scholarly journals Profiles of vagal withdrawal to challenging interactions: Links with preschoolers’ conceptual shifting ability

2018 ◽  
Vol 61 (1) ◽  
pp. 116-124 ◽  
Author(s):  
Sara Scrimin ◽  
Elisabetta Patron ◽  
Silvia Lanfranchi ◽  
Ughetta Moscardino ◽  
Daniela Palomba ◽  
...  
Keyword(s):  

Author(s):  
Steven E. Perkins ◽  
Herbert F. Jelinek ◽  
Beverlie de Jong ◽  
David J. Cornforth ◽  
Mika P. Tarvainen ◽  
...  


1990 ◽  
Vol 69 (2) ◽  
pp. 407-418 ◽  
Author(s):  
L. B. Rowell ◽  
D. S. O'Leary

The overall scheme for control is as follows: central command sets basic patterns of cardiovascular effector activity, which is modulated via muscle chemo- and mechanoreflexes and arterial mechanoreflexes (baroreflexes) as appropriate error signals develop. A key question is whether the primary error corrected is a mismatch between blood flow and metabolism (a flow error that accumulates muscle metabolites that activate group III and IV chemosensitive muscle afferents) or a mismatch between cardiac output (CO) and vascular conductance [a blood pressure (BP) error] that activates the arterial baroreflex and raises BP. Reduction in muscle blood flow to a threshold for the muscle chemoreflex raises muscle metabolite concentration and reflexly raises BP by activating chemosensitive muscle afferents. In isometric exercise, sympathetic nervous activity (SNA) is increased mainly by muscle chemoreflex whereas central command raises heart rate (HR) and CO by vagal withdrawal. Cardiovascular control changes for dynamic exercise with large muscles. At exercise onset, central command increases HR by vagal withdrawal and "resets" the baroreflex to a higher BP. As long as vagal withdrawal can raise HR and CO rapidly so that BP rises quickly to its higher operating point, there is no mismatch between CO and vascular conductance (no BP error) and SNA does not increase. Increased SNA occurs at whatever HR (depending on species) exceeds the range of vagal withdrawal; the additional sympathetically mediated rise in CO needed to raise BP to its new operating point is slower and leads to a BP error. Sympathetic vasoconstriction is needed to complete the rise in BP. The baroreflex is essential for BP elevation at onset of exercise and for BP stabilization during mild exercise (subthreshold for chemoreflex), and it can oppose or magnify the chemoreflex when it is activated at higher work rates. Ultimately, when vascular conductance exceeds cardiac pumping capacity in the most severe exercise both chemoreflex and baroreflex must maintain BP by vasoconstricting active muscle.



Author(s):  
Pravati Pal ◽  
Jagadeeswaran Indumathy ◽  
GopalKrushna Pal
Keyword(s):  


2017 ◽  
Vol 65 (2) ◽  
pp. 363-366
Author(s):  
Ligia Helena Rodríguez-Mendieta ◽  
Jerson Quitián-Moreno ◽  
Guillermo Mora-Pabón

Introducción. Los pacientes con síndrome de Down sin enfermedad cardiaca estructural pueden presentar disfunción de la regulación autonómica cardiaca, lo cual se manifiesta mediante una contestación reducida de la frecuencia cardiaca (FC) frente a los estímulos. Con base en las respuestas hemodinámicas, se postuló que dichos pacientes tienen una reducción en las retirada vagales y la activación simpática. En esta revisión se explica el rol del sistema autonómico en el control de la FC y la respuesta cronotrópica atenuada observada en esta población.Objetivo. Describir, mediante la presentación de un caso clínico, la disfunción autonómica presente en los pacientes con síndrome de Down a fin de identificar las causas atribuidas por la evidencia científicaMateriales y métodos.Se describió un caso clínico y se realizó una búsqueda a través de PubMed con los términos: “Down Syndrome” AND “Bradycardia”, “VO2peak”, “Heart Rate Variability”, “Vagal Withdrawal”, “Sympathetic Activation”.Resultados. Los hallazgos sugieren que el ejercicio físico puede ser una intervención efectiva para mejorar la función cardiaca autonómica en personas con síndrome de Down. Además, las mejoras inducidas por el entrenamiento fueron alcanzadas por los participantes con niveles más bajos de modulación vagal al inicio del estudio en pacientes con y sin discapacidad, por lo que el entrenamiento puede ser eficaz para mejorar la aptitud cardiorespiratoria en quienes tienen un mayor grado de disfunción autonómica.Conclusión. Se presentó un caso clínico de síndrome de Down con disfunción sinusal, que podía estar relacionado con la disfunción de la regulación de la función cardiaca autonómica, dada por una FC reducida frente a los estímulos.



2019 ◽  
Vol 126 (1) ◽  
pp. 124-131 ◽  
Author(s):  
Christoph Siebenmann ◽  
Camilla K. Ryrsø ◽  
Laura Oberholzer ◽  
James P. Fisher ◽  
Linda M. Hilsted ◽  
...  

