Carotid Baroreflex Responsiveness Research Articles

Carotid Baroreflex Responsiveness in Patients with Heart Failure with a Preserved Ejection Fraction

The carotid baroreflex (CBR) plays an important role in blood pressure regulation by modulating heart rate (HR) and vasomotor tone. In humans, CBR function can be investigated non‐invasively using the variable pressure neck collar, which alters carotid sinus transmural pressure through application of positive and negative pressure within the neck chamber. Using this technique, derangements in CBR function have been identified in a variety of patient populations, but whether patients with heart failure with a preserved ejection fraction (HFpEF) suffer from disease‐related changes in CBR responsiveness has yet to be determined. We evaluated beat‐to‐beat changes in HR and mean arterial pressure (MAP) in response to 5‐sec pulses of neck pressure (NP, +40 Torr) and neck suction (NS, ‐80 Torr) to simulate carotid hypotension and hypertension, respectively in 5 patients with HFpEF (69±3 yrs and BMI: 38±4) and 4 healthy, older controls (68±2 yrs and BMI: 26±3). Resting HR was lower in patients with HFpEF compared to control subjects (77±7 vs. 68±6 bpm, respectively; p<0.005), while MAP was similar between groups (88±2 vs. 88±5mmHg, HFpEF vs controls). Following NP, a disease‐related decrement in CBR responsiveness was evident, with diminished changes in HR (2±1 vs 9±1 bpm, HFpEF vs controls, p=0.041) and MAP (4±2 vs 8±1 mmHg, p=0.095) in the HFpEF group. Similarly, changes in both HR (‐6±1 vs ‐8±1 bpm, HFpEF vs controls, p=0.21) and MAP (‐5±1 vs ‐8±1 mmHg, HFpEF vs controls, p=0.16) in response to carotid hypertension provoked by NS were reduced in patient with HFpEF. Though preliminary in nature, these initial findings appear to indicate a decline in carotid baroreflex‐mediated cardiac and vasomotor control in patients with HFpEF that is likely to contribute significantly to autonomic nervous system dysregulation in this patient group.

Carotid baroreflex control of central and peripheral hemodynamics during recovery after moderate leg cycling exercise.

This study aimed to examine the carotid baroreflex (CBR) control of the central and peripheral hemodynamics after exercise using the neck pressure (NP) and neck suction (NS) technique. Sixteen healthy young male participants (age: 27 ± 1.5 yr) were in a supine position for 30 min preexercise, followed by 60 min of cycling exercise, and then returned to a supine position for an additional 60 min postexercise. Both pre- and postexercise, the CBR-mediated responses of the central and peripheral hemodynamics were evaluated using 5-s periods of NP and NS (-60, -40, or +40 mmHg). As the central hemodynamics measurements, heart rate (HR), mean arterial pressure (MAP), cardiac output, and total vascular conductance were assessed. To determine peripheral circulation, vascular conductance in active and inactive limbs was measured. Eight participants [responder (RE) group] showed substantial postexercise hypotension (PEH) during recovery from exercise (Δ MAP: approximately -5 ± 0.9 mmHg, P < 0.05). The other eight participants did not display a reduction in MAP after exercise (non-RE group). In the non-RE group, the responsiveness of CBR-mediated changes in HR, MAP, and vascular conductance increased, particularly in response to -40 mmHg NS during postexercise compared with preexercise. However, in the RE group, any alterations in responsiveness to NP and NS were unchanged during PEH compared with preexercise. In conclusion, some normotensive individuals do not show PEH because the responsiveness of the CBR in central and peripheral hemodynamics following exercise is augmented, particularly to high blood pressure.NEW & NOTEWORTHY The carotid baroreflex (CBR) control of central and peripheral hemodynamics was investigated after exercise in both the presence and absence of postexercise hypotension (PEH). In individuals with no PEH, the responsiveness of CBR-mediated changes in all hemodynamics was augmented after exercise, particularly to high blood pressure; conversely, the CBR responsiveness remained unchanged in individuals with PEH. These findings provide insight into the mechanism of CBR control after exercise.

Neural control of cardiovascular function in black adults: implications for racial differences in autonomic regulation.

