Carotid baroreflex responsiveness during dynamic exercise in humans

Potts, Jeffrey T.; Shi, Xiangrong; Raven, Peter B.

doi:10.1152/ajpheart.1993.265.6.h1928

Cited by 224 publications

(378 citation statements)

References 15 publications

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“…The resulting secondary reflex effects will tend to counteract the responses evoked via the carotid sinus baroreflex itself (10, 12, 26 -28). However, the HR and MAP responses to a brief (5 s) neck chamber stimulus are regarded as being only minimally affected by extracarotid sinus baroreceptors (21,23). In addition, the use of Doppler ultrasound in the present study provided a noninvasive blood flow measurement with beat-by-beat resolution, and this facilitated measurement of transient, yet marked, changes in vascular conductance.…”

Section: Discussionmentioning

confidence: 90%

Muscle metaboreflex modulates the arterial baroreflex dynamic effects on peripheral vascular conductance in humans

Ichinose¹,

Nishiyasu²

2005

American Journal of Physiology-Heart and Circulatory Physiology

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by the ultrasound Doppler method), leg vascular conductance (LVC), mean arterial blood pressure (MAP), and heart rate (HR)] in humans. In 12 healthy subjects (10 men and 2 women), who performed sustained 1-min handgrip exercise at 50% maximal voluntary contraction followed immediately by an imposed postexercise muscle ischemia (PEMI), 5-s periods of neck pressure (NP; 50 mmHg) or neck suction (NS; Ϫ60 mmHg) were used to evaluate carotid baroreflex function both at rest (Con) and during PEMI. First, the decreases in LVC and LBF and the augmentation of MAP elicited by NP were all greater during PEMI than in Con (⌬LVC, Ϫ1.2 Ϯ 0.2 vs. Ϫ1.9 Ϯ 0.2 ml ⅐ min Ϫ1 ⅐ mmHg Ϫ1 ; ⌬LBF, Ϫ97.3 Ϯ 11.2 vs. Ϫ177.0 Ϯ 21.8 ml/min; ⌬MAP, 6.7 Ϯ 1.2 vs. 11.5 Ϯ 1.4 mmHg, Con vs. PEMI; each P Ͻ 0.05). Second, in Con, NS significantly increased both LVC and LBF (⌬LVC, 0.9 Ϯ 0.2 ml ⅐ min Ϫ1 ⅐ mmHg Ϫ1 ; ⌬LBF, 46.6 Ϯ 9.8 ml/min; significant change from baseline: each P Ͻ 0.05), and, whereas during PEMI no significant increases in LVC and LBF occurred during NS itself (⌬LVC, 0.2 Ϯ 0.1 ml ⅐ min Ϫ1 ⅐ mmHg Ϫ1 ; ⌬LBF, 10.8 Ϯ 9.6 ml/min; each P Ͼ 0.05), a decrease was evident in each parameters at 5 s after the cessation of NS. Third, during PEMI, the decrease in MAP elicited by NS was smaller (⌬MAP, Ϫ8.4 Ϯ 1.0 vs. Ϫ5.8 Ϯ 0.4 mmHg, Con vs. PEMI; P Ͻ 0.05), and it recovered to its initial level more quickly after NS (vs. Con). Finally, however, the HR responses to NS and NP were not different between PEMI and Con. These results suggest that during muscle metaboreflex activation in humans, the arterial baroreflex dynamic effect on peripheral vascular conductance is modulated, as exemplified by 1) an augmentation of the NP-induced LVC decrease, and 2) a loss of the NS-induced LVC increase. skeletal muscle metaboreflex; carotid baroreflex; exercise DURING HEAVY EXERCISE, the arterial baroreflexes and the reflexes evoked by activation of those afferent nerve endings in the working skeletal muscles that are sensitive to metabolic changes (the so-called muscle metaboreflex) are hypothesized to be activated and, moreover, to interact in ways that lead to modulation of the primary cardiovascular reflex responses (6 -9, 15, 19, 20, 24, 25, 29, 31). Two types of interaction between these reflexes have been demonstrated to lead to such modulation. In the first type, the arterial baroreflexes act to oppose the pressor response elicited via the muscle metaboreflex (15,19,29,31). Evidence for this effect has been obtained during dynamic exercise in dogs (31) as well as during static handgrip exercise (29) and postexercise muscle ischemia (PEMI) in humans (15). The second type of interaction involves a modulation of arterial baroreflex function during muscle metaboreflex activation (6 -9, 20). However, these interactions (especially the second: viz. modulation of arterial baroreflex function by the muscle metaboreflex) and their consequences are not fully understood.Papelier et al. (20) found that during PEMI-induced muscle metaboreflex activation, the carotid sin...

