scholarly journals GLP-1 and Insulin Recruit Muscle Microvasculature and Dilate Conduit Artery Individually But Not Additively in Healthy Humans

2018 ◽  
Vol 2 (2) ◽  
pp. 190-206 ◽  
Author(s):  
Alvin W K Tan ◽  
Sharmila C Subaran ◽  
Matthew A Sauder ◽  
Weidong Chai ◽  
Linda A Jahn ◽  
...  

Abstract Context Glucagon-like peptide-1 (GLP-1) and insulin increase muscle microvascular perfusion, thereby increasing tissue endothelial surface area and nutrient delivery. Objective To examine whether GLP-1 and insulin act additively on skeletal and cardiac microvasculature and conduit artery. Design Healthy adults underwent three study protocols in random order. Setting Clinical Research Unit at the University of Virginia. Methods Overnight-fasted participants received an intravenous infusion of GLP-1 (1.2 pmol/kg/min) or normal saline for 150 minutes with or without a 2-hour euglycemic insulin clamp (1 mU/kg/min) superimposed from 30 minutes onward. Skeletal and cardiac muscle microvascular blood volume (MBV), flow velocity, and flow; brachial artery diameter, flow velocity, and blood flow; and pulse wave velocity (PWV) were measured. Results GLP-1 significantly increased skeletal and cardiac muscle MBV and microvascular blood flow (MBF) after 30 minutes; these remained elevated at 150 minutes. Insulin also increased skeletal and cardiac muscle MBV and MBF. Addition of insulin to GLP-1 did not further increase skeletal and cardiac muscle MBV and MBF. GLP-1 and insulin increased brachial artery diameter and blood flow, but this effect was not additive. Neither GLP-1, insulin, nor GLP-1 and insulin altered PWV. Combined GLP-1 and insulin infusion did not result in higher whole-body glucose disposal. Conclusion GLP-1 and insulin at physiological concentrations acutely increase skeletal and cardiac muscle microvascular perfusion and dilate conduit artery in healthy adults; these effects are not additive. Thus, GLP-1 and insulin may regulate skeletal and cardiac muscle endothelial surface area and nutrient delivery under physiological conditions.

2014 ◽  
Vol 127 (3) ◽  
pp. 163-170 ◽  
Author(s):  
Sharmila C. Subaran ◽  
Matthew A. Sauder ◽  
Weidong Chai ◽  
Linda A. Jahn ◽  
Dale E. Fowler ◽  
...  

GLP-1 increases microvascular perfusion in both skeletal and cardiac muscle, and brachial artery diameter and blood flow in humans. These vascular actions may contribute to the beneficial actions of the GLP-1 receptor analogues.


2007 ◽  
Vol 293 (5) ◽  
pp. E1250-E1255 ◽  
Author(s):  
Zhenqi Liu

Vascular endothelium regulates vascular tone and tissue perfusion in response to various physiological and pathological stimuli. Insulin and meal feeding increase microvascular perfusion and thus oxygen, nutrient, and hormone delivery to human skeletal muscle. Meal feeding also increases cardiac microvascular perfusion in healthy humans. To examine whether insulin at physiological concentrations increases microvascular perfusion in human myocardium, we studied 13 healthy, overnight-fasted, lean, young human volunteers by using myocardial contrast echocardiography (MCE) and insulin-clamp techniques. We measured cardiac microvascular blood volume (MBV), microvascular flow velocity (MFV), and microvascular blood flow (MBF) at baseline, 60 min, and 120 min after initiating insulin infusion at 1 mU·kg−1·min−1. MBF is the product of MBV and MFV and represents microvascular perfusion. Insulin increased myocardial MBV by 23% at 60 min ( P < 0.01) and by 41% at 120 min ( P = 0.001) without changing MFV. As a result, insulin-mediated myocardial MBF increased significantly at both 60 min ( P < 0.01) and 120 min ( P < 0.0005). Insulin also significantly increased brachial artery diameter, flow velocity, and total blood flow at 60 and 120 min ( P < 0.05 for all). The changes in cardiac MBV correlated positively with quantitative insulin sensitivity check index (QUICKI) and negatively with body mass index but not with the steady-state glucose-infusion rates or the changes in brachial artery parameters. We conclude that insulin, at physiologically relevant concentrations, increases microvascular perfusion in human heart muscle by increasing cardiac MBV in healthy, insulin-sensitive adults. This insulin-mediated cardiac microvascular perfusion may play an important role in normal human myocardial oxygen and substrate physiology.