Black adults are at increased risk for developing hypertension and cardiovascular and chronic kidney disease and have greater associated morbidity/mortality than white adults who are otherwise demographically similar. Despite the key role of the autonomic nervous system in the regulation of cardiovascular function, the mechanistic contributions of sympathetic nerves to racial differences in cardiovascular dysfunction and disease remain poorly understood. In this review, we present an update and synthesis of current understanding regarding the roles of autonomic neural mechanisms in normal and pathophysiological cardiovascular control in black and white adults. At rest, many hemodynamic and autonomic variables, including blood pressure, cardiac output, and sympathetic nerve activity, are similar in healthy black and white adults. However, resting sympathetic vascular transduction and carotid baroreflex responses are altered in ways that tend to promote increased vasoconstriction and higher blood pressure, even in healthy, normotensive black adults. Acute sympathoexcitatory maneuvers, including exercise and cold pressor test, often result in augmented sympathetic and hemodynamic responses in healthy black adults. Clinically, although mechanistic evidence is scarce in this area, existing data support the idea that excessive sympathetic activation and/or transduction into peripheral vasoconstriction contribute importantly to the pathophysiology of hypertension and chronic kidney disease in black compared with white adults. Important areas for future work include more detailed study of sympathetic and hemodynamic reactivity to exercise and other stressors in male and female black adults and, particularly, sympathetic control of renal function, an important area of clinical concern in black patients.

Carotid baroreflex responses to simulated hypotension are blunted during passive whole‐body heat stress in young women

Previous studies have proposed that carotid baroreflex (CBR) function is potentially compromised during heat stress, thus possibly disrupting the ability to maintain arterial blood pressure in the heat (e.g., decreased orthostatic tolerance during hyperthermia). Recently, we demonstrated that CBR function is preserved, if not enhanced, during a passive whole‐body heat stress (WBH) in young healthy men. What remains unknown is how CBR function is impacted by hyperthermia in women. Therefore, the purpose of this study was to test the hypothesis that CBR‐mediated responses are preserved during a passive WBH in young women. Changes in mean arterial pressure (MAP) and HR were assessed in 7 healthy women (age: 21±1 yrs, height: 171±5 cm, weight: 66±5 kg, BMI: 23±2 kg/m2) using 5‐s trials of neck pressure (NP, carotid hypotension) and neck suction (NS, carotid hypertension) ranging from +40 to −80 Torr during normothermia (NT) and WBH (increased core temp ~1.0 °C) conditions. To assess the CBR control of MAP and HR, a separate two‐way repeated measures ANOVA was utilized for 1) hypertensive stimuli (i.e., NS: −20, −40, −60 &amp; −80 Torr) and 2) hypotensive‐stimuli (i.e., NP: +20 &amp; +40 Torr). Additionally, the time‐to‐peak responses for HR and MAP, separately, in response +40 Torr &amp; −80 Torr trials were examined between thermal conditions using paired t‐tests. During WBH, the CBR‐mediated increases in MAP and HR in response to NP were blunted (main effect of thermal condition p=0.02 and p=0.02, respectively). While the CBR‐mediated decreases in MAP in response to NS were not different between thermal conditions (main effect of thermal condition p=0.34), decreases in HR were markedly greater during WBH (main effect of thermal condition p&lt;0.001). Additionally, the time‐to‐peak responses for MAP and HR were not altered between thermal conditions for either NP or NS trials (p &gt; 0.05 for all comparisons). Taken together, these data suggest the CBR control of MAP and HR during simulated hypotension is blunted in females during passive WBH, while the control of MAP and HR seems to be preserved, if not enhanced, during simulated hypertension. Contrary to our findings in young men, these results suggest there are sex differences in CBR function during WBH. This diminished ability to increase MAP and HR in response to a hypotensive stimulus during hyperthermia may be a key component in reduced orthostatic tolerance in females during WBH.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Identifying the role of group III/IV muscle afferents in the carotid baroreflex control of mean arterial pressure and heart rate during exercise.

