scholarly journals Instructed reappraisal and cardiovascular habituation to recurrent stress

2021 ◽  
Author(s):  
Siobhán M Griffin ◽  
Siobhán Howard
Keyword(s):  
Emotion Regulation ◽  
Cardiac Output ◽  
Cardiovascular Response ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Control Group ◽  
Stress Exposure ◽  
Response Profile ◽  
Single Stress ◽  
The Relationship

Instructed reappraisal has previously been associated with a challenge-oriented cardiovascular response profile, indexed by greater cardiac output (CO) and lower total peripheral resistance (TPR), in response to a single stress exposure. The present study builds on this research by employing a stress habituation paradigm where participants completed a speech task twice; in which prior to the second task participants heard reappraisal instructions (i.e., view feelings of stress arousal as something that is beneficial) or control instructions. This paradigm allowed us to (a) test if reappraisal aids cardiovascular habituation to recurrent stress, and (b) examine if reappraisal leads to a within-participant change in CO/TPR responding from an uninstructed task to an instructed reappraisal task. Habitual use of reappraisal was assessed using the Emotion Regulation Questionnaire. The analyses report upon 173 young adults (121 women, 52 men). Cardiovascular parameters were measured continuously using the Finometer Pro. All participants demonstrated similar cardiovascular habituation during the second stress exposure (lower SBP, CO, and HR); suggesting reappraisal did not aid cardiovascular habituation to recurrent stress. Reappraisal instructions did not lead to a challenge-oriented response compared to both the control group and responses to the uninstructed task. This study is the first to examine the relationship between instructed reappraisal and cardiovascular habituation and identifies that habitual use of reappraisal does not interact with reappraisal instructions to influence cardiovascular responses to stress.

scholarly journals Reappraising Threat: How to Optimize Performance Under Pressure

2015 ◽  
Vol 37 (3) ◽  
pp. 339-343 ◽  
Author(s):  
Lee J. Moore ◽  
Samuel J. Vine ◽  
Mark R. Wilson ◽  
Paul Freeman
Keyword(s):  
Cardiac Output ◽  
Motor Performance ◽  
Cardiovascular Response ◽  
Peripheral Resistance ◽  
Motor Task ◽  
Cardiovascular Responses ◽  
Control Group ◽  
Potential Solution ◽  
Single Trial ◽  
Performance Under Pressure

Competitive situations often hinge on one pressurized moment. In these situations, individuals’ psychophysiological states determine performance, with a challenge state associated with better performance than a threat state. But what can be done if an individual experiences a threat state? This study examined one potential solution: arousal reappraisal. Fifty participants received either arousal reappraisal or control instructions before performing a pressurized, single-trial, motor task. Although both groups initially displayed cardiovascular responses consistent with a threat state, the reappraisal group displayed a cardiovascular response more reflective of a challenge state (relatively higher cardiac output and/or lower total peripheral resistance) after the reappraisal manipulation. Furthermore, despite performing similarly at baseline, the reappraisal group outperformed the control group during the pressurized task. The results demonstrate that encouraging individuals to interpret heightened physiological arousal as a tool that can help maximize performance can result in more adaptive cardiovascular responses and motor performance under pressure.

scholarly journals INDIVIDUAL DIFFERENCES IN EMOTION REGULATION AND CARDIOVASCULAR RESPONDING TO STRESS

2021 ◽  
Author(s):  
Siobhán M Griffin ◽  
Siobhán Howard
Keyword(s):  
Blood Pressure ◽  
Emotion Regulation ◽  
Individual Differences ◽  
Acute Stress ◽  
Negative Emotion ◽  
Cardiovascular Response ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Emotional Valence ◽  
Emotion Words

