FIGURE 4.

Potential consequences of acute intense exercise, unhealthy diet (e.g., high-fat diet) or dysbiosis on the intestinal barrier. Acute intense exercise contributes to the development of heat stress that the body cannot cope with, as well as a decrease in oxygen concentration, which causes hypoxia and the associated activation of HIF-1α. At the same time, hypoxia-related oxidative stress caused by an increase in the level of ROS can be observed. In general, these changes can cause the development of dysbacteriosis that can be associated with decreased expression of tight junction proteins and mucus degradation probably due to overgrowth of mucolytic bacteria. A high-fat diet also contributes to a decrease in tight junction proteins in combination with an increase in ROS production and the development of dysbacteriosis. In general, this contributes to a decrease in mucus thickness, an increase in the distance between neighboring epithelial cells and, as a result, an increase in the permeability of the intestinal barrier. This causes the development of an immune imbalance. Bacterial lipopolysaccharides are available as a result of increased permeability of the intestinal barrier and are recognized by TLR4 of the host’s epithelial and immune cells. This leads to the activation of NF-κB and production of pro-inflammatory cytokines such as IL-1β, IL-2, IL-6 triggering the development of inflammation. Abbreviations: ROS, reactive oxygen species; HIF-1α, hypoxia-inducible factor 1α; TLR4, toll-like receptor 4; NF-κB, nuclear factor κB; IL-1β/2/6, interleukin 1β/2/6. ↓, decreasing; ↑, increasing. Details of the structure of the intestinal barrier are shown in Figure 1.