Potential research gaps
Association of shifts in salivary IgA with modified susceptibility to respiratory infections has been established. However, unresolved issues still remain with regard to the role of factors often accompanying strenuous exercise (to list just a few: psychological stress, sleep deprivation, concomitant medication and dietary supplements) and potentially influencing immune status. In what regards exercise-associated changes in serum levels of other immunoglobulin isotypes, results of not abundant studies are often contradictory, therefore, a potential, largely not addressed research area is still open.
Exercise load and susceptibility to infections
Association of exercise load and URTI susceptibility can be presented as the so-called “J-shaped curve model” hypothesizing that although regular moderate doses of physical activity have beneficial effects on health, excessive amounts or intensities of physical activity have opposite, negative consequences (69) (Figure 1) . Although the “J” shaped curve hypothesis relating amount of exercise and risk of disease has been accepted by athletes, coaches and scientists, the available evidence is insufficient to support it (93). Recently, a modification was proposed to the J-curve model and an “S-shaped” graphic presentation of interactions between exercise intensity and URTI susceptibility was proposed (94,95) (Figure 2) . This S-curve model takes into account suggestions based on previous reports on increased infection rate only in athletes reporting pre-race symptoms (96). Moreover, these authors postulate that athletes with high training load should be analyzed separately from the “true” elite athletes. Assumption that in the latter ones an excessive training volume does not coincide with increased susceptibility to infections can be supported by data from pilot training log analysis covering a 16-year time span (95). Furtherly, a combined model has been proposed that includes additional issues highlighted by Moreira et al, indicating that J-curve model may be applicable solely to less-fit individuals whereas the classical curve would tend to flatten as the fitness level increases (97). It should also be mentioned that acute bout of exercise may be considered as a set of positive stimuli leading to enhancement of immune response and immune protection, contributing to enhanced performance (98).
In the context of exercise load-related infection susceptibility, several issues may be considered not yet elucidated and requiring further research. The role of pre-existing, sometimes latent or clinically silent, URTI in the development of what is later reported as upper respiratory symptoms, should be cleared up in order to avoid blurring of the clinical picture and interpretation of irrelevant data. Establishing a uniform definition of “elite” athlete will help to compare results from different studies and settings.
In the context of URTI susceptibility, the influence of exercise on the microbiome cannot be neglected. There are data confirming that exercise (recreational and endurance) modifies gut microbial diversity (99,100) and that prebiotic supplementation may influence exercise-induced bronchial hyperresponsiveness (101), although not influencing allergic inflammation markers (102). Although several environmental factors (e.g., smoking) have been identified as possible modifiers of airway microbiome, data on influence of exercise are not abundant and not conclusive with regard to specific taxa (103).
Finally, not only clinical data and reports, but also immunological parameters should be addressed in more numerous studies assuming stratification based on training load.