Sympathetic neural reactivity to stress does not increase with age in healthy humans

1994 ◽  
Vol 267 (1) ◽  
pp. H344-H353 ◽  
Author(s):  
A. V. Ng ◽  
R. Callister ◽  
D. G. Johnson ◽  
D. R. Seals
Keyword(s):  
Heart Rate ◽  
Nervous System ◽  
Arterial Pressure ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Handgrip Exercise ◽  
Isometric Handgrip ◽  
Isometric Handgrip Exercise ◽  
Sympathetic Nervous ◽  
Older Subjects

Sympathetic nervous system reactivity to stress is though to increase with age in humans. We tested this hypothesis by recording postganglionic sympathetic nerve activity to skeletal muscle (MSNA) (peroneal microneurography) and by measuring plasma norepinephrine concentrations (PNE), heart rate, and arterial pressure before (prestress control) and during cognitive challenge (mental arithmetic and colored word test), thermal stress (i.e., the cold pressor test), and exhaustive isometric handgrip exercise (40% of maximum voluntary force)/postexercise ischemia in 15 older (60-74 yr, mean +/- SE = 64 +/- 1) and 15 young (19–30 yr, mean +/- SE = 25 +/- 1) healthy men and women (8 males, 7 females each). The initial prestress control level of MSNA was higher in the older subjects (P < 0.01 vs. young), but there were no significant differences for PNE, heart rate, or arterial pressure. The MSNA and PNE responses to mental stress were small and not different in the two groups. MSNA and PNE increased markedly in response to the cold pressor test and isometric handgrip exercise/post exercise ischemia in both groups. The absolute unit increases in MSNA were similar in the two groups, but the relative (percentage) increases were actually smaller in the older subjects (P < 0.05 vs. young) due to their elevated baseline levels. The stress-evoked increases in arterial pressure were similar in the groups, but the older subjects tended to demonstrate smaller increases in heart rate. In general, no gender differences were noted in either age group. These findings fail to support the long-held concept that stress-induced sympathetic nervous system stimulation becomes exaggerated with age. Thus, sympathetic neural hyperreactivity does not appear to be a fundamental property of the aging process in humans.

scholarly journals Developmental Changes in Hemodynamic Responses and Cardiovagal Modulation during Isometric Handgrip Exercise

2010 ◽  
Vol 2010 ◽  
pp. 1-11 ◽  
Author(s):  
Styliani Goulopoulou ◽  
Bo Fernhall ◽  
Jill A. Kanaley
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Isometric Contraction ◽  
Pressor Response ◽  
Reflex Response ◽  
Group Differences ◽  
Handgrip Exercise ◽  
Isometric Handgrip ◽  
Isometric Handgrip Exercise ◽  
Pressor Reflex

The purpose of this study was to examine differences in pressor response and cardiovagal modulation during isometric handgrip exercise (IHG) between children and adults. Beat-to-beat heart rate (HR) and blood pressure were measured in 23 prepubertal children and 23 adults at baseline and during IHG. Cardiovagal modulation was quantified by analysis of HR variability. Mean arterial pressure responses to IHG were greater in adults compared to children (P<.05) whereas there were no group differences in HR responses (P>.05). Children had a greater reduction in cardiovagal modulation in response to IHG compared to adults (P<.05). Changes in mean arterial pressure during IHG were correlated with baseline cardiovagal modulation and force produced during isometric contraction (P<.05). In conclusion, differences in pressor reflex response between children and adults cannot be solely explained by differences in autonomic modulation and appear to be associated with factors contributing to the force produced during isometric contraction.

scholarly journals Altered Autonomic Nervous System Reactivity to Pain in Trigeminal Neuralgia

2015 ◽  
Vol 42 (2) ◽  
pp. 125-131 ◽  
Author(s):  
Guillaume Léonard ◽  
Philippe Chalaye ◽  
Philippe Goffaux ◽  
David Mathieu ◽  
Isabelle Gaumond ◽  
...  
Keyword(s):  
Heart Rate ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Trigeminal Neuralgia ◽  
Cold Pressor Test ◽  
Cardiac Activity ◽  
Cold Pressor ◽  
Healthy Controls ◽  
P Values ◽  
Autonomic Nervous

