Postprandial Walking is Better for Lowering the Glycemic Effect of Dinner than Pre-Dinner Exercise in Type 2 Diabetic Individuals
In prior studies of exercise done before or after breakfast and lunch, postprandial activity generally reduces glycemia more than pre-meal. This study sought to examine the effects of exercise before or after an evening meal.
Examined the differing effects of a single bout of pre- or postprandial moderate exercise or no exercise on the glycemic response to an evening (dinner) meal in individuals with type 2 diabetes.
Community-dwelling participants tested at a research university in Virginia.
Twelve men and women subjects (mean age of 61.4+/-2.7 years) with type 2 diabetes treated with diet and/or oral medications.
Three trials conducted on separate days consisting of a rest day when subjects consumed a standardized dinner with a moderate glycemic effect and 2 exercise days when they undertook 20 minutes of self-paced treadmill walking immediately before or 15 to 20 minutes after eating.
Blood samples taken every 30 minutes over a 4-hour period and later assayed for plasma glucose; from these data both absolute and relative changes in glucose levels were determined, as well as the total glucose area under the curve (AUC) of the 4-hour testing period. Initial samples were additionally assayed for glycated hemoglobin and lipid levels.
Twenty minutes of self-paced walking done shortly after meal consumption resulted in lower plasma glucose levels at the end of exercise compared to values at the same time point when subjects had walked pre-dinner. Total glucose AUC over 4-hours was not significantly different among trials.
Postprandial walking may be more effective at lowering the glycemic impact of the evening meal in individuals with type 2 diabetes compared with pre-meal or no exercise and may be an effective means to blunt postprandial glycemic excursions.
Available from: Bryan Gibson
- "We aggregated data from three prior diabetes and exercise studies to determine the significant predictors and to test potential model structures. These prior studies were conducted in Virginia, USA ; Sao Paolo, Brazil ; and Quebec, Canada . The aggregated dataset represents 56 individuals with T2DM performing 488 exercise sessions. "
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ABSTRACT: Our purpose was to develop and test a predictive model of the acute glucose response to exercise in individuals with type 2 diabetes.Design and Methods: Data from three previous exercise studies (56 subjects, 488 exercise sessions) were combined and used as a development dataset. A mixed-effects Least Absolute Shrinkage Selection Operator (LASSO) was used to select predictors among 12 potential predictors. Tests of the relative importance of each predictor were conducted using the Lindemann Merenda and Gold (LMG) algorithm. Model structure was tested using likelihood ratio tests. Model accuracy in the development dataset was assessed by leave-one-out cross-validation.Prospectively captured data (47 individuals, 436 sessions) was used as a test dataset. Model accuracy was calculated as the percentage of predictions within measurement error. Overall model utility was assessed as the number of subjects with <=1 model error after the third exercise session. Model accuracy across individuals was assessed graphically. In a post-hoc analysis, a mixed-effects logistic regression tested the association of individuals' attributes with model error.
Minutes since eating, a non-linear transformation of minutes since eating, post-prandial state, hemoglobin A1c, sulfonylurea status, age, and exercise session number were identified as novel predictors. Minutes since eating, its transformations, and hemoglobin A1c combined to account for 19.6% of the variance in glucose response. Sulfonylurea status, age, and exercise session each accounted for <1.0% of the variance.In the development dataset, a model with random slopes for pre-exercise glucose improved fit over a model with random intercepts only (likelihood ratio 34.5, p < 0.001). Cross-validated model accuracy was 83.3%.In the test dataset, overall accuracy was 80.2%. The model was more accurate in pre-prandial than postprandial exercise (83.6% vs. 74.5% accuracy respectively). 31/47 subjects had <=1 model error after the third exercise session. Model error varied across individuals and was weakly associated with within-subject variability in pre-exercise glucose (Odds ratio 1.49, 95% Confidence interval 1.23-1.75).
The preliminary development and test of a predictive model of acute glucose response to exercise is presented. Further work to improve this model is discussed.