Instructed use of reappraisal to regulate stress in the laboratory is typically associated with a more adaptive cardiovascular response to stress, indexed by either: (i) lower cardiovascular reactivity (CVR; e.g., lower blood pressure); or (ii) a challenge-oriented response profile (i.e., greater cardiac output paired with lower total peripheral resistance). In contrast, instructed use of suppression is associated with exaggerated CVR (e.g., greater heart rate, blood pressure). Despite this, few studies have examined if the habitual use of these strategies are related to cardiovascular responding during stress. The current study examined the relationship between cardiovascular responses to acute stress and individual differences in emotion regulation style: trait reappraisal, suppression, and emotion regulation difficulties. Forty-eight participants (25 women, 23 men) completed a standardised laboratory stress paradigm incorporating a 20-minute acclimatization period, a 10-minute baseline, and two 5-minute speech tasks separated by a 10-minute inter-task rest period. The emotional valence of the speech task was examined as a potential moderating factor; participants spoke about a block of negative-emotion words and a block of neutral-emotion words. Cardiovascular parameters were measured using the Finometer Pro. Greater habitual use of suppression was associated with exaggerated blood pressure responding to both tasks. However, only in response to the negative-emotion task was greater use of reappraisal associated with a challenge-oriented cardiovascular response. The findings suggest that individual differences in emotion regulation translate to differing patterns of CVR to stress, but the emotional valence of the stressor may play a role.

Role of vasopressin in the cardiovascular response to hypoxia in the conscious rat

1986 ◽  
Vol 251 (6) ◽  
pp. H1316-H1323 ◽  
Author(s):  
B. R. Walker
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Cardiovascular Response ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Hypoxic Exposure ◽  
Conscious Rat ◽  
Time Control ◽  
Hemodynamic Variables

Previous experiments have demonstrated that hypoxia stimulates the release of arginine vasopressin in conscious animals including the rat. The present study was designed to test whether AVP may exert a vasoconstrictor influence during hypoxia at varying levels of CO2. Systemic hemodynamics were assessed in conscious rats for 30 min under hypocapnic hypoxic, isocapnic hypoxic, hypercapnic hypoxic, and room air conditions. Progressive effects on heart rate (HR), cardiac output (CO), and total peripheral resistance (TPR) were observed with varying CO2 under hypoxic conditions. Hypocapnic hypoxia [arterial PO2 (PaO2) = 32 Torr; arterial PCO2 (PaCO2) = 22 Torr] caused HR and CO to rise and TPR to fall. Isocapnic hypoxia (PaO2 = 36 Torr; PaCO2 = 35 Torr) was associated with no significant changes in HR and CO or TPR, whereas hypercapnic hypoxia (PaO2 = 35 Torr; PaCO2 = 51 Torr) caused HR and CO to fall and TPR to rise. Room air time control experiments were associated with no change in measured hemodynamic variables. To determine the possible role of circulating AVP on these cardiovascular responses, additional experiments were performed where the specific V1-vasopressinergic antagonist d(CH2)5Tyr(Me)AVP (10 micrograms/kg iv) was administered at the midpoint of hypoxic exposure. Antagonist administration had no effect on hypocapnic hypoxic animals or animals breathing room air; however, blood pressure and TPR were significantly reduced by d(CH2)5Tyr(Me)AVP in both isocapnic and hypercapnic hypoxic animals. The heart rate response to hypoxia at the various CO2 levels was unaffected; however, cardiac output and stroke volume were increased after V1-antagonism in the isocapnic and hypercapnic hypoxic animals.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Abnormal cardiovascular response to nitroglycerin in migraine

Cephalalgia ◽  
2019 ◽  
Vol 40 (3) ◽  
pp. 266-277
Author(s):  
Willebrordus PJ van Oosterhout ◽  
Guus G Schoonman ◽  
Dirk P Saal ◽  
Roland D Thijs ◽  
Michel D Ferrari ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Cardiovascular Response ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Initial Increase

Introduction Migraine and vasovagal syncope are comorbid conditions that may share part of their pathophysiology through autonomic control of the systemic circulation. Nitroglycerin can trigger both syncope and migraine attacks, suggesting enhanced systemic sensitivity in migraine. We aimed to determine the cardiovascular responses to nitroglycerin in migraine. Methods In 16 women with migraine without aura and 10 age- and gender-matched controls without headache, intravenous nitroglycerin (0.5 µg·kg−1·min−1) was administered. Finger photoplethysmography continuously assessed cardiovascular parameters (mean arterial pressure, heart rate, cardiac output, stroke volume and total peripheral resistance) before, during and after nitroglycerin infusion. Results Nitroglycerin provoked a migraine-like attack in 13/16 (81.2%) migraineurs but not in controls ( p = .0001). No syncope was provoked. Migraineurs who later developed a migraine-like attack showed different responses in all parameters vs. controls (all p < .001): The decreases in cardiac output and stroke volume were more rapid and longer lasting, heart rate increased, mean arterial pressure and total peripheral resistance were higher and decreased steeply after an initial increase. Discussion Migraineurs who developed a migraine-like attack in response to nitroglycerin showed stronger systemic cardiovascular responses compared to non-headache controls. The stronger systemic cardiovascular responses in migraine suggest increased systemic sensitivity to vasodilators, possibly due to insufficient autonomic compensatory mechanisms.