We investigated the contribution of group III/IV muscle afferents to carotid baroreflex resetting during electrically evoked (no central command) and voluntary (requiring central command) isometric knee extension exercise. Lumbar intrathecal fentanyl was used to attenuate the central projection of μ-opioid receptor-sensitive group III/IV leg muscle afferent feedback. Spontaneous carotid baroreflex control was assessed by loading and unloading the carotid baroreceptors with a variable pressure neck chamber. Group III/IV muscle afferents did not influence spontaneous carotid baroreflex responsiveness at rest or during exercise. Afferent feedback accounted for at least 50% of the exercise-induced increase in the carotid baroreflex blood pressure and heart rate operating points, adjustments that are critical for an appropriate cardiovascular response to exercise. These findings suggest that group III/IV muscle afferent feedback is, independent of central command, critical for the resetting of the carotid baroreflex blood pressure and heart rate operating points, but not for spontaneous baroreflex responsiveness. This study sought to comprehensively investigate the role of metabolically and mechanically sensitive group III/IV muscle afferents in carotid baroreflex responsiveness and resetting during both electrically evoked (EVO, no central command) and voluntary (VOL, requiring central command) isometric single-leg knee-extension (15% of maximal voluntary contraction; MVC) exercise. Participants (n=8) were studied under control conditions (CTRL) and following lumbar intrathecal fentanyl injection (FENT) to inhibit μ-opioid receptor-sensitive lower limb muscle afferents. Spontaneous carotid baroreflex control of mean arterial pressure (MAP) and heart rate (HR) were assessed following rapid 5s pulses of neck pressure (NP, +40mmHg) or suction (NS, -60mmHg). Resting MAP (87±10mmHg) and HR (70±8bpm) were similar between CTRL and FENT conditions (P>0.4). In terms of spontaneous carotid baroreflex responsiveness, FENT did not alter the change in MAP or HR responses to NP (+13±5mmHg, P=0.85; +9±3bpm; P=0.99) or NS (-13±5mmHg, P=0.99; -24±11bpm; P=0.49) at rest or during either exercise protocol, which were of a remarkably similar magnitude to rest. In contrast, FENT administrationreduced the exercise-induced resetting of the operating point for MAP and HR during both EVO (116±10mmHg to 100±15mmHg and 93±14bpm to 82±10bpm) and VOL (107±13mmHg to 100±17mmHg and 89±10bpm to 72±10bpm) exercise bouts. Together, these findings document that group III/IV muscle afferent feedback is critical for the resetting of the carotid baroreflex MAP and HR operating points, independent of exercise-induced changes in central command, but not for spontaneous carotid baroreflex responsiveness.

Group III/IV muscle afferents contribute to carotid baroreflex resetting during evoked contractions in humans

BackgroundArterial baroreflexes play an important role in the control and regulation of the cardiovascular response to exercise. In fact, carotid baroreflex control of arterial blood pressure needs to be reset during exercise to tolerate the higher blood pressures associated with physical activities. This resetting of carotid baroreflex control to operate at a higher blood pressure during exercise is thought to be mediated by both feedback and feed forward mechanisms.PurposeTo investigate the contribution of group III/IV muscle afferents to the carotid baroreflex control during evoked quadriceps contractions, devoid of feed forward input (i.e. no central command).MethodsEight recreationally active males (29 ± 5 yrs) performed electrically evoked isometric quadriceps contractions for 10 min (femoral nerve stimulation, 40 Hz, 50‐s on, 10‐s off) under control conditions (CTRL) and following lumbar intrathecal fentanyl (FENT) injection to impair feedback from μ‐opioid receptor sensitive lower limb muscle afferents. Carotid baroreflex function was assessed by applying rapid 5‐s pulses of neck pressure (NP, +40 mmHg) or suction (NS, −60 mmHg) via a customized collar. Heart rate (HR) and mean arterial pressure (MAP) were derived from a 12‐lead ECG and a radial arterial catheter, respectively. The carotid baroreflex operating point was determined using the average pre‐stimulus values for HR and MAP.ResultsResting HR (~70 bpm) and MAP (~87 mmHg) were similar between CTRL and FENT conditions (P &gt; 0.4). FENT administration did not alter the cardiac response to NP (+9 ± 3 bpm; P = 0.99) or NS (−24 ± 11 bpm; P = 0.49) at rest. Similarly, FENT did not alter changes in MAP in response to NP (+13 ± 5 mmHg; P = 0.85) or NS (−13 ± 5 mmHg; P = 0.99) at rest. During exercise, FENT attenuated both HR (82 ± 10 bpm vs 93 ± 14 bpm; P &lt; 0.05) and MAP (100 ± 14 mmHg vs 112 ± 14 mmHg; P &lt; 0.05). However, similar to resting responses (P &gt; 0.4), the cardiac response to NP (+11 ± 4 bpm) or NS (−23 ± 9 bpm) was similar during CTRL and FENT exercise (P &gt; 0.5). Furthermore, changes in MAP in response to NP (+12 ± 4 mmHg) or NS (−14 ± 5 mmHg) were similar during CTRL and FENT exercise (P &gt; 0.4).ConclusionInhibition of group III/IV muscle afferents during evoked muscle contractions reduced the operating point for both HR and MAP, suggesting this feedback pathway is important for carotid baroreflex resetting during exercise. However, carotid baroreflex responsiveness at rest and during exercise was preserved despite muscle afferent blockade, indicating that group III/IV muscle afferents do not govern the carotid baroreflex control of HR and MAP.Support or Funding InformationThe authors were supported by National Heart, Lung, and Blood Institute grants (HL‐103786 and HL‐116579) and a Veterans Affairs Spire grant (E1572P).

