Document Detail


Exercise preconditioning of the myocardium.
MedLine Citation:
PMID:  19827860     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Diseases of the heart (e.g. myocardial ischaemia reperfusion injury) remain the major cause of death in the industrialized world. Therefore, developing a pragmatic countermeasure to reduce myocardial ischaemia reperfusion injury is vital. In this regard, a plethora of evidence indicates that regular exercise can protect the heart during an ischaemia reperfusion insult (i.e. cardioprotection). This review summarizes studies indicating that both short-term (i.e. 1-5 days) and long-term (i.e. weeks to months) endurance exercise provides cardioprotection. Data are presented showing that exercise duration and exercise intensity are both important factors in achieving a cardioprotective phenotype. Importantly, it appears that the exercise duration of a single exercise session should last for 60 minutes and should be performed at about 75% maximum oxygen consumption in order to achieve exercise-induced cardioprotection. Furthermore, data are presented showing that exercise-induced cardioprotection against myocardial stunning can persist for at least 9 days after the cessation of exercise training, but is lost 18 days after exercise. This review also summarizes the exercise-induced adaptations that occur to the myocardium. In particular, extrinsic changes observed in human and animal models include neural, hormonal, humoral, vascular and reduced body fat. Other anatomical and biochemical/molecular changes that have been studied as putative mechanisms in exercise-induced cardioprotection include alterations in anatomic coronary arteries, induction of myocardial heat shock proteins, increased myocardial cyclooxygenase-2 activity, elevated endoplasmic reticulum stress proteins, nitric oxide production, improved function of sarcolemmal and/or mitochondrial adenosine triphosphate (ATP)-sensitive potassium channels and increased myocardial antioxidant capacity. However, the most compelling evidence for exercise-induced cardioprotection is the fact that exercise training upregulates key antioxidant enzymes that have been shown to promote cardioprotection. Moreover, data are presented showing that exercise training induces cardiac mitochondrial changes that result in reduced oxidant production. In addition, recently our laboratory has shown that exercise training evokes changes in mitochondrial phenotype that are protective against apoptotic stimuli. Specifically, data are presented showing that several mitochondrial proteins are altered following repeated bouts of endurance exercise and several of these differentially expressed proteins are potential important cardioprotective mediators. Finally, in hopes of stimulating debate and future research, this review concludes with a discussion of unanswered questions related to exercise-induced cardioprotection.
Authors:
Andreas N Kavazis
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Sports medicine (Auckland, N.Z.)     Volume:  39     ISSN:  0112-1642     ISO Abbreviation:  Sports Med     Publication Date:  2009  
Date Detail:
Created Date:  2009-10-15     Completed Date:  2010-01-07     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8412297     Medline TA:  Sports Med     Country:  New Zealand    
Other Details:
Languages:  eng     Pagination:  923-35     Citation Subset:  IM    
Affiliation:
Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, Florida 32611, USA. andreas@hhp.ufl.edu
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MeSH Terms
Descriptor/Qualifier:
Adaptation, Physiological
Animals
Antioxidants / metabolism
Exercise / physiology*
Exercise Therapy*
Exercise Tolerance
Humans
Ischemic Preconditioning, Myocardial*
Mitochondria
Models, Animal
Myocardial Reperfusion Injury / etiology,  mortality,  prevention & control*
Myocardium* / enzymology
Physical Endurance
Time Factors
Grant Support
ID/Acronym/Agency:
R01HL067855/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Antioxidants

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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