Comparison of cardiovascular response to passive tilt in young and elderly men

1988 ◽  
Vol 66 (11) ◽  
pp. 1425-1432 ◽  
Author(s):  
D. A. Cunningham ◽  
R. J. Petrella ◽  
D. H. Paterson ◽  
P. M. Nichol
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Cardiovascular Response ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Left Ventricular ◽  
Age Effects ◽  
Hemodynamic Responses ◽  
Arterial Blood ◽  
Postural Changes

To test the hypothesis that altered hemodynamic responses to postural changes are associated with aging, cardiovascular responses to head-up tilt (HUT) and head-down tilt (HDT) were examined in 12 healthy young (average age, 24.6 ± 1.7 years) and 12 healthy elderly (average age, 68.6 ± 2.2 years) men. Subjects were passively tilted from supine to 30°, 60°, and 90° HUT and HDT. Responses to these perturbations were determined 5 min after tilting with measures of heart rate (HR), blood pressure (SBP, DBP), and echocardiographically determined left ventricular diameter in systole and diastole (LVIDs, LVIDd). In HUT there were no significant age effects. In both young and elderly, SBP decreased significantly (p < 0.05), and DBP and HR increased significantly. Ejection fraction (EF), mean arterial blood pressure (MABP), and rate-pressure product (RPP) were unchanged in both groups. In HDT, the hemodynamic responses of the young and elderly were in opposite directions and significant age effects were found for SBP, DBP, HR, LVIDs, EF, MABP, and RPP. In HDT, the young appear to increase cardiac output primarily due to an increase in EF and end-diastolic volume (LVIDd), while HR is unchanged and SBP is decreased. MABP is unchanged, suggesting a small decrease in total peripheral resistance. The elderly may increase cardiac output slightly, owing to an increase in LVIDd with no change in EF, and a large increase in HR. Afterload increased markedly, therefore attenuating any increase in cardiac output. These results suggest that in healthy men, the cardiovascular response to HUT is not age related, while conversely there appear to be significant differences between young and elderly in response to HDT.

Cardiovascular responses to static exercise in distance runners and weight lifters

1980 ◽  
Vol 49 (4) ◽  
pp. 676-683 ◽  
Author(s):  
J. C. Longhurst ◽  
A. R. Kelly ◽  
W. J. Gonyea ◽  
J. H. Mitchell
Keyword(s):  
Exercise Training ◽  
Cardiovascular Response ◽  
Cardiovascular Responses ◽  
Weight Lifting ◽  
Volume Index ◽  
Control Group ◽  
Static Exercise ◽  
Distance Runners ◽  
Long Distance ◽  
Weight Lifters

Sixty individuals including 17 competitive weight lifters (CWL), 12 competitive long-distance runners (LDR), 7 amateur (noncompetitive) weight lifters (AWL), 14 heavy controls (HC), and 10 light controls (LC) were studied at supine rest and during static exercise at 40% of maximal voluntary contraction. Blood pressures were similar in all groups at rest (R) and exercise (EX), but the heart rate (HR) and calculated double product (DP) of the LDR were lower at rest (HR: 53 +/- 2.9 beats/min, DP: 6,346 +/- 402) and at fatigue (HR: 78 +/- 5.4 beats/min. DP: 12,739 +/- 1,011) compared to the control group (R-HR: 69 +/- 2.2 beats/min, DP: 8,553 +/- 372; EX-HR: 97 +/- 3.5 beats/min, DP: 16,345 +/- 836). The LDR demonstrated higher end-diastolic volume index (EDVI) and higher end-systolic volume index (ESVI) at rest (EDVI: 84 +/- 3.7, ESVI: 31 +/- 2.7 ml/m2) and at the time of fatigue (EDVI: 90 +/- 5, ESVI: 37 +/- 2.7 ml/m2) compared to the LC group (R-EDVI: 61 +/- 4.4, ESVI: 22 +/- 2.2; EX-EDVI: 75 +/- 3.4, ESVI: 27 +/- 3.2 ml/m2). The CWL, AWL, and control groups had similar HR, DP, and cardiac volumes at rest and during exercise. These data suggest that competitive endurance (dynamic exercise) training alters the cardiovascular response to static exercise. On the other hand, weight lifting (static exercise) training does not alter the cardiovascular response to static exercise.

