Attenuating blood glucose excursions in the postprandial state have the capacity to reduce the risk for cardiovascular disease, type 2 diabetes, and mortality, even in apparently healthy populations. Nearly a century ago, it was reported that oral glucose tolerance is improved by prior glucose consumption. This was termed the second-meal phenomenon and is also seen with consumption of mixed-macronutrient-containing meals. In this context, a number of mechanisms probably contribute to the attenuation of glycemia, including gastric emptying, early-phase insulin secretion, hepatic glucose output, and muscle glucose uptake. More recently, a paradoxical second-meal phenomenon has been observed in the immediate postexercise period whereby prior meal consumption deteriorated glucose tolerance. The mechanisms regulating the postexercise second-meal phenomenon are less clear, but are likely to involve an increase in intestinal absorption, greater hepatic glucose output, and under circumstances of muscle damage, reductions in muscle glucose uptake. Further work is required to confirm these mediating factors and to characterize the time course of this paradox, which is likely to only exist within the first 4 h following exercise. Critically, this acute postexercise phenomenon should be maintained in the perspective of the benefits of chronic exercise training, which for the majority of individuals improves glycemic control and reduces many health risks including those associated with exaggerated postprandial glycemia.
Keywords: Exercise; Fatty acids; Glucose; Insulin; Metabolism; Postprandial; Type 2 diabetes.
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