Exercise training improves myocardial tolerance to  in vivo ischemia-reperfusion in the rat

Powers, Scott K.; Demirel, Haydar A.; Vincent, H. K.; Coombes, Jeff S.; Naito, Hisashi; Hamilton, Karyn L.; Shanely, R. Andrew; Jessup, James V.

doi:10.1152/ajpregu.1998.275.5.r1468

Cited by 141 publications

(237 citation statements)

References 36 publications

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“…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. For example, Posel et al (76) documented a reduced accumulation of cyclic AMP in the ischemic left ventricular zone in hearts from trained rats.…”

Section: Discussionmentioning

confidence: 99%

“…Other investigators (13,14,35,36,39) using isolated rat heart preparations as well as cardiomyocytes have documented that exercise training improved cardiac and metabolic function after ischemia or anoxia. Exercise training also improved myocardial tolerance to ischemia in anesthetized rats (63,77). It is important to note that, with few exceptions (69,76), studies using isolated heart preparations or anesthetized rats do not document the incidence of arrhythmias despite prolonged periods of ischemia.…”

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confidence: 99%

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

Lujan

Britton²,

Koch

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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. Reduced susceptibility to ventricular tachyarrhythmias in rats selectively bred for high aerobic capacity. Am J Physiol Heart Circ Physiol 291: H2933-H2941, 2006. First published August 4, 2006 doi:10.1152/ajpheart.00514.2006.-Reperfusion after a brief period of cardiac ischemia can lead to potentially lethal arrhythmias. Human epidemiological studies and experimental work with animals indicate that regular physical activity is associated with reductions in cardiovascular disease (CVD) risk factors and sudden cardiac death. Similarly, artificial selection of rats for high aerobic treadmill-running capacity (high-capacity runners; HCR) has been shown to reduce CVD risk factors relative to rats selected as lowcapacity runners (LCR). Therefore, we tested the hypothesis that HCR, relative to LCR rats, would be less susceptible to ischemiareperfusion-mediated ventricular tachyarrhythmias. To test this hypothesis, we measured the susceptibility to ventricular tachyarrhythmias produced by 3 min of occlusion and reperfusion of the left main coronary artery in conscious LCR and HCR rats. Results document a significantly lower incidence of ventricular tachyarrhythmias in HCR (3 of 11, 27.3%) relative to LCR (6 of 7, 85.6%) rats. The decreased susceptibility to tachyarrhythmias in HCR rats was associated with a reduced cardiac metabolic demand during ischemia (lower rate-pressure product and ST segment elevation) as well as a wider range for the autonomic control of heart rate. The HCR and LCR represent a unique substrate for evaluation of the mechanisms underlying ischemia-mediated cardiac arrhythmogenesis. artificial selection; cardiovascular risks; arrhythmia; exercise TEMPORARY OCCLUSION of the coronary arteries can lead to potentially lethal arrhythmias (66,82). Coronary artery occlusion-induced arrhythmias are triggered by the ischemic insult directly or on relief of the ischemic insult during the reperfusion phase. The mechanisms underlying the ventricular arrhythmias during ischemia and reperfusion are related but distinct (5,56,75,82). Although ischemia is a more common trigger of sudden death than is reperfusion, life-threatening reperfusion arrhythmias are observed during relief of coronary spasm, during angioplasty or thrombolysis, and after cardiac surgery with ischemic arrest (24).

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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

Lujan

Britton²,

Koch

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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“…8,10 ± 12,32 Previous studies have reported the induction of HSP72 in response to ischemia, 11 acute exercise 8 and regular exercise training. 10 A common stimulus among these conditions is oxidative stress. When ROS are generated at greater rates by acute or chronic stimuli, HSP expression is induced.…”

Section: Hsp and Obesitymentioning

confidence: 99%

“…8 Previous studies have reported that myocardial levels of both enzymatic (for example, superoxide dismutase, SOD) and non-enzymatic (for example, glutathione) antioxidants are elevated following chronic or repeated exposure to ROS. 9,10 Furthermore, exposure to heat andaor ROS has been shown to increase the expression of HSP72 in cardiac myocytes. 9,11,12 It follows that if obesity is associated with an increased ROS production in cardiac myocytes, the myocardium could respond by increasing the levels of HSP72 and enzymatic and non-enzymatic antioxidant defenses.…”