Cardiovascular responses to diving and their relation to lung and blood oxygen stores in vertebrates

1988 ◽  
Vol 66 (1) ◽  
pp. 20-28 ◽  
Author(s):  
Warren Burggren
Keyword(s):  
Cardiac Output ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Lung Perfusion ◽  
Blood Oxygen ◽  
Arterial Blood ◽  
Resistance Reduction ◽  
Lower Vertebrates ◽  
Oxygen Stores ◽  
Cardiovascular Performance

Air-breathing vertebrates generally respond to apnea during diving by adjusting cardiovascular performance (e.g., bradycardia, selective increases in peripheral resistance, reduction and redistribution of cardiac output). In mammals, and to a lesser extent in birds, the major O2 stores at the beginning of a dive reside within blood and tissues rather than in lung gas. Consequently, there is limited respiratory benefit during apnea in either maintaining or transiently restoring extensive lung perfusion to predive levels, and so cardiac output (and thus lung perfusion) remains low during the dive. In contrast, in most amphibians and reptiles the major O2 stores at the beginning of a dive reside within lung gas rather than in blood and tissues. Recent experiments on frogs and turtles reveal that pulmonary blood flow during diving can transiently increase to or above predive levels when it becomes necessary during the dive to transfer O2 from lung gas to arterial blood. In this regard, cardiovascular responses to diving in lower vertebrates are qualitatively different from those of higher vertebrates.

scholarly journals Cardiovascular Responses to the Induction of Mild Hypothermia in the Presence of Epidural Anesthesia

2001 ◽  
Vol 94 (4) ◽  
pp. 678-682 ◽  
Author(s):  
Masahiro Yoshida ◽  
Keizo Shibata ◽  
Hironori Itoh ◽  
Ken Yamamoto
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Ejection Fraction ◽  
General Anesthesia ◽  
Epidural Anesthesia ◽  
Mild Hypothermia ◽  
Cardiovascular Response ◽  
Cardiovascular Responses ◽  
Plasma Catecholamine ◽  
Plasma Catecholamine Concentrations

Background The combining of epidural anesthesia with general anesthesia impairs central and peripheral thermoregulatory control and therefore is often accompanied by unintended intraoperative hypothermia. However, little is known about the cardiovascular response to hypothermia during combined epidural and general anesthesia. The authors assessed the effects of hypothermia during such combined anesthesia. Methods The authors randomly assigned 30 mongrel dogs anesthetized with isoflurane (1.0%) to three groups of 10: control, receiving general anesthesia alone; thoracic injection, additionally receiving thoracic epidural anesthesia; and lumbar injection, additionally receiving thoracolumbar epidural anesthesia. Core temperature was lowered from 38.5 degrees C to approximately 34 degrees C (mild hypothermia) using a femoral arteriovenous shunt in an external cool water bath. During hypothermia, the authors measured heart rate, cardiac output, and plasma catecholamine concentrations in each group. Ejection fraction was also measured using echocardiography. Results Compared with measurements during baseline conditions (general anesthesia alone with no epidural injection and no hypothermia) in the control, thoracic, and lumbar injection groups, the injections followed by hypothermia produced 17, 32, and 41% decreases in heart rate; 22, 32, and 47% reductions in cardiac output; 66, 85, and 92% decreases in the epinephrine concentrations; and 27, 44, and 85% decreases in the norepinephrine concentrations. In contrast, ejection fraction did not change in any group. Conclusion Mild hypothermia during combined epidural anesthesia and general anesthesia markedly reduced cardiac output in dogs, mainly by decreasing heart rate.

scholarly journals Elevated vascular resistance and afterload reduce the cardiac output response to dobutamine in early growth-restricted rats in adulthood

