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.