Dietary salt, airway inflammation, and diffusion capacity in exercise-induced asthma.

PURPOSE

Recent studies have supported a role for dietary salt as a modifier of the severity of exercise-induced asthma. The main aim of this study was to demarcate a possible mechanism by which dietary salt modification may alter exercise-induced airway narrowing in asthmatic patients.

METHODS

Twenty-four patients participated in a randomized, double-blind crossover study. Subjects entered the study on their normal salt diet (NSD) and were then placed on either a low-salt diet (LSD) or high-salt diet (HSD) for 2 wk with a 1-wk washout period occurring between diets. Pre- and postexercise spirometry, pulmonary diffusion capacity (DLCO) and its subdivisions, and induced sputum were obtained on the NSD and at the end of each 2-wk treatment period (LSD and HSD).

RESULTS

FEV1 decreased by 7.9 +/- 2.8% on LSD, 18.3 +/- 4.0% on NSD, and 27.4 +/- 3.2% on HSD at 20 min postexercise. The NSD and HSD induced significant reductions (P < 0.05) in DLCO and its subdivisions. However, postexercise pulmonary capillary blood volume significantly increased (P < 0.05) by 6.3 and 9.6 mL on NSD and HSD, respectively, compared with baseline values, with no significant change (P > 0.05) being observed on LSD. Postexercise-induced sputum neutrophil and eosinophil differential cell counts and induced sputum supernatant concentration of eosinophil cationic protein, interleukin (IL)-1beta, IL-8, leukotriene (LT) C(4)-E(4), LTB(4), and prostaglandin D(2) were significantly elevated (P < 0.05) on NSD and HSD compared with LSD.

CONCLUSION

Our findings indicate that dietary salt loading enhances airway inflammation following exercise in asthmatic subjects, and that small salt-dependent changes in vascular volume and microvascular pressure might have substantial effects on airway function following exercise in the face of mediator-induced increased vascular permeability.