The negative effects of chronic hypertension on vascular endothelial function are well documented; however, less is understood about the effects of transient elevations in blood pressure on vascular reactivity. Fluctuations in blood pressure occur on a minute-to-minute basis throughout daily living, and more dramatically, blood pressure substantially increases during resistance exercise (19). In a landmark study by Lamping and Dole (18), brief exposure to hypertension (1–5 min) was sufficient to potentiate vasoconstriction in the coronary vasculature, and this potentiation could last for at least 2.5 h. This raises the question whether elevations in blood pressure that occur with isometric exercise also impair endothelial function in human conduit and resistance arteries. This is important because systolic blood pressure can surpass 400 mm Hg during high-intensity isometric exercise (19). Consistent with this observation, when young, healthy sedentary (SED) subjects perform resistance exercise at maximal effort, significant increases in systolic blood pressure are observed along with the impairment of both endothelium-dependent brachial artery flow-mediated dilation (FMD) (9,10,16,23) and microvascular vasodilation in response to acetylcholine (8).
In a review of the effects of acute exercise on FMD in healthy humans by Dawson et al. (5), there appears to be a biphasic FMD pattern in response to exercise that varies according to fitness level, exercise duration, intensity, and mode. Previous work from our group and others would support the idea that fitness level predicts the FMD response after maximal-exertion exercise, as exercise-trained (ET) individuals are protected from reductions in conduit and resistance artery function postexercise whereas young, healthy SED subjects are not (8,16). Although the specific mechanism responsible for the protective effect of exercise training on endothelial function is not known, it is well established that exercise increases endothelial nitric oxide synthase (12) and superoxide dismutase enzyme expression (24), both of which would increase nitric oxide bioavailability.
The reduction in FMD in SED subjects could be explained by either barotrauma to the brachial artery from the rise in arterial pressure during exercise (8,16,23) or possibly because of the exercise-induced release of neurohumoral agents and catecholamines (1,7) that reduce nitric oxide bioavailability. In addition, exercise acutely increases numerous factors that can also have direct vasoconstrictor properties, including angiotensin II (21), endothelin 1 (20), and norepinephrine (7). The purpose of this study is to determine whether the rise in intraluminal pressure contributes to the impaired FMD after resistance exercise in healthy SED subjects. We aimed to measure brachial artery FMD in young SED subjects who have a cuff around the upper arm inflated to 100 mm Hg during a leg bench press exercise to protect the distal brachial artery from the exercise-induced increase in intra-arterial pressure. Because the inflation pressure of the cuff is never greater than the systolic pressure, neither at rest nor during exercise, the distal vasculature of the cuffed arm will still be exposed to the same circulating factors. Our hypothesis is that increased intraluminal pressure within the brachial artery is responsible for impaired FMD after resistance exercise in healthy SED subjects.
All subjects issued written informed consent before any study procedures, and all methods were approved by the Institutional Review Board at the Medical College of Wisconsin.
Nine SED and six ET healthy male and female subjects between the ages of 18 and 38 yr were recruited by posting flyers at local universities and through Craigslist advertisement. All subjects acted as their own controls. Our study defined healthy individuals as having no known history of cardiovascular disease and a body mass index ≤25 kg·m−2. SED subjects included individuals who self-reported regular strength and resistance exercises once a week or less for at least the past 6 months. ET subjects included individuals who self-reported concurrent strength and resistance exercises three times a week or more for at least the past 6 months. Exclusion criteria for all subjects included hypercholesterolemia (total cholesterol >200 mg·dL−1), hypertension (resting blood pressure >140/90 mm Hg), diabetes (blood glucose >200 mg·dL−1), tobacco use in the previous 6 months, subjects who were currently abusing alcohol or drugs, history of lower extremity injury, and female subjects who were pregnant or nursing. All subjects had a skinfold test performed by the same licensed nutritionist to determine percent body fat. The average of three measurements at selected anatomical skinfold sites based on sex were used to estimate body density. Each body density measurement was then used in a population specific equation for either men (14) or women (15) to estimate body fat percent. All skinfold measurements were taken with a Lange Skinfold Caliper (Beta Technology Inc., Santa Cruz, CA).
