Exercise training reduces pulmonary ischemia-reperfusion-induced inflammatory responses

¹ Dept of Thoracic Surgery, Faculty of Medical Sciences, P.O. Box 6111, State University of Campinas (UNICAMP), 13084-971, Campinas (SP), Brazil
² Dept of Pharmacology, Faculty of Medical Sciences, P.O. Box 6111, State University of Campinas (UNICAMP), 13084-971, Campinas (SP), Brazil
³ Dept of Physical Education, Institute of Biosciences, University of São Paulo State (UNESP), Rio Claro (SP), Brazil

^* To whom correspondence should be addressed. E-mail: rkm{at}unicamp.br.

	Abstract

Physical exercise reduces the deleterious effects of cardiovascular and inflammatory disorders. The purpose of this study was to evaluate the beneficial effects of physical training on the inflammatory responses after lung ischemia-reperfusion (I/R) in rats.

Male Wistar rats were divided in sham-operated, sedentary and trained animals undergoing lung I/R. Run training program consisted of 60-min·day^-1, 5- days·week^-1 sessions, 66% VO_2max during 8 weeks. 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 the myeloperoxidase activity.

The lung I/R in sedentary rats resulted in marked increases in protein extravasation and neutrophil influx, and in significant elevations of serum TNF- and IL-1 levels. Physical preconditioning attenuated the increased I/R-induced protein leakage, without affecting the neutrophil influx. Physical preconditioning reduced the serum TNF- (and IL-1) levels, but had no effect on IL-10 levels. The plasma superoxide dismutase (SOD) activity was significantly increased in I/R trained rats.

Our data show that physical preconditioning protects the rat lung I/R injury by attenuating the pulmonary vascular permeability that may be a consequence of reduced levels of TNF- and IL-1, and elevated SOD activity.