2005 ◽  
Vol 98 (6) ◽  
pp. 2311-2315 ◽  
Author(s):  
Louise H. Naylor ◽  
Cara J. Weisbrod ◽  
Gerry O'Driscoll ◽  
Daniel J. Green

The purpose of this study was to establish valid indexes of conduit and resistance vessel structure in humans by using edge detection and wall tracking of high-resolution B-mode arterial ultrasound images, combined with synchronized Doppler waveform envelope analysis, to calculate conduit artery blood flow and diameter continuously across the cardiac cycle. Nine subjects aged 36.7 (9.2) yr underwent, on separate days, assessment of brachial artery blood flow and diameter response to 5-, 10-, and 15-min periods of forearm ischemia in the presence and absence of combined sublingual glyceryl trinitrate (GTN) administration. Two further sessions examined responses to ischemic exercise, one in combination with GTN. The peak brachial artery diameter was observed in response to the combination of ischemic exercise and GTN; a significant difference existed between resting brachial artery diameter and peak brachial artery diameter, indicating that resting diameter may be a poor measure of conduit vessel structure in vivo. Peak brachial artery flow was also observed in response to a combination of forearm ischemia exercise and GTN administration, the response being greater than that induced by periods of ischemia, GTN, or ischemic exercise alone. These data indicate that noninvasive indexes of conduit and resistance vessel structure can be simultaneously determined in vivo in response to a single, brief, stimulus and that caution should be applied in using resting arterial diameter as a surrogate measure of conduit artery structure in vivo.


2012 ◽  
Vol 112 (6) ◽  
pp. 956-961 ◽  
Author(s):  
Julie E. A. Hunt ◽  
Lucy A. Walton ◽  
Richard A. Ferguson

Low load resistance training with blood flow restriction (BFR) can increase muscle size and strength, but the implications on the conduit artery are uncertain. We examined the effects of low-load dynamic handgrip training with and without BFR, and detraining, on measures of brachial artery function and structure. Nine male participants (26 ± 4 yr, 178 ± 3 cm, 78 ± 10 kg) completed 4 wk (3 days/wk) of dynamic handgrip training at 40% 1 repetition maximum (1RM). In a counterbalanced manner, one forearm trained under BFR (occlusion cuff at 80 mmHg) and the other under nonrestricted (CON) conditions. Brachial artery function [flow-mediated dilation (FMD)] and structure (diameter) were assessed using Doppler ultrasound. Measurements were made before training (pretraining), after training (posttraining), and after 2-wk no training (detraining). Brachial artery diameter at rest, in response to 5-min ischemia (peak diameter), and ischemic exercise (maximal diameter) increased by 3.0%, 2.4%, and 3.1%, respectively, after BFR training but not after CON. FMD did not change at any time point in either arm. Vascular measures in the BFR arm returned to baseline after 2 wk detraining with no change after CON. The data demonstrate that dynamic low-load handgrip training with BFR induced transient adaptations to conduit artery structure but not function.


Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Daniela K Andaku ◽  
Bruno Archiza ◽  
Flavia C Caruso ◽  
Katiany T Zangrando ◽  
Humberto Lanzotti ◽  
...  

Background: Recent evidence has indicated a ceiling to the benefits of exercise training that, if chronically surpassed, may have a negative effect on cardiac function. Conversely, improvements in peripheral arterial function may respond positively to chronic high volume training. Recent studies have shown that flow-mediated dilation (FMD) is decreased immediately after maximal exercise in sedentary subjects and is unaltered in subjects who participate in moderate volume exercise. We investigated the acute effects of maximal exercise on vascular function of elite female athletes with a high-volume training history. Methods: Fifteen elite female soccer players (mean age: 22.1 ± 4.4 years; BMI: 20.76 ± 1.75 kg/m2), with a high volume/intensity training history (4-6 hours per day) were evaluated. Subjects underwent maximal cardiopulmonary exercise testing (CPX) on a treadmill (VO2max 41.1 ± 3.9 mLO2•kg-1•min-1). Brachial artery FMD was determined using high-resolution ultrasound before and immediately after CPX. Flow velocity were measured at baseline (BSL) and during reactive hyperemia (RH) both prior to and following exercise. Results: Brachial artery diameter increased during RH before (3.42 ± 0.38mm vs. 3.03 ± 0.28mm, p<0.001) and after CPX (3.61 ± 0.44mm vs. 3.10 ± 0.37mm, p<0.001). Importantly, FMD was increased following CPX compared to BSL (16.86 ± 9.04% vs. 12.95 ± 7.03%, p=0.027). There was significant increase in peak flow velocity during RH before (135.28 ± 42.19cm/s vs. 79.19 ± 28.14cm/s, p=0.001) and after CPX (139.15 ± 41.07cm/s vs. 87.64 ± 21.23cm/s, p<0.001) (Table). Conclusion: The results of the current study indicate that arterial function is improved following acute aerobic exercise in elite female athletes with a chronic high volume training history. These findings deviate from the emerging literature suggesting chronic high volume training may be detrimental to cardiovascular function in the long term.