Weight Lifting Protocol
All subjects were instructed to fast for 12 h before each study visit and asked to abstain from exercise for 48 h before their visit. Each subject performed the same weight lifting protocol during both study visits, and the visits were separated by at least 7 d to allow for recovery. Before the lifting protocol, subjects were instructed to stretch their leg muscles for approximately 5 min to avoid injury.
The weight lifting protocol was performed on a recumbent leg press machine. Subjects performed two sets each of 10 repetitions of leg press exercise at 35%, 50%, and 90% of their approximate one-repetition maximum or until fatigue as previously described (16). Briefly, after each set of 10 lifts, subjects were asked to rate their perceived level of exertion on a 10-point scale. Weight was then added to the next set of lifts at the discretion of the study team. All subjects performed repetitions until failure on the last two sets of lifts. On the last repetition of each set, subjects were instructed to continue to breathe regularly and perform an isometric hold with the knees bent at approximately 45° while blood pressure was measured in the left arm using a sphygmomanometer and stethoscope.
During one of the visits, a second blood pressure cuff was placed proximal to the site of brachial artery measurement and inflated to 100 mm Hg to protect the distal vasculature from the acute rise in blood pressure observed during weight lifting exercise. A cuff inflation pressure of 100 mm Hg was chosen based on studies which demonstrated that upper arm cuff inflation pressures of 60 and 100 mm Hg blunted increased shear stress during handgrip exercise (27) and reactive hyperemia in response to forearm heating (11), respectively. The placement of the “protective” cuff on visit one or two was randomized for all participants. The cuff remained inflated for 1 min after the last repetition of each set of 10 lifts to allow adequate time for blood pressure to return to baseline values. After 1 min, the cuff was then released for a period of 1 min before the next set of weight lifting to avoid venous engorgement in the test arm. To confirm that a cuff inflation pressure of 100 mm Hg on the upper arm blunted the rise in systolic pressure in the distal vasculature during maximal exertion, in a separate group of five healthy individuals, blood pressure was measured distal to the protective cuff by determining the pressure at which the radial pulse returned after forearm occlusion with a blood pressure cuff.
Brachial Artery FMD Protocol
All FMD procedures were performed in a temperature-controlled room between the hours of 7:00 a.m. and 9:00 a.m., and all subjects had been fasting for ≥12 h. Subjects reported to the study site and were instructed to lie quietly in a supine position for 15 min before beginning FMD assessment. In the supine state, imaging of the brachial artery on the right arm was performed by the same person each visit using a Sonosite MicroMaxx (Bothell, WA) portable ultrasound machine. The brachial artery was visualized in a longitudinal plane at a site proximal to the antecubital fossa of the supinated right arm abducted ~80°. The ultrasound probe (10.5 mHz) was positioned at 90° to the vessel to visualize anterior and posterior lumen–intimal interfaces. Three 6-s video clips of the brachial artery were recorded to determine resting artery diameter, and one Doppler image of arterial blood flow was captured to compare baseline and peak hyperemic flow responses in the artery. The clips and images were stored on the ultrasound machine for offline analysis. After recording baseline images, a forearm blood pressure cuff was inflated to 250 mm Hg for 5 min. After releasing the cuff, brachial artery flow velocity was measured during peak hyperemia, and 6-s clips of brachial artery diameter were recorded every minute for 5 min after cuff release. The probe position was marked with a surgical pen to ensure transducer placement over the brachial artery was consistent between measurements. The probe position in relation to the antecubital fossa was also recorded to ensure the same segment of the brachial artery was visualized during the second visit.
The postlift FMD was assessed approximately 30 min after the weight lifting session. After the second FMD assessment, endothelium-independent vasodilation was determined by administering 0.4 mg sublingual nitroglycerin (NTG) and recording the change in brachial artery diameter after 3, 4, and 5 min.