Section: Introductionmentioning

confidence: 99%

Obesity is associated with increased myocardial oxidative stress

et al. 1999

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OBJECTIVE: To determine: 1) whether obesity predisposes the myocardium to oxidative stress as evidenced by higher tissue levels of myocardial lipid peroxidation, and 2) what cellular mechanisms are responsible for this predisposition. DESIGN: Comparative, descriptive study of the myocardial tissue of lean and obese Fatty Zucker animals. ANIMALS: 12 month old lean ( 7 afa; n 6; mean body weight 590 g) and obese (faafa; na 7; mean body weight 882 g) male Fatty Zucker rats. MEASUREMENTS: Basal lipid peroxidation (assessed using thiobarbituric reactive acid substances (TBARS) and cumene hydroperoxide equivalents), oxidative and antioxidant enzyme activities (citrate synthase (CS), superoxide dismutase (SOD), glutathione peroxidase (GPX) and catalase (CAT), thiol content, heat shock protein expression (HSP72a73) and TBARS concentrations following an iron-mediated challenge in vitro. RESULTS: Compared to lean, lipid peroxidation was greater (P`0.05) in the left ventricle (LV) from obese rats as indicated by higher levels of lipid hydroperoxides (mean 11.48 vs 13.7 cumene hydroperoxide equivalents (CHPE)amg lipid) and TBARS (mean 11.1 vs 13.9 nMolamg lipid.). The activity of the manganese isoform of superoxide dismutase in the LV was higher (P`0.05) in obese animals, compared to controls (mean 135 vs 117 Uamg protein). In contrast, LV catalase and glutathione peroxidase activities did not differ (P b 0.05) between groups. Also, LV levels of HSP 72 (inducible) and 73 (constitutive) did not differ (P b 0.05)( between lean and obese animals. Following an iron-stimulated oxidative challenge in vitro, TBARS concentration was signi®cantly greater (P`0.05) in LV of obese rats compared to the lean (mean 12.7 vs 16.7 nMolamg lipid). CONCLUSIONS: These results support the notion that obesity predisposes the myocardium to oxidative stress. However, the postulate that obesity is associated with elevated myocardial antioxidant enzyme activities and HSPs was only partially supported by these ®ndings.

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“…Unaltered or even decreased CS activities have been reported in skeletal muscles shortly after a single bout of exercise. Several studies have been conducted to determine the influence of exercise training in the mitochondrial enzyme adaptation in cardiac muscles (2,10,11,18,19). Although the majority of previous studies suggest that the traininginduced alteration of mitochondrial enzymes is not noticeable in cardiac muscle (1,2,17,18,30), a few discrepant results regarding the changes were reported (10).…”

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confidence: 99%

Citrate synthase expression and enzyme activity after endurance training in cardiac and skeletal muscles

Siu

Donley

Bryner

2003

Journal of Applied Physiology

114

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. Citrate synthase expression and enzyme activity after endurance training in cardiac and skeletal muscles. J Appl Physiol 94: 555-560, 2003; 10.1152/ japplphysiol.00821.2002.-The present study was designed to examine the acute and chronic effects of endurance treadmill training on citrate synthase (CS) gene expression and enzymatic activity in rat skeletal and cardiac muscles. Adult rats were endurance trained for 8 wk on a treadmill. They were killed 1 h (T1, n ϭ 8) or 48 h (T48, n ϭ 8) after their last bout of exercise training. Eight rats were sedentary controls (C) during the training period. CS mRNA levels and enzymatic activities of the soleus and ventricle muscles were determined. Training resulted in higher CS mRNA levels in both the soleus muscles (21% increase in T1; 18% increase in T48, P Ͻ 0.05) and ventricle muscles (23% increase in T1; 17% increase in T48, P Ͻ 0.05) when compared with the C group. The CS enzyme activities were 42 (P Ͻ 0.01) and 25% (P Ͻ 0.01) greater in the soleus muscles of T1 and T48 groups, respectively, when compared with that of the C group. Soleus CS enzyme activity was significantly greater in the T1 vs. T48 groups (P Ͻ 0.05). However, no appreciable alterations in CS enzyme activities were observed in the ventricle muscles in both training groups. These findings suggest differential responses of skeletal and cardiac muscles in CS enzymatic activity but similar responses in CS gene expression at 1 and 48 h after the last session of endurance training. Moreover, our data support the existence of an acute effect of exercise on the training-induced elevation in CS activity in rat soleus but not ventricle muscles. physical activity; oxidative enzyme; gene transcriptional expression; soleus muscle; heart muscle CITRATE SYNTHASE (CS) is one of the key regulatory enzymes in the energy-generating metabolic pathway that catalyzes the condensation of oxaloacetate and acetyl coenzyme A to form citrate in the tricarboxylic acid cycle. It has been extensively used as a metabolic marker in assessing oxidative and respiratory capacity (22). More than 30 years ago, Holloszy and his colleagues (8) reported that endurance exercise training increases the oxidative enzyme activities in skeletal muscle. After that, numerous studies were conducted to examine the effect of exercise training on muscle oxidative capacity and metabolic characteristics (7,15,20,22,29). It is generally recognized that the skeletal muscle oxidative capacity and the activities of mitochondrial enzymes are elevated by endurance exercise training.

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Exercise training improves myocardial tolerance to in vivo ischemia-reperfusion in the rat

Cited by 141 publications

References 36 publications

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

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

Obesity is associated with increased myocardial oxidative stress

Citrate synthase expression and enzyme activity after endurance training in cardiac and skeletal muscles

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