Impaired central hemodynamic response and exaggerated vasoconstriction during muscle metaboreflex activation in heart failure patients

Crisafulli, Antonio; Salis, Enrico; Tocco, Filippo; Melis, Franco; Milia, Raffaele; Pittau, Gianluigi; Caría, M. A.; Solinas, Roberto; Meloni, Luigi; Pagliaro, Pasquale; Concu, Alberto

doi:10.1152/ajpheart.00008.2007

Cited by 106 publications

(185 citation statements)

References 51 publications

Supporting

Mentioning

156

Contrasting

Unclassified

Order By: Relevance

“…This response is achieved as the result of an elevation in sympathetic tone, which produces arteriolar constriction and enhancement in myocardial performance and in cardiac preload (18,35,39). Differently, in several cardiovascular diseases, such as chronic heart failure and hypertension, although not universally reported (37,50), it has been demonstrated that excessive sympathetic activity can occur during the metaboreflex (7,11,16,41,42). This fact leads to detrimental effects, such as elevated SVR, which in turn causes excessive vasoconstriction and elevated blood pressure (46,47).…”

Section: The Main New Finding Of the Present Investigation Is That Obmentioning

confidence: 99%

“…An impedance device (NCCOM 3; BoMed, Irvine, CA) previously used in similar experimental settings was used (9,11,12). This technique assumes that when an electrical current circulates through the thorax, the pulsatile aortic blood flow causes a proportional fluctuation in electrical conductivity.…”

Section: Study Populationmentioning

confidence: 99%

“…Afterward, SV was calculated beat-to-beat from stored trans-thoracic impedance traces. Moreover, the pre-ejection period/left ejection time ratio (PEP/VET) was calculated from impedance traces to have a parameter inversely related with myocardial performance (8,9,11). This ratio has been found to correlate well with the angiographic ejection fraction (27).…”

Section: Study Populationmentioning

confidence: 99%

See 2 more Smart Citations

Differences in hemodynamic response to metaboreflex activation between obese patients with metabolic syndrome and healthy subjects with obese phenotype

Milia

Velluzzi

Roberto

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

Self Cite

View full text Add to dashboard Cite

Patients suffering from obesity and metabolic syndrome (OMS) manifest a dysregulation in hemodynamic response during exercise, with an exaggerated systemic vascular increase. However, it is not clear whether this is the consequence of metabolic syndrome per se or whether it is due to concomitant obesity. The aim of the present investigation was to discover whether OMS and noncomplicated obesity resulted in different hemodynamic responses during the metaboreflex. Twelve metabolically healthy but obese subjects (MHO; 7 women), 13 OMS patients (5 women), and 12 normal age-matched controls (CTL; 6 women) took part in this study. All participants underwent a postexercise muscle ischemia protocol to evaluate the metaboreflex activity. Central hemodynamics were evaluated by impedance cardiography. The main result shows an exaggerated increase in systemic vascular resistance from baseline during the metaboreflex in the OMS patients as compared with the other groups (481.6 ± 180.3, -0.52 ± 177.6, and -60.5 ± 58.6 dynes·s(-1)·cm(-5) for the OMS, the MHO, and the CTL groups, respectively; P < 0.05). Moreover, the MHO subjects and the CTL group showed an increase in cardiac output during the metaboreflex (288.7 ± 325.8 and 703.8 ± 276.2 ml/m increase with respect to baseline), whereas this parameter tended to decrease in the OMS group (-350 ± 236.5 ml/m). However, the blood pressure response, which tended to be higher in the OMS patients, was not statistically different between groups. The results of the present investigation suggest that OMS patients have an exaggerated vasoconstriction in response to metaboreflex activation and that this fact is not due to obesity per se

show abstract

Section: The Main New Finding Of the Present Investigation Is That Obmentioning

confidence: 99%

Section: Study Populationmentioning

confidence: 99%

Section: Study Populationmentioning

confidence: 99%

See 1 more Smart Citation

Differences in hemodynamic response to metaboreflex activation between obese patients with metabolic syndrome and healthy subjects with obese phenotype

