Forearm vascular responses to baroreceptor unloading at the onset of dynamic exercise

1993 ◽  
Vol 75 (2) ◽  
pp. 979-985 ◽  
Author(s):  
T. Nishiyasu ◽  
X. Shi ◽  
G. W. Mack ◽  
E. R. Nadel
Keyword(s):  
Lower Body Negative Pressure ◽  
Dynamic Exercise ◽  
Central Command ◽  
Lower Body ◽  
Physically Active ◽  
Vascular Responses ◽  
Vasoconstrictor Response ◽  
The Relationship ◽  
Forearm Vascular Resistance ◽  
Cardiac Stroke Volume

To determine the extent to which reflexes accompanying muscular exercise (associated with central command) interact with cardiopulmonary (CP) baroreceptor-mediated reflexes controlling forearm vascular resistance (FVR), we examined the forearm vasoconstrictor response at the onset of dynamic exercise, with and without CP baroreflex unloading, in 10 physically active men. CP baroreceptors were unloaded by application of lower body negative pressure (LBNP) at rest and during five 4-min bouts of supine exercise at 25 and 32 degrees C. Exercise intensities were 10 (essentially no load) and 100 W, and LBNP was applied at -10, -20, -30, and -40 mmHg during rest and at -20 and -40 mmHg during exercise. Resting FVR was 33.0 +/- 3.2 and 14.0 +/- 2.7 resistance units, and cardiac stroke volume (SV) was 117 +/- 7 and 126 +/- 9 ml/beat at 25 and 32 degrees C, respectively. We found a linear relationship between the increase in FVR and decrease in SV during LBNP; the slope of the relationship was significantly lower at 32 degrees C (FVR = 51.7–0.29SV) than at 25 degrees C (FVR = 123–0.79SV). At the onset of 100-W exercise without LBNP, FVR increased significantly to 50.2 +/- 9.0 and 21.2 +/- 3.2 units at 25 and 32 degrees C, respectively, whereas SV was unchanged. Application of -40-mmHg LBNP reduced SV significantly to 68 +/- 5 and 71 +/- 6 ml/beat and increased FVR significantly to 89.0 +/- 11.3 and 36.3 +/- 7.6 units at 25 and 32 degrees C, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Natriuretic Factor Potentiates the Human Forearm Vasoconstrictor Response to Sympathetic Stimulation

1994 ◽  
Vol 86 (3) ◽  
pp. 275-283 ◽  
Author(s):  
Tim L. Th. A. Jansen ◽  
Dr Paul Smits ◽  
Jacques W. M. Lenders ◽  
Marie-Cécile G. S. Jacobs ◽  
Jacques Willemsen ◽  
...  
Keyword(s):  
Sodium Nitroprusside ◽  
Negative Pressure ◽  
Atrial Natriuretic Factor ◽  
Lower Body Negative Pressure ◽  
Sympathetic Stimulation ◽  
Lower Body ◽  
Natriuretic Factor ◽  
Vasoconstrictor Response ◽  
Forearm Vascular Resistance ◽  
Atrial Natriuretic

