Respiratory symptoms
Competitive and synchronized swimming ranked second among sport
disciplines associated with increased prevalence of asthma
symptoms38. The long-term exposure to CBPs in a sport
setting underlines some aspects: 1) the role in inducing and sustaining
airway inflammation; 2) the contribution to airway remodeling; and 3)
possible promotion of allergic sensitization in regularly exposed
competitive swimmers.
A significantly higher rate of BHR with increased inflammatory
parameters have been observed in elite swimmers. Long-term swimming-pool
exposure effects included increase in both eosinophilic and neutrophilic
inflammation, as reflected not only in sputum cell counts but also in
higher concentration of sputum eosinophil peroxidase and human
neutrophil lipocalin, respectively39. Inflammatory and
remodeling changes reported in bronchial biopsies of competitive
swimmers were similar to non-exercising mild asthmatics and were present
also during off-training period. Discontinuation of a swimming career
decreases eosinophilic and neutrophilic inflammation and reduces BHR,
although these findings should be interpreted with caution given the
small sample sizes40,41. These inflammatory changes
did not seem, however, to correlate with BHR. A study carried out in a
mixed population of competitive athletes including mostly non-asthmatic
swimmers and speed skaters indicated that the baseline pattern of
proinflammatory cytokine TNF-α and anti-inflammatory IL-1ra
concentrations in the lower airways appear to be similar in top level
athletes and asthmatic patients, but different in healthy
controls42.
Increased airway edema due to CBPs-induced vascular leakage has been
also hypothesized for airway inflammation in swimmers. A significant
association of vascular permeability index (quotient of albumin levels
in sputum and in serum) with increased sputum eosinophil and neutrophil
counts was found43, although vascular leakage did not
correlate with lung function and BHR. In synchronized swimmers no
evidence was found for negative influence of CBPs on the pulmonary
function44.
A study assessing rhinitis in swimmers showed 44% presented baseline
allergic rhinitis and 35% had inflammation with neutrophilic
predominance45. Neutrophilic influx is mainly
attributed to irritation through CBPs exposure and is possibly reversed
– contrarily to eosinophil infiltration – after nose clip
introduction45. Mucociliary transport impairment and
reduced ciliary beats frequency have been described in swimmers and also
attributed to irritation by CBPs. Nasal lavage fluid (NLF) collected
immediately after competitive swimming contains more neutrophils with
decreased phagocytic activity. However, NLF changes tend to subside in
swimmers shortly after training cessation or introduction of protective
measures, such as nose clip46. In the
study42 involving swimmers and speed skaters, TNF-α
concentrations in nasal secretions were similar between athletes,
asthmatics and healthy controls. However, IL-1ra levels in upper airways
were higher in athletes and asthmatics than healthy subjects. Seemingly
paradoxical, this fact may reflect a local anti-inflammatory response of
the nasal mucosa.