Dynamic Carotid Baroreflex Function at the Onset of Leg Cycling

Carotid baroreflex (CBR) controls blood pressure (BP) by altering heart rate (HR), cardiac output (CO) and total vascular conductance (TVC) on a beat‐to‐beat basis at rest and during exercise. However, functional changes in CBR are known to occur during exercise. For example, the decrease in HR during CBR stimulation with neck suction (NS) is attenuated in the first 5 s of static handgrip exercise. In contrast, BP decrease by NS in the first 5 s of static handgrip exercise is similar to that obtained in resting conditions, and the decrease in both HR and BP by NS are similar to rest after 40 s of static handgrip exercise, evidencing a dynamic modulation of CBR control of HR at the onset of handgrip and a differential CBR control of HR and BP. Considering that regulatory mechanisms and physiological responses to exercise are affected by muscle mass, type and intensity of muscle contraction, we investigated whether CBR function is dynamically modulated during 45‐s leg cycling. Fifteen male healthy subjects (age: 24 ± 1 years (mean ± SEM); height: 182 ± 2 cm; weight: 74 ± 3 kg) were screened for CBR responsiveness at rest, using an adjustable collar around the anterior portion of the neck for application of 5‐s NS pulses at −60 mmHg. In addition, workloads for steady‐state low‐ (90 heart beats/min; LI) and moderate‐intensity (130 heart beats/min; MI) exercise at 60 rpm were determined by 3‐min cycling bouts. These workloads were used in a second visit, when subjects performed 45‐s LI and MI leg cycling bouts, without (CTRL) or with NS application during 0–5 s (NS 0–5), 10–15 s (NS 10–15) or 30–35 s (NS 30–35) after the onset of cycling. NS was applied at the end of a normal expiration. Each combination of exercise intensity and NS application was repeated for three exercise bouts and data were averaged for individual responses. Resting CBR was also assessed during a breath hold. Beat‐to‐beat HR (ECG) and BP (Finometer) were measured, stroke volume (SV) was obtained by Modelflow, CO and TVC were calculated (CO = HR SV; TVC = CO/BP), and the respiratory movements were monitored (Pneumobelt). Compared to CTRL cycling, reflex bradycardia was obtained at all exercising NS applications (P &lt; 0.05). The reflex response was small at NS 0–5 in both cycling intensities, as compared to resting NS (LI and MI: −7 ± 1 vs. Rest: −9 ± 1 beats/min; P &lt; 0.05). NS 10–15 and NS 30–35 in both cycling intensities resulted in bradycardia similar to resting NS (P &gt; 0.05). Transient BP decrease was observed at all exercising NS applications (P &lt; 0.05), compared to CTRL cycling. The NS‐induced BP decrease at NS 0–5 (LI and MI: −9 ± 1 mmHg) and NS 10–15 (LI and MI: −8 ± 1 mmHg) was significantly greater than at rest (−5 ± 1 mmHg; P &lt; 0.05 vs. NS 0–5 and NS 10–15). NS 30–35 in both cycling intensities resulted in BP decrease similar to resting NS (P &gt; 0.05). The NS‐induced exaggerated BP decrease during cycling was accompanied by a greater increase of TVC at NS 0–5 (LI: +13 ± 4; MI: +15 ± 3 mL/min/mmHg) and at NS 10–15 of MI cycling (+12 ± 2 mL/min/mmHg) than that obtained at rest (+3 ± 2 mL/min/mmHg; P &lt; 0.05), while the decrease in CO during NS was similar to rest (P &gt; 0.05). Cardiovascular responses to NS were similar between exercise intensities (P &gt; 0.05). A differential dynamic CBR control of HR and BP was detected in the transition from rest to cycling, i.e., CBR control of HR was blunted in the first 5 s, while CBR control of BP was exaggerated in the first 15 s cycling.Support or Funding InformationCAPES Foundation, Science without Borders Program, Brazil; Ehrenreich Fond, Denmark.

