Reduced ischemia and reperfusion injury following exercise training

Libonati, Joseph R.; Gaughan, John; Hefner, Colleen; Gow, Andrew J.; Paolone, A. M.; Houser, Steven R.

doi:10.1097/00005768-199704000-00013

Cited by 66 publications

(64 citation statements)

References 29 publications

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“…In the present study, hearts obtained from endurance exercise-trained animals exhibited a better recovery of contractile function after a brief period of ischemia and reperfusion than hearts obtained from sedentary rats. In agreement with the present study, some studies have reported that exercise training elicited an improved functional recovery, as measured in whole hearts, in response to ischemia-reperfusion (6,7,19,22,24), whereas other studies did not (19,21). These conflicting results may result from diverse experimental protocols (e.g., ischemic duration, global vs. regional ischemia), as well as differences in exercise protocols.…”

Section: Discussionsupporting

confidence: 79%

Effects of exercise training on contractile function in myocardial trabeculae after ischemia-reperfusion

Hwang¹,

Reiser²

2005

Journal of Applied Physiology

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Effects of exercise training on contractile function in myocardial trabeculae after ischemia-reperfusion. J Appl Physiol 99: 230 -236, 2005. First published March 17, 2005; doi:10.1152/japplphysiol.00850.2004.-Potential protective effects of aerobic exercise training on the myocardium, before an ischemic event, are not completely understood. The purpose of the study was to investigate the effects of exercise training on contractile function after ischemia-reperfusion (Langendorff preparation with 15-min global ischemia/30-min reperfusion). Trabeculae were isolated from the left ventricles of both sedentary control and 10-to 12-wk treadmill exercisetrained rats. The maximal normalized isometric force (force/cross-sectional area; P o/CSA) and shortening velocity (Vo) in isolated, skinned ventricular trabeculae were measured using the slack test. Ischemiareperfusion induced significant contractile dysfunction in hearts from both sedentary and trained animals; left ventricular developed pressure (LVDP) and maximal rates of pressure development and relaxation (ϮdP/dt max) decreased, whereas end-diastolic pressure (EDP) increased. However, this dysfunction (as expressed as percent change from the last 5 min before ischemia) was attenuated in trained myocardium [LVDP: sedentary Ϫ60.8 Ϯ 6.4% (32.0 Ϯ 5.5 mmHg) vs. trained Ϫ15.6 Ϯ 8.6% (64.9 Ϯ 6.6 mmHg); ϩdP/dt max: sedentary Ϫ54.1 Ϯ 4.7% (1,058.7 Ϯ 124.2 mmHg/s) vs. trained Ϫ16.7 Ϯ 8.4% (1,931.9 Ϯ 188.3 mmHg/s); ϪdP/dt max: sedentary Ϫ44.4 Ϯ 2.5% (Ϫ829.3 Ϯ 52.0 mmHg/s) vs. trained Ϫ17.9 Ϯ 7.2% (Ϫ1,341.3 Ϯ 142.8 mmHg/s); EDP: sedentary 539.5 Ϯ 147.6%; (41.3 Ϯ 6.0 mmHg) vs. trained 71.6 Ϯ 30.6%; 11.4 Ϯ 1.2 mmHg]. There was an average 26% increase in P o/CSA in trained trabeculae compared with sedentary controls, and this increase was not affected by ischemia-reperfusion. Ischemia-reperfusion reduced V 0 by 39% in both control and trained trabeculae. The relative amount of the ␤-isoform of myosin heavy chain (MHC-␤) was twofold greater in trained trabeculae as well as in the ventricular free walls. Despite a possible increase in the economy in the trained heart, presumed from a greater amount of MHC-␤, ischemia-reperfusion reduced V o, to a similar extent in both control and trained animals. Nevertheless, the trained myocardium appears to have a greater maximum force-generating ability that may, at least partially, compensate for reduced contractile function induced by a brief period of ischemia.

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Section: Discussionsupporting

confidence: 79%

Effects of exercise training on contractile function in myocardial trabeculae after ischemia-reperfusion

Hwang¹,

Reiser²

2005

Journal of Applied Physiology

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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.…”

Section: Discussionmentioning

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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. 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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“…126 -128 Studies that use less intense training programs have not consistently observed protection from ischemia and reperfusion. 124,127,129,130 In summary, in the majority of clinical and experimental studies, endurance-type exercise training has improved indices of diastolic function in elderly and younger humans and in rats with LVH. Thus, exercise training may have beneficial potential in clinically significant, symptomatic diastolic dysfunction.…”

Section: Long-term Exercise Training and Protection Against Hypoxic Amentioning

confidence: 97%

Exercise and Heart Failure

Piña¹,

Apstein²,

Balady³

et al. 2003

Circulation

872

286

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Reduced ischemia and reperfusion injury following exercise training

Cited by 66 publications

References 29 publications

Effects of exercise training on contractile function in myocardial trabeculae after ischemia-reperfusion

Effects of exercise training on contractile function in myocardial trabeculae after ischemia-reperfusion

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

Exercise and Heart Failure

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