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Dietary salt, airway inflammation, and diffusion capacity in exercise-induced asthma.
Med Sci Sports Exerc 2005; 37(6):904-14MS

Abstract

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.

Authors+Show Affiliations

Human Performance and Exercise Biochemistry Laboratory, Department of Kinesiology, Indiana University, Bloomington, IN 47401, USA. tmickleb@indiana.eduNo affiliation info availableNo affiliation info available

Pub Type(s)

Clinical Trial
Journal Article
Randomized Controlled Trial

Language

eng

PubMed ID

15947713

Citation

Mickleborough, Timothy D., et al. "Dietary Salt, Airway Inflammation, and Diffusion Capacity in Exercise-induced Asthma." Medicine and Science in Sports and Exercise, vol. 37, no. 6, 2005, pp. 904-14.
Mickleborough TD, Lindley MR, Ray S. Dietary salt, airway inflammation, and diffusion capacity in exercise-induced asthma. Med Sci Sports Exerc. 2005;37(6):904-14.
Mickleborough, T. D., Lindley, M. R., & Ray, S. (2005). Dietary salt, airway inflammation, and diffusion capacity in exercise-induced asthma. Medicine and Science in Sports and Exercise, 37(6), pp. 904-14.
Mickleborough TD, Lindley MR, Ray S. Dietary Salt, Airway Inflammation, and Diffusion Capacity in Exercise-induced Asthma. Med Sci Sports Exerc. 2005;37(6):904-14. PubMed PMID: 15947713.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Dietary salt, airway inflammation, and diffusion capacity in exercise-induced asthma. AU - Mickleborough,Timothy D, AU - Lindley,Martin R, AU - Ray,Shahla, PY - 2005/6/11/pubmed PY - 2005/9/10/medline PY - 2005/6/11/entrez SP - 904 EP - 14 JF - Medicine and science in sports and exercise JO - Med Sci Sports Exerc VL - 37 IS - 6 N2 - 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. SN - 0195-9131 UR - https://www.unboundmedicine.com/medline/citation/15947713/Dietary_salt_airway_inflammation_and_diffusion_capacity_in_exercise_induced_asthma_ L2 - http://Insights.ovid.com/pubmed?pmid=15947713 DB - PRIME DP - Unbound Medicine ER -