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Section: Discussionmentioning

confidence: 90%

Muscle metaboreflex modulates the arterial baroreflex dynamic effects on peripheral vascular conductance in humans

Ichinose¹,

Nishiyasu²

2005

American Journal of Physiology-Heart and Circulatory Physiology

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“…In closed-loop context, in which the sequence method is used, different definitions of baroreflex sensitivity provide F I G U R E 1 Graphical representations of: A, Equation (1), constructed using published data; 6 B, Equation (A1), constructed using the same data of panel (A); 6 C, Equation (2), constructed using published data; 5 D, Equation (A3), constructed using the same data of panel (C). 5 Black and grey lines refer to resting and exercising humans, respectively. For panels (A) and (B), dots represent the operating points and the solid lines highlight the relationships, encompassing 2 standard deviations around the mean pressure value at the operating point.…”

Section: Discussionmentioning

confidence: 99%

“…However, the maximum baroreflex gain is equal to ab 4d aþd ð Þ . Thus, with respect to the HR-vs-P relationship represented by Equation (2), the maximum baroreflex gain (i) is positive instead of negative, (ii) depends also on d and (iii) is lower at exercise than at rest (in fact 3 times lower for the data of Potts et al 5 ). Moreover, the sigmoid midpoint corresponds to a centring pressure of c þ À Á , thus higher than c. This means that if we use RR instead of HR, the steepest slope and the centring pressure change quantitatively and qualitatively, quod erat demonstrandum.…”

Section: Baroreflex Sensitivity and The Logistic Modelmentioning

confidence: 94%

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Baroreflex sensitivity: An algebraic dilemma

et al. 2017

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The baroreflex system is a complex mechanism for short-term regulation of arterial blood pressure, involving the heart rate (HR), the heart contractility and the vascular tone in its efferent branches. The study of arterial baroreflexes relies on two different experimental approaches. On the one hand, the closed-loop approach analyses the mutual relationship between HR and arterial blood pressure, both in steady state and in dynamic conditions. The most classical method for the study of arterial baroreflexes with a closed-loop approach is the sequence method.1 The typical representation uses the R-

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“…Carotid baroreflex (CBR) control of leg hemodynamics was assessed at rest by determining changes in HR, mean arterial blood pressure (MAP), and LBF before and during a single, 5-s pulse of neck pressure (NP) at +40 Torr, as described previously (Potts et al, 1993). NP was applied during a 10-15 s breath hold at end-expiration in order to minimize the respiratory modulation of HR and MAP.…”

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confidence: 99%

Diminished baroreflex-induced vasoconstriction following alpha-2 adrenergic receptor blockade in humans

Wray

Raven

Sander³

2008

Autonomic Neuroscience

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The relative contribution of alpha adrenergic receptor subtypes in the transduction of sympathetic nerve activity (SNA) during carotid baroreflex (CBR) engagement is not well understood. Therefore, we compared the hemodynamic consequence of CBR-mediated sympatho-excitation via neck pressure (NP) before and after alpha-2 adrenergic blockade with intra-arterial yohimbine. Leg blood flow was measured using 2D and Doppler ultrasound, and arterial blood pressure was determined directly. NP caused the expected vasoconstriction, and this response was significantly reduced (by 50-60%) when NP was repeated after yohimbine. These data indicate that alpha-2 adrenergic receptors contribute significantly to CBR-induced vasoconstriction in the human leg under resting conditions. KeywordsBaroreflex; Yohimbine; Leg Blood Flow; ultrasound Doppler In response to a hypotensive stimulus, the carotid baroreceptors respond with a reflex increase in sympathetic nerve activity (SNA). In the peripheral circulation, this results in vasoconstriction and subsequent decreased systemic vascular conductance via binding of norepinephrine (NE) to both alpha-1 and alpha-2 adrenergic receptors on vascular smooth muscle. However, the relative contribution of adrenergic receptor subtypes in the transduction of SNA during carotid baroreflex (CBR) engagement is not well understood in humans.While the principle action of the CBR is towards arterial blood pressure homeostasis, we have demonstrated that acute CBR-mediated changes in sympathetic outflow and the subsequent impact on systemic vascular conductance also heavily influence beat-to-beat regulation of skeletal muscle blood flow Wray et al., 2004a). From a clinical perspective, CBR sensitivity has been demonstrated to be diminished in heart failure (Eckberg et al., 1971), hypertension (Bristow et al., 1969), and chronic obstructive pulmonary disease (Patakas et al., 1982), conditions also characterized by dysfunction in skeletal muscle perfusion. In this

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Carotid baroreflex responsiveness during dynamic exercise in humans

Cited by 224 publications

References 15 publications

Muscle metaboreflex modulates the arterial baroreflex dynamic effects on peripheral vascular conductance in humans

Muscle metaboreflex modulates the arterial baroreflex dynamic effects on peripheral vascular conductance in humans

Baroreflex sensitivity: An algebraic dilemma

Diminished baroreflex-induced vasoconstriction following alpha-2 adrenergic receptor blockade in humans

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