Brachial artery diameter was measured using the automatic edge detection feature of Brachial Analyzer (Medical Imaging Applications LLC, Coralville, IA) at a sampling rate of 10 frames per second. The resting diameter of the brachial artery was determined by averaging the values of the three resting measurements. Peak FMD was determined by reporting the largest value from the average resting diameter. The brachial artery was remeasured 10 min postcuff release to determine average resting baseline diameter before NTG administration. NTG-mediated dilation was determined by reporting the largest value from the new series of baseline measurements. Percent change in FMD was defined as 100 × (maximum diameter during reactive hyperemia − resting diameter)/resting diameter. Peak brachial artery shear stress was calculated using the following equation (2,6,28,29): shear rate (s−1) = 4 × blood velocity (cm·s−1)/vessel diameter (cm).
All data are presented as mean ± SEM. Differences between subjects were determined using an unpaired Student's t-test. Differences in pre- and postlift FMD and NTG-mediated dilation as well as pre- and postlift hemodynamic values were determined using a two-way repeated-measures ANOVA with the presence of the cuff and weight lifting as independent variables. A post hoc Student–Newman–Keuls test was used to determine differences between individual means. To determine the effect size of either weight lifting or the presence of the cuff during weight lifting, Cohen's d was calculated using the means and standard deviations of FMD before and after the lifting exercise. An ANCOVA was performed to test if covariates affected the FMD response after weight lifting. P < 0.05 was considered statistically significant.
Previous studies by Phillips et al. (23) and Jurva et al. (16) have shown that relative brachial FMD is reduced between 29% and 65% from prelift values in SED subjects with similar inclusion criteria who undergo leg press exercise to maximal exertion (absolute FMD was reduced in those studies by 2.3% and 4.7%, respectively). On the basis of these effect sizes, and an interobserver variation of 1.3% ± 0.7% for repeated measures from our group using the FMD method described previously (25), our sample size of SED subjects (n = 9) could detect a relative difference in FMD of 20% (or an absolute difference of 1.6% assuming a prelift FMD of 8.0%) with 80% power and α = 0.05 using paired analysis.
Nine SED (two males and seven females) and six ET subjects (three males and three females), ages 18–38 yr, were consented and completed the study protocol (Table 1). Two SED subjects (one male and one female) were screened but not enrolled in the study because they had total cholesterol levels >200 mg·dL−1.
The maximum weight lifted during the session with the protective upper arm blood pressure cuff was 122 ± 5.9 kg for the SED group and 140 ± 12.2 kg for the ET group (P = 0.175) (Table 1). Similarly, the maximum weight lifted during the session without the protective cuff was 119 ± 8.8 kg for SED group and 142 ± 10.8 kg for the ET group (P = 0.132).
The maximum systolic blood pressure measured during the isometric hold during the session without the protective cuff was 194 ± 8 mm Hg and 235 ± 11 mm Hg for the SED and ET subjects, respectively (P = 0.010) (Table 1). The presence of the protective cuff had no effect on maximum systemic systolic blood pressure measured in the opposite uncuffed arm in either group (SED 194 ± 8 mm Hg without cuff vs 198 ± 10 mm Hg with cuff, P = 0.350; ET 235 ± 11 mm Hg without cuff vs 235 ± 7 mm Hg with cuff; P = 0.964). We confirmed that the inflation of the upper arm cuff to 100 mm Hg reduced distal systolic blood pressure in the cuffed arm in a subset of five healthy subjects (two males and three females; age = 27 ± 2.0 yr, body mass index = 24 ± 1.5, resting SBP = 110 ± 4 mm Hg) during consecutive maximal-exertion lifts (maximum weight lifted = 123 ± 9.0 kg). The upper arm cuff reduced distal systolic blood pressure by 64 ± 12 mm Hg in these subjects (159 ± 4 mm Hg without cuff vs 94 ± 13 mm Hg with cuff, P = 0.005).
Without the protective cuff, brachial artery FMD in SED subjects was reduced after weight lifting (9.0% ± 1.2% prelift vs 6.6% ± 0.8% postlift; P = 0.005), whereas in ET individuals FMD was unchanged (7.4% ± 0.7% prelift vs 8.0% ± 0.9% postlift; P = 0.543) (Fig. 1). With the protective cuff, FMD increased in both SED (8.7% ± 1.2% prelift vs 10.5% ± 1.0% postlift; P = 0.025) and ET (6.6% ± 0.7% prelift vs 10.9% ± 1.5% postlift; P < 0.001) subjects (Fig. 1). Of the cardiometabolic factors presented in Table 1, percent body fat was found to be the only covariate that had an influence on the FMD response after weight lifting. The absolute change in brachial artery FMD in SED and ET individuals after weight lifting ± the protective cuff is shown in Figure 2. When the protective cuff was present, FMD increased after weight lifting in both groups compared with prelift values.