Carotid baroreflex responsiveness in normotensive African Americans is attenuated at rest and during dynamic leg exercise

Evidence suggests differences between African Americans (AAs) and Caucasian Americans (CAs) in cardiovascular responsiveness to physiological stressors. This study tested the hypothesis that carotid baroreflex (CBR) control of heart rate (HR) and blood pressure is reduced in AAs compared to CAs during exercise. Mean arterial pressure (MAP) and HR were continuously recorded at rest and during leg cycling in 23 non-hypertensive male subjects (12 AA; 11 CA; age 19–26 years). CBR control of HR and MAP was assessed with 5-s pulses of neck pressure (NP, simulated hypotension) and neck suction (NS, simulated hypertension) ranging from +45 to −80 Torr. Across all NS stimuli (−20, −40, −60, −80 Torr) at rest, the AA group demonstrated attenuated CBR-mediated reductions in HR (AA, −8.9 ± 1.9 vs. CA, −14.1 ± 2.3 bpm; P < 0.001) and MAP (AA, −6.4 ± 1 vs. CA, −7.8 ± 0.8 mmHg; P < 0.05). Despite similar gain and magnitude of resetting observed in the modeled stimulus response curves, an attenuation among AAs persisted in HR (AA, −8.2 ± 1.6 vs. CA, −11.8 ± 3 bpm; P < 0.05) and MAP (AA, −6.8 ± 0.9 vs. CA, −8.2 ± 1.1 mmHg; P < 0.05) responses to NS during exercise. No differences in CBR-mediated HR and MAP responses to NP were detected between groups at rest or during exercise. These data suggest impairment in the ability to defend against a hypertensive challenge among AAs during steady-state exercise compared to their CA counterparts.

Role of Carotid Baroreflex and Sympathetic Responses in the Push-Pull Effect: A Simulation Study

The push-pull maneuver (PPM) can lead to loss of consciousness in pilots of high-performance aircraft. This paper presents a mathematical model for the simulation of carotid baroreflex function and sympathetic responses during PPM. The previous model was first modified by incorporating a submodel of the carotid baroreflex and then validated by comparing the simulation results with experimental data. Then the role of the carotid baroreflex was evaluated by varying the time delay and gain of the baroreflex independently during PPM and control runs, and the influence of different PPM profiles on sympathetic efferent activities were predicted. Model outputs suggest that the effects of carotid baroreflex regulation with different time delays and gain factors on the push-pull effect (PPE) are almost the same as those on the control run. Meanwhile, simulation of sympathetic responses indicates that the frequency of spikes in the efferent sympathetic nerves increases with higher magnitude and longer duration of -Gz exposure, as well as with higher magnitude of +Gz exposure. However, the effect of changed sympathetic responses may be alleviated when transferred to baroreflex effectors. The simulation results support that the carotid baroreflex and sympathetic responses might have little specific influences on the PPE. It also suggests that the limited range of G alteration and transition rate should be considered when using tilting experiments to investigate sympathetic response to PPE. The limitation of the present model due to the lack of sufficient data on the contribution of different peripheral vascular beds and their myogenic response is discussed.

Baroreflex responsiveness is attenuated in African Americans during steady‐state leg exercise

Carotid baroreflex (CBR) responsiveness is impaired in African Americans (AA) compared to Caucasian Americans (CA) at rest. In addition, AA exhibit greater blood pressure responses to exercise compared to CA. We tested the hypothesis that CBR control of heart rate (HR) and mean arterial pressure (MAP) is reduced in AA compared to CA during steady‐state leg exercise. CBR control of HR and MAP was assessed in 11 AA and 11 CA subjects using 5s trials of neck pressure (NP, simulated hypotension: +45, +30, +15 Torr) and neck suction (NS, simulated hypertension: −20, −40, −60, −80 Torr). At rest, no racial differences were found in either the mean HR or the mean MAP responses to NP. While MAP responses to NS were similar between races at rest, the mean HR response to NS was attenuated in the AA group (−8.6±2.0bpm) compared to the CA group (−14.4±2.3bpm, p&lt;0.05). During exercise (50% VO2peak), again no racial differences were found in either the mean HR or mean MAP responses to NP. However, the mean HR response to NS tended to be reduced in the AA group (−7.9±1.7bpm) compared to the CA group (− 11.0±3.1bpm, p=0.069) during exercise. Interestingly, the mean MAP response to NS was impaired in the AA group (− 6.5±0.8mmHg) compared to the CA group (−8.0±1.2mmHg, p&lt;0.05) during exercise. These findings support inherent differences in CBR responsiveness in AA compared to CA during both rest and exercise.Support by NIH Grant R15HL096103

Arterial baroreflex control of muscle sympathetic nerve activity under orthostatic stress in humans

