Attenuated forearm vascular conductance responses to rhythmic handgrip in young African-American compared with Caucasian-American men

Previous studies have demonstrated that African-American (AA) individuals have heightened vasoconstrictor and reduced vasodilator responses under resting conditions compared with Caucasian-American (CA) individuals. However, potential differences in vascular responses to exercise remain unclear. Therefore, we tested the hypothesis that, compared with CA subjects, AA subjects would present an attenuated increase in forearm vascular conductance (FVC) during rhythmic handgrip exercise. Forearm blood flow (FBF; duplex Doppler ultrasound) and mean arterial pressure (MAP; finger photoplethysmography) were measured in healthy young CA ( n = 10) and AA ( n = 10) men during six trials of rhythmic handgrip performed at workloads of 4, 8, 12, 16, 20, and 24 kg. FVC (calculated as FBF/MAP), FBF, and MAP were similar between groups at rest (FVC: 63 ± 7 ml·min−1·100 mmHg−1 in CA subjects vs. 62 ± 7 ml·min−1·100 mmHg−1 in AA subjects, P = 0.862). There was an intensity-dependent increase in FVC during exercise in both groups; however, AA subjects presented lower FVC (interaction P < 0.001) at 8-, 12-, 16-, 20-, and 24-kg workloads (e.g., 24 kg: 324 ± 20 ml·min−1·100 mmHg−1 in CA subjects vs. 241 ± 21 ml·min−1·100 mmHg−1 in AA subjects, P < 0.001). FBF responses to exercise were also lower in AA subjects (interaction P < 0.001), whereas MAP responses did not differ between groups (e.g., ∆MAP at 24 kg: +19 ± 2 mmHg in CA subjects vs. +19 ± 2 mmHg in AA subjects, interaction P = 0.950). These findings indicate lower hyperemic responses to rhythmic handgrip exercise in AA men compared with CA men. NEW & NOTEWORTHY It is known that African-American individuals have heightened vasoconstriction and reduced vasodilation under resting conditions compared with Caucasian-American individuals. Here, we identified that the hyperemic response to moderate and high-intensity rhythmic handgrip exercise was lower in healthy young African-American men.

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Hypohydration affects forearm vascular conductance independent of heart rate during exercise

Journal of Applied Physiology ◽

10.1152/jappl.1992.73.4.1232 ◽

1992 ◽

Vol 73 (4) ◽

pp. 1232-1237 ◽

Cited By ~ 9

Author(s):

C. G. Tankersley ◽

D. H. Zappe ◽

T. G. Meister ◽

W. L. Kenney

Keyword(s):

Heart Rate ◽

Blood Flow ◽

Mean Arterial Pressure ◽

Forearm Blood Flow ◽

Body Core Temperature ◽

Esophageal Temperature ◽

Vascular Conductance ◽

Cutaneous Vasodilation ◽

Forearm Vascular Conductance ◽

Body Core

Elevated body core temperature stimulates cutaneous vasodilation, which can be modified by nonthermal factors. To test whether hypohydration affects forearm vascular conductance discretely from relative alterations in heart rate (HR), eight trained cyclists exercised progressively for 20 min each at 60, 120, and 180 W [approximately 22, 37, and 55% of maximal cycling O2 consumption (VO2peak), respectively] in a warm humid environment (dry bulb temperature 30 degrees C; wet bulb temperature 24 degrees C). Esophageal temperature and forearm blood flow were measured every 30 s, and mean arterial pressure and HR were measured at rest and during each exercise intensity (minutes 15, 35, and 55). In the hypovolemic (HP) compared with the euvolemic (EU) state, blood volume was contracted by 24-h fluid restriction an average of 510 ml, and this difference was sustained throughout exercise. The esophageal temperature and HR responses were similar between EU and HP states at 60 and 120 W but were significantly (P < 0.05) higher in HP by the end of 180 W. In contrast, the forearm blood flow response was significantly (P < 0.05) depressed during exercise at 120 and 180 W in HP, whereas mean arterial pressure remained similar between conditions. When body core temperature is elevated in a hypohydrated state, forearm vascular conductance is reduced at exercise intensities of approximately 37% VO2peak, which is independent of relative changes in HR. These findings are consistent with the notion that during exercise an attenuated cutaneous vasodilation is elicited by alterations in regionalized sympathetic outflow, which is unaccompanied by activation of cardiac pacemaker cells.