The presence of the protective cuff during the lifting protocol had no effect on peak hyperemic shear stress (immediately postcuff release) during the FMD protocol performed 30 min after lifting (Table 2). When FMD was normalized to peak shear stress, both ET and SED subjects still demonstrated augmented FMD when the protective cuff was present during the lifting protocol. Endothelium-independent vasodilation was unaffected by either weight lifting or blood pressure cuff as all subjects demonstrated appropriate and similar endothelial-independent vasodilation (≥20% in all groups) after NTG administration (Table 2). There were also no differences in NTG-mediated dilation between SED and ET subjects. Peak hyperemic shear stress after the release of the cuff was also not different between SED and ET subjects, or between cuff- and no-cuff sessions.
Table 3 shows the effect size of weight lifting and the presence of the protective cuff on FMD in SED and ET subjects as estimated by the Cohen method. This analysis indicates that resistance exercise (without the protective cuff) had a larger effect on FMD in SED subjects (d = 0.78) compared with ET subjects (d = 0.27). Conversely, although the lifting session had a positive and medium-to-large effect on FMD in both groups when the cuff was present, the larger effect was observed in ET subjects compared with SED subjects (d = 1.49 and 0.55, respectively). This is in agreement with the larger increase in FMD, which was observed in ET subjects when the protective cuff was present (Fig. 2). When comparing postlift FMD in SED and ET subjects with and without the protective cuff, a large-to-very large effect of the cuff was seen in both groups (d = 1.43 and 0.96, respectively).
Previously, we have shown that systemic endothelial-dependent vasodilation is impaired in healthy SED subjects, but not ET subjects, after they perform isometric exercise to maximal exertion (8,16,23). The major finding of this study is that the impairment in SED subjects is abrogated when the brachial artery is protected from the marked rise in blood pressure that occurs with weight lifting, indicating that the barostress on the vessel is responsible for the reduced brachial FMD observed in SED subjects after maximal exertion.
This is the first study to our knowledge to control systolic blood pressure to a limb during high-intensity isometric exercise. Interestingly, when the rise in blood pressure within the brachial artery during exercise was blunted, an increase in brachial artery FMD was observed in both athletes and nonathletes, indicating that in the absence of increased intra-arterial pressure within the arm during exertion, vascular endothelial function is augmented in both groups. This observation is consistent with numerous studies (as reviewed by Dawson et al. (5) that demonstrate postexercise FMD is augmented after medium- to light-intensity aerobic exercise (where the pressor response is low) but reduced in high-intensity aerobic and resistance exercise (where the pressor response is high). The increased FMD seen in both ET and SED groups could be explained by a systemically circulating dilatory factor whose effect dominates in the vasculature which was not exposed to the high intraluminal pressures during maximal-exertion resistance exercise. Alternatively, it has been proposed that acute, high shear levels during acute bouts of hypertension directly reduce NO release from the endothelium (3,5), although this hypothesis has not been explored in terms of exercise-induced FMD changes.
Atkinson et al. (1) demonstrated that alpha-one adrenoreceptor blockade with prazosin during cycle ergometer exercise prevented exercise-induced reductions in FMD, suggesting a competing mechanism between sympathetic constriction and endothelium-dependent dilator capacity. In that study, it should be noted that mean arterial pressure during exercise was lower in prazosin-treated subjects; however, this finding was not statistically significant, possibly because of the relatively small sample size of 10 individuals. The results from that study, in addition to our data, would indicate a possible combined mechanism of increased sympathetic activity with elevated intraluminal pressure as the critical factors for reducing FMD after maximum effort resistance exercise. Our data would however suggest it is primarily the increased intra-arterial pressure that is responsible for reducing FMD as the brachial artery was exposed to the same levels of circulating factors in both the cuff and the no-cuff sessions.
