Perspectives in innate and acquired cardioprotection: cardioprotection acquired through exercise

Brown, David A.; Moore, Russell L.

doi:10.1152/japplphysiol.00464.2007

Cited by 42 publications

(36 citation statements)

References 73 publications

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“…This is exemplified in animal models, which are devoid of confounding risk factors for cardiovascular disease, where exercise has consistently been shown to improve coronary vascular reactivity, decrease myocardial stunning, and reduce arrhythmias in hearts subjected to I/R injury (26). Moreover, exercise confers sustainable protection against myocardial infarction following both long-term and short-term training regimens (9) and improves survival after an ischemic event in humans (37,50). A review of the literature indicates that reductions in cell death following exercise range from 4 to 75% depending on the ischemic model studied (permanent ischemia or I/R) and the training strategy employed (1, 6 -8, 13, 16, 27, 35, 47, 71, 72, 74, 75, 77) (Table 1).…”

Section: Cardioprotective Effects Of Exercisementioning

confidence: 99%

Role of β-Adrenergic Receptors and Nitric Oxide Signaling in Exercise-Mediated Cardioprotection

Calvert

Lefer

2013

Physiology

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Exercise promotes cardioprotection in both humans and animals not only by reducing risk factors associated with cardiovascular disease but by reducing myocardial infarction and improving survival following ischemia. This article will define the role that nitric oxide and ␤-adrenergic receptors play in mediating the cardioprotective effects of exercise in the setting of ischemiareperfusion injury.

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Section: Cardioprotective Effects Of Exercisementioning

confidence: 99%

Role of β-Adrenergic Receptors and Nitric Oxide Signaling in Exercise-Mediated Cardioprotection

Calvert

Lefer

2013

Physiology

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“…The beneficial effects of physical training for the cardiovascular system in the range 50-80% of maximum O 2 uptake _ VO 2 max À Á are well known (Brown and Moore 2007). In animal models, this effect translates into greater tolerance to ischemia/reperfusion (I/R) challenge.…”

Section: Introductionmentioning

confidence: 99%

Myocardial tolerance to ischemia–reperfusion injury, training intensity and cessation

et al. 2010

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Training has been shown to induce cardioprotection. The mechanisms involved remain still poorly understood. Aims of the study were to examine the relevance of training intensity on myocardial protection against ischemia/reperfusion (I/R) injury, and to which extent the beneficial effects persist after training cessation in rats. Sprague-Dawley rats trained at either low (60% [Formula: see text]) or high (80% [Formula: see text]) intensity for 10 weeks. An additional group of highly trained rats was detrained for 4 weeks. Untrained rats served as controls. At the end of treatment, rats of all groups were split into two subgroups. In the former, rats underwent left anterior descending artery (LAD) ligature for 30 min, followed by 90-min reperfusion, with subsequent measurement of the infarct size. In the latter, biopsies were taken to measure heat-shock proteins (HSP) 70/72, vascular endothelial growth factor (VEGF) protein levels, and superoxide dismutase (SOD) activity. Training reduced infarct size proportionally to training intensity. With detraining, infarct size increased compared to highly trained rats, maintaining some cardioprotection with respect to controls. Cardioprotection was proportional to training intensity and related to HSP70/72 upregulation and Mn-SOD activity. The relationship with Mn-SOD was lost with detraining. VEGF protein expression was not affected by either training or detraining. Stress proteins and antioxidant defenses might be involved in the beneficial effects of long-term training as a function of training intensity, while HSP70 may be one of the factors accounting for the partial persistence of myocardial protection against I/R injury in detrained rats.

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“…Experimental studies using trained rat models (e.g treadmill running) have demonstrated that these epidemiological observations can be, at least partly, attributed to an exercise-induced cardioprotection against a variety of cellular mechanisms involved in deleterious effects of ischemia and reperfusion (Brown and Moore, 2007;Powers et al, 2008). However, these studies were carried out on young adult rats (< 6 month of age) whereas most cardiac complications occur in late adulthood.…”

Section: Introductionmentioning

confidence: 99%

Exercise training improves functional post-ischemic recovery in senescent heart

Page

Noirez

Courty

et al. 2009

Experimental Gerontology

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This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. and eNOS myocardial contents. ACCEPTED MANUSCRIPT

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Perspectives in innate and acquired cardioprotection: cardioprotection acquired through exercise

Cited by 42 publications

References 73 publications

Role of β-Adrenergic Receptors and Nitric Oxide Signaling in Exercise-Mediated Cardioprotection

Role of β-Adrenergic Receptors and Nitric Oxide Signaling in Exercise-Mediated Cardioprotection

Myocardial tolerance to ischemia–reperfusion injury, training intensity and cessation

Exercise training improves functional post-ischemic recovery in senescent heart

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