1. Atrial natriuretic factor has been suggested to affect human sympathetic nervous system activity. The interaction between atrial natriuretic factor and the sympathetic nervous system has not been fully elucidated yet, but may occur at different sites. We studied this modulator effect at the level of the forearm vascular bed: the forearm vasoconstrictor response was examined after α-adrenergic sympathetic stimulation in healthy subjects during the loco-regional administration of atrial natriuretic factor, sodium nitroprusside and placebo. As a sympathetic stimulation test, the technique of the lower body negative pressure (–20 mmHg) was used. 2. Lower body negative pressure increased the forearm vascular resistance by +37 ± 8% during concomitant intra-arterial infusion of placebo (n = 10). During a predilator state achieved by infusion of atrial natriuretic factor (10 ng min−1 100 ml−1 forearm volume) into the brachial artery, lower body negative pressure subsequently induced a forearm vasoconstrictor response of +153 ± 22% (P < 0.05 versus placebo), whereas this was +64 ± 14% when predilatation was achieved by infusion of an equipotent vasodilator dose of sodium nitroprusside (P > 0.1 versus placebo; P < 0.05 versus atrial natriuretic factor). The potentiation of the forearm vasoconstrictor response to lower body negative pressure by atrial natriuretic factor only occurred in the experimental and not in the contralateral arm. According to calculations on simultaneously sampled arterial and venous plasma catecholamine concentrations, the augmented forearm vasoconstrictor response seemed not to be caused by an increased release of noradrenaline. 3. In a second experiment (n = 10), we demonstrated that atrial natriuretic factor did not alter the forearm vasoconstrictor response to the intra-arterial administration of exogenous noradrenaline, thereby excluding a postsynaptic modulation by atrial natriuretic factor. In the presence of atrial natriuretic factor, the subsequent infusion of two dosages of noradrenaline (0.1 and 1.0 ng min−1 100 ml−1 forearm volume) increased the forearm vascular resistance by +118 ± 29% and +387 ± 79%, respectively, whereas these numbered +129 ± 18% and + 316 ± 41% when atrial natriuretic factor was replaced by an equipotent dose of sodium nitroprusside. 4. We conclude that atrial natriuretic factor potentiates the forearm vasoconstrictor response to α-adrenergic sympathetic stimulation in man, and that this effect may be located at the level of the forearm vascular bed. This potentiation cannot be explained by an increased vascular α-adrenergic sensitivity. More detailed studies are needed to analyse the effects of atrial natriuretic factor on local noradrenaline kinetics to elucidate influences on sympathetic neurotransmission.

VASOCONSTRICTOR RESPONSE TO LOWER BODY NEGATIVE PRESSURE DURING AUTONCMIC BLOCKADE

1986 ◽  
Vol 18 (supplement) ◽  
pp. S15
Author(s):  
H. L. Smith ◽  
D. L. Hudson ◽  
H. M. Graitzer ◽  
P. B. Raven
Keyword(s):  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Vasoconstrictor Response

scholarly journals Differential Effects of Low- and High-Intensity Lower Body Negative Pressure on Noradrenaline and Adrenaline Kinetics in Humans

1996 ◽  
Vol 90 (5) ◽  
pp. 337-343 ◽  
Author(s):  
Marie-Cecile Jacobs ◽  
David S. Goldstein ◽  
Jacques J. Willemsen ◽  
Paul Smits ◽  
Theo Thien ◽  
...  
Keyword(s):  
Heart Rate ◽  
Vascular Resistance ◽  
Pulse Pressure ◽  
Negative Pressure ◽  
High Intensity ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Total Body ◽  
Noradrenaline And Adrenaline ◽  
Forearm Vascular Resistance

1. Lower body negative pressure provides a means to examine neurocirculatory reflexive responses to decreases in venous return to the heart. We assessed whether the pattern of catecholaminergic responses to lower body negative pressure depends on the intensity of the stimulus (−15 versus −40 mmHg). 2. In 14 healthy subjects, responses of forearm blood flow and noradrenaline spillover and of total body noradrenaline and adrenaline spillover were assessed during infusion of [3H]noradrenaline and [3H]adrenaline during −15 and −40 mmHg of lower body negxative pressure. 3. During lower body negative pressure at −15 mmHg, heart rate and pulse pressure did not change, but forearm vascular resistance increased by 25–50%. Forearm noradrenaline spillover increased by about 50%, from 0.63 ± 0.16 to 0.94 ± 0.23 pmol min−1 100 ml−1 (P<0.05). Total body noradrenaline spillover did not change, and total body adrenaline spillover increased significantly by about 30%. Clearances of noradrenaline and adrenaline were unchanged. 4. During lower body negative pressure at −40 mmHg, heart rate increased and pulse pressure decreased. Forearm vascular resistance increased by about 100%, and forearm noradrenaline spillover increased by 80%, from 0.73 ± 0.19 to 1.32 ± 0.36 pmol min−1 100 ml−1 (P<0.05). Total body noradrenaline spillover increased by 30%, and total body adrenaline spillover increased by about 50%. Clearances of both noradrenaline and adrenaline decreased. 5. The results are consistent with the view that selective deactivation of cardiopulmonary baroreceptors during low-intensity lower body negative pressure increases sympathoneural traffic to forearm skeletal muscle and increases adrenomedullary secretion without a concomitant generalized increase in sympathoneural outflows. Concurrent deactivation of cardiopulmonary and arterial baroreceptors during high-intensity lower body negative pressure evokes a more generalized increase in sympathoneural activity, accompanied by further increased adrenomedullary secretion and decreased plasma clearances of noradrenaline and adrenaline. The findings support differential increases in skeletal sympathoneural and adrenomedullary outflows during orthostasis, with more generalized sympathoneural responses to systemic hypotension.