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Elevated extracellular potassium prior to muscle contraction reduces onset and steady-state exercise hyperemia in humans

Journal of Applied Physiology ◽

10.1152/japplphysiol.00183.2018 ◽

2018 ◽

Vol 125 (2) ◽

pp. 615-623 ◽

Cited By ~ 3

Author(s):

Janée D. Terwoord ◽

Christopher M. Hearon ◽

Gary J. Luckasen ◽

Jennifer C. Richards ◽

Michael J. Joyner ◽

...

Keyword(s):

Steady State ◽

Voluntary Contraction ◽

Extracellular Potassium ◽

Handgrip Exercise ◽

Exercise Hyperemia ◽

Forearm Vascular Conductance ◽

Response To Exercise ◽

Exercise In Humans ◽

Hyperemic Response

The increase in interstitial potassium (K+) during muscle contractions is thought to be a vasodilatory signal that contributes to exercise hyperemia. To determine the role of extracellular K+ in exercise hyperemia, we perfused skeletal muscle with K+ before contractions, such that the effect of any endogenously-released K+ would be minimized. We tested the hypothesis that local, intra-arterial infusion of potassium chloride (KCl) at rest would impair vasodilation in response to subsequent rhythmic handgrip exercise in humans. In 11 young adults, we determined forearm blood flow (FBF) (Doppler ultrasound) and forearm vascular conductance (FVC) (FBF/mean arterial pressure) during 4 min of rhythmic handgrip exercise at 10% of maximal voluntary contraction during 1) control conditions, 2) infusion of KCl before the initiation of exercise, and 3) infusion of sodium nitroprusside (SNP) as a control vasodilator. Infusion of KCl or SNP elevated resting FVC similarly before the onset of exercise (control: 39 ± 6 vs. KCl: 81 ± 12 and SNP: 82 ± 13 ml·min−1·100 mmHg−1; both P < 0.05 vs. control). Infusion of KCl at rest diminished the hyperemic (ΔFBF) and vasodilatory (ΔFVC) response to subsequent exercise by 22 ± 5% and 30 ± 5%, respectively (both P < 0.05 vs. control), whereas SNP did not affect the change in FBF ( P = 0.74 vs. control) or FVC ( P = 0.61 vs. control) from rest to steady-state exercise. These findings implicate the K+ ion as an essential vasodilator substance contributing to exercise hyperemia in humans. NEW & NOTEWORTHY Our findings support a significant and obligatory role for potassium signaling in the local vasodilatory and hyperemic response to exercise in humans.

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Comparison of the vasodilatory effects of sodium nitroprusside vs. nitroglycerin

Journal of Applied Physiology ◽

10.1152/japplphysiol.00167.2017 ◽

2017 ◽

Vol 123 (2) ◽

pp. 402-406 ◽

Cited By ~ 4

Author(s):

Sushant M. Ranadive ◽

Andy R. Eugene ◽

Gabrielle Dillon ◽

Wayne T. Nicholson ◽

Michael J. Joyner

Keyword(s):

