Short-term exercise training can improve myocardial tolerance to I/R without elevation in heat shock proteins

Citation
Kl. Hamilton et al., Short-term exercise training can improve myocardial tolerance to I/R without elevation in heat shock proteins, AM J P-HEAR, 281(3), 2001, pp. H1346-H1352
Citations number
28
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
ISSN journal
03636135 → ACNP
Volume
281
Issue
3
Year of publication
2001
Pages
H1346 - H1352
Database
ISI
SICI code
0363-6135(200109)281:3<H1346:SETCIM>2.0.ZU;2-6
Abstract
We examined the effects of 3 days of exercise in a cold environment on the expression of left ventricular (LV) heat shock proteins (HSPs) and contract ile performance during in vivo ischemia-reperfusion (I/R). Sprague-Dawley r ats were divided into the following three groups (n = 12/group): 1) control , 2) exercise (60 min/day) at 4 degreesC (E-Cold), and 3) exercise (60 min/ day) at 25 degreesC (E-Warm). Left anterior descending coronary occlusion w as maintained for 20 min, followed by 30 min of reperfusion. Compared with the control group, both the E-Cold and E-Warm groups maintained higher (P < 0.05) LV developed pressure, first derivative of pressure development over time (+dP/dt), and pressure relaxation over time (-dP/dt) throughout I/R. Relative levels of HSP90, HSP72, and HSP40 were higher (P < 0.05) in E-Warm . animals compared with both control and E-Cold. HSP10, HSP60, and HSP73 di d not differ between groups. Exercise increased manganese superoxide dismut ase (MnSOD) activity in both E-Warm. and E-Cold hearts (P < 0.05). Protecti on against I/R-induced lipid peroxidation in the LV paralleled the increase in MnSOD activity whereas lower levels of lipid peroxidation were observed in both E-Warra and E-Cold groups compared with control. We conclude that exercise-induced myocardial protection against a moderate duration I/R insu lt is not dependent on increases in myocardial HSPs. We postulate that exer cise-associated cardioprotection may depend, in part, on increases in myoca rdial antioxidant defenses.