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Exercise training reduces pulmonary ischaemia–reperfusion-induced inflammatory responses

Depts of ¹ Thoracic Surgery, and ² Pharmacology, Faculty of Medical Sciences, State University of Campinas, Campinas, and ³ Dept of Physical Education, Institute of Biosciences, University of São Paulo State, Rio Claro, Brazil.

CORRESPONDENCE: R. K. Mussi, Dept of Thoracic Surgery, Faculty of Medical Sciences, UNICAMP P.O. Box 6111, 13084-971, Campinas (SP), Brazil. Fax: 55 1932892968. E-mail: rkm{at}unicamp.br

Keywords: Exercise training, inflammation, ischaemia–reperfusion, lung

Received: February 8, 2007
Accepted October 26, 2007

Physical exercise reduces the deleterious effects of cardiovascular and inflammatory disorders. The purpose of the present study was to evaluate the beneficial effects of physical training on the inflammatory responses following lung ischaemia–reperfusion (IR) in rats.

Male Wistar rats were divided into sham-operated animals and sedentary and trained animals submitted to lung IR. The run training programme consisted of 5 sessions·week^–1, each lasting 60 min·day^–1, at 66% of maximal oxygen consumption for 8 weeks. The left pulmonary artery, bronchus and pulmonary vein were occluded for 90 min and reperfused for 2 h. Lung protein extravasation was measured as ¹²⁵I-human albumin accumulation, whereas lung neutrophil infiltration was measured as myeloperoxidase activity.

Lung IR in sedentary rats resulted in marked increases in protein extravasation and neutrophil influx, and in significant elevations of serum tumour necrosis factor (TNF)- and interleukin (IL)-1β levels. Physical preconditioning attenuated the increased IR-induced protein leakage without affecting neutrophil influx. It also reduced serum TNF- (and IL-1β) levels, but had no effect on IL-10 levels. Plasma superoxide dismutase activity was significantly increased in trained IR rats.

The present data show that physical preconditioning protects the rat lung from ischaemia–reperfusion injury by attenuating the pulmonary vascular permeability that may be a consequence of reduced levels of tumour necrosis factor- and interleukin-1β and elevated superoxide dismutase activity.