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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Low-Intensity Swimming Training Partially Inhibits Lipopolysaccharide-Induced Acute Lung Injury

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Author(s):
Ramos, Daniel Souza [1] ; Olivo, Clarice Rosa [2] ; Quirino Santos Lopes, Fernanda Degobbi Tenorio [2] ; Toledo, Alessandra Choqueta [2] ; Martins, Milton Arruda [2] ; Lazo Osorio, Rodrigo Alexis [1] ; Dolhnikoff, Marisa [3] ; Ribeiro, Wellington [1] ; Vieira, Rodolfo De Paula [4, 5, 6]
Total Authors: 9
Affiliation:
[1] Univ Vale Paraiba, Lab Physiol & Pharmacodynam, Inst Res & Dev, Sao Paulo - Brazil
[2] Univ Sao Paulo, Dept Med LIM 20, Sch Med, BR-01246903 Sao Paulo - Brazil
[3] Univ Sao Paulo, Dept Pathol LIM 05, Sch Med, BR-01246903 Sao Paulo - Brazil
[4] Univ Sao Paulo, Fac Med, Sch Med, Dept Phys Therapy LIM 34, BR-01246903 Sao Paulo - Brazil
[5] Univ Freiburg, Dept Pneumol, COPD, Freiburg - Germany
[6] Univ Freiburg, Asthma Res Grp, Freiburg - Germany
Total Affiliations: 6
Document type: Journal article
Source: MEDICINE AND SCIENCE IN SPORTS AND EXERCISE; v. 42, n. 1, p. 113-119, JAN 2010.
Web of Science Citations: 28
Abstract

RAMOS, D. S. C. R. OLIVO. F. D. QUIRINO SANTOS LOPES, A. C. TOLEDO, M. A. MARTINS, R. A. LAZO OSORIO. M. DOLHNIKOFF, W. RIBEIRO, and R. R VIEIRA. Low-Intensity Swimming Training Partially Inhibits Lipopolysaccharide-Induced Acute Lung Injury. Med. Sci. Sports Exerc.. Vol. 42, No. 1, pp. 113-119, 2010. Background: Aerobic exercise-decreases pulmonary inflammation and remodeling in experimental models of allergic asthma. However, the effects of aerobic exercise oil pulmonary inflammation of nonallergic Origin, such as in experimental models of acute long injury induced by lipopolysaccharide (LPS), have not been evaluated. Objective: The present study evaluated file effects of aerobic exercise in a model of LPS-induced acute lung injury. Methods: BALB/c mice were divided into four groups: Control, Aerobic Exercise, LPS, and Aerobic Exercise + LPS. Swimming tests were conducted at baseline and at 3 and 6 wk. Low-Intensity swimming training was performed for 6 wk, four times per week, 60 min per session. Intranasal LPS (1 mg.kg(-1) (60 mu g per mouse)) was instilled 24 It after the last swimming physical test in the LPS and Aerobic Exercise + LPS mice, and the animals were studied 24 It after LPS instillation. Exhaled nitric oxide, respiratory mechanics, total and differential cell Counts in bronchoalveolar lavage, and lung parenchymal inflammation and remodeling were evaluated. Results: LPS instillation resulted in increased levels of exhaled nitric oxide (P < 0.001), higher numbers of neutrophils in file bronchoalveolar lavage (P < 0.001) and in the lung parenchyma (P < 0.001), and decreased lung tissue resistance (P < 0.05) and volume proportion of elastic fibers (P < 0.01) compared with the Control group. Swim training in LPS-instilled animals resulted in significantly lower exhaled nitric oxide levels (P < 0.001) and fewer nelltrophils in the bronchoalveolar lavage (P < 0.001) and the lung parenchyma (P < 0.01) compared with the LPS group. Conclusions: These results Suggest that low-intensity swimming training inhibits lung neutrophilic inflammation, but not remodeling and impaired lung mechanics, in a model of LPS-induced acute lung injury. (AU)