Sodium Nitroprusside ◽

Doppler Ultrasound ◽

Forearm Blood Flow ◽

Venous Occlusion ◽

Similar Concentration ◽

Vascular Conductance ◽

Significant Difference ◽

Forearm Vascular Conductance ◽

Higher Doses ◽

Healthy Participants

The vasodilatory mechanism of Nntroglycerin (NTG) is similar to sodium nitroprusside (SNP) in regard to action on guanosine 3′5′-monophosphate (cyclic GMP) via nitric oxide. However, it is unknown whether NTG can achieve the same magnitude of vasodilation in the forearm as SNP. Therefore, the purpose of the study was to evaluate the differences in forearm blood flow (FBF) and forearm vascular conductance (FVC) during escalating infusions of NTG vs. SNP at similar concentration doses and rates. We measured FBF using venous occlusion plethysmography (VOP) and Doppler ultrasound in eight young, healthy participants (mean age = 28 ± 2 yr) during four forearm volume (FAV)-specific doses (0.25, 0.5, 1, and 2 µg·100 ml FAV−1·min−1) of SNP and NTG infused via a brachial artery catheter. There was a significant difference in FVC of SNP vs. NTG only at the higher doses, as measured by VOP (14.9 ± 1.4 and 18.3 ± 1.5 vs. 11.6 ± 1.2 and 12.5 ± 1.2 ml/dl FAV−1·min−1·100 mmHg−1). FVC as measured by Doppler ultrasound unadjusted for FAV was significantly different at the lowest and the higher two doses of SNP compared with NTG (202.1 ± 25.8, 329.4 ± 46.7, and 408 ± 63.5 vs. 142.9 ± 22.4, 217.2 ± 18.8, and 247.5 ± 18.2 ml·min−1·100 mmHg−1). SNP induces significantly higher vasodilatory actions compared with NTG. However, NTG is comparable in eliciting equivalent vasodilator effects to SNP during low concentration doses when measured by VOP. Importantly, for forearm pharmacology studies, NTG can elicit marked endothelium-independent forearm vasodilation. NEW & NOTEWORTHY We compared the vasodilatory capacities of NTG vs. SNP at similar concentration doses and rates into the forearm. Based on the results of the study, it may be feasible to use intra-arterial NTG as a measure of endothelial-independent vasodilator in research studies. However, NTG dosing may need to be higher if used as an endothelial-independent vasodilator due to significant differences in the vasodilatory effects during higher doses of SNP compared with NTG.

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Neurovascular responses to mental stress in prehypertensive humans

Journal of Applied Physiology ◽

10.1152/japplphysiol.00912.2010 ◽

2011 ◽

Vol 110 (1) ◽

pp. 76-82 ◽

Cited By ~ 23

Author(s):

Christopher E. Schwartz ◽

John J. Durocher ◽

Jason R. Carter

Keyword(s):

Heart Rate ◽

Mental Stress ◽

Sympathetic Nerve Activity ◽

Mental Arithmetic ◽

Pressor Response ◽

Muscle Sympathetic Nerve Activity ◽

Vascular Conductance ◽

Nerve Activity ◽

Vascular Responses ◽

Forearm Vascular Conductance

Neurovascular responses to mental stress have been linked to several cardiovascular diseases, including hypertension. Mean arterial pressure (MAP), muscle sympathetic nerve activity (MSNA), and forearm vascular responses to mental stress are well documented in normotensive (NT) subjects, but responses in prehypertensive (PHT) subjects remain unclear. We tested the hypothesis that PHT would elicit a more dramatic increase of MAP during mental stress via augmented MSNA and blunted forearm vascular conductance (FVC). We examined 17 PHT (systolic 120–139 and/or diastolic 80–89 mmHg; 22 ± 1 yr) and 18 NT (systolic < 120 and diastolic < 80 mmHg; 23 ± 2 yr) subjects. Heart rate, MAP, MSNA, FVC, and calf vascular conductance were measured during 5 min of baseline and 5 min of mental stress (mental arithmetic). Mental stress increased MAP and FVC in both groups, but the increases in MAP were augmented (Δ 10 ± 1 vs. Δ14 ± 1 mmHg; P < 0.05), and the increases in FVC were blunted (Δ95 ± 14 vs. Δ37 ± 8%; P < 0.001) in PHT subjects. Mental stress elicited similar increases in MSNA (Δ7 ± 2 vs. Δ6 ± 2 bursts/min), heart rate (Δ21 ± 3 vs. Δ18 ± 3 beats/min), and calf vascular conductance (Δ29 ± 10 vs. Δ19 ± 5%) in NT and PHT subjects, respectively. In conclusion, mental stress elicits an augmented pressor response in PHT subjects. This augmentation appears to be associated with altered forearm vascular, but not MSNA, responses to mental stress.

