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.