The mechanisms by which blood pressure is maintained against the orthostatic stress caused by gravity's effect on the fluid distribution within the body are important issues in physiology, especially in humans who usually adopt an upright posture. Peripheral vasoconstriction and increased heart rate (HR) are major cardiovascular adjustments to orthostatic stress and comprise part of the reflex response elicited via the carotid sinus and aortic baroreceptors (arterial baroreflex: ABR) and cardiopulmonary stretch receptors (cardiopulmonary baroreflex). In a series of studies, we have been characterizing the ABR-mediated regulation of cardiovascular hemodynamics and muscle sympathetic nerve activity (MSNA) while applying orthostatic stress in humans. We have found that under orthostatic stress, dynamic carotid baroreflex responses are modulated as exemplified by the increases in the MSNA, blood pressure, and HR responses elicited by carotid baroreflex unloading and the shorter period of MSNA suppression, comparable reduction and faster recovery of mean arterial blood pressure (MAP) and greater HR response to carotid baroreflex stimulation. Our results also show that ABR-mediated beat-to-beat control over burst incidence, burst strength and total MSNA is progressively modulated as orthostatic stress is increased until induction of syncope, and that the sensitivity of ABR control over the aforementioned MSNA variables is substantially reduced during the development of syncope. We suggest that in humans, the modulation of ABR function under orthostatic stress may be one of the mechanisms by which blood pressure is maintained and orthostatic hypotension limited, and impairment of ABR control over sympathetic vasomotor activity leads to the severe hypotension associated with orthostatic syncope.

Carotid baroreflex responsiveness is impaired in normotensive African American men

There are important differences in autonomic function and cardiovascular responsiveness between African Americans (AA) and Caucasian Americans (CA). This study tested the hypothesis that carotid baroreflex (CBR) responsiveness is impaired in normotensive AA compared with normotensive CA at rest. CBR control of heart rate (HR) and mean arterial blood pressure (MAP) was assessed in 30 nonhypertensive male subjects (15 AA; 15 CA; age 18-33 yr) with 5-s periods of neck pressure (NP; simulated hypotension) and neck suction (NS; simulated hypertension) ranging from +45 to -80 Torr during rest. Carotid-cardiac stimulus-response curves revealed a significantly lower minimum HR response in the CA compared with AA (40.8 ± 2.4 vs. 49.8 ± 2.9 beats/min, respectively; P < 0.05). In addition, the magnitude of the mean HR response to all trials of NS (-20, -40, -60, and -80 Torr) was attenuated in the AA group (AA, -10.1 ± 1.7 vs. CA, -14.9 ± 2.2 beats/min; P < 0.05), while no significant differences were found in the magnitude of the mean HR response to NP (+15, +30, and +45 Torr) between racial groups. There were no significant differences in the carotid-vasomotor stimulus-response curves between racial groups. Also, while no racial differences were found in the magnitude of the mean MAP response to all trials of NS, the magnitude of the mean MAP response to all trials of NP was attenuated in the AA group (AA, 7.2 ± 1.3 vs. CA, 9.3 ± 1.1 mmHg; P < 0.05). Together, these findings support inherent differences in short-term blood pressure regulation between racial groups that exhibit different relative risk for the development of hypertension.

Exercise in hypertension: do skeletal muscle reflexes make this a dangerous proposition?

the benefits of exercise and exercise training are numerous, varying from increasing skeletal muscle strength to enhancing cardiovascular and respiratory fitness. These attributes of exercise are key elements to the maintenance of good health and the improvement of athletic performance. But are

Alterations in carotid baroreflex control of arterial blood pressure during the menstrual cycle in young women

Limited studies have suggested that menstrual cycle variations in sex hormones may influence arterial baroreflex control of heart rate (HR) and sympathetic nerve activity; however, results are equivocal. In addition, the baroreflex control of blood pressure (BP) has not been directly examined as pharmacological perturbations were mainly used to assess baroreflex function. Therefore, 5s pulses of neck suction (NS, −60 Torr) and neck pressure (NP, +40 Torr) were applied to load and unload the carotid baroreflex (CBR), respectively in young women during the early follicular (EF, day 1–5, low estrogen, low progesterone), late follicular (LF, day 10–12, high estrogen, low progesterone), and mid luteal (ML, day 20–24, high estrogen, high progesterone) menstrual cycle phases. Resting HR and BP were not different between the 3 phases. Similarly, HR responses to NP and NS were not significantly different between phases. In contrast, mean BP responses to NP were significantly greater in the ML phase (Δ17±1 vs. Δ13±1 EF; Δ13±2 LF mmHg; P&lt;0.05); however, responses to NS were not significantly different between phases (EF Δ−10±2, LF Δ−10±1, and ML Δ−10±1 mmHg). These preliminary findings suggest a maintained CBR control of HR throughout the menstrual cycle whereas concomitant elevations in estrogen and progesterone selectively augment CBR‐mediated BP responses to hypotension without effect on CBR responses to hypertension.Supported by R01HL093167.