2019 ◽  
Vol 97 (10) ◽  
pp. 1006-1011
Author(s):  
Ayelen Rodriguez-Portelles ◽  
Delfin Rodriguez-Leyva

Smoking is associated with endothelial and left ventricular diastolic disfunction. We aimed to determine the endothelial and diastolic function in young adults exposed to tobacco smoke and the effects of acute exposure to it. Smokers were considered as cases and non-smokers as controls. Brachial artery diameter, brachial artery flow velocity, and echocardiographic variables were measured. Mean age of the participants was 21 years. Smokers showed significant endothelial dysfunction compared with non-smokers. Arterial dilation mediated by the endothelium was significantly higher in non-smokers than in smokers (p = 0.005). Non-endothelium-mediated arterial dilation was significantly impaired in smokers compared with non-smokers (p = 0.02). After reactive hyperaemia, there was a significant increase in blood flow in non-smokers (61%) compared with that in smokers (29%). Acute cigarette exposure showed a trend towards left ventricle diastolic disfunction in smokers. Left atrium diameter was significantly higher in smokers than in non-smokers. After acute exposure to cigarette smoke, arterial dilation and brachial flow velocity were lower than those achieved in the abstinence phase (p = 0.005). We concluded that endothelium-dependent arterial dilation is impaired in young smokers and it worsens even after acute exposure to cigarette smoke.


2012 ◽  
Vol 32 (3) ◽  
pp. 227-233 ◽  
Author(s):  
Susann J. Järhult ◽  
Tomas Hansen ◽  
Håkan Ahlström ◽  
Lars Johansson ◽  
Johan Sundström ◽  
...  

2009 ◽  
Vol 14 (4) ◽  
pp. 351-360 ◽  
Author(s):  
Hassan A Chami ◽  
Michelle J Keyes ◽  
Joseph A Vita ◽  
Gary F Mitchell ◽  
Martin G Larson ◽  
...  

2000 ◽  
Vol 99 (4) ◽  
pp. 261-267 ◽  
Author(s):  
Karen L. BERRY ◽  
R. Andrew P. SKYRME-JONES ◽  
Ian T. MEREDITH

Non-invasive ultrasound techniques to assess flow-mediated vasodilation (FMD) are frequently used to assess arterial endothelial vasodilator function. However, the range of normal values varies considerably, possibly due to differences in methodological factors. We sought to determine the effect of occlusion cuff position on the time course and magnitude of brachial artery blood flow and flow-mediated dilation. Twelve healthy subjects underwent measurements of forearm blood flow using venous occlusion plethysmography (VOP) before and after 5 min of susprasystolic cuff inflation, using two randomly assigned occlusion cuff positions (upper arm and forearm). An additional 16 subjects underwent two brachial ultrasound studies, using the two cuff positions, to assess the extent and time course of changes in brachial artery diameter and blood flow. Maximum increase in blood flow (peak reactive hyperaemia), measured by VOP, occurred immediately upon each cuff deflation, but was greater after upper arm compared with forearm arterial occlusion (33.1±3.1 versus 22.8±2.2 ml/min per forearm tissue, P = 0.001). Maximal brachial artery FMD was significantly greater following upper arm occlusion (9.0±1.2%, mean±S.E.M.) compared with forearm occlusion (5.9±0.7%, P = 0.01). The time course of the change in brachial artery diameter was affected differently in response to each protocol. The time to peak dilation following upper arm occlusion was delayed by 22 s compared with forearm occlusion. Occlusion cuff position is thus a powerful determinant of peak reactive hyperaemia, volume repaid and the extent and time course of brachial artery FMD. Positioning the cuff on the upper arm produces a greater FMD. These results highlight the need for comparisons between FMD studies to be made with care.


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