Occupational Physical Activity as an Indicator of Health and Fitness

2001 ◽  
Vol 92 (1) ◽  
pp. 121-127 ◽  
Author(s):  
Jon Hammermeister ◽  
Randy M. Page ◽  
Dennis Dolny ◽  
Tim Burnham
Keyword(s):  
Physical Activity ◽  
Pacific Northwest ◽  
United States Forest Service ◽  
Lower Body ◽  
Physically Active ◽  
Work Related ◽  
The Pacific ◽  
Health And Fitness ◽  
The Relationship ◽  
Recent Government

Recent government guidelines suggest that simply increasing physical activity, regardless of mode, leads to improved health profiles. This study examined the relationship between amount of work-related physical activity of United States Forest Service (USFS) workers and 12 indicators of health and fitness. Subjects were 110 USFS workers recruited from 8 separate USFS ranger stations in the Pacific Northwest. The associations between work-related physical activity and indicators of health and fitness indicated the 63 workers who were physically active on the job displayed better overall health and fitness patterns as evidenced by higher aerobic capacity, lower body fat, and greater muscular flexibility than their 47 inactive peers.

scholarly journals Forehead versus forearm skin vascular responses at presyncope in humans

2014 ◽  
Vol 307 (7) ◽  
pp. R908-R913 ◽  
Author(s):  
Daniel Gagnon ◽  
R. Matthew Brothers ◽  
Matthew S. Ganio ◽  
Jeffrey L. Hastings ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Heat Stress ◽  
Lower Body Negative Pressure ◽  
Lower Body ◽  
Facial Skin ◽  
Vascular Responses ◽  
Radial Artery Catheterization ◽  
Forearm Skin ◽  
Cutaneous Vasoconstriction

Facial pallor is commonly observed at presyncope in humans, suggestive of reductions in facial skin blood flow (SkBF). Yet, cutaneous vasoconstriction is usually minimal at presyncope when measured at the forearm. We tested the hypothesis that reductions in forehead SkBF at presyncope are greater than in the forearm. Forehead and forearm SkBF (laser-Doppler) and blood pressure (Finometer or radial artery catheterization) were measured during lower body negative pressure (LBNP) to presyncope in 11 normothermic and 13 heat-stressed subjects (intestinal temperature increased ∼1.4°C). LBNP reduced mean arterial pressure from 91 ± 5 to 57 ± 7 mmHg during normothermia ( P ≤ 0.001) and from 82 ± 5 to 57 ± 7 mmHg during heat stress ( P ≤ 0.001). During normothermia, LBNP decreased forehead SkBF 55 ± 14% compared with 24 ± 11% at the forearm ( P = 0.002), while during heat stress LBNP decreased forehead SkBF 39 ± 11% compared with 28 ± 8% in the forearm ( P = 0.007). In both conditions, most (≥68%) of the decreases in SkBF were due to decreases in blood pressure. However, a greater contribution of actively mediated reductions in SkBF was observed at the forehead, relative to the forearm during normothermia (32 ± 13% vs. 11 ± 11%, P = 0.031) and heat stress (30 ± 13% vs. 10 ± 13%, P = 0.004). These data suggest that facial pallor at presyncope is due to a combination of passive decreases in forehead SkBF secondary to reductions in blood pressure and to active decreases in SkBF, the latter of which are relatively greater than in the forearm.

