Objective To evaluate the effect of exercise training on heat shock protein 70 (HSP70) expression during endotoxin-induced acute lung injury (ALI) in rats. Methods Thirty-two SPF healthy male Sprague-Dawley rats, aged 8 weeks, weighing 175-220 g, were divided into 4 groups (n=8 each) using a random number table method: control group (group C), group ALI, low-intensity exercise training group (group ET1) and high-intensity exercise training group (group ET2). The rats in ET1 and ET2 groups received 2- and 4-week treadmill exercise training before establishing the ALI model, while the rats in C and ALI groups received no training.ALI was induced by intravenously injecting 5 mg/kg lipopolysaccharide via the tail vein in ALI, ET1 and ET2 groups, and the equal volume of normal saline was given instead in group C. The animals were sacrificed, and the lungs were harvested for microscopic examination of the pathological changes of lung tissues which were also scored and for determination of wet to dry weight ratio (W/D ratio), concentrations of total protein, interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) in bronchoalveolar lavage fluid (BALF), and expression of HSP70 and nuclear factor kappa B (NF-κB) in lung tissues by Western blot. Results Compared with group C, the W/D ratio and pathological changes of lung tissues were significantly increased, the concentrations of total protein, IL-1β and TNF-α in BALF were increased, the expression of NF-κB was up-regulated (P 0.05). Compared with group ALI, the W/D ratio and pathological changes of lung tissues were significantly decreased, the concentrations of total protein, IL-1β and TNF-α in BALF were decreased, the expression of HSP70 was up-regulated, and the expression of NF-κB was down-regulated in ET1 and ET2 groups (P<0.05). Conclusion Exercise training can attenuate the endotoxin-induced ALI through relieving the inflammatory responses, which may be related to up-regulating HSP70 expression in the lung of rats. Key words: Exercise; Endotoxemia; Acute lung injury; HSP70 heat-shock proteins