title: Low-intensity swimming training partially inhibits lipopolysaccharide-induced acute lung injury.
abstract: BACKGROUND
  Aerobic exercise decreases pulmonary inflammation and remodeling in experimental models of allergic asthma. However, the effects of aerobic exercise on pulmonary inflammation of nonallergic origin, such as in experimental models of acute lung injury induced by lipopolysaccharide (LPS), have not been evaluated.
  
  
  OBJECTIVE
  The present study evaluated the 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 x kg(-1) (60 microg per mouse)) was instilled 24 h after the last swimming physical test in the LPS and Aerobic Exercise + LPS mice, and the animals were studied 24 h 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 the 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 neutrophils 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.
authors.affiliation: Laboratory of Physiology and Pharmacodynamics, Institute of Research and Development, University of Vale do Paraíba, Săo Paulo, Brazil.
authors.forename: Daniel Souza
authors.initials: DS
authors.lastname: Ramos
authors.forename: Clarice Rosa
authors.initials: CR
authors.lastname: Olivo
authors.forename: Fernanda Degobbi Tenório
authors.initials: FD
authors.lastname: Quirino Santos Lopes
authors.forename: Alessandra Choqueta
authors.initials: AC
authors.lastname: Toledo
authors.forename: Milton Arruda
authors.initials: MA
authors.lastname: Martins
authors.forename: Rodrigo Alexis
authors.initials: RA
authors.lastname: Lazo Osório
authors.forename: Marisa
authors.initials: M
authors.lastname: Dolhnikoff
authors.forename: Wellington
authors.initials: W
authors.lastname: Ribeiro
authors.forename: Rodolfo de Paula
authors.initials: RP
authors.lastname: Vieira
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001992:Bronchoalveolar Lavage Fluid; D018836:Inflammation Mediators / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009504:Neutrophils / Q000187:drug effects; D009569:Nitric Oxide / Q000378:metabolism; D010805:Physical Conditioning, Animal; D012128:Respiratory Distress Syndrome / Q000139:chemically induced* / Q000517:prevention & control*; D015656:Respiratory Mechanics; D013550:Swimming / Q000502:physiology*
chemical_list: D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D009569:Nitric Oxide