Milia

Velluzzi

Roberto

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

Self Cite

View full text Add to dashboard Cite

show abstract

“…With the limited ability to raise cardiac output during metaboreflex activation, the mechanism of the pressor response shifts from a flow-mediated rise in arterial pressure to peripheral vasoconstriction (18,35). What causes this shift is unclear but may involve impaired arterial baroreflex buffering of the metaboreflex pressor response.…”

Section: Impaired Baroreflex Buffering Of Muscle Metaboreflex In Hearmentioning

confidence: 99%

Neural control of circulation and exercise: a translational approach disclosing interactions between central command, arterial baroreflex, and muscle metaboreflex

Michelini

O’Leary

Raven

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Michelini LC, O'Leary DS, Raven PB, Nobrega AC. Neural control of circulation and exercise: a translational approach disclosing interactions between central command, arterial baroreflex, and muscle metaboreflex*. Am J Physiol Heart Circ Physiol 309: H381-H392, 2015. First published May 29, 2015; doi:10.1152/ajpheart.00077.2015.-The last 100 years witnessed a rapid and progressive development of the body of knowledge concerning the neural control of the cardiovascular system in health and disease. The understanding of the complexity and the relevance of the neuroregulatory system continues to evolve and as a result raises new questions. The purpose of this review is to articulate results from studies involving experimental models in animals as well as in humans concerning the interaction between the neural mechanisms mediating the hemodynamic responses during exercise. The review describes the arterial baroreflex, the pivotal mechanism controlling mean arterial blood pressure and its fluctuations along with the two main activation mechanisms to exercise: central command (parallel activation of central somatomotor and autonomic descending pathways) and the muscle metaboreflex, the metabolic component of exercise pressor reflex (feedback from ergoreceptors within contracting skeletal muscles). In addition, the role of the cardiopulmonary baroreceptors in modulating the resetting of arterial baroreflex is identified, and the mechanisms in the central nervous system involved with the resetting of baroreflex function during dynamic exercise are also described. Approaching a very relevant clinical condition, the review also presents the concept that the impaired arterial baroreflex function is an integral component of the metaboreflex-mediated exaggerated sympathetic tone in subjects with heart failure. This increased sympathetic activity has a major role in causing the depressed ventricular function observed during submaximal dynamic exercise in these patients. The potential contribution of a metaboreflex arising from respiratory muscles is also considered. autonomic; baroreflex; central command; exercise; metaboreflex THIS ARTICLE is part of a collection on 1st Pan American Congress of Physiological Sciences: Physiology Without Borders. Other articles appearing in this collection, as well as a full archive of all collections, can be found online at http://ajpheart.physiology.org/.A wide range of complex but routine behaviors such as feeding, shivering, locomotion, aggressive/defensive, and sexual behaviors triggers concomitant activation of somatomotor and autonomic outflows (47). Dynamic exercise is a complex physiological challenge involving highly coordinated activity of skeletal muscles, rapid and immediate increases in respiratory function, heart rate (HR), stroke volume and cardiac output associated with changes in regional vascular resistance, and redistribution of systemic blood flow that cause a slight increase in mean blood pressure (108). The increased blood flow to active muscles provides the necessary o...

show abstract

“…These data should also contribute to a better understanding of the pathophysiology of heart failure. Increasing evidence suggests the metaboreflex is exaggerated or tonically activated in heart failure (9,13,28) and that hypercapnia plays a key role (5,6,16,12) in the disease complications. Furthermore, because heart failure is characterized by an inability to increase SV, hemodynamic effects related to the interactions between the muscle metaboreflex and hypercapnia, such as those observed in this study, could explain in part the heart failure-linked exercise intolerance.…”

Section: Perspectives and Significancementioning

confidence: 99%

Cardiovascular responses to forearm muscle metaboreflex activation during hypercapnia in humans