Dissociation between reflex sympathetic and forearm vascular responses to lower body negative pressure in heart failure patients with coronary artery disease

2009 ◽  
Vol 297 (5) ◽  
pp. H1760-H1766 ◽  
Author(s):  
Catherine F. Notarius ◽  
Beverley L. Morris ◽  
John S. Floras
Keyword(s):  
Heart Failure ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Muscle Sympathetic Nerve Activity ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Plasma Norepinephrine ◽  
Lower Body ◽  
Ventricular Ejection Fraction ◽  
Vascular Responses

Many heart failure (HF) patients exhibit paradoxical forearm vasodilation when central blood volume is reduced by lower body negative pressure (LBNP). We tested the hypothesis that this response results from reflex sympathetic withdrawal. We recorded simultaneously forearm blood flow, muscle sympathetic nerve activity (MSNA), and plasma norepinephrine (PNE) during four random applications of LBNP, −5, −10, −20, and −40 mmHg, in 12 men with HF (mean left ventricular ejection fraction = 24 ± 2%) and 10 healthy, normal, age-matched men (N). Compared with N, MSNA burst frequency ( P = 0.001) and PNE ( P = 0.005) were significantly higher in the HF group, both at rest and during LBNP. As anticipated in N, LBNP −40 mmHg significantly increased MSNA (+14.2 ± 2.5 bursts/min; P < 0.05) and PNE (+0.83 ± 0.22 nmol/l; P < 0.05) and decreased forearm vascular conductance (FVC) (−11.7 ± 3.2 ml·min−1·mmHg−1; P < 0.05). In the HF group, LBNP elicited similar increases in MSNA (+11.5 ± 2.0; P < 0.05) and PNE (+0.85 ± 0.12; P < 0.05), without affecting FVC significantly (−4.1 ± 2.4; P = 0.01 vs. N, interaction P = 0.03). However, within the HF group, responses were bimodal: LBNP −40 mmHg increased MSNA in all subjects ( P < 0.001), yet the six patients with nonischemic or dilated cardiomyopathy (DCM) exhibited significant vasoconstriction (decrease in FVC; P = 0.001), whereas the six patients with ischemic cardiomyopathy (ICM) exhibited significant vasodilation (increase in FVC; P < 0.02 vs. DCM and N; interaction P = 0.02). Cold pressor testing increased MSNA and decreased FVC in ICM ( n = 4). Thus paradoxical forearm vasodilator responses to LBNP in HF are not mediated by reflex sympathetic withdrawal. ICM and DCM patients differ qualitatively in their vascular responses to hypotensive LBNP.

Orthostatic intolerance during a 13-day bed rest does not result from increased leg compliance

1993 ◽  
Vol 74 (1) ◽  
pp. 286-292 ◽  
Author(s):  
F. M. Melchior ◽  
S. M. Fortney
Keyword(s):  
Orthostatic Intolerance ◽  
Lower Body Negative Pressure ◽  
Bed Rest ◽  
Venous Occlusion ◽  
Orthostatic Tolerance ◽  
Lower Body ◽  
Pressure Test ◽  
Before And After ◽  
Negative Pressure Test ◽  
The Relationship

Increased leg compliance (LC) has been proposed as a mechanism for orthostatic intolerance after spaceflight or bed rest. Using venous occlusion plethysmography with mercury-in-Silastic strain gauge, we evaluated LC before, during, and after a 13-day head-down (-6 degrees) bed rest in 10 men. LC was measured by the relationship between the increased calf areas (in cm2) at thigh cuff occlusions of 20, 30, 50, 70, and 80 mmHg. Orthostatic tolerance was evaluated by a presyncopal-limited lower body negative pressure test (PSL-LBNP) before and after bed rest. The 10 subjects were divided into TOL (n = 5) and INT (n = 5) groups for which the orthostatic tolerance was similar and lower after bed rest, respectively. For TOL (INT) before bed rest, calf area increases were 2.2 +/- 0.5 (SE) (1.3 +/- 0.4), 3.5 +/- 0.7 (2.3 +/- 0.5), 5.0 +/- 0.9 (3.5 +/- 0.6), 5.6 +/- 0.9 (4.4 +/- 0.6), and 6.4 +/- 1.1 (4.7 +/- 0.6) cm2 for thigh occlusion pressures of 20, 30, 50, 70, and 80 mmHg, respectively. Neither for INT nor for TOL were these results significantly changed by bed rest. These results suggest that other mechanisms than increased LC have to be taken into account to explain the decreased orthostatic tolerance induced by this 13-day bed rest.

