Abstract
The carbohydrate deficit induced by exercise is thought to play a key role in increased post-exercise insulin action. However, the effects of replacing carbohydrate utilized during exercise on postprandial glycaemia and insulin sensitivity are yet to be determined. This study therefore isolated the extent to which the insulin-sensitizing effects of exercise are dependent on the carbohydrate deficit induced by exercise, relative to other exercise-mediated mechanisms. Fourteen healthy adults performed a 90-min run at 70% max starting at 1600–1700 h before ingesting either a non-caloric artificially-sweetened placebo solution (CHO-DEFICIT) or a 15% carbohydrate solution (CHO-REPLACE; 221.4 ± 59.3 g maltodextrin) to precisely replace the measured quantity of carbohydrate oxidized during exercise. The alternate treatment was then applied one week later in a randomized, placebo-controlled, and double-blinded crossover design. A standardized low-carbohydrate evening meal was consumed in both trials before overnight recovery ahead of a two-hour oral glucose tolerance test (OGTT) the following morning to assess glycemic and insulinemic responses to feeding. Compared to the CHO-DEFICIT condition, CHO-REPLACE increased the incremental area under the plasma glucose curve by a mean difference of 68 mmol·L−1 (95% CI: 4 to 132 mmol·L−1; p = 0.040) and decreased the Matsuda insulin sensitivity index by a mean difference of −2 au (95% CI: −1 to −3 au; p = 0.001). This is the first study to demonstrate that post-exercise feeding to replaceme the carbohydrate expended during exercise can attenuate glucose tolerance and insulin sensitivity the following morning. The mechanism through which exercise improves insulin sensitivity is therefore (at least in part) dependent on carbohydrate availability and so the day-to-day metabolic health benefits of exercise might be best attained by maintaining a carbohydrate deficit overnight.
Highlights
Physical activity is a powerful tool to improve insulin sensitivity and glycemic control [1].increasing physical activity is a crucial counter-measure in reducing T2D prevalence [2,3].On an acute level, single bouts of exercise consistently enhance insulin sensitivity and muscle glucose uptake in both insulin-resistant [4] and healthy individuals [5], the acute effects of exercise on glucose tolerance are less clear [6,7].Nutrients 2018, 10, 123; doi:10.3390/nu10020123 www.mdpi.com/journal/nutrientsMetabolic flexibility is a key aspect of insulin sensitivity and reflects the ability to switch between substrate sources for oxidation according to availability
Following ingestion of the oral glucose tolerance test (OGTT), plasma glucose concentrations rose to a greater extent in CHO-REPLACE versus CHO-DEFICIT
The present study demonstrates that replacement of the carbohydrate utilized during a single bout of exercise impairs both insulin sensitivity and glucose tolerance by ~20–25% the following morning, relative to when the exercise-induced carbohydrate deficit is maintained
Summary
Physical activity is a powerful tool to improve insulin sensitivity and glycemic control [1].increasing physical activity is a crucial counter-measure in reducing T2D prevalence [2,3].On an acute level, single bouts of exercise consistently enhance insulin sensitivity and muscle glucose uptake in both insulin-resistant [4] and healthy individuals [5], the acute effects of exercise on glucose tolerance are less clear [6,7].Nutrients 2018, 10, 123; doi:10.3390/nu10020123 www.mdpi.com/journal/nutrientsMetabolic flexibility is a key aspect of insulin sensitivity and reflects the ability to switch between substrate sources for oxidation according to availability. Physical activity is a powerful tool to improve insulin sensitivity and glycemic control [1]. Single bouts of exercise consistently enhance insulin sensitivity and muscle glucose uptake in both insulin-resistant [4] and healthy individuals [5], the acute effects of exercise on glucose tolerance are less clear [6,7]. Metabolic flexibility is a key aspect of insulin sensitivity and reflects the ability to switch between substrate sources for oxidation according to availability. Individuals with robust metabolic flexibility display high rates of fat oxidation in the fasted state, switching to high rates of carbohydrate oxidation in the fed (or insulin-stimulated) state. Substrate selection in the fasted and fed state may be an important mechanism by which exercise alters insulin sensitivity and postprandial glycemia
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