels for several months, it does not necessarily reflect the magnitude of changes in glucose levels for shorter periods of time, such as during the course of a day when meals of varying macronutrient content are consumed.[19,26,27] During the course of a day, blood glucose levels can rise and fall several times, depending on frequency of feeding and the type of food that is consumed as well as the level of physical activity.[19,26–28,41] Fasting glucose levels, another common indicator of glycemic control, also fails to assess changes in glucose in response to feeding. Therefore, both HbA1c and fasting glucose may not adequately capture changes in blood glucose concentrations experienced over a typical day.[19,28,41] Recently, it has been reported that postprandial (or postglucose challenge) glucose excursions (PPG) may be more tightly linked to risk for CVD than HbA1c or fasting glucose levels.[6,33] Therefore, therapies that limit the magnitude of PPG should also lower risk for CVD.[4,6,7,21,33]

Exercise is a powerful method to improve long-term glycemic control.[3,11,14,15,18,30,32,34,35] It has been demonstrated that exercise can 1) act in an acute manner to increase glucose uptake in the absence of insulin and 2) acutely improve insulin-stimulated glucose uptake in skeletal muscle.[30] Moreover, exercise transiently improves insulin sensitivity for a prolonged period, suggesting that PPG may also be improved for several meals after one bout of exercise depending on the health status of the population.[15,16,22] We have recently shown that 7 d of exercise training improves postprandial glucose levels measured by a continuous glucose monitoring system (CGMS) in free-living humans with T2D;[24] however, the design did not allow us to determine the residual effects of each exercise bout on PPG. Because of the known effects of exercise to transiently improve skeletal muscle insulin sensitivity, we next questioned if, and for how many subsequent meals (identical in composition and caloric load), one bout of exercise would improve PPG measured by CGMS in free-living individuals with T2D. Importantly, PPG is driven by not just muscle insulin sensitivity but also by hepatic insulin sensitivity, pancreatic β-cell function, and other physiological responses. Although other laboratories have shown reduced concentrations in PPG and postprandial insulin at a specific time points postprandially (2.5 h),[40] the total area under the glucose curve has not been assessed, nor did subjects consume the same foods at each meal after the exercise bout. We hypothesized that a single, morning exercise session would only improve PPG area under the curve (AUC) for meals consumed during the same day (meals 1–3), and PPG-AUC would subsequently return to preexercise levels on day 2 (meals 4–6). Our hypothesis for a 1-d effect was based on 1) previous data showing one bout of exercise may not improve insulin sensitivity for as long as duration in T2D as in health cohorts 2) and that subsequent meals would replete muscle glycogen thus reducing the positive effects of exercise on PPG.[9,15,22] If proven correct, this hypothesis would indicate that exercise on a daily basis may be needed to most effectively improve PPG in individuals with T2D, at least in the initial stages of training.