Exercise, heat shock proteins, and myocardial protection from I-R injury

Heat shock proteins (HSPs) play a critical role in maintaining cellular hom eostasis and protecting cells during episodes of acute stress. Specifically , HSPs of the 70 kDa family (i.e.. HSP72) are important in preventing ische mia-reperfusion induced apoptosis. necrosis. and oxidative injury in a vari ety of cell types including the cardiac myocyte. Evidence indicates that HS P72 may contribute to cellular protection against a variety of stresses by preventing protein aggregation. assisting in the refolding of damaged prote ins, and chaperoning nascent polypeptides along ribosomes. Endurance exerci se is a physiological stress that can be used to elevate myocardial levels of HSP72. It is now clear that endurance exercise training can elevate myoc ardial HSP72 by 400-500%% in young adult animals. Importantly, an exercise- induced elevation in myocardial HSPs is associated with a reduction in isch emia-reperfusion (I-R) injury in the heart. Although it seems likely that e xercise-induced elevations in myocardial levels of HSPs play an important r ole in this protection against an I-R insult, new evidence suggests that ot her factors may also be involved. This is an important area for future rese arch.