TITLE

Exercise pretraining attenuates endotoxin-induced hemodynamic alteration in type I diabetic rats

AUTHOR(S)
Chen, Yu-Wen; Shao, Dong-Zi; Chang, Che-Ning; Tsai, Yung-Yuh; Cheng, Juei-Tang; Hung, Ching-Hsia
PUB. DATE
October 2008
SOURCE
Applied Physiology, Nutrition & Metabolism;Oct2008, Vol. 33 Issue 5, p976
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Higher expression of heat shock protein 72 (HSP72) reduces the mortality rate and organ damage in septic shock and prevents cardiac mitochondrial dysfunction due to lipopolysaccharide (LPS). Our hypothesis is that exercise preconditioning may increase the expression of HSP72 in heart and the nucleus tractus solitarii (NTS) of the brain to alleviate the cardiovascular dysfunction in type I diabetic rats receiving endotoxin. Wistar rats were randomly assigned to the following groups: sedentary normal, sedentary type I diabetic rats, and type I diabetic rats with exercise training. The trained rats ran on a treadmill 5 d·week-1, 30-60 min·d-1, at an intensity of 1.0 mile·h-1 (1 mile = 1.6 km) over a 3 week period. Twenty-four hours after the last training session, we compared the temporal profiles of mean arterial pressure, heart rate, cardiac output, stroke volume, and serum tumor necrosis factor α level in rats receiving an injection of LPS. In addition, HSP72 expression in heart and NTS from each group was determined. We found that HSP72 expression in the heart and NTS was significantly increased in diabetic rats with exercise training. After administration of LPS, the survival time was significantly longer in diabetic rats with exercise training. Additionaly, serum tumor necrosis factor α levels decreased as compared with those rats not receiving exercise training. Exercise training also diminished cardiovascular dysfunction in diabetic rats during endotoxemia. These data suggest that exercise may increase the expression of HSP72 in the heart and NTS to protect against the high mortality rate and attenuate cardiovascular dysfunction in diabetic rats during endotoxemia.
ACCESSION #
34716314

 

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