Exercise, heat shock proteins, and myocardial protection from I-R injury.
Heat shock proteins (HSPs) play a critical role in maintaining cellular homeostasis and protecting cells during episodes of acute stress. Specifically, HSPs of the 70 kDa family (i.e., HSP72) are important in preventing ischemia-reperfusion induced apoptosis, necrosis, and oxidative injury in a variety of cell types including the cardiac myocyte. Evidence indicates that HSP72 may contribute to cellular protection against a variety of stresses by preventing protein aggregation, assisting in the refolding of damaged proteins, and chaperoning nascent polypeptides along ribosomes. Endurance exercise is a physiological stress that can be used to elevate myocardial levels of HSP72. It is now clear that endurance exercise training can elevate myocardial HSP72 by 400-500% in young adult animals. Importantly, an exercise-induced elevation in myocardial HSPs is associated with a reduction in ischemia-reperfusion (I-R) injury in the heart. Although it seems likely that exercise-induced elevations in myocardial levels of HSPs play an important role in this protection against an I-R insult, new evidence suggests that other factors may also be involved. This is an important area for future research.
Department of Exercise and Sport Sciences and Physiology, Center for Exercise Science, University of Florida, Gainesville, FL 32611, USA. spowers@hhp.ufl.edu
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D017209:Apoptosis; D015444:Exercise / Q000502:physiology*; D005786:Gene Expression Regulation; D018882:Heat Stress Disorders; D006360:Heat-Shock Proteins / Q000096:biosynthesis* / Q000494:pharmacology; D006801:Humans; D018482:Muscle, Skeletal / Q000502:physiology; D009206:Myocardium / Q000473:pathology*; D009336:Necrosis; D018384:Oxidative Stress; D015427:Reperfusion Injury / Q000503:physiopathology / Q000517:prevention & control*
D006360:Heat-Shock Proteins