Carotid baroreflex pressor responses at rest and during exercise: cardiac output vs. regional vasoconstriction

Collins, Heidi L.; Augustyniak, Robert A.; Ansorge, Eric J.; O’Leary, Donal S.

doi:10.1152/ajpheart.2001.280.2.h642

Cited by 45 publications

(76 citation statements)

References 28 publications

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“…Although the major target vascular bed(s) for this increased peripheral vasoconstriction with metaboreflex activation after SAD were not revealed in the present study, previous observations from our laboratory (3,20) have shown that, as workload increases, vasoconstriction in active skeletal muscle becomes a progressively more important component of the pressor response to carotid occlusion. Indeed, as skeletal muscle blood flow becomes a progressively larger fraction of CO, the potential ability of this vascular bed to regulate arterial pressure also increases proportionally (15), and at high workloads the majority of the carotid pressor response is due to vasoconstriction in the active skeletal muscle.…”

Section: Discussioncontrasting

confidence: 61%

“…As observed previously, in normal animals the major mechanism utilized by the muscle metaboreflex to raise arterial pressure during submaximal exercise is an increase in CO, with little if any net change in peripheral vascular conductance to nonischemic areas (16,18,39). This increase in arterial pressure is attenuated by arterial and cardiopulmonary baroreflexes (3,32). However, the arterial baroreflex not only modifies the strength of the muscle metaboreflex but markedly changes the mechanisms mediating the muscle metaboreflex pressor response.…”

Section: Discussionmentioning

confidence: 58%

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Arterial baroreflex alters strength and mechanisms of muscle metaboreflex during dynamic exercise

Kim¹,

Sala‐Mercado²,

Rodrı́guez³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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. Arterial baroreflex alters strength and mechanisms of muscle metaboreflex during dynamic exercise. Am J Physiol Heart Circ Physiol 288: H1374 -H1380, 2005. First published November 11, 2004; doi:10.1152/ajpheart.01040. 2004.-Previous studies showed that the arterial baroreflex opposes the pressor response mediated by muscle metaboreflex activation during mild dynamic exercise. However, no studies have investigated the mechanisms contributing to metaboreflex-mediated pressor responses during dynamic exercise after arterial baroreceptor denervation. Therefore, we investigated the contribution of cardiac output (CO) and peripheral vasoconstriction in mediating the pressor response to graded reductions in hindlimb perfusion in conscious, chronically instrumented dogs before and after sinoaortic denervation (SAD) during mild and moderate exercise. In control experiments, the metaboreflex pressor responses were mediated via increases in CO. After SAD, the metaboreflex pressor responses were significantly greater and significantly smaller increases in CO occurred. During control experiments, nonischemic vascular conductance (NIVC) did not change with muscle metaboreflex activation, whereas after SAD NIVC significantly decreased with metaboreflex activation; thus SAD shifted the mechanisms of the muscle metaboreflex from mainly increases in CO to combined cardiac and peripheral vasoconstrictor responses. We conclude that the major mechanism by which the arterial baroreflex buffers the muscle metaboreflex is inhibition of metaboreflex-mediated peripheral vasoconstriction. sinoaortic denervation; cardiac output; pressor response THE MUSCLE METABOREFLEX is activated when intramuscular metabolites accumulate because of a mismatch between blood flow and metabolism, and this accumulation stimulates group III and IV afferent neurons within the active muscle. Activation of these nerves transmits signals to the brain stem, which elicits a reflex increase in sympathetic nerve activity and systemic arterial blood pressure (10,11,27). The reflex acts to partially restore blood flow to the hypoperfused muscle (22). This muscle metaboreflex mediated-pressor response is attributable to increases in cardiac output (CO) and peripheral vasoconstriction (12,18,39).Previous studies showed that during mild to moderate exercise the pressor response primarily depends on increased CO to improve the ischemic condition in active skeletal muscles (16,18,39). If a reduction in blood flow to active skeletal muscle occurs when there is sufficient cardiac reserve during mild to moderate exercise, the metaboreflex will increase CO and thus the total amount of blood flow available to active skeletal muscle. O'Leary and Augustyniak (18) demonstrated that activation of the muscle metaboreflex in conscious dogs during dynamic exercise produced significant increases in CO via the reflex tachycardia with constant stroke volume (SV), and this was the major mechanism causing the reflex increase in arterial pressure. However, when CO is at or near maximal l...

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Section: Discussioncontrasting

confidence: 61%

Section: Discussionmentioning

confidence: 58%

Arterial baroreflex alters strength and mechanisms of muscle metaboreflex during dynamic exercise

Kim¹,

Sala‐Mercado²,

Rodrı́guez³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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“…Thus the arterial baroreflex buffers the muscle metaboreflex mainly by preventing peripheral vasoconstriction. This is consistent with studies in canines as well as in humans showing that unloading of the arterial baroreceptors during exercise raises arterial pressure mainly via peripheral vasoconstriction (13,80). In heart failure, the strength of the arterial baroreflex is depressed and sinoaortic denervation neither markedly increases the magnitude nor alters mechanisms of the metaboreflex pressor response; a somewhat larger rise in arterial pressure occurs via even more peripheral vasoconstriction (48,49).…”

Section: Impaired Baroreflex Buffering Of Muscle Metaboreflex In Hearsupporting

confidence: 89%

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

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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...

