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Carbohydrate availability is important to maximize endurance performance during prolonged bouts of moderate- to high-intensity exercise as well as for acute post-exercise recovery. The primary form of carbohydrates that are typically ingested during and after exercise are glucose (polymers). However, intestinal glucose absorption can be limited by the capacity of the intestinal glucose transport system (SGLT1). Intestinal fructose uptake is not regulated by the same transport system, as it largely depends on GLUT5 as opposed to SGLT1 transporters. Combining the intake of glucose plus fructose can further increase total exogenous carbohydrate availability and, as such, allow higher exogenous carbohydrate oxidation rates. Ingesting a mixture of both glucose and fructose can improve endurance exercise performance compared to equivalent amounts of glucose (polymers) only. Fructose co-ingestion can also accelerate post-exercise (liver) glycogen repletion rates, which may be relevant when rapid (1.2 g/kg/h) are ingested during post-exercise recovery. In conclusion, combined ingestion of fructose with glucose may be preferred over the ingestion of glucose (polymers) only to help trained athletes maximize endurance performance during prolonged moderate- to high-intensity exercise sessions and accelerate post-exercise (liver) glycogen repletion.

Carbohydrate availability is important to maximize endurance performance during prolonged bouts of moderate‐ to high‐intensity exercise as well as for acute post‐exercise recovery. The primary form of carbohydrates that are typically ingested during and after exercise are glucose (polymers). However, intestinal glucose absorption can be limited by the capacity of the intestinal glucose transport system (SGLT1). Intestinal fructose uptake is not regulated by the same transport system, as it largely depends on GLUT5 as opposed to SGLT1 transporters. Combining the intake of glucose plus fructose can further increase total exogenous carbohydrate availability and, as such, allow higher exogenous carbohydrate oxidation rates. Ingesting a mixture of both glucose and fructose can improve endurance exercise performance compared to equivalent amounts of glucose (polymers) only. Fructose co‐ingestion can also accelerate post‐exercise (liver) glycogen repletion rates, which may be relevant when rapid (1.2 g/kg/h) are ingested during post‐exercise recovery. In conclusion, combined ingestion of fructose with glucose may be preferred over the ingestion of glucose (polymers) only to help trained athletes maximize endurance performance during prolonged moderate‐ to high‐intensity exercise sessions and accelerate post‐exercise (liver) glycogen repletion., Fructose (Fru) co‐ingestion with glucose (Glu) appears to increase the total capacity to absorb carbohydrates. In addition, fructose can be converted within the intestine and the liver into glucose and lactate (Lac). This can be used as an additional fuel source during exercise and also as a substrate for (liver) glycogen repletion during post‐exercise recovery. Therefore, fructose co‐ingestion may benefit athletes by maximizing carbohydrate availability during exercise and during acute post‐exercise recovery.

We recently showed that patients with mitochondrial diabetes are insulin resistant in skeletal muscle before the decline in insulin secretion is observed. In this study, we further evaluate whether insulin resistance is associated with increased ectopic fat accumulation and altered adipose and hepatic tissue insulin sensitivity. We studied 15 nonobese patients with the m.3243A > G mutation. Five were without diabetes (group 1), three had newly diagnosed diabetes (group 2), and seven had previously diagnosed diabetes (group 3). Thirteen healthy volunteers of similar age and body mass index (BMI) served as controls. Insulin-stimulated glucose uptake was measured with positron emission tomography using 2- [F-18]-fluoro-2-deoxyglucose during euglycemic hyperinsulinemia. Fat masses and liver fat content were measured with magnetic resonance imaging and spectroscopy. Compared with controls, insulin-stimulated glucose uptake in adipose tissue was decreased by similar to 50% in all groups with the m.3243A > G mutation. In addition, fat masses were not different, but insulin-mediated suppression of lipolysis and adiponectin metabolism were blunted in patients with the m.3243A > G mutation. Hepatic fat content was normal ( G did not differ from that of controls. In conclusion, m.3243A > G mutation affects subcutaneous adipose tissue metabolism. This seems to occur before aberrant liver metabolism, if any, can be observed or before beta-cell failure results in mitochondrial diabetes.