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

Med Sci Sports Exerc. 2001 Mar;33(3):386-92. doi: 10.1097/00005768-200103000-00009.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Apoptosis
  • Exercise / physiology*
  • Gene Expression Regulation
  • Heat Stress Disorders*
  • Heat-Shock Proteins / biosynthesis*
  • Heat-Shock Proteins / pharmacology
  • Humans
  • Muscle, Skeletal / physiology
  • Myocardium / pathology*
  • Necrosis
  • Oxidative Stress
  • Reperfusion Injury / physiopathology
  • Reperfusion Injury / prevention & control*


  • Heat-Shock Proteins