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


Medicine & Science in Sports & Exercise: June 2005 - Volume 37 - Issue 6 - p 904-914
doi: 10.1249/01.mss.0000166949.11296.2b
Clinical Sciences: Clinical Investigations

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.

1Human Performance and Exercise Biochemistry Laboratory, Department of Kinesiology, and 2Department of Applied Health Science, Indiana University, Bloomington, IN

Address for correspondence: Timothy D. Mickleborough, Ph.D., Department of Kinesiology, Indiana University, 1025 East 7th Street, HPER 112, Bloomington, IN 47401; E-mail:

Submitted for publication November 2004.

Accepted for publication January 2005.

©2005The American College of Sports Medicine