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Diabetologia. 2012 May;55(5):1417-23. doi: 10.1007/s00125-012-2490-8. Epub 2012 Feb 4.

Glycaemic control is improved by 7 days of aerobic exercise training in patients with type 2 diabetes.

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  • 1Department of Nutrition and Exercise Physiology, 10A McKee, University of Missouri, Columbia, MO, 65211, USA.



Cardiovascular events and death are better predicted by postprandial glucose (PPG) than by fasting blood glucose or HbA(1c). While chronic exercise reduces HbA(1c) in patients with type 2 diabetes, short-term exercise improves measures of insulin sensitivity but does not consistently alter responses to the OGTT. The purpose of this study was to determine whether short-term exercise training improves PPG and glycaemic control in free-living patients with type 2 diabetes, independently of the changes in fitness, adiposity and energy balance often associated with chronic exercise training.


Using continuous glucose monitors, PPG was quantified in previously sedentary patients with type 2 diabetes not using exogenous insulin (n = 13, age 53 ± 2 years, HbA(1c) 6.6 ± 0.2% (49.1 ± 1.9 mmol/mol)) during 3 days of habitual activity and during the final 3 days of a 7 day aerobic exercise training programme (7D-EX) which does not elicit measurable changes in cardiorespiratory fitness or body composition. Diet was standardised across monitoring periods, with modifications during 7D-EX to offset increases in energy expenditure. OGTTs were performed on the morning following each monitoring period.


7D-EX attenuated PPG (p < 0.05) as well as the frequency, magnitude and duration of glycaemic excursions (p < 0.05). Conversely, average 24 h blood glucose did not change, nor did glucose, insulin or C-peptide responses to the OGTT.


7D-EX attenuated glycaemic variability and PPG in free-living patients with type 2 diabetes but did not significantly alter responses to the laboratory-based OGTT. These effects appeared to be independent of changes in fitness, body composition or energy balance. numbers: NCT00954109 and NCT00972452.


This project was funded by the University of Missouri Institute for Clinical and Translational Sciences (CRM), NIH grant T32 AR-048523 (CRM), Diabetes Action Research and Education Foundation (JPT). Medtronic supplied CGMS sensors at a discounted rate.

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