Dietary Salt, Airway Inflammation, and Diffusion Capacity in Exercise-Induced Asthma

Timothy D. Mickleborough; Martin R. Lindley; Shahla Ray

Disclosures

Med Sci Sports Exerc. 2005;37(6):904-914. 

In This Article

Abstract and Introduction

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)-1β, IL-8, leukotriene (LT) C4-E4, LTB4, and prostaglandin D2 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.

Exercise-induced asthma (EIA) describes a condition in which vigorous physical activity triggers acute airway obstruction in individuals with heightened airway reactivity. Up to 90% of those with chronic asthma, 3-10% of the general population, and 11-50% of elite athletes[26] may experience EIA.[27] Significant numbers of asthmatics demonstrate signs and symptoms of EIA, including cough, wheeze, dyspnea, shortness of breath, chest tightness, and chest pain, normally beginning after a brief period of exercise (5-8 min) and resolving spontaneously within 30-60 min after stopping exercise.[27] Exercise is a powerful trigger of asthma symptoms and may result in asthmatic patients avoiding physical activity resulting in detrimental consequences to their health.

The mechanism(s) unique to exercise that triggers EIA in asthmatic patients have been extensively investigated.[3,18] It has been suggested that transient dehydration of the airways activates inflammatory mediators such as histamine, neuropeptides, and the arachidonic acid metabolites, leukotrienes, and prostanoids from airway cells, resulting in bronchial smooth muscle contraction.[3] Alternatively, it has been suggested that rapid rewarming of the airways following exercise leads to reactive hyperemia resulting in vascular engorgement and perivascular edema,[18] which would further contribute to airway narrowing caused by bronchoconstriction.

There is accumulating evidence that dietary modification has the potential to reduce the prevalence and incidence of EIA.[19] Recent studies have supported a role for dietary salt as a modifier of airway narrowing following exercise in EIA subjects, as it has previously been shown that a high-salt diet (HSD) worsens and a low-salt diet (LSD) improves postexercise pulmonary function in EIA.[9,20]

The mechanism(s) by which dietary salt may modify EIA is not known. However, possible mechanisms include a direct effect of the sodium[28] and/or chloride ion[20] on airway smooth muscle contractility, the release of bronchoconstrictor mediators from airway cells either directly or through changes in airway osmolarity as a result of dietary salt modification,[21] and the potential influence of dietary salt on vascular volume and microvascular pressure, resulting in mucosal edema and narrowing of the airway lumen.[8] How dietary salt is involved in any or some of these probable mechanisms remains to be determined.

Therefore, the main aim of this study was to demarcate a possible mechanism by which dietary salt modification may alter airway narrowing following exercise in EIA subjects. We sought to characterize airway inflammation directly via induced sputum by measuring differential cell counts and fluid phase mediators, and to compare inflammatory markers on different salt-loading regimens. In addition, we wished to determine whether intravascular volume expansion, as a result of dietary salt loading, may have an effect on the diffusion capacity of the lung (DLCO) and its subdivisions, and therefore be a causative factor in exercise-induced airway narrowing in asthmatic subjects. We hypothesized that DLCO and its subdivisions and the degree of airway inflammation would be dependent on the amount of dietary salt intake in EIA subjects.

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