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Augmented Muscle Vasodilatory Responses in Obese Children with Glu27 β2-Adrenoceptor Polymorphism

Pediatric Exercise Science ◽

10.1123/pes.20.2.157 ◽

2008 ◽

Vol 20 (2) ◽

pp. 157-168 ◽

Cited By ~ 2

Author(s):

Alexandre G. da Silva ◽

Mauricio M. Ribeiro ◽

Ivani C. Trombetta ◽

Christiane Nicolau ◽

Eliana Frazzatto ◽

...

Keyword(s):

Blood Flow ◽

Forearm Blood Flow ◽

Color Word ◽

Isometric Exercise ◽

Obese Children ◽

Vascular Conductance ◽

Word Test ◽

Forearm Vascular Conductance ◽

Stroop Color Word Test

This study examined forearm vasodilatation during mental challenge and exercise in 72 obese children (OC; age = 10 ± 0.1 years) homozygous with polymorphism in the allele 27 of the β2-adrenoceptors: Gln27 (n = 61) and Glu27 (n = 11). Forearm blood flow was recorded during 3 min of each using the Stroop color-word test (MS) and handgrip isometric exercise. Baseline hemodynamic and vascular measurements were similar. During the MS, peak forearm vascular conductance was significantly greater in group Glu27 (Δ = 0.35 ± 0.4 vs. 0.12 ± 0.1 units, respectively, p = .042). Similar results were found during exercise (Δ = 0.64 ± 0.1 vs. 0.13 ± 0.1 units, respectively, p = .035). Glu27 OC increased muscle vasodilatory responsiveness upon the MS and exercise.

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Gly16 + Glu27 β2-adrenoceptor polymorphisms cause increased forearm blood flow responses to mental stress and handgrip in humans

Journal of Applied Physiology ◽

10.1152/japplphysiol.00503.2004 ◽

2005 ◽

Vol 98 (3) ◽

pp. 787-794 ◽

Cited By ~ 33

Author(s):

Ivani C. Trombetta ◽

Luciana T. Batalha ◽

Maria U. P. B. Rondon ◽

Mateus C. Laterza ◽

Eliana Frazzatto ◽

...

Keyword(s):

Blood Flow ◽

Sympathetic Nerve ◽

Mental Stress ◽

Sympathetic Nerve Activity ◽

Forearm Blood Flow ◽

Muscle Sympathetic Nerve Activity ◽

Isometric Exercise ◽

Vascular Conductance ◽

Nerve Activity ◽

Forearm Vascular Conductance

We hypothesized that the muscle vasodilatation during mental stress and exercise would vary among humans who are polymorphic at alleles 16 and 27 of the β2-adrenoceptors. From 216 preselected volunteers, we studied 64 healthy, middle-aged normotensive women selected to represent three genotypes: homozygous for the alleles Arg16 and Gln27 (Arg16/Gln27, n = 34), Gly16 and Gln27 (Gly16/Gln27, n = 20), and Gly16 and Glu27 (Gly16/Glu27, n = 10). Forearm blood flow (plethysmography) and muscle sympathetic nerve activity (microneurography) were recorded during 3-min Stroop color-word test and 3-min handgrip isometric exercise (30% maximal voluntary contraction). Baseline muscle sympathetic nerve activity, forearm vascular conductance, mean blood pressure, and heart rate were not different among groups. During mental stress, the peak forearm vascular conductance responses were greater in Gly16/Glu27 group than in Gly16/Gln27 and Arg16/Gln27 groups (1.79 ± 0.66 vs. 0.70 ± 0.11 and 0.58 ± 0.12 units, P = 0.03). Similar results were found during exercise (0.80 ± 0.25 vs. 0.28 ± 0.08 and 0.31 ± 0.08 units, P = 0.02). Further analysis in a subset of subjects showed that brachial intra-arterial propranolol infusion abolished the difference in vasodilatory response between Gly16/Glu27 ( n = 6) and Arg16/Gln27 ( n = 7) groups during mental stress (0.33 ± 0.20 vs. 0.46 ± 0.21 units, P = 0.50) and exercise (0.08 ± 0.06 vs. 0.03 ± 0.03 units, P = 0.21). Plasma epinephrine concentration in Arg16/Gln27 and Gly16/Glu27 groups was similar. In conclusion, women who are homozygous for Gly16/Glu27 of the β2-adrenoceptors have augmented muscle vasodilatory responsiveness to mental stress and exercise.