Mathematical Modeling of the Push-Pull Effect for Various Acceleration Profiles and Countermeasures

The push-pull maneuver (PPM) can lead to loss of consciousness in pilots of high-performance aircraft. Modeling of the physical and physiological aspects of this phenomenon should allow improved countermeasures. A structurally based mechanistic computer model was developed to incorporate dynamic carotid baroreflex responses and detailed modeling of vessel segments for different anatomic regions. The model was used to predict the effect of the PPM on cardiovascular responses and the protection afforded by extended coverage anti-G suits (ECGS) and neck pressure. The model was validated by comparing the simulation results with previously published experimental data obtained during centrifuge and tilt-table studies. Simulations of various PPM acceleration profiles indicated that +Gz tolerance was reduced in the presence of higher +Gz levels prior to the push phase, more -Gz levels during the push phase, and prolongation of the push phase. On the other hand, the onset rate for the two phases had only minor effects on +Gz tolerance. Model output suggested that improved protection could be provided by an ECGS with minimal inflation delay and a multilevel pressure schedule in which the leg bladders inflated to a higher pressure than the abdominal bladder. Modeling application of a 100-mmHg neck pressure during the push phase partly inactivated the carotid baroreflex, but induced only a small increase in tolerance. Mathematical modeling and simulation showed that +Gz tolerance for the PPM might be increased by improving the design and inflation schedule of the ECGS.

Adventitial Stripping for Carotid Sinus Syndrome

Patients with a carotid sinus syndrome (CSS) suffer from spells of dizziness and loss of conscience due to an exaggerated carotid baroreflex response. Three types of the syndrome are described: cardioinhibitory, vasodepressor and a mixed form. The gold standard for treatment is insertion of a pacemaker, but this therapy may be effective only in a pure cardioinhibitory type. In contrast, surgically interrupting afferent nerves at the origin may offer relief of symptoms in all three types. The present review analyzes the results of a surgical technique termed "adventitial stripping" of the carotid sinus. Data from 130 procedures demonstrate that carotid denervation is effective in 85% of CSS cases with low complication rates. Postoperative monitoring is mandatory as transient alterations in blood pressure and heart rate may occur.

Baroreflex and Muscle Metaboreflex

During heavy exercise, the arterial baroreflex and the reflexes evoked by the 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 the modulation of the primary cardiovascular reflex responses. For the past few years, our group has been investigating the interaction between the arterial baroreflex and the muscle metaboreflex. We have focused our efforts in identifying the effects of muscle metaboreflex activation on the arterial baroreflex regulation of the cardiovascular hemodynamics and muscle sympathetic nerve activity (MSNA) in humans. In a series of studies, we have found that during muscle metaboreflex activation, dynamic carotid baroreflex responses are modulated, as exemplified by the augmentation of the MSNA, leg vascular conductance and blood pressure responses to carotid baroreflex unloading and the shorter suppression period of MSNA, diminished vasodilation, and reduced blood pressure response to carotid baroreflex stimulation. Furthermore, we have found that the modification of the arterial baroreflex-mediated beat-to-beat control of MSNA, which is seen during activation of the muscle metaboreflex (i.e., resetting and an increase in sensitivity), could be a consequence of the alteration in the arterial baroreflex control of both the occurrence and strength of the MSNA burst. In addition, we have demonstrated that the arterial baroreflex beat-to-beat control of MSNA is time-dependently modulated during isometric exercise. We suggest that the modulation of arterial baroreflex function during the activation of muscle metaboreflex is one of the mechanisms for increasing, or maintaining, blood pressure at the required pressure and thereby contributes to the regulation of the cardiovascular system during exercise.

Carotid-Cardiac Baroreflex Function Does Not Influence Blood Pressure Regulation during Head-Up Tilt in Humans

