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Endurance Training Damages Small Airway Epithelium in Mice

¹ Department of Experimental Medicine (DIMES), University of Palermo, Italy; ² Institute of Biomedicine and Molecular Immunology (IBIM), National Research Council (CNR), Palermo, Italy; and ³ Department of Medicine, Pneumology, Physiology, and Nutrition (DIMPEFINU), University of Palermo, Italy

Correspondence and requests for reprints should be addressed to Laura Chimenti, Ph.D., Department of Experimental Medicine, University of Palermo, Corso Tukory, 129, 90134 Palermo, Italy. E-mail: chimenti{at}ibim.cnr.it

Rationale: In athletes, airway inflammatory cells were found to be increased in induced sputum or bronchial biopsies. Most data were obtained after exposure to cold and dry air at rest or during exercise. Whether training affects epithelial and inflammatory cells in small airways is unknown.

Objectives: To test whether endurance training under standard environmental conditions causes epithelial damage and inflammation in the small airways of mice.

Methods and Measurements: Formalin-fixed, paraffin-embedded lung sections were obtained in sedentary (n = 14) and endurance-trained (n = 16) Swiss mice at baseline and after 15, 30, and 45 days of training. The following variables were assessed (morphometry and immunohistochemistry) in small airways (basement membrane length < 1 mm): (1) integrity, proliferation, and apoptosis of bronchiolar epithelium; and (2) infiltration, activation, and apoptosis of inflammatory cells.

Main Results: Compared with sedentary mice, bronchiolar epithelium of trained mice showed progressive loss of ciliated cells, slightly increased thickness, unchanged goblet cell number and appearance, and increased apoptosis and proliferation (proliferating cell nuclear antigen) (p < 0.001 for all variables). Leukocytes (CD45⁺ cells) infiltrated airway walls (p < 0.0001) and accumulated within the lumen (p < 0.001); however, apoptosis of CD45⁺ cells did not differ between trained and sedentary mice. Nuclear factor-B translocation and inhibitor-alpha of NF-B (IB) phosphorylation were not increased in trained compared with sedentary mice.

Conclusions: Bronchiolar epithelium showed damage and repair associated with endurance training. Training increased inflammatory cells in small airways, but inflammatory activation was not increased. These changes may represent an adaptive response to increased ventilation during exercise.

Key Words: exercise • airway damage • remodeling • inflammation • apoptosis

AT A GLANCE COMMENTARY Scientific Knowledge on the Subject Studies in endurance athletes of winter and summer sports documented increased inflammatory cells in large airways. However, whether training affects the small airways is unknown. What This Study Adds to the Field Endurance training in mice causes epithelial damage and repair but does not appear to be a powerful proinflammatory stimulus.

 

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