Enhanced postischemic myocardial recovery following exercise induction of HSP 72

Abstract

The inducible isoform of the 70-kDa heat shock protein (HSP) family, HSP 72, has been shown to protect cells from protein-damaging stressors and has been associated with myocardial protection. Because exercise is capable of increasing HSP 72 content, we determined whether exercise induction of HSP 72 also provided myocardial protection. Twenty-eight rats (n = 7 per group) were divided into control, heat-shocked (15 min at 42 degrees C), and two exercised groups. Exercise consisted of either one or three bouts (on 3 consecutive days) of treadmill running for 60 min at 30 m/min. Twenty-four hours after heat shock or exercise, hearts were placed on a Langendorff apparatus and subjected to 30 min of global ischemia followed by 30 min of reperfusion. Left ventricular developed pressure (LVDP), maximal rate of contraction and relaxation (+/- dP/dt, respectively), coronary flow, catalase activity, and HSP 72 content were determined. During reperfusion, hearts from heat-shocked animals and animals subjected to three bouts of exercise recovered a greater percentage of preischemic LVDP and +/- dP/dt compared with controls or animals that exercised only once. Compared with hearts from controls, HSP 72 content was significantly elevated in the hearts of heat-shocked animals and in animals subjected to three bouts of exercise, but not in animals that exercised only once. These results suggest that exercise induction of HSP 72 can confer an enhanced postischemic recovery and may explain, at least in part, the myocardial protection associated with exercise.

Exercise improves postischemic function in aging hearts

“…In the youngest group, there was an exercise-induced increase in HSP70 (105%) and catalase (26%) accompanying the improved cardioprotection. It could be concluded that HSP70 is the primary mediator of protection in this age group because the magnitude of the increase was similar to that reported by other studies supporting this chaperone as the primary mechanism of exercise-induced cardioprotection (23,27), and there is considerable data indicating that an elevation of HSP70 is cardioprotective against I/R (for reviews, see Refs. 18, 30, and 31).…”

“…ENHANCED CARDIOPROTECTION against ischemia-reperfusion (I/R) injury has been observed after one to three exercise bouts (4,11,13,15,23,27,34,36,38). Exercise, along with brief heat shock or ischemia, is among a group of the manipulations that have been reported to induce the late phase of preconditioning against I/R (for reviews, see Refs.…”

“…These manipulations may share some common protective pathways, especially exercise and heat shock, because exercise can significantly increase core temperature. Proteins reported to have prominent roles in exerciseinduced preconditioning against I/R include inducible heat shock protein (HSP70), superoxide dismutase (SOD), and catalase (11,13,15,23,27,31,34,38). The antioxidant enzymes function to prevent protein denaturation during the oxidative stress associated with both exercise and I/R, whereas HSP70 aids in the subsequent recovery by promoting restoration of dysfunctional enzymes and preventing aggregation of severely denatured proteins (for reviews, see Refs.…”

Reduced susceptibility to ventricular tachyarrhythmias in rats selectively bred for high aerobic capacity

“…Furthermore, experimental studies have documented that both short-and long-term endurance exercise provides myocardial protection against ischemia-reperfusion injury in rats (6,14,23,30,53,54,77). Several factors, including an increase in calcium handling (14), endogenous antioxidants (50,77), heat shock proteins (50,81), and increased expression of myosin heavy chain-␤ (34) as well as intrinsic metabolic factors and reduced content of the arrhythmogenic substance cyclic AMP, have been implicated as mechanisms responsible for the protective effects of exercise.…”

Obesity is associated with increased myocardial oxidative stress

“…Therefore, LV levels of HSP72 and HSP73 were assessed by performing polyacrylamide gel electrophoresis and western blotting techniques. 19 In brief, LV samples were homogenized in a buffer containing 10 mM Tris, 10 mM NaCl, 0.1 mM EDTA, 15 mM mercaptoethanol at pH 7.6. Samples (30 mg) were loaded into wells of a 4% polyacrylamide stacking gela12% separating gel (Bio-Rad Mini Protean II Gel apparatus).…”