The influence of the carotid-cardiac baroreflex on blood pressure regulation was evaluated during supine rest and 40 degrees head-up tilt (HUT) in 9 healthy young subjects with and without full cardiac vagal blockade. The carotid baroreflex responsiveness, or maximal gain (G(MAX)), was assessed from the beat-to-beat changes in heart rate (HR) and mean arterial pressure (MAP) by the variable neck pressure and suction technique ranging in pressure from +40 to -80 Torr, with and without glycopyrrolate (12.0 +/- 1.0 microg/kg body weight; mean +/- SE). In the supine position, glycopyrrolate increased the HR to 91 +/- 3 bpm, from 54 +/- 3; MAP to 89 +/- 2 mmHg, from 76 +/- 2; and cardiac output to 6.8 +/- 0.3 l.min(-1), from 4.9 +/- 0.3 (P < 0.05). The G(MAX) of the carotid baroreflex control of HR was reduced to -0.06 +/- 0.01 bpm.mmHg(-1), from -0.30 +/- 0.02 (P < 0.05) with no significant effect on the G(MAX) of the carotid baroreflex control of MAP. During HUT the carotid baroreflex control of MAP was unchanged, though the G(MAX) of the carotid baroreflex control of HR was increased (P < 0.05). During HUT, central blood volume, assessed by electrical thoracic admittance, and total vascular conductance were decreased with and without glycopyrrolate. Furthermore, glycopyrrolate reduced G(MAX) of the carotid baroreflex control of HR during HUT (P < 0.05) with no significant effect on G(MAX) of the carotid baroreflex control of MAP. These data suggest that during supine rest and HUT-induced decreases in central blood volume, the carotid baroreflex control of HR is mediated primarily via parasympathetic activity. Furthermore, the maintenance of arterial blood pressure during postural stress is primarily mediated by arterial and cardiopulmonary reflex regulation of sympathetic activity and its effects on the systemic vasculature.

Whole-body heating slows carotid baroreflex response in human subjects

Heat stress increases sympathetic activity and decreases parasympathetic activity to the heart. To test the hypothesis that carotid baroreflex responses of heart rate (HR) and systemic blood pressure become slowed with altered autonomic nerve activities during whole-body heat stress, we determined changes in HR and mean arterial pressure (MAP) in response to approximately 5 s of 40 mmHg neck pressure (NP) and of -65 mmHg neck suction (NS) in normothermia and during whole-body heating produced by a hot water-perfused suit. The NP and NS stimuli were triggered by R waves of an ECG during held expiration in the supine position. Whole-body heating did not alter the onset time of the HR and MAP responses during NP and NS. Whole-body heating significantly increased the time from onset of the HR response until peak of the response during NP (2.53 +/- 0.33 s in normothermia and 3.46 +/- 0.28 s during heating, P<0.05) and NS (1.20 +/- 0.23 s and 2.24 +/- 0.29 s, P<0.05). Whole-body heating significantly increased the time from onset of the MAP response until peak of the response during NP (4.31+/-0.46 s in normothermia, 6.67 +/- 0.56 s during heating, P<0.05) but not during NS (5.06 +/- 0.47 s and 4.50 +/- 0.60 s). These findings suggest that heat stress prolongs the response time of carotid-cardiac and carotid-vasomotor baroreflexes.

The Effect Of Aerobic Fitness On The Carotid Baroreflex Function During Exercise

Chronic endurance exercise training induces changes in cardiovascular structure and haemodynamic function that result in an attenuation of the baroreflex control of the vasculature at rest. PURPOSE This investigation examined the effect of aerobic fitness on the carotid baroreflex (CBR) function during exercise. METHOD Eight average fit (AF) individuals, with a mean maximal oxygen uptake (VO2max) of 44±1 (ml O2) kg−1 min−1, and eight elite rowers (HF), with a VO2max of 72±1 (ml O2) kg−1 min−1, voluntarily participated in the investigation. CBR function was determined at rest and during 15 min of cycle exercise at a heart rate (HR) of 120 beats min−1. Acute changes in carotid sinus transmural pressure were evoked using 5 s pulses of neck pressure (NP) and neck suction (NS) from +40 to −80 Torr (+5.33 to −10.67 kPa). Beat-to-beat changes in HR and mean arterial pressure (MAP) were recorded throughout. The maximal gain of the carotidDHR (GmaxDHR) and carotidDMAP (GmaxDMAP) baroreflex function curves was identified as measures of CBR responsiveness. RESULTS During exercise the CBR-HR response ranges (15±1, vs. 17±1 bpm) and GmaxDHR (−0.41±0.09 vs. −0.44±0.11 bpm mmHg−1, for the HF and AF, respectively) were similar in the two groups. In contrast, both the CBR-MAP response range (17.7±5.4 vs. 26.7±5.4 mmHg, p < 0.05) and the GmaxDMAP (−0.63±0.19 vs. −0.43±0.12 mmHg mmHg−1, p < 0.05) were smaller in the HF compared with the AF. CONCLUSION The data suggest that endurance training results in an attenuated CBR control of blood pressure during exercise, while the CBR control of HR is maintained.