Training the Gut for Athletes

Abstract

The gastrointestinal (GI) tract plays a critical role in delivering carbohydrate and fluid during prolonged exercise and can therefore be a major determinant of performance. The incidence of GI problems in athletes participating in endurance events is high, indicating that GI function is not always optimal in those conditions. A substantial body of evidence suggests that the GI system is highly adaptable. Gastric emptying as well as stomach comfort can be "trained" and perceptions of fullness decreased; some studies have suggested that nutrient-specific increases in gastric emptying may occur. Evidence also shows that diet has an impact on the capacity of the intestine to absorb nutrients. Again, the adaptations that occur appear to be nutrient specific. For example, a high-carbohydrate diet will increase the density of sodium-dependent glucose-1 (SGLT1) transporters in the intestine as well as the activity of the transporter, allowing greater carbohydrate absorption and oxidation during exercise. It is also likely that, when such adaptations occur, the chances of developing GI distress are smaller. Future studies should include more human studies and focus on a number of areas, including the most effective methods to induce gut adaptations and the timeline of adaptations. To develop effective strategies, a better understanding of the exact mechanisms underlying these adaptations is important. It is clear that "nutritional training" can improve gastric emptying and absorption and likely reduce the chances and/or severity of GI problems, thereby improving endurance performance as well as providing a better experience for the athlete. The gut is an important organ for endurance athletes and should be trained for the conditions in which it will be required to function.

Fig. 1

Absorption of glucose and fructose. Glucose and fructose are absorbed from the intestinal lumen (on the left) through the enterocyte (luminal and basolateral membrane) into the circulation (on the right), via different pathways involving SGLT1 and GLUT5, respectively. SGLT1 sodium-dependent glucose transporter 1, GLUT5 glucose transporter 5 (fructose transporter), GLUT2 glucose transporter 2

Fig. 2

Schematic of exogenous carbohydrate oxidation from a single carbohydrate (black) and multiple transportable carbohydrates (blue), based on data presented elsewhere [3, 7, 51, 52]. It is clear that higher oxidation rates can be achieved with multiple transportable carbohydrates, especially at high intakes. At intakes up to 60 g/h, there is no difference between single and multiple transportable carbohydrates, but when intake increases above 60 g/h and the sodium-dependent glucose transporter 1 (SGLT1) becomes saturated, added fructose will result in higher exogenous carbohydrate oxidation rates. The recommended intake for single and multiple transportable carbohydrates are indicated with a circle. If single carbohydrate sources are ingested at rates higher than 60 g/h, gastrointestinal problems are likely. With multiple transportable carbohydrates, fewer symptoms have been observed, but “training the gut” (and getting used to high intakes) is recommended

Fig. 3

A proposed mechanism for upregulation of sodium-dependent glucose transporter 1 (SGLT1) protein. Sweet receptors T1R2 + T1R3, expressed on the luminal membrane of villus endocrine cells, sense luminal concentration of glucose. When this glucose concentration reaches a threshold, it activates a signaling cascade in endocrine cells that involves T1R2 + T1R3 receptors, gustducin, and other signaling elements. This will result in the secretion of GLP-1, GLP-2, and GIP. GLP-2 binding to its receptor GLP-2R on enteric neurons elicits an action potential. This stimulus, in turn, is transmitted to sub-epithelial regions by axonal projections, which will evoke the release of a neuropeptide in the absorptive enterocytes. The binding of this neuropeptide to its receptor increases intracellular cAMP concentrations, thereby increasing the stability of mRNA of SGLT1 and increasing the SGLT1 protein concentration. AAAAA amino acid chain, AC adenylate cyclase, cAMP cycling AMP, cAMPRE cyclic AMP response element, GIP glucose-dependent insulinotropic peptide, GLP glucagon-like peptide, GLP-2R receptor for GLP-2, mRNA messenger RNA., SGLT1 sodium dependent glucose transporter 1, T1R2 + T1R3 taste receptor formed as a dimer of the T1R2 and T1R3 proteins. Adapted from Shirazi-Beechey et al. [24] with permission

Fig. 4

A summary of methods to “train the gut”, the adaptations that may occur in the gut, and implications for performance