Mechanisms Involved in Exercise-Induced Cardioprotection: A Systematic Review

Borges, Juliana Pereira; Lessa, Marcos Adriano

doi:10.5935/abc.20150024

Cited by 29 publications

(33 citation statements)

References 70 publications

(133 reference statements)

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“…Despite some mechanisms being known to operate in EICP – including an increment in antioxidant capacity, changes in mitochondrial phenotype and glycolytic flux, promotion of nitric oxide signalling, promotion of ATP‐dependent potassium channel function, and an increase in endoplasmic reticulum stress proteins and myocardial cyclooxygenase 2 activity – knowledge of the mechanisms responsible for EICP is limited (Borges, 2015; Kavazis et al., 2008; Powers et al., 2014; Powers et al., 2008; Quindry et al., 2012). Moreover, most studies have focused on the effects of moderate intensity continuous training, and there are limited studies on the effects of HIIT and its cardioprotective mechanisms (Fallahi et al, 2015; Rahimi et al., 2015; Ghanimati et al, 2020).…”

Section: Discussionmentioning

confidence: 99%

High‐intensity interval training increases myocardial levels of Klotho and protects the heart against ischaemia–reperfusion injury

Ramez

Ramezani

Nasirinezhad

et al. 2020

Experimental Physiology

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Cardiovascular disease, especially coronary artery disease, remains a major cause of morbidity and mortality in the world, and ischaemia-reperfusion (IR) insult is the main pathological cause leading to death. Exercise training is associated with a reduced risk of cardiovascular disease and the development of cardioprotection against IR injury. Therefore, the purpose of this study was to investigate the effect of preconditioning with high-intensity interval training (HIIT) on myocardial and plasma levels of Klotho and its related axes as novel mechanisms of exercise-induced cardioprotection against IR injury. Seventy male Wistar rats were randomly divided into five groups of control, HIIT, sham, IR and HIIT group that underwent IR injury (H-IR). The training group performed five sessions of HIIT on the treadmill. The cardiac IR injury was induced by ligation of the left anterior descending coronary artery for 30 min followed by 24 h reperfusion. Infarct size and histopathological assessment of cardiac tissues were determined through Evans Bluetriphenyltetrazolium chloride and haematoxylin-eosin staining, respectively. We investigated lipid peroxidation and markers of cardiac injury, antioxidant enzymes and the plasma levels of Klotho using enzyme-linked immunosorbent assays. Also, myocardial levels of Klotho and TRPC6 expression were determined by western blot assays. The results demonstrated a significant increase in myocardial and plasma levels of Klotho following HIIT and a significant decrease during IR injury. Myocardial TRPC6 channel expression increased following IR. HIIT also prevented a significant reduction of Klotho during IR and consequently reduced the expression of the TRPC6 channel in the H-IR group compared with the IR group. Furthermore, HIIT decreased the infarct size, cardiac injury, lipid peroxidation, lactate dehydrogenase, creatine kinase myocardial band and cardiac troponin-I, and improved total antioxidant capacity and catalase, superoxide dismutase and glutathione peroxidase activities following IR injury. The findings of the present study suggest that HIIT improves cardioprotection against IR injury and reduces cardiac damages through an increase in myocardial and plasma levels of Klotho and its related axes (TRPC6 and antioxidant defence). These findings can help to develop preventive and therapeutic approaches. K E Y W O R D SAntioxidant defence, cardioprotection, high-intensity interval training, Klotho, TRPC6 channels wileyonlinelibrary.com/journal/eph Experimental Physiology. 2020;105:652-665.

