title: Loss of exercise-induced cardioprotection after cessation of exercise.
abstract: Endurance exercise provides cardioprotection against ischemia-reperfusion (I/R) injury. Exercise-induced cardioprotection is associated with increases in cytoprotective proteins, including heat shock protein 72 (HSP72) and increases in antioxidant enzyme activity. On the basis of the reported half-life of these putative cardioprotective proteins, we hypothesized that exercise-induced cardioprotection against I/R injury would be lost within days after cessation of exercise. To test this, male rats (4 mo) were randomly assigned to one of five experimental groups: 1). sedentary control, 2). exercise followed by 1 day of rest, 3). exercise followed by 3 days of rest, 4). exercise followed by 9 days of rest, and 5). exercise followed by 18 days of rest. Exercise-induced increases (P < 0.05) in left ventricular catalase activity and HSP72 were evident at 1 and 3 days postexercise. However, at 9 days postexercise, myocardial HSP72 and catalase levels declined to sedentary control values. To evaluate cardioprotection during recovery from I/R, hearts were isolated, placed in working heart mode, and subjected to 20.5 min of global ischemia followed by 30 min of reperfusion. Compared with sedentary controls, exercised animals sustained less I/R injury as evidenced by maintenance of a higher (P < 0.05) percentage of preischemia cardiac work during reperfusion at 1, 3, and 9 days postexercise. The exercise-induced cardioprotection vanished by 18 days after exercise cessation. On the basis of the time course of the loss of cardioprotection and the return of HSP72 and catalase to preexercise levels, we conclude that HSP72 and catalase are not essential for exercise-induced protection during myocardial stunning. Therefore, other cytoprotective molecules are responsible for providing protection during I/R.
authors.affiliation: Department of Exercise and Sport Sciences, University of Florida, Gainesville, Florida 32611, USA. slennon@bu.edu
authors.forename: Shannon L
authors.initials: SL
authors.lastname: Lennon
authors.forename: John
authors.initials: J
authors.lastname: Quindry
authors.forename: Karyn L
authors.initials: KL
authors.lastname: Hamilton
authors.forename: Joel
authors.initials: J
authors.lastname: French
authors.forename: Jessica
authors.initials: J
authors.lastname: Staib
authors.forename: Jawahar L
authors.initials: JL
authors.lastname: Mehta
authors.forename: Scott K
authors.initials: SK
authors.lastname: Powers
mesh_terms: D000818:Animals; D002374:Catalase / Q000378:metabolism; D050884:HSP72 Heat-Shock Proteins; D006321:Heart / Q000502:physiology*; D006352:Heart Ventricles; D006360:Heat-Shock Proteins / Q000378:metabolism; D019157:Ischemic Preconditioning, Myocardial; D008297:Male; D009043:Motor Activity / Q000502:physiology*; D009206:Myocardium / Q000378:metabolism; D010088:Oxidoreductases / Q000378:metabolism; D010805:Physical Conditioning, Animal; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000517:prevention & control*; D012146:Rest; D013997:Time Factors
chemical_list: D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins; D010088:Oxidoreductases; D002374:Catalase