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Abstract P172: Endothelial Function In The Early Years After Delivery: Effect Of Adverse Pregnancy Outcomes And Activity Behaviors

Circulation ◽

10.1161/circ.143.suppl_1.p172 ◽

2021 ◽

Vol 143 (Suppl_1) ◽

Author(s):

Abbi D Lane-Cordova ◽

Erin O'Connor ◽

Janet M Catov ◽

Bo Fernhall ◽

Jihong Liu ◽

...

Keyword(s):

Blood Flow ◽

Endothelial Function ◽

Pregnancy Outcomes ◽

Forearm Blood Flow ◽

Reactive Hyperemia ◽

Adverse Pregnancy Outcomes ◽

Early Years ◽

Vascular Conductance ◽

Forearm Vascular Conductance ◽

Adverse Pregnancy

Introduction: Adverse pregnancy outcomes (APOs) are independently associated with cardiovascular disease (CVD). Endothelial dysfunction may indicate early CVD and can be influenced by physical activity (PA) and sedentary behavior (SED). Hypothesis: We hypothesized women with a past APO would have worse endothelial function versus controls and that mid-pregnancy and current PA would be directly related while SED would be inversely related to endothelial function in the years soon after delivery. Methods: We used venous occlusion plethysmography to measure baseline forearm blood flow, reactive hyperemia, and vascular conductance (forearm blood flow/mean arterial pressure) in a case control study of 53 women 6 mo to 3 yrs after a singleton birth; 26% with past APO, 21% African American, mean age=33±1 yrs, mean BMI=27.4±0.9 kg/m 2 . Current and mid-pregnancy leisure time PA and weekday SED were assessed with validated questionnaires. We evaluated differences in endothelial function by APO exposure with t-tests and relations of endothelial function with PA and SED with Spearman correlations. Results: Baseline forearm blood flow (APO: 1.6±0.2; non-APO: 1.8±0.1 ml*min -1 *100 ml -1 tissue, p=0.3) and reactive hyperemia (APO: 13.2±2; non-APO: 11.4±1 ml*min -1 *100 ml -1 , p=0.8) were similar between groups. Vascular conductance was non-significantly lower in women with a past APO: 1.7x10 -2 versus 2.1x10 -2 ml*min -1 *100 ml -1 mmHg -1 in women without a past APO, p<0.10. Vascular conductance was related to current and mid-pregnancy SED (figure) but not PA (r=0.2 and r=0.06, p>0.05 for mid-pregnancy and current PA). Associations of mid-pregnancy and current SED with vascular conductance after delivery persisted after adjustment for age and BMI. Conclusions: Forearm vascular conductance tended to be lower soon after delivery in women with an APO. Mid-pregnancy and current SED were inversely related to forearm vascular conductance and may represent targets for interventions aimed at improving endothelial function after delivery.

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Thermoregulatory reflexes and cutaneous active vasodilation during heat stress in hypertensive humans

Journal of Applied Physiology ◽

10.1152/jappl.1998.85.1.175 ◽

1998 ◽

Vol 85 (1) ◽

pp. 175-180 ◽

Cited By ~ 22

Author(s):

D. L. Kellogg ◽

S. R. Morris ◽

S. B. Rodriguez ◽

Y. Liu ◽

M. Grossmann ◽

...