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Section: Discussionmentioning

confidence: 99%

High‐intensity interval training increases myocardial levels of Klotho and protects the heart against ischaemia–reperfusion injury

Ramez

Ramezani

Nasirinezhad

et al. 2020

Experimental Physiology

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“…Hydrogen ions and lactate levels increase, decreasing pH below 6.5. Na + /H + exchange and Na + /K + pumps are compromised as ATP levels are challenged (Borges & Lessa, 2015).…”

Section: Exercise Preconditioning and Ischaemia-reperfusionmentioning

confidence: 99%

Mitochondria in the middle: exercise preconditioning protection of striated muscle

Lawler¹,

Rodriguez²,

Hord³

2016

The Journal of Physiology

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Cellular and physiological adaptations to an atmosphere which became enriched in molecular oxygen spurred the development of a layered system of stress protection, including antioxidant and stress response proteins. At physiological levels reactive oxygen and nitrogen species regulate cell signalling as well as intracellular and intercellular communication. Exercise and physical activity confer a variety of stressors on skeletal muscle and the cardiovascular system: mechanical, metabolic, oxidative. Transient increases of stressors during acute bouts of exercise or exercise training stimulate enhancement of cellular stress protection against future insults of oxidative, metabolic and mechanical stressors that could induce injury or disease. This phenomenon has been termed both hormesis and exercise preconditioning (EPC). EPC stimulates transcription factors such as Nrf‐1 and heat shock factor‐1 and up‐regulates gene expression of a cadre of cytosolic (e.g. glutathione peroxidase and heat shock proteins) and mitochondrial adaptive or stress proteins (e.g. manganese superoxide dismutase, mitochondrial KATP channels and peroxisome proliferator activated receptor γ coactivator‐1 (PGC‐1)). Stress response and antioxidant enzyme inducibility with exercise lead to protection against striated muscle damage, oxidative stress and injury. EPC may indeed provide significant clinical protection against ischaemia–reperfusion injury, Type II diabetes and ageing. New molecular mechanisms of protection, such as δ‐opioid receptor regulation and mitophagy, reinforce the notion that mitochondrial adaptations (e.g. heat shock proteins, antioxidant enzymes and sirtuin‐1/PGC‐1 signalling) are central to the protective effects of exercise preconditioning.

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“…The relationship between physical activity and health status has stimulated an increasing number of researchers looking at the role of chronic exercise training on telomere biology. It has been shown that regular exercise exerts a protective effect against cellular and molecular damage, attenuating the decline in physiological functions during aging, leading to a greater quality of life and lowered mortality [4,33,34,41].…”

Section: Introductionmentioning

confidence: 99%

Training Performed Above Lactate Threshold Decreases p53 and Shelterin Expression in Mice

et al. 2018

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Telomere shortening is associated to sarcopenia leading to functional impairment during aging. There are mechanisms associated with telomere attrition, as well to its protection and repair. Physical training is a factor that attenuates telomere shortening, but little is known about the effects of different exercise intensities on telomere biology. Thus, we evaluated the effects of exercise intensity (moderate vs. high-intensity domain) on gene expression of senescence markers Checkpoint kinase 2 and tumor suppressor ( and , respectively), shelterin telomere repeat binding 1 and 2 (/), DNA repair (), telomerase reverse transcriptase () and telomere length in middle aged mice. Three groups were studied: a control group (CTL) and two groups submitted to swimming at intensities below the lactate threshold (LI group) and above the lactate threshold (HI group) for 40 and 20 min respectively, for 12 weeks. After training, the HI group showed reduction in p53 expression in the muscle, and decreased shelterin complex expression when compared to LI group. No differences were observed between groups for expression and telomere length. Thus, exercise training in high-intensity domain was more effective on reducing markers of senescence and apoptosis. The higher intensity exercise training also diminished shelterin expression, with no differences in telomere length and mTERT expression. Such results possibly indicate a more effective DNA protection for the higher-intensity exercise training.

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Mechanisms Involved in Exercise-Induced Cardioprotection: A Systematic Review

Cited by 29 publications

References 70 publications

High‐intensity interval training increases myocardial levels of Klotho and protects the heart against ischaemia–reperfusion injury

High‐intensity interval training increases myocardial levels of Klotho and protects the heart against ischaemia–reperfusion injury

Mitochondria in the middle: exercise preconditioning protection of striated muscle

Training Performed Above Lactate Threshold Decreases p53 and Shelterin Expression in Mice

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