Diabetology and Metabolic Syndrome 07/2013; 5(1):33. DOI:10.1186/1758-5996-5-33 · 2.17 Impact Factor
Available from: Andrei Gribok
- "Other studies have investigated the role of exercise timing on glycemic responses to meals, primarily among younger or middle-aged people with type 2 diabetes and with the exercise timing ranging from premeal (26,27), immediately postmeal (25,28), 15–45 min postmeal (29,30), and 2 h postmeal (31). Studies of premeal (i.e., postabsorptive) exercise generally report either no effect on postchallenge glycemia (29,30) or an increase in the glycemic effect of a meal (26), which corroborates our findings regarding the effects of exercise performed at 4:30 p.m. on the subsequent dinner meal. "
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The purpose of this study was to compare the effectiveness of three 15-min bouts of postmeal walking with 45 min of sustained walking on 24-h glycemic control in older persons at risk for glucose intolerance.RESEARCH DESIGN AND METHODS
Inactive older (≥60 years of age) participants (N = 10) were recruited from the community and were nonsmoking, with a BMI <35 kg m(-2) and a fasting blood glucose concentration between 105 and 125 mg dL(-1). Participants completed three randomly ordered exercise protocols spaced 4 weeks apart. Each protocol comprised a 48-h stay in a whole-room calorimeter, with the first day serving as the control day. On the second day, participants engaged in either 1) postmeal walking for 15 min or 45 min of sustained walking performed at 2) 10:30 a.m. or 3) 4:30 p.m.. All walking was on a treadmill at an absolute intensity of 3 METs. Interstitial glucose concentrations were determined over 48 h with a continuous glucose monitor. Substrate utilization was measured continuously by respiratory exchange (VCO2/VO2).RESULTSBoth sustained morning walking (127 ± 23 vs. 118 ± 14 mg dL(-1)) and postmeal walking (129 ± 24 vs. 116 ± 13 mg dL(-1)) significantly improved 24-h glycemic control relative to the control day (P < 0.05). Moreover, postmeal walking was significantly (P < 0.01) more effective than 45 min of sustained morning or afternoon walking in lowering 3-h postdinner glucose between the control and experimental day.CONCLUSIONS
Short, intermittent bouts of postmeal walking appear to be an effective way to control postprandial hyperglycemia in older people.
Diabetes care 06/2013; 36(10). DOI:10.2337/dc13-0084 · 8.42 Impact Factor
Available from: PubMed Central
- "Controlling hyperglycemia is the most important factor for reducing the risks associated with diabetes and diabetic complications. Management of type 2 diabetes usually begins with a change of diet and exercise , and most patients ultimately require pharmacotherapy such as an oral antidiabetic drug (OAD) . OADs include sulfonylurea, non-sulfonylurea secretagogues, biguanides, thiazolidinediones, glucosidase inhibitors, and glucagon-like peptide-1 (GLP-1) inhibitors. "
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ABSTRACT: Leaf of Sasa borealis, a species of bamboo, has been reported to exhibit anti-hyperglycemic effect. However, its antidiabetic mechanism is not fully understood. In this study, we examined whether an extract of S. borealis activates AMP-activated protein kinase (AMPK) and exerts anti-hyperglycemic effects. Treatment with the S. borealis extract increased insulin signaling and phosphorylation of AMPK and stimulated the expression of its downstream targets, including PPARα, ACO, and CPT-1 in C2C12 cells and PPARα in HepG2 cells. However, inhibition of AMPK activation attenuated insulin signaling and prevented the stimulation of AMPK target genes. The S. borealis extract increased glucose uptake in C2C12 cells and suppressed expression of the gluconeogenic gene, PEPCK in HepG2 cells. The extract significantly reduced blood glucose and triglyceride levels in STZ-induced diabetic mice. The extract enhanced AMPK phosphorylation and increased Glut-4 expression in the skeletal muscle of the mice. These findings demonstrated that the S. borealis extract exerts its anti-hyperglycemic effect through activation of AMPK and enhancement of insulin signaling.
Nutrition research and practice 02/2013; 7(1):15-21. DOI:10.4162/nrp.2013.7.1.15 · 1.44 Impact Factor
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