Our findings suggest that a gradual approach should be undertaken (from the standpoint of systemic vascular endothelial function) when initiating resistance exercise training in an untrained individual. ET individuals, in contrast, are protected from the negative effects of exercise-induced hypertension on the vasculature (8,16,23). This begs the question of whether repeated exposures to high arterial pressure are necessary to condition the vasculature to maintain vasodilation after maximal exertion. Because the time necessary for this conditioning process to occur has yet to be determined, more gradual resistance training programs should be recommended for previously SED subjects to limit the potential for damage which occurs to the vascular endothelium during the initial training period.
We recognize several limitations in our study. First, the sample size of nine SED and six ET subjects is small. Previous studies by Jurva et al. (16) and Phillips et al. (23) have demonstrated that FMD is reduced in SED subjects after leg press exercise to maximal exertion, whereas FMD is maintained in ET subjects. The goal of this study was to determine whether protecting the distal vasculature from barostress during the same lifting protocol using a protective cuff would result in maintained or augmented FMD in SED and ET subjects. As shown by the individual responses plotted in Figure 1, FMD increased in 8/9 SED and 6/6 ET subjects; therefore, it is unlikely that increasing enrollment numbers would change the interpretation of our findings. Our study was also not designed to examine gender-specific differences in FMD or blood pressure, so our relatively small sample size does preclude this analysis.
A second limitation was that brachial artery diameter and Doppler flow were not continuously measured postcuff release per established guidelines (26); thus, the time to peak dilation and the total shear rate (area under the curve) were not calculated. As shown in Table 2, peak hyperemic shear stress immediately after cuff release did not change either after weight lifting or when the protective cuff was present during the lifting protocol. When FMD was normalized to peak shear stress, normalized FMD was still greater in the cuff versus no-cuff session in both ET and SED subjects. Although continuous measurement of arterial diameter may give a more robust measure of FMD (26), measurements of diameter at 1, 2, and 3 min postcuff release have been shown to have high levels of agreement with traditional QRS-gated continuous measurements. Thus, it is unlikely that the peak FMD response was underestimated (17).
We did not control the stage in the menstrual cycle when female subjects participated. Because subjects served as their own controls, and FMD responses were only compared with pre- and postlift values taken on the same day, the effects of hormone changes during the different stages of menses are expected to be minimal.
A final limitation of the study is that NTG-mediated dilation was not tested after the first FMD procedure and before weight lifting to avoid lingering effects of the drug on the second FMD measurement, and potentially the pressor response during lifting. All subjects showed robust dilation to NTG (>20%) after weight lifting, so it is unlikely that weight lifting reduced endothelium-independent vasodilation compared with normal prelift values.
This is the first study to our knowledge that directly examines the effects of increased arterial pressure on endothelium-dependent dilation after maximal-exertion resistance exercise. It is well established by our group (8,16,23) and by others (9,10) that high-intensity resistance exercise causes both increases in systolic blood pressure and a postexercise decline in endothelial function in untrained subjects. As the results of this study indicate, when the blood pressure increase is prevented in a controlled limb, FMD in that limb increases in both SED and ET subjects. This response is similar to what is observed in subjects after low- to moderate-intensity aerobic exercise (4,13,22), during which systolic blood pressure does not significantly increase. Together, these findings suggest that a circulating prodilatory factor may be present, and its effects are dampened by the increased barostress on the blood vessels which occurs during weight lifting.
This project was supported by the National Center for Advancing Translational Sciences, National Institutes of Health, through grant number 8UL1TR000055 and the National Institutes of Health Training Grant T35 HL072483. Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the National Institutes of Health. The authors thank the staff at the Sports Medicine Center at the Medical College of Wisconsin for allowing the use of their facilities and leg press machine. They also thank the nursing and bionutritional staff at the Translational Research Unit of the Medical College of Wisconsin for performing anthropomorphic measurements of all subjects and administrating NTG.
The authors have no conflicts of interest to disclose. The results of the present study do not constitute endorsement by the American College of Sports Medicine. The results of the study are presented clearly, honestly, and without fabrication, falsification, or inappropriate data manipulation.
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Keywords:© 2017 American College of Sports Medicine
EXERCISE; ENDOTHELIUM; VASODILATION; BRACHIAL ARTERY