AbstractBackground: In the past two decades, there has been increasing evidence to suggest that trigeminal neuralgia (TN) may be linked to a dysfunction of the autonomic nervous system (ANS). The aim of the present study was to formally test this hypothesis by comparing the reactivity of the ANS to experimental pain in a population of TN patients and healthy controls. Methods: Twelve patients diagnosed with classical TN and 12 healthy controls participated in the study. Cardiac activity was assessed while participants were instructed to rest and again during a cold pressor test (CPT). Heart rate variability analyses were performed off-line to obtain parasympathetic (high-frequency) and sympathetic (low-frequency) indices. Results: At baseline, ANS measures did not differ between healthy controls and TN patients, and both groups showed a similar increase in heart rate during the CPT (all p values >0.05). However, TN patients showed a greater increase in cardiac sympathetic activity and a greater decrease in cardiac parasympathetic activity during CPT compared with healthy controls (all p values <0.05). Importantly, changes in sympathetic reactivity, from baseline to CPT, were negatively associated with the number of pain paroxysms experienced each day by TN patients in the preceding week (r=−.58, p<0.05). Conclusions: These results suggest that TN, like many other short-lasting, unilateral facial pain conditions, is linked to ANS alterations. Future studies are required to determine if the altered ANS response observed in TN patients is a cause or a consequence of TN pain

Individual differences in cardiac and vascular components of the pressor response to isometric handgrip exercise in humans

2014 ◽  
Vol 306 (2) ◽  
pp. H251-H260 ◽  
Author(s):  
Kazuhito Watanabe ◽  
Masashi Ichinose ◽  
Rei Tahara ◽  
Takeshi Nishiyasu
Keyword(s):  
Individual Differences ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Voluntary Contraction ◽  
Handgrip Exercise ◽  
Isometric Handgrip ◽  
Muscle Metaboreflex ◽  
Coefficients Of Variation ◽  
Isometric Handgrip Exercise ◽  
Induced Changes

We tested the hypotheses that, in humans, changes in cardiac output (CO) and total peripheral vascular resistance (TPR) occurring in response to isometric handgrip exercise vary considerably among individuals and that those individual differences are related to differences in muscle metaboreflex and arterial baroreflex function. Thirty-nine healthy subjects performed a 1-min isometric handgrip exercise at 50% of maximal voluntary contraction. This was followed by a 4-min postexercise muscle ischemia (PEMI) period to selectively maintain activation of the muscle metaboreflex. All subjects showed increases in arterial pressure during exercise. Interindividual coefficients of variation (CVs) for the changes in CO and TPR between rest and exercise periods (CO: 95.1% and TPR: 87.8%) were more than twofold greater than CVs for changes in mean arterial pressure (39.7%). There was a negative correlation between CO and TPR responses during exercise ( r = −0.751, P < 0.01), but these CO and TPR responses correlated positively with the corresponding responses during PEMI ( r = 0.568 and 0.512, respectively, P < 0.01). The CO response during exercise did not correlate with PEMI-induced changes in an index of cardiac parasympathetic tone and cardiac baroreflex sensitivity. These findings demonstrate that the changes in CO and TPR that occur in response to isometric handgrip exercise vary considerably among individuals and that the two responses have an inverse relationship. They also suggest that individual differences in components of the pressor response are attributable in part to variations in muscle metaboreflex-mediated cardioaccelerator and vasoconstrictor responses.

Chemoreflex and metaboreflex control during static hypoxic exercise

2005 ◽  
Vol 288 (4) ◽  
pp. H1724-H1729 ◽  
Author(s):  
Anne Houssiere ◽  
Boutaina Najem ◽  
Agniezka Ciarka ◽  
Sonia Velez-Roa ◽  
Robert Naeije ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Circulatory Arrest ◽  
Handgrip Exercise ◽  
Isometric Handgrip ◽  
Isometric Handgrip Exercise ◽  
Baseline Values ◽  
Hypoxic Exercise

To investigate the effects of muscle metaboreceptor activation during hypoxic static exercise, we recorded muscle sympathetic nerve activity (MSNA), heart rate, blood pressure, ventilation, and blood lactate in 13 healthy subjects (22 ± 2 yr) during 3 min of three randomized interventions: isocapnic hypoxia (10% O2) (chemoreflex activation), isometric handgrip exercise in normoxia (metaboreflex activation), and isometric handgrip exercise during isocapnic hypoxia (concomitant metaboreflex and chemoreflex activation). Each intervention was followed by a forearm circulatory arrest to allow persistent metaboreflex activation in the absence of exercise and chemoreflex activation. Handgrip increased blood pressure, MSNA, heart rate, ventilation, and lactate (all P < 0.001). Hypoxia without handgrip increased MSNA, heart rate, and ventilation (all P < 0.001), but it did not change blood pressure and lactate. Handgrip enhanced blood pressure, heart rate, MSNA, and ventilation responses to hypoxia (all P < 0.05). During circulatory arrest after handgrip in hypoxia, heart rate returned promptly to baseline values, whereas ventilation decreased but remained elevated ( P < 0.05). In contrast, MSNA, blood pressure, and lactate returned to baseline values during circulatory arrest after hypoxia without exercise but remained markedly increased after handgrip in hypoxia ( P < 0.05). We conclude that metaboreceptors and chemoreceptors exert differential effects on the cardiorespiratory and sympathetic responses during exercise in hypoxia.

