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Articles in PresS, published online ahead of print October 24, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00513.2002
Submitted on August 26, 2002
Accepted on October 18, 2002
1 KAPH, University of Colorado, Boulder, CO, USA; Center for Neuroscience, University of Colorado, Boulder, CO, USA
2 KAPH, University of Colorado, Boulder, CO, USA
* To whom correspondence should be addressed. E-mail: fleshner{at}colorado.edu.
The mechanism(s) for how physically active organisms are resistant to many damaging effects of acute stressor exposure is unknown. Cellular induction of heat-shock proteins (e.g., HSP72) is one successful strategy used by the cell to survive the damaging effects of stress. It is possible, therefore, that the stress-buffering effect of physical activity may be due to an improved HSP72 response to stress. Thus, the purpose of the current study was to determine whether prior voluntary freewheel running facilitates the stress-induced induction of HSP72 in central (brain), peripheral, and immune tissues. Adult, male Fischer 344 rats were housed with either a mobile running wheel (Active) or a locked, immobile wheel (Sed) for 8 weeks prior to stressor exposure. Rats were exposed to either inescapable tailshock stress (IS; 100, 1.6 mA tailshocks, 5-sec duration, 60-sec ITI), exhaustive exercise stress (EXS; treadmill running to exhaustion), or no stress (controls). Blood, brain, and peripheral tissues were collected 2-h after stressor termination. The kinetics of HSP72 induction after IS was determined in cultured mesenteric lymph node cells. Activation of the stress response was verified by measuring serum corticosterone (RIA). Tissue and cellular HSP72 content were measured using HSP72 ELISA in cell lysates. Both Active and Sed rats had elevated levels of serum corticosterone after stress. In contrast, Active but not Sed rats exposed to IS and/or EXS had elevated HSP72 in dorsal vagal complex, frontal cortex, hippocampus, pituitary, adrenal, liver, spleen, mesenteric lymph nodes, and heart. In addition, physically active rats exposed to IS demonstrated a faster induction of lymphocyte HSP72 compared with Sed rats. Thus, Active rats responded to stress with both greater and faster HSP72 responses, compared to Sed rats. These results indicate that previous physical activity potentiates HSP72 expression following a wide range of stressors. Facilitated induction of HSP72 may contribute to the increased stress resistance previously reported in physically active organisms.
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