Abstract
1- Introduction
2- Salivary secretory immunoglobulin A (SIgA), T-cells and URTI
3- Stressors that team-sport athletes face on a continual basis
4- Interactive effect of stressors on immunity and infection risk
5- Strategies to reduce immunodepression and avoid illness in team-sport athletes
6- Conclusions
Practical implications
Acknowledgments
References
Abstract
Objectives: Elite team-sport athletes are frequently exposed to stressors that have the potentialto depress immunity and increase infection risk. Therefore, the purpose of this review is to describe how team-sport stressors impact upon immune responses, along with exploring whether alterations in these markers have the potential to predict upper respiratory tract illness symptoms. Design: Narrative review. Methods: Salivary secretory immunoglobulin A (SIgA) and T-cell markers have been shown to predict infection risk in individual endurance athletes. Papers discussing the impact of team-sport stressors on SIgA and T-cells were discussed in the review, studies discussing other aspects of immunity were excluded. Journal articles were sourced from PubMed, Web of science and Scopus. Key search terms included team-sport athletes, stressors, immunity, T-cells, cytokines, SIgA and upper respiratory illness. Results: Most team-sport stressors appear to increase risk for illness. An association between reduced SIgA and increased illness incidence has been demonstrated. Intensive training and competition periods have been shown to reduce SIgA, however, itis less clear how additional stressors including extreme environmental conditions, travel, psychological stress, sleep disturbance and poor nutrition affect immune responses. Conclusions: Monitoring SIgA may provide an assessment of a team-sport athletes risk status for developing upper respiratory tract symptoms, however there is currently not enough evidence to suggest SIgA alone can predict illness. Team-sport stressors challenge immunity and it is possible that the combination of stressors could have a compounding effect on immunodepression and infection risk. Given that illness can disrupt training and performance, further research is required to better elucidate how stressors individually and collectively influence immunity and illness
Introduction
Athletes are continually exposed to stressors that have the potential to depress immune functions and increase infection risk, particularly upper respiratory tract infections (URTI) or the common cold. Indeed, acute URTI is the most common infectious illness reportedinelite athletes.1 Illness is of great concernfor athletes as it can disrupttraining and performance.1 To understand why athletes appear to have a heightened risk for infection, the field of exercise immunology emerged. Studies in this area have been largely concerned with identifying immune markers that can be used to predict athletes’ susceptibility to illness, mostly in endurance athletes. Specifically, mucosal immunity and T-cell cytokine responses have been found to be key determinants of URTI risk in athletes participating in individual endurance sports.2 However, there is comparatively little research in team-sport athletes, therefore whether such immune markers influence a team-sport athletes risk for URTI remains unclear. Team-sport athletes are an important populationto investigate as their closeproximity to teammates and other athletes (e.g. shaking hands, contact sports, changing rooms) may increase their exposure to infection-causing pathogens. Furthermore, team-sport athletes are continually exposed to a range of stressors which may depress immune responses. Such stressors include training, competition,travel, environmental extremes, psychological stress, sleep deprivation, poor nutrition and excessive alcohol consumption. It is possible that the combination of these stressors could amplify immunodepression, resulting in greater URTI risk than if each stressor were applied alone. The purpose of this review is to describe how team-sport stressors impact upon salivary secretory immunoglobulin A (SIgA) and T-cell responses, along with exploring whether alterations in these markers have the potential to predict infection risk. Finally, strategies to counteract the potential immunodepression evoked by these stressors will be proposed.