Journal article
Exercise Protects Cardiac Mitochondria against Ischemia-Reperfusion Injury
Medicine and science in sports and exercise, Vol.44(3), pp.397-405
03/01/2012
DOI: 10.1249/MSS.0b013e318231c037
PMID: 21857373
Abstract
LEE, Y., K. MIN, E. E. TALBERT, A. N. KAVAZIS, A. J. SMUDER, W. T. WILLIS, AND S. K. POWERS. Exercise Protects Cardiac Mitochondria against Ischemia-Reperfusion Injury. Med. Sci. Sports Exerc., Vol. 44, No. 3, pp. 397-405, 2012. Purpose: Three to five consecutive days of endurance exercise can protect the heart against an ischemia-reperfusion (IR) insult. However, the mechanisms responsible for this exercise-mediated cardioprotection remain unknown. Given the important role that mitochondria play in IR-induced cardiac myocyte injury, we hypothesized that exercise training promotes cardioprotection, at least in part, by increasing mitochondrial antioxidants, preventing mitochondrial release of reactive oxygen species, and protecting cardiac mitochondria against IR-induced oxidative damage and functional impairment. Methods: To test our hypothesis, Sprague-Dawley rats were assigned to either sedentary (n = 16) or exercise-trained (n = 16) groups. Exercise-trained animals performed 5 d of treadmill running for 60 min.d(-1) at 30 m.s(-1). Hearts were excised from sedentary and exercised-trained animals and were either perfused for 80 min or exposed to 40 min of global ischemia followed by 45 min of reperfusion by using an ex vivo isolated working heart model. After the protocol, cardiac subsarcolemmal and intermyofibrillar mitochondria were isolated and used to determine respiratory control ratio, reactive oxygen species emission, and indices of oxidative stress and apoptosis. Results: Our results support our hypothesis because exercise training protected both cardiac subsarcolemmal and intermyofibrillar mitochondria from IR-induced uncoupling and oxidative damage. Specifically, the levels of cardiac mitochondrial 4-hydroxynonenal-conjugated proteins were elevated in hearts from sedentary animals exposed to IR compared with cardiac mitochondria isolated from exercise-trained animals. Exercise also resulted in an increase in mitochondrial antioxidant enzymes (copper-zinc superoxide dismutase, manganese superoxide dismutase, and glutathione peroxidase) and prevented the IR-induced release of proapoptotic proteins from the mitochondria. Conclusions: Collectively, these novel findings reveal that exercise-induced cardioprotection is mediated, at least in part, through mitochondrial adaptations resulting in a mitochondrial phenotype that resists IR-induced damage.
Details
- Title: Subtitle
- Exercise Protects Cardiac Mitochondria against Ischemia-Reperfusion Injury
- Creators
- Youngil Lee - University of FloridaKisuk Min - University of FloridaErin E. Talbert - University of FloridaAndreas N. Kavazis - Mississippi State UniversityAshley J. Smuder - University of FloridaWayne T. Willis - Arizona State UniversityScott K. Powers - University of Florida
- Resource Type
- Journal article
- Publication Details
- Medicine and science in sports and exercise, Vol.44(3), pp.397-405
- Publisher
- Lippincott Williams & Wilkins
- DOI
- 10.1249/MSS.0b013e318231c037
- PMID
- 21857373
- ISSN
- 0195-9131
- eISSN
- 1530-0315
- Number of pages
- 9
- Grant note
- R01 HL067855 / National Institutes of Health (NIH); United States Department of Health & Human Services; National Institutes of Health (NIH) - USA R01HL067855 / NATIONAL HEART, LUNG, AND BLOOD INSTITUTE; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Heart Lung & Blood Institute (NHLBI)
- Language
- English
- Date published
- 03/01/2012
- Academic Unit
- Fraternal Order of Eagles Diabetes Research Center; Health and Human Physiology; Internal Medicine
- Record Identifier
- 9984259644602771
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