Hypoxia increases heart rate (HR) in humans by sympathetic activation and vagal withdrawal. However, in anaesthetized dogs hypoxia increases vagal activity and reduces HR if pulmonary ventilation does not increase and we evaluated whether that observation applies to awake humans. Ten healthy males were exposed to 15 min of normoxia and hypoxia (10.5% O2), while respiratory rate and tidal volume were volitionally controlled at values identified during spontaneous breathing in hypoxia. End-tidal CO2 tension was clamped at 40 mmHg by CO2 supplementation. β-Adrenergic blockade by intravenous propranolol isolated vagal regulation of HR. During spontaneous breathing, hypoxia increased ventilation by 3.2 ± 2.1 l/min ( P = 0.0033) and HR by 8.9 ± 5.5 beats/min ( P < 0.001). During controlled breathing, respiratory rate (16.3 ± 3.2 vs. 16.4 ± 3.3 breaths/min) and tidal volume (1.05 ± 0.27 vs. 1.06 ± 0.24 l) were similar for normoxia and hypoxia, whereas the HR increase in hypoxia persisted without (8.6 ± 10.2 beats/min) and with (6.6 ± 5.6 beats/min) propranolol. Neither controlled breathing ( P = 0.80), propranolol ( P = 0.64), nor their combination ( P = 0.89) affected the HR increase in hypoxia. Arterial pressure was unaffected ( P = 0.48) by hypoxia across conditions. The hypoxia-induced increase in HR during controlled breathing and β-adrenergic blockade indicates that hypoxia reduces vagal activity in humans even when ventilation does not increase. Vagal withdrawal in hypoxia seems to be governed by the arterial chemoreflex rather than a pulmonary inflation reflex in humans. NEW & NOTEWORTHY Hypoxia accelerates the heart rate of humans by increasing sympathetic activity and reducing vagal activity. Animal studies have indicated that hypoxia-induced vagal withdrawal is governed by a pulmonary inflation reflex that is activated by the increased pulmonary ventilation in hypoxia. The present findings, however, indicate that humans experience vagal withdrawal in hypoxia even if ventilation does not increase, indicating that vagal withdrawal is governed by the arterial chemoreflex rather than a pulmonary inflation reflex.



2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
G. K. Pal ◽  
Pravati Pal ◽  
Nivedita Nanda ◽  
V. Lalitha ◽  
T. K. Dutta ◽  
...  

Objective. Though prehypertension has strong familial predisposition, difference in pathophysiological mechanisms in its genesis in offspring of both parents and single parent hypertensive have not been elucidated.Methods. Body mass index (BMI), waist-hip ratio (WHR), basal heart rate (BHR), blood pressure (BP), HR and BP response to standing, deep breathing difference, BP response to handgrip and spectral indices of heart rate variability (HRV) were analyzed in normotensive offspring of two parents hypertensive (Group I), normotensive offspring of one parent hypertensive (Group II), prehypertensive offspring of two parents hypertensive (Group III) and prehypertensive offspring of one parent hypertensive (Group IV).Results. Sympathovagal imbalance (SVI) in prehypertensive offspring was observed due to increased sympathetic and decreased vagal activity. In group III, SVI was more prominent with greater contribution by vagal withdrawal. LF-HF ratio, the marker of SVI was correlated more with diastolic pressure, 30 : 15 ratio and E : I ratio in prehypertensives and the degree of correlation was more in group III prehypertensives.Conclusion. Vagal withdrawal plays a critical role in development of SVI in prehypertensive offspring of hypertensive parents. The intensity of SVI was more in offspring of two parents hypertensive compared to single parent hypertensive.



2011 ◽  
Vol 81 (3) ◽  
pp. 218-224 ◽  
Author(s):  
Nanna Hurwitz Eller ◽  
Morten Blønd ◽  
Martin Nielsen ◽  
Jesper Kristiansen ◽  
Bo Netterstrøm


2008 ◽  
Vol 295 (2) ◽  
pp. R624-R632 ◽  
Author(s):  
Frédéric Lador ◽  
Enrico Tam ◽  
Marcel Azabji Kenfack ◽  
Michela Cautero ◽  
Christian Moia ◽  
...  

We tested the hypothesis that vagal withdrawal plays a role in the rapid (phase I) cardiopulmonary response to exercise. To this aim, in five men (24.6 ± 3.4 yr, 82.1 ± 13.7 kg, maximal aerobic power 330 ± 67 W), we determined beat-by-beat cardiac output (Q̇), oxygen delivery (Q̇aO2), and breath-by-breath lung oxygen uptake (V̇o2) at light exercise (50 and 100 W) in normoxia and acute hypoxia (fraction of inspired O2 = 0.11), because the latter reduces resting vagal activity. We computed Q̇ from stroke volume (Qst, by model flow) and heart rate ( fH, electrocardiography), and Q̇aO2 from Q̇ and arterial O2 concentration. Double exponentials were fitted to the data. In hypoxia compared with normoxia, steady-state fH and Q̇ were higher, and Qst and V̇o2 were unchanged. Q̇aO2 was unchanged at rest and lower at exercise. During transients, amplitude of phase I (A1) for V̇o2 was unchanged. For fH, Q̇ and Q̇aO2, A1 was lower. Phase I time constant (τ1) for Q̇aO2 and V̇o2 was unchanged. The same was the case for Q̇ at 100 W and for fH at 50 W. Qst kinetics were unaffected. In conclusion, the results do not fully support the hypothesis that vagal withdrawal determines phase I, because it was not completely suppressed. Although we can attribute the decrease in A1 of fH to a diminished degree of vagal withdrawal in hypoxia, this is not so for Qst. Thus the dual origin of the phase I of Q̇ and Q̇aO2, neural (vagal) and mechanical (venous return increase by muscle pump action), would rather be confirmed.



2005 ◽  
Vol 64 (2) ◽  
pp. 252-255 ◽  
Author(s):  
Anthony J. Yun ◽  
Kimberly A. Bazar ◽  
Patrick Y. Lee
Keyword(s):  




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