Keyword(s):

Blood Flow ◽

Heat Stress ◽

Skin Blood Flow ◽

Forearm Blood Flow ◽

Venous Occlusion ◽

Vascular Conductance ◽

Doppler Flowmetry ◽

Forearm Vascular Conductance ◽

Normotensive Subjects ◽

Cutaneous Vascular Conductance

During dynamic exercise in the heat, increases in skin blood flow are attenuated in hypertensive subjects when compared with normotensive subjects. We studied responses to passive heat stress (water-perfused suits) in eight hypertensive and eight normotensive subjects. Forearm blood flow was measured by venous-occlusion plethysmography, mean arterial pressure (MAP) was measured by Finapres, and forearm vascular conductance (FVC) was calculated. Bretylium tosylate (BT) iontophoresis was used to block active vasoconstriction in a small area of skin. Skin blood flow was indexed by laser-Doppler flowmetry at BT-treated and untreated sites, and cutaneous vascular conductance was calculated. In normothermia, FVC was lower in hypertensive than in normotensive subjects ( P < 0.01). During heat stress, FVC rose to similar levels in both groups ( P > 0.80); concurrent cutaneous vascular conductance increases were unaffected by BT treatment ( P > 0.60). MAP was greater in hypertensive than in normotensive subjects during normothermia ( P < 0.05, hypertensive vs. normotensive subjects). During hyperthermia, MAP fell in hypertensive subjects but showed no statistically significant change in normotensive subjects ( P < 0.05, hypertensive vs. normotensive subjects). The internal temperature at which vasodilation began did not differ between groups ( P> 0.80). FVC is reduced during normothermia in unmedicated hypertensive subjects; however, they respond to passive heat stress in a fashion no different from normotensive subjects.

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Exogenous NO administration and α-adrenergic vasoconstriction in human limbs

Journal of Applied Physiology ◽

10.1152/japplphysiol.00634.2003 ◽

2003 ◽

Vol 95 (6) ◽

pp. 2370-2374 ◽

Cited By ~ 35

Author(s):

Jaya B. Rosenmeier ◽

Sandy J. Fritzlar ◽

Frank A. Dinenno ◽

Michael J. Joyner

Keyword(s):

Blood Flow ◽

Skeletal Muscles ◽

Forearm Blood Flow ◽

Norepinephrine Release ◽

Vascular Conductance ◽

No Donor ◽

Exercise Hyperemia ◽

Functional Sympatholysis ◽

Human Forearm ◽

Forearm Vascular Conductance

Nitric oxide (NO) is capable of blunting α-adrenergic vasoconstriction in contracting skeletal muscles of experimental animals (functional sympatholysis). We therefore tested the hypothesis that exogenous NO administration can blunt α-adrenergic vasoconstriction in resting human limbs by measuring forearm blood flow (FBF; Doppler ultrasound) and blood pressure in eight healthy males during brachial artery infusions of three α-adrenergic constrictors (tyramine, which evokes endogenous norepinephrine release; phenylephrine, an α1-agonist; and clonidine, an α2-agonist). To simulate exercise hyperemia, the vasoconstriction caused by the α-agonists was compared during adenosine-mediated (>50% NO independent) and sodium nitroprusside-mediated (SNP; NO donor) vasodilation of the forearm. Both adenosine and SNP increased FBF from ∼35–40 to ∼200–250 ml/min. All three α-adrenergic constrictor drugs caused marked reductions in FBF and calculated forearm vascular conductance ( P < 0.05). The relative reductions in forearm vascular conductance caused by the α-adrenergic constrictors during SNP infusion were similar (tyramine, –74 ± 3 vs. –65 ± 2%; clonidine, –44 ± 6 vs. –44 ± 6%; P > 0.05) or slightly greater (phenylephrine, –47 ± 6 vs. –33 ± 6%; P < 0.05) compared with the responses during adenosine. In conclusion, these results indicate that exogenous NO sufficient to raise blood flow to levels simulating those seen during exercise does not blunt α-adrenergic vasoconstriction in the resting human forearm.

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