Delliaux

Ichinose

Watanabe

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

Ten healthy males participated under three experimental conditions: 1) hypercapnia (HCA, PET CO 2 : ϩ10 mmHg, by inhalation of a CO 2-enriched gas mixture); 2) muscle metaboreflex activation (MMA, by 5 min of local circulatory occlusion after 1 min of 50% maximum voluntary contraction isometric handgrip under normocapnia); and 3) HCAϩMMA. We measured mean arterial pressure (MAP), heart rate (HR), and cardiac output (CO); calculated stroke volume (SV), and total peripheral resistance (TPR); and evaluated myocardial oxygen consumption (MV O2) and cardiac work (CW) noninvasively. MAP increased in the three experimental conditions but HCAϩMMA led to the highest MAP, CO, and HR. Moreover, HCAϩMMA increased SV and was associated with the highest MV O2 and CW. HCA and MMA exhibited inhibitory interactions with MAP, HR, TPR, MV O2, and CW, increases of which were smaller during HCAϩMMA than the sum of the increases during HCA and MMA alone (MAP: ϩ28 Ϯ 2 vs. ϩ34 Ϯ 2 mmHg, P Ͻ 0.001; HR: ϩ15 Ϯ 2 vs. ϩ22 Ϯ 3 bpm, P Ͻ 0.01; TPR: ϩ1.1 Ϯ 1.4 vs. ϩ3.0 Ϯ 1.5 mmHg·l·min Ϫ1 , P Ͻ 0.05; MV O2: ϩ50.25 Ϯ 4.74 vs. ϩ59.48 Ϯ 5.37 mmHg·min Ϫ1 ·10 Ϫ2 , P Ͻ 0.01; CW: ϩ59.10 Ϯ 7.52 vs. ϩ63.67 Ϯ 7.71 ml mmHg·min Ϫ1 ·10 Ϫ4 , P Ͻ 0.05). Oppositely, HCA and MMA interactions were linearly additive for CO (ϩ2.3 Ϯ 0.4 l/min) and SV (ϩ13 Ϯ 4 ml). We showed that muscle metaboreflex and hypercapnia interact in healthy humans, reducing vasoconstriction but enhancing SV.hypercapnia; muscle metaboreflex; hypertension; stroke volume; myocardial oxygen consumption REGULATION OF ARTERIAL BLOOD pressure involves the integration of humoral, hormonal, and neurogenic components. For example, whereas hypercapnia has direct humoral vasodilatory effects (19,20), the neurally mediated central chemoreflex increases cardiovascular sympathetic nervous system activity, leading heart rate (HR), stroke volume (SV), cardiac output (CO), vascular resistance, and then blood pressure all to increase (31). During exercise, blood pressure is also regulated by muscle reflexes (2, 17). The muscle metaboreflex forms a second direct excitatory input for the neural control of cardiovascular function (21, 29, 42) that also stimulates sympathetic pathways (29,30,33) leading to increases in HR, SV, CO, vascular resistance, and then blood pressure.It is known that central chemoreflex and muscle metaboreflex signals converge to common areas in the brain (43) and exert similar excitatory effects through the cardiovascular autonomic nervous system. On the other hand, little is known about the hemodynamic effects of muscle metaboreflex activation during hypercapnia. Ponikowski (35) showed that muscle ergoreflex activation was an independent predictor of ventilation sensitivity to hypercapnia in chronic heart failure and argued for the existence of interactions between the muscle metaboreflex and hypercapnic chemoreflex. Despite the likelihood that these two reflexes interact during exercise, this topic received little direct attention before the pioneering work of Lykidis et al. (22,23),...

show abstract

Impaired central hemodynamic response and exaggerated vasoconstriction during muscle metaboreflex activation in heart failure patients

Abstract: A. Impaired central hemodynamic response and exaggerated vasoconstriction during muscle metaboreflex activation in heart failure patients.

Cited by 106 publications

References 51 publications

Differences in hemodynamic response to metaboreflex activation between obese patients with metabolic syndrome and healthy subjects with obese phenotype

Differences in hemodynamic response to metaboreflex activation between obese patients with metabolic syndrome and healthy subjects with obese phenotype

Neural control of circulation and exercise: a translational approach disclosing interactions between central command, arterial baroreflex, and muscle metaboreflex

Cardiovascular responses to forearm muscle metaboreflex activation during hypercapnia in humans

Contact Info

Product

Resources

About