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“…In addition, the majority of these studies used pharmacological approaches to examine arterial baroreflex function, which do not permit an assessment of BP responses to baroreflex perturbation. Thus, to date, no studies have investigated whether there are sex-related differences in BP responses elicited by the arterial baroreflex.Previous studies (12,41,42) have suggested that alterations in vasomotor activity are the primary means by which the arterial baroreflex regulates BP. In dogs, the pressor response to carotid sinus hypotension via bilateral carotid occlusion was mediated solely by changes in TVC (12).…”

mentioning

confidence: 99%

“…Previous studies (12,41,42) have suggested that alterations in vasomotor activity are the primary means by which the arterial baroreflex regulates BP. In dogs, the pressor response to carotid sinus hypotension via bilateral carotid occlusion was mediated solely by changes in TVC (12).…”

mentioning

confidence: 99%

Sex differences in carotid baroreflex control of arterial blood pressure in humans: relative contribution of cardiac output and total vascular conductance

Kim

Deo²,

Vianna³

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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Kim A, Deo SH, Vianna LC, Balanos GM, Hartwich D, Fisher JP, Fadel PJ. Sex differences in carotid baroreflex control of arterial blood pressure in humans: relative contribution of cardiac output and total vascular conductance. Am J Physiol Heart Circ Physiol 301: H2454 -H2465, 2011. First published September 30, 2011 doi:10.1152/ajpheart.00772.2011.-It is presently unknown whether there are sex differences in the magnitude of blood pressure (BP) responses to baroreceptor perturbation or if the relative contribution of cardiac output (CO) and total vascular conductance (TVC) to baroreflex-mediated changes in BP differs in young women and men. Since sympathetic vasoconstrictor tone is attenuated in women, we hypothesized that carotid baroreflex-mediated BP responses would be attenuated in women by virtue of a blunted vascular response (i.e., an attenuated TVC response). BP, heart rate (HR), and stroke volume were continuously recorded during the application of 5-s pulses of neck pressure (NP; carotid hypotension) and neck suction (NS; carotid hypertension) ranging from ϩ40 to Ϫ80 Torr in women (n ϭ 20, 21 Ϯ 0.5 yr) and men (n ϭ 20, 21 Ϯ 0.4 yr). CO and TVC were calculated on a beat-to-beat basis. Women demonstrated greater depressor responses to NS (e.g., Ϫ60 Torr, Ϫ17 Ϯ 1%baseline in women vs. Ϫ11 Ϯ 1%baseline in men, P Ͻ 0.05), which were driven by augmented decreases in HR that, in turn, contributed to larger reductions in CO (Ϫ60 Torr, Ϫ15 Ϯ 2%baseline in women vs. Ϫ6 Ϯ 2%baseline in men, P Ͻ 0.05). In contrast, pressor responses to NP were similar in women and men (e.g., ϩ40 Torr, ϩ14 Ϯ 2%baseline in women vs. ϩ10 Ϯ 1%baseline in men, P Ͼ 0.05), with TVC being the primary mediating factor in both groups. Our findings indicate that sex differences in the baroreflex control of BP are evident during carotid hypertension but not carotid hypotension. Furthermore, in contrast to our hypothesis, young women exhibited greater BP responses to carotid hypertension by virtue of a greater cardiac responsiveness. arterial baroreceptors; gender; heart rate; stroke volume; total peripheral resistance THE ARTERIAL BAROREFLEX plays an important role in the beatto-beat regulation of arterial blood pressure (BP). These rapid baroreflex adjustments are mediated by alterations in autonomic neural activity to the heart and vasculature, which modulates cardiac output (CO) and total vascular conductance (TVC), respectively (19,48). Studies (7, 10) in animals have demonstrated that baroreflex-mediated heart rate (HR) responses are greater in female rodents compared with male rodents. However, limited studies have been performed in humans, and equivocal results have been reported. Indeed, compared with young men, young women have been reported to exhibit similar, increased, or decreased cardiac baroreflex control (1, 8, 13, 59). In addition, the majority of these studies used pharmacological approaches to examine arterial baroreflex function, which do not permit an assessment of BP responses to baroreflex perturbation. Thus, to date,...

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Carotid baroreflex pressor responses at rest and during exercise: cardiac output vs. regional vasoconstriction

Cited by 45 publications

References 28 publications

Arterial baroreflex alters strength and mechanisms of muscle metaboreflex during dynamic exercise

Arterial baroreflex alters strength and mechanisms of muscle metaboreflex during dynamic exercise

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

Sex differences in carotid baroreflex control of arterial blood pressure in humans: relative contribution of cardiac output and total vascular conductance

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