Delayed vasoconstrictor response to venous pooling in the calf is associated with high orthostatic tolerance to LBNP

2010 ◽  
Vol 109 (4) ◽  
pp. 996-1001 ◽  
Author(s):  
T. Hachiya ◽  
M. L. Walsh ◽  
M. Saito ◽  
A. P. Blaber
Keyword(s):  
Blood Volume ◽  
Negative Pressure ◽  
Near Infrared ◽  
Lower Body Negative Pressure ◽  
Orthostatic Stress ◽  
Orthostatic Tolerance ◽  
Lower Body ◽  
High Tolerance ◽  
Venous Pooling ◽  
Vasoconstrictor Response

Central blood volume loss to venous pooling in the lower extremities and vasoconstrictor response are commonly viewed as key factors to distinguish between individuals with high and low tolerance to orthostatic stress. In this study, we analyzed calf vasoconstriction as a function of venous pooling during simulated orthostatic stress. We hypothesized that high orthostatic tolerance (OT) would be associated with greater vasoconstrictor responses to venous pooling compared with low OT. Nineteen participants underwent continuous stepped lower body negative pressure at −10, −20, −30, −40, −50, and −60 mmHg each for 5 min or until exhibiting signs of presyncope. Ten participants completed the lower body negative pressure procedure without presyncope and were categorized with high OT; the remaining nine were categorized as having low OT. Near-infrared spectroscopy measurements of vasoconstriction (Hachiya T, Blaber A, Saito M. Acta Physiologica 193: 117–127, 2008) in calf muscles, along with heart rate (HR) responses for each participant, were evaluated in relation to calf blood volume, estimated by plethysmography. The slopes of this relationship between vasoconstriction and blood volume were not different between the high- and low-tolerance groups. However, the onset of vasoconstriction in the high-tolerance group was delayed. Greater HR increments in the low-tolerance group were also observed as a function of lower limb blood pooling. The delayed vasoconstriction and slower HR increments in the high-tolerance group to similar venous pooling in the low group may suggest a greater vascular reserve and possible delayed reduction in venous return.

Effects of graded LBNP on MSNA and interstitial norepinephrine

2002 ◽  
Vol 283 (5) ◽  
pp. H2038-H2044 ◽  
Author(s):  
Mazhar H. Khan ◽  
Lawrence I. Sinoway ◽  
David A. MacLean
Keyword(s):  
Nervous System ◽  
Sympathetic Nerve Activity ◽  
Lower Body Negative Pressure ◽  
Vastus Lateralis ◽  
Muscle Sympathetic Nerve Activity ◽  
Plasma Norepinephrine ◽  
Lower Body ◽  
Nerve Activity ◽  
Sympathetic Nervous ◽  
The Relationship

Exposure to lower body negative pressure (LBNP) leads to an increased activation of the sympathetic nervous system (SNS) and an increase in muscle sympathetic nerve activity (MSNA). In this study, we examined the relationship between MSNA and interstitial norepinephrine (NEi) concentrations during LBNP. Twelve healthy volunteers were studied (26 ± 6 yr). Simultaneous MSNA and microdialysis data were collected in six of these subjects. Measurements of MSNA (microneurography) and NEi (microdialysis, vastus lateralis) were performed at rest and then during an incremental LBNP paradigm (−10, −30, and −50 mmHg). MSNA rose as a function of LBNP ( P < 0.001, n = 12). The plasma norepinephrine (NEp) concentration was 0.9 ± 0.1 nmol/l at rest ( n = 12). NEi measured in six subjects rose from 5.2 ± 0.8 nmol/l at rest to 17.0 ± 1.7 nmol/l at −50 mmHg ( P < 0.001). Of note, the rise in NEp with LBNP was considerably less compared with the changes in NEi (Δ21 ± 6% vs. Δ197 ± 52%, n = 6, P < 0.015). MSNA and NEi showed a significant linear relationship ( r = 0.721, P < 0.004). Activation of the SNS increased MSNA and NEi levels. The magnitude of the NEi increase was far greater than that seen for NEp suggesting that NE movement into the circulation decreases with baroreceptor unloading.

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