Abstract

Endurance-sport athletes have a high incidence of gastrointestinal disorders, compromising performance and impacting overall health status. An increase in several proinflammatory cytokines and proteins (LPS, I-FABP, IL-6, IL-1β, TNF-α, IFN-γ, C-reactive protein) has been observed in ultramarathoners and triathlon athletes. One of the most common effects of this type of physical activity is the increase in intestinal permeability, known as leaky gut. The intestinal mucosa's degradation can be identified and analyzed by a series of molecular biomarkers, including the lactulose/rhamnose ratio, occludin and claudin (tight junctions), lipopolysaccharides, and I-FABP. Identifying the molecular mechanisms involved in the induction of leaky gut by physical exercise can assist in the determination of safe exercise thresholds for the preservation of the gastrointestinal tract. It was recently shown that 60 min of vigorous endurance training at 70% of the maximum work capacity led to the characteristic responses of leaky gut. It is believed that other factors may contribute to this effect, such as altitude, environmental temperature, fluid restriction, age and trainability. On the other hand, moderate physical training and dietary interventions such as probiotics and prebiotics can improve intestinal health and gut microbiota composition. This review seeks to discuss the molecular mechanisms involved in the intestinal mucosa's adaptation and response to exercise and discuss the role of the intestinal microbiota in mitigating these effects.

Highlights

  • Physical exercise is a non-pharmacologic agent in preventing and managing non-communicable chronic diseases, where its beneficial effect is well-documented in the musculoskeletal and cardiovascular systems

  • It is believed that intestinal ischemia is considered the leading cause of abdominal pain, nausea, vomiting, and diarrhea, occurring 2-fold more in running athletes compared to other endurance sports, and 1.5–3 times more in elite athletes compared to amateurs [7]

  • After exploring the main molecular changes caused by exercise, the next topic aims to highlight whether it is possible to determine an exercise “threshold” that leads to the “leaky gut” phenomenon

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Summary

INTRODUCTION

Physical exercise is a non-pharmacologic agent in preventing and managing non-communicable chronic diseases, where its beneficial effect is well-documented in the musculoskeletal and cardiovascular systems. Splanchnic hypoperfusion and subsequent ischemia can damage the specialized antimicrobial protein-secreting cells (Paneth cells), the mucus-producing cells (such as goblet cells), and the tight junction proteins (claudin and occludin) that prevent the infiltration of pathogenic organisms into the systemic circulation [8] Endotoxins such as lipopolysaccharide (LPS) and proinflammatory cytokines may pass through epithelial cells due to their permeability, an effect known as “leaky gut” [20, 21]. Strenuous exercise may affect the intestinal epithelial cells [31], tight junction (TJs) proteins [32], smooth muscle cells [33], and the composition and function of the gut microbiota (GM) [34], compromising gastrointestinal homeostasis This phenomenon has been observed in ultramarathon athletes, where the profile of proinflammatory proteins and cytokines such as C-reactive protein, interleukin-6 (IL-6), IL-1β, TNF-α, and interferon-gamma (IFN-γ) increased [20]. After exploring the main molecular changes caused by exercise, the next topic aims to highlight whether it is possible to determine an exercise “threshold” that leads to the “leaky gut” phenomenon

A Possible Exercise “Treshold” to Avoid Leaky Gut
Findings
CONCLUSION

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