Aerobic exercise acutely prevents the endothelial dysfunction induced by mental stress among subjects with metabolic syndrome: the role of shear rate

Sales, Allan Robson Kluser; Fernandes, Igor A.; Rocha, Nazareth de Novaes; Costa, Lucas S. Nova da; Rocha, Helena; Mattos, João D.; Vianna, Lauro C.; Silva, Bruno M.; Nóbrega, Antônio Cláudio Lucas da

doi:10.1152/ajpheart.00811.2013

Cited by 26 publications

(31 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…) or induced by mental stress (Sales et al . ). Likewise, a single bout of lower limb interval exercise prevents endothelial dysfunction due to ischaemia–reperfusion injury (Seeger et al .…”

Section: Nitric Oxidementioning

confidence: 97%

Endothelial dysfunction and vascular disease - a 30th anniversary update

Vanhoutte¹,

et al. 2016

View full text Add to dashboard Cite

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.

show abstract

Section: Nitric Oxidementioning

confidence: 97%

Endothelial dysfunction and vascular disease - a 30th anniversary update

Vanhoutte¹,

et al. 2016

View full text Add to dashboard Cite

show abstract

“…Type 2 diabetes is associated with endothelial dysfunction as well as elevated retrograde SR (Gibbs et al, 2011). Increased SR is one of the key mechanisms that affect endothelial function (Sales et al, 2014).…”

Section: New Findingsmentioning

confidence: 99%

“…Type 2 diabetes is associated with endothelial dysfunction as well as elevated retrograde SR (Gibbs et al., ). Increased SR is one of the key mechanisms that affect endothelial function (Sales et al., ). Changes in blood flow and SR in conduit arteries of inactive limbs after acute exercise reflect adaptive vascular functioning induced by exercise (Iwamoto, Bock, & Casey, ).…”

Section: Introductionmentioning

confidence: 99%

Improved brachial artery shear patterns and increased flow‐mediated dilatation after low‐volume high‐intensity interval training in type 2 diabetes

Afousi

Izadi

Rakhshan

et al. 2018

Experimental Physiology

View full text Add to dashboard Cite

Atherosclerosis in patients with type 2 diabetes is characterized by endothelial dysfunction associated with impaired flow-mediated dilatation (FMD) and increases retrograde and oscillatory shear. The present study investigated endothelium-dependent vasodilatation and shear rate in patients with type 2 diabetes at baseline and follow-up after 12 weeks of low-volume high-intensity interval training (LV-HIIT) or continuous moderate-intensity training (CMIT). Seventy-five sedentary patients with type 2 diabetes and untreated pre- or stage I hypertension were randomly divided into LV-HIIT, CMIT and control groups. The LV-HIIT group intervention was 12 intervals of 1.5 min at 85-90% maximal heart rate (HR ) and 2 min at 55-60% HR . The CMIT group intervention was 42 min of exercise at 70% HR for three sessions per week during 12 weeks. High-resolution Doppler ultrasound was used to measure FMD, arterial diameter, anterograde and retrograde blood flow, and shear rate patterns. Brachial artery FMD increased significantly in the LV-HIIT group (3.83 ± 1.13 baseline, 7.39 ± 3.6% follow-up), whereas there was no significant increase in the CMIT group (3.45 ± 0.97 baseline, 4.81 ± 2.36% follow-up) compared to the control group (3.16 ± 0.78 baseline, 4.04 ± 1.28% follow-up) (P < 0.05). Retrograde shear in the LV-HIIT group decreased significantly (P < 0.05), and no significant decrease in retrograde shear was seen in the CMIT group. Anterograde shear after LV-HIIT increased significantly (P < 0.05) but was unchanged in the CMIT group. However, oscillatory shear index in both exercise groups decreased significantly (P = 0.029). Nitrite/nitrate (NOx) level increased in both exercise groups, but the increase was greater in the LV-HIIT group (P < 0.001). The results indicate that by increasing NOx, HIIT decreases the oscillatory shear-induced improvement in FMD and outward artery remodelling in patients with type 2 diabetes.

show abstract

“…Eligibility criteria for all were: age between 20 and 49 years, no smoking history, sedentary lifestyle, no diagnosis of chronic diseases (except MetS), no regular use of medications, and normal resting electrocardiogram. MetS was diagnosed following criteria of the Joint Interim Statement , as previously reported by our group . HCs did not present any MetS criteria.…”

Section: Methodsmentioning

confidence: 94%