Habitual low-intensity exercise does not protect against myocardial dysfunction after ischemia in rats.
BACKGROUND
It is well established that participation in a chronic exercise program can reduce coronary heart disease (CHD) risk factors and improve myocardial tolerance to ischemia-reperfusion (I-R) injury. Low-intensity exercise programs are known to be effective in reducing CHD risk factors in humans and rats, but whether similar programs are of sufficient intensity to improve intrinsic tolerance to I-R injury has not been established. Thus, the purpose of this study is to determine whether low-intensity exercise provides self-protection to the heart against I-R injury.


METHODS
Male, Sprague-Dawley rats were exercised on a treadmill at an intensity of 55-60% VO2max, 40 min/day, 5 days/week for 16 weeks. Reperfusion injury following 20 min of global ischemia was evaluated using the isolated perfused working heart model. Left ventricular content of the cytoprotective protein heat shock protein 70 (HSP70) was determined by Western blotting.


RESULTS
The exercise program elevated HSP70 2.7-fold, but did not provide enhanced protection following 20 min of ischemia. Final post-ischemic recovery of cardiac external work was 63+/-9% of pre-ischemic value in the sedentary group (n=9) and 51+/-11% in the exercising group (n=9) (P>0.05). Post-ischemic lactate dehydrogenase release was also similar between groups and the magnitude of release was low, consistent with stunning.


CONCLUSIONS
Regular exercise at 55-60% VO2max is below the threshold intensity necessary to induce intrinsic cardioprotection against I-R injury. Furthermore, elevated myocardial HSP70 is not necessarily a marker of improved protection against dysfunction associated with stunning.
Starnes
Joseph W
JW
Department of Kinesiology and Health Education, Cardiac Metabolism Laboratory, University of Texas, Austin, Texas 78712, USA. jstarnes@mail.utexas.edu
Taylor
Ryan P
RP
Ciccolo
Joseph T
JT
D000818:Animals; D015415:Biomarkers / Q000032:analysis; D015153:Blotting, Western; D004195:Disease Models, Animal; D006334:Heart Function Tests; D006360:Heat-Shock Proteins / Q000032:analysis*; D019157:Ischemic Preconditioning, Myocardial; D007770:L-Lactate Dehydrogenase / Q000032:analysis*; D008297:Male; D017202:Myocardial Ischemia; D010805:Physical Conditioning, Animal; D011336:Probability; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012016:Reference Values; D015427:Reperfusion Injury / Q000503:physiopathology* / Q000517:prevention & control*; D012307:Risk Factors; D012680:Sensitivity and Specificity
D015415:Biomarkers; D006360:Heat-Shock Proteins; D007770:L-Lactate Dehydrogenase