Literature DB >> 21252216

Resistance and aerobic exercise protects against acute endothelial impairment induced by a single exposure to hypertension during exertion.

Shane A Phillips1, Emon Das, Jingli Wang, Kirkwood Pritchard, David D Gutterman.   

Abstract

Resistance and aerobic exercise is recommended for cardiovascular health and disease prevention. However, the accompanying increase in arterial pressure during resistance exercise may be detrimental to vascular health. This study tests the vascular benefits of aerobic compared with resistance exercise on preventing impaired vascular function induced by a single weight lifting session that is associated with acute hypertension. Healthy, lean sedentary (SED) subjects, weight lifters, runners (>15 miles/wk), and cross trainers (chronic aerobic and resistance exercisers), underwent a single progressive leg press weight lifting session with blood pressure measurements. Brachial artery flow-mediated vasodilation (FMD; an index of arterial endothelial function) was determined using ultrasonography immediately before and after weight lifting. Sublingual nitroglycerin (0.4 mg) was used to determine endothelium-independent dilation after weight lifting. All subjects were normotensive with similar blood pressure responses during exercise. Baseline FMD was lower in runners (5.4 ± 0.5%; n = 13) and cross trainers (4.44 ± 0.3%; n = 13) vs. SED (8.5 ± 0.8%; n = 13; P = 0.037). Brachial FMD improved in conditioned weight lifters (to 8.8 ± 0.9%; P = 0.007) and runners (to 7.6 ± 0.6%; P < 0.001) but not cross trainers (to 5.3 ± 0.6%; P = NS) after acute hypertension. FMD was decreased in SED (to 5.7 ± 0.4%; P = 0.019). Dilation to nitroglycerin was similar among groups. These data suggest that endothelial responses are maintained after exposure to a single bout of weight lifting in resistance and aerobic athletes. Resistance and aerobic exercise may confer similar protection against acute vascular insults such as exertional hypertension.

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Year:  2011        PMID: 21252216      PMCID: PMC3075126          DOI: 10.1152/japplphysiol.00438.2010

Source DB:  PubMed          Journal:  J Appl Physiol (1985)        ISSN: 0161-7567


  48 in total

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4.  Ultrasound assessment of flow-mediated dilation.

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  39 in total

1.  Acute exertion elicits a H2O2-dependent vasodilator mechanism in the microvasculature of exercise-trained but not sedentary adults.

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2.  Relationship between muscle sympathetic nerve activity and aortic wave reflection characteristics in aerobic- and resistance-trained subjects.

Authors:  Michael M Smith; C A Tony Buffington; Robert L Hamlin; Steven T Devor
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3.  An acute rise in intraluminal pressure shifts the mediator of flow-mediated dilation from nitric oxide to hydrogen peroxide in human arterioles.

Authors:  Andreas M Beyer; Matthew J Durand; Joseph Hockenberry; T Clark Gamblin; Shane A Phillips; David D Gutterman
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4.  Circuit resistance training attenuates acute exertion-induced reductions in arterial function but not inflammation in obese women.

Authors:  Nina C Franklin; Austin T Robinson; Jing-Tan Bian; Mohamed M Ali; Edita Norkeviciute; Patrick McGinty; Shane A Phillips
Journal:  Metab Syndr Relat Disord       Date:  2015-04-06       Impact factor: 1.894

5.  The vascular renin-angiotensin system contributes to blunted vasodilation induced by transient high pressure in human adipose microvessels.

Authors:  Matthew J Durand; Shane A Phillips; Michael E Widlansky; Mary F Otterson; David D Gutterman
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Review 10.  Diversity in mechanisms of endothelium-dependent vasodilation in health and disease.

Authors:  Matthew J Durand; David D Gutterman
Journal:  Microcirculation       Date:  2013-04       Impact factor: 2.628

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