2011 ◽  
Vol 106 (9) ◽  
pp. 1374-1382 ◽  
Author(s):  
Vladislava Zohdi ◽  
M. Jane Black ◽  
James T. Pearson
Keyword(s):  
Cardiac Output ◽  
Cardiac Function ◽  
Peripheral Resistance ◽  
Early Growth ◽  
Left Ventricular ◽  
Growth Restriction ◽  
Protein Diet ◽  
Ventricular Pressure ◽  
Control Group ◽  
Increased Risk

Epidemiological studies have linked intra-uterine growth restriction (IUGR) with an increased risk of CVD later in life. The aim of the present study was to examine the effect of maternal protein restriction on cardiac function in adulthood during dobutamine (DOB) stimulation. IUGR was induced in Wistar Kyoto dams through administration of a low-protein diet (LPD; 8·7 % casein) during pregnancy and lactation; the control group received a normal-protein diet (NPD; 20 % casein). At 14 weeks of age, cardiac function was assessed in male and female NPD (eight females and eight males) and LPD offspring (ten females and ten males) by pressure volumetry using an anaesthetised closed-chest approach. We determined mean arterial pressure (MAP), heart rate and left ventricular pressure–volume indices under baseline conditions and DOB stimulation (2 and 4 μg/kg per min). During β-adrenergic activation in LPD offspring, increases in cardiac output (CO, P < 0·018) and stroke volume (SV, P < 0·005) were attenuated in comparison with NPD offspring, while increases in ejection fraction and the maximal rate of ventricular pressure development were not affected. LPD females maintained a smaller end-diastolic volume (P < 0·017). MAP did not differ between the groups and did not change significantly during DOB infusion. Arterial elastance and total peripheral resistance decreased in all rats but remained significantly elevated in LPD offspring (P < 0·015 and < 0·01). Early growth restriction did not affect ventricular contractility but led to an increased afterload and impaired the ability to increase SV and CO during β-adrenergic stimulation.

scholarly journals Aging alters muscle reflex control of autonomic cardiovascular responses to rhythmic contractions in humans

2015 ◽  
Vol 309 (9) ◽  
pp. H1479-H1489 ◽  
Author(s):  
Simranjit K. Sidhu ◽  
Joshua C. Weavil ◽  
Massimo Venturelli ◽  
Matthew J. Rossman ◽  
Benjamin S. Gmelch ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Cardiovascular Response ◽  
Knee Extensor ◽  
Cardiovascular Responses ◽  
Muscle Afferents ◽  
Group Iii ◽  
Exercise Pressor Reflex ◽  
Pressor Reflex ◽  
Exercise Induced ◽  
The Impact

We investigated the influence of aging on the group III/IV muscle afferents in the exercise pressor reflex-mediated cardiovascular response to rhythmic exercise. Nine old (OLD; 68 ± 2 yr) and nine young (YNG; 24 ± 2 yr) males performed single-leg knee extensor exercise (15 W, 30 W, 80% max) under control conditions and with lumbar intrathecal fentanyl impairing feedback from group III/IV leg muscle afferents. Mean arterial pressure (MAP), cardiac output, leg blood flow (QL), systemic (SVC) and leg vascular conductance (LVC) were continuously determined. With no hemodynamic effect at rest, fentanyl blockade during exercise attenuated both cardiac output and QL ∼17% in YNG, while the decrease in cardiac output in OLD (∼5%) was significantly smaller with no impact on QL ( P = 0.8). Therefore, in the face of similar significant ∼7% reduction in MAP during exercise with fentanyl blockade in both groups, LVC significantly increased ∼11% in OLD, but decreased ∼8% in YNG. The opposing direction of change was reflected in SVC with a significant ∼5% increase in OLD and a ∼12% decrease in YNG. Thus while cardiac output seems to account for the majority of group III/IV-mediated MAP responses in YNG, the impact of neural feedback on the heart may decrease with age and alterations in SVC become more prominent in mediating the similar exercise pressor reflex in OLD. Interestingly, in terms of peripheral hemodynamics, while group III/IV-mediated feedback plays a clear role in increasing LVC during exercise in the YNG, these afferents seem to actually reduce LVC in OLD. These peripheral findings may help explain the limited exercise-induced peripheral vasodilation often associated with aging.

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