The Effects of Increasing Plasma Concentrations of Dexmedetomidine in Humans

2000 ◽  
Vol 93 (2) ◽  
pp. 382-394 ◽  
Author(s):  
Thomas J. Ebert ◽  
Judith E. Hall ◽  
Jill A. Barney ◽  
Toni D. Uhrich ◽  
Maelynn D. Colinco
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Plasma Concentrations ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Central Venous ◽  
Pressor Test

Background This study determined the responses to increasing plasma concentrations of dexmedetomidine in humans. Methods Ten healthy men (20-27 yr) provided informed consent and were monitored (underwent electrocardiography, measured arterial, central venous [CVP] and pulmonary artery [PAP] pressures, cardiac output, oxygen saturation, end-tidal carbon dioxide [ETCO2], respiration, blood gas, and catecholamines). Hemodynamic measurements, blood sampling, and psychometric, cold pressor, and baroreflex tests were performed at rest and during sequential 40-min intravenous target infusions of dexmedetomidine (0.5, 0.8, 1.2, 2.0, 3.2, 5.0, and 8.0 ng/ml; baroreflex testing only at 0.5 and 0.8 ng/ml). Results The initial dose of dexmedetomidine decreased catecholamines 45-76% and eliminated the norepinephrine increase that was seen during the cold pressor test. Catecholamine suppression persisted in subsequent infusions. The first two doses of dexmedetomidine increased sedation 38 and 65%, and lowered mean arterial pressure by 13%, but did not change central venous pressure or pulmonary artery pressure. Subsequent higher doses increased sedation, all pressures, and calculated vascular resistance, and resulted in significant decreases in heart rate, cardiac output, and stroke volume. Recall and recognition decreased at a dose of more than 0.7 ng/ml. The pain rating and mean arterial pressure increase to cold pressor test progressively diminished as the dexmedetomidine dose increased. The baroreflex heart rate slowing as a result of phenylephrine challenge was potentiated at both doses of dexmedetomidine. Respiratory variables were minimally changed during infusions, whereas acid-base was unchanged. Conclusions Increasing concentrations of dexmedetomidine in humans resulted in progressive increases in sedation and analgesia, decreases in heart rate, cardiac output, and memory. A biphasic (low, then high) dose-response relation for mean arterial pressure, pulmonary arterial pressure, and vascular resistances, and an attenuation of the cold pressor response also were observed.

scholarly journals Acute Cardiovascular Effects of Epidural Spinal Cord Stimulation

2007 ◽  
Vol 5;10 (9;5) ◽  
pp. 677-685
Author(s):  
David M. Schultz
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Spinal Cord Stimulation ◽  
Statistical Significance ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Arterial Blood

Background: Several animal studies support the contention that thoracic spinal cord stimulation (SCS) might decrease arterial blood pressure. Objective: To determine if electrical stimulation of the dorsal spinal cord in humans will lower mean arterial pressure (MAP) and heart rate (HR). Design: Case Series Methods: Ten normotensive subjects that were clinically indicated for SCS testing were studied. Two of the 10 patients who underwent testing were excluded from the analysis because they did not respond to the Cold Pressor Test (CPT). Systolic blood pressure, diastolic blood pressure, and heart rate were measured continuously at the wrist (using the Vasotrac device). SCS was administered with quadripolar leads implanted into the epidural space under fluoroscopic guidance. SCS was randomly performed either in the T1-T2 or T5-T6 region of the spinal cord during normal conditions as well as during transient stress induced by CPT. The CPT was conducted by immersing the non-dominant hand in ice-cold water for 2 minutes. Results: There were moderate decreases in MAP and HR during SCS at the T5-T6 region compared to baseline that did not reach statistical significance. However, SCS at the T1-T2 region tended to increase MAP and HR compared to baseline but the change did not reach statistical significance. Arterial blood pressure was transiently elevated by 9.4 ± 3.8 mmHg using CPT during the control period with SCS turned off and also during SCS at either the T1-T2 region or T5-T6 region of the spinal cord (by 9.2 ± 5 mmHg and 10.7 ± 8.4 mmHg, respectively). During SCS at T5-T6, the CPT significantly increased MAP by 5.9±7.1 mmHg compared to control CPT (SCS off). Conclusion: This study demonstrated that SCS at either the T1-T2 or T5-T6 region did not significantly alter MAP or HR compared to baseline (no SCS). However, during transcient stress (elevated sympathetic tone) induced by CPT, there was a significant increase in MAP and moderate decrease in HR during SCS at T5-T6 region, which is not consistent with previous data in the literature. Acute SCS did not result in adverse cardiovascular responses and proved to be safe. Key words: Spinal cord stimulation, mean arterial pressure, heart rate, cold pressor test

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