Interval exercise, but not endurance exercise, prevents endothelial ischemia-reperfusion injury in healthy subjects

Seeger, Joost P. H.; Lenting, Charlotte J.; Schreuder, Tim H. A.; Landman, Thijs; Cable, N. Timothy; Hopman, Maria T. E.; Thijssen, Dick H. J.

doi:10.1152/ajpheart.00647.2014

Cited by 33 publications

(32 citation statements)

References 34 publications

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“…We induced I–R injury in the brachial artery using an experimental approach that has been extensively utilized in humans (Brunt et al., ; Kharbanda et al., , ; Seeger et al., ; van den Munckhof et al., ). Importantly, the brachial artery can be used as a surrogate for the coronary artery given the strong relationship between brachial and coronary vasodilator function (Anderson et al., ; Takase et al., , ; Vallbracht‐Israng, Morguet, & Schwimmbeck, ).…”

Section: Discussionmentioning

confidence: 99%

Acute lower leg hot water immersion protects macrovascular dilator function following ischaemia–reperfusion injury in humans

Engelland

Hemingway

Tomasco

et al. 2019

Experimental Physiology

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Reperfusion that follows a period of ischaemia paradoxically reduces vasodilator function in humans and contributes to the tissue damage associated with an ischaemic event. Acute wholebody hot water immersion protects against vascular ischaemia-reperfusion (I-R) injury in young healthy humans. However, the effect of acute lower leg heating on I-R injury is unclear. Therefore, wileyonlinelibrary.com/journal/eph Experimental Physiology. 2020;105:302-311.

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Section: Discussionmentioning

confidence: 99%

Acute lower leg hot water immersion protects macrovascular dilator function following ischaemia–reperfusion injury in humans

Engelland

Hemingway

Tomasco

et al. 2019

Experimental Physiology

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“…Likewise, a single bout of lower limb interval exercise prevents endothelial dysfunction due to ischaemia–reperfusion injury (Seeger et al . ). Cardiac patients with lower physical activity levels exhibit endothelial dysfunction, to judge from reduced flow‐mediated vasodilatations (Luk et al .…”

Section: Nitric Oxidementioning

confidence: 97%

Endothelial dysfunction and vascular disease - a 30th anniversary update

Vanhoutte¹,

et al. 2016

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The endothelium can evoke relaxations of the underlying vascular smooth muscle, by releasing vasodilator substances. The best-characterized endothelium-derived relaxing factor (EDRF) is nitric oxide (NO) which activates soluble guanylyl cyclase in the vascular smooth muscle cells, with the production of cyclic guanosine monophosphate (cGMP) initiating relaxation. The endothelial cells also evoke hyperpolarization of the cell membrane of vascular smooth muscle (endothelium-dependent hyperpolarizations, EDH-mediated responses). As regards the latter, hydrogen peroxide (H O ) now appears to play a dominant role. Endothelium-dependent relaxations involve both pertussis toxin-sensitive G (e.g. responses to α -adrenergic agonists, serotonin, and thrombin) and pertussis toxin-insensitive G (e.g. adenosine diphosphate and bradykinin) coupling proteins. New stimulators (e.g. insulin, adiponectin) of the release of EDRFs have emerged. In recent years, evidence has also accumulated, confirming that the release of NO by the endothelial cell can chronically be upregulated (e.g. by oestrogens, exercise and dietary factors) and downregulated (e.g. oxidative stress, smoking, pollution and oxidized low-density lipoproteins) and that it is reduced with ageing and in the course of vascular disease (e.g. diabetes and hypertension). Arteries covered with regenerated endothelium (e.g. following angioplasty) selectively lose the pertussis toxin-sensitive pathway for NO release which favours vasospasm, thrombosis, penetration of macrophages, cellular growth and the inflammatory reaction leading to atherosclerosis. In addition to the release of NO (and EDH, in particular those due to H O ), endothelial cells also can evoke contraction of the underlying vascular smooth muscle cells by releasing endothelium-derived contracting factors. Recent evidence confirms that most endothelium-dependent acute increases in contractile force are due to the formation of vasoconstrictor prostanoids (endoperoxides and prostacyclin) which activate TP receptors of the vascular smooth muscle cells and that prostacyclin plays a key role in such responses. Endothelium-dependent contractions are exacerbated when the production of nitric oxide is impaired (e.g. by oxidative stress, ageing, spontaneous hypertension and diabetes). They contribute to the blunting of endothelium-dependent vasodilatations in aged subjects and essential hypertensive and diabetic patients. In addition, recent data confirm that the release of endothelin-1 can contribute to endothelial dysfunction and that the peptide appears to be an important contributor to vascular dysfunction. Finally, it has become clear that nitric oxide itself, under certain conditions (e.g. hypoxia), can cause biased activation of soluble guanylyl cyclase leading to the production of cyclic inosine monophosphate (cIMP) rather than cGMP and hence causes contraction rather than relaxation of the underlying vascular smooth muscle.

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“…Using this model, Seeger et al explored the ability of exercise, similar to limb-ischaemic preconditioning, to prevent endothelial ischemia-reperfusion injury in vivo. 51 A single episode of interval, but not an isocaloric endurance, exercise induced protection against endothelial ischemia-reperfusion injury. While this observation indicates the potency of exercise preconditioning, it also raises questions regarding the stimuli mediating these responses.…”

Section: Can Exercise Training Precondition Arteries?mentioning

confidence: 99%