Habitual physical activity facilitates stress-induced HSP72 induction in brain, peripheral, and immune tissues.
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 [sedentary (Sed)] for 8 wk before stressor exposure. Rats were exposed to either inescapable tail-shock stress (IS; 100 1.6-mA tail shocks, 5-s duration, 60-s intertrial interval), 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, 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 with Sed rats. These results indicate that previous physical activity potentiates HSP72 expression after a wide range of stressors. Facilitated induction of HSP72 may contribute to the increased stress resistance previously reported in physically active organisms.
Campisi
Jay
J
Department of Kinesiology and Applied Physiology and the Center for Neuroscience, University of Colorado, Boulder, Colorado 80309-0354, USA.
Leem
Ted H
TH
Greenwood
Ben N
BN
Hansen
Michael K
MK
Moraska
Albert
A
Higgins
Karianne
K
Smith
Taro P
TP
Fleshner
Monika
M
D000311:Adrenal Glands / Q000378:metabolism; D000818:Animals; D001835:Body Weight; D001921:Brain / Q000378:metabolism*; D002478:Cells, Cultured; D003345:Corticosterone / Q000097:blood; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins / Q000032:analysis / Q000097:blood / Q000378:metabolism*; D007107:Immune System / Q000378:metabolism*; D008099:Liver / Q000378:metabolism; D008198:Lymph Nodes / Q000378:metabolism; D008214:Lymphocytes / Q000378:metabolism; D008297:Male; D009043:Motor Activity / Q000502:physiology*; D009206:Myocardium / Q000378:metabolism; D010805:Physical Conditioning, Animal / Q000502:physiology*; D051381:Rats; D011916:Rats, Inbred F344; D013154:Spleen / Q000378:metabolism; D013312:Stress, Physiological / Q000097:blood / Q000503:physiopathology*; D013997:Time Factors; D015854:Up-Regulation
D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins; D003345:Corticosterone