Carotid Baroreflex Control Of Heart Rate Research Articles

Interaction between graviception and carotid baroreflex function in humans during parabolic flight-induced microgravity.

The aim of the present study was to assess carotid baroreflex (CBR) function during acute changes in otolithic activity in humans. To address this question, we designed a set of experiments to identify the modulatory effects of microgravity on CBR function at a tilt angle of -2°, which was identified to minimize changes in central blood volume during parabolic flight. During parabolic flight at 0 and 1 g, CBR function curves were modeled from the heart rate (HR) and mean arterial pressure (MAP) responses to rapid pulse trains of neck pressure and neck suction ranging from +40 to -80 Torr; CBR control of HR (carotid-HR) and MAP (carotid-MAP) function curves, respectively. The maximal gain of both carotid-HR and carotid-MAP baroreflex function curves were augmented during microgravity compared with 1 g (carotid-HR, -0.53 to -0.80 beats·min-1·mmHg-1, P < 0.05; carotid-MAP, -0.24 to -0.30 mmHg/mmHg, P < 0.05). These findings suggest that parabolic flight-induced acute change of otolithic activity may modify CBR function and identifies that the vestibular system contributes to blood pressure regulation under fluctuations in gravitational forces. NEW & NOTEWORTHY The effect of acute changes in vestibular activity on arterial baroreflex function remains unclear. In the present study, we assessed carotid baroreflex function without changes in central blood volume during parabolic flight, which causes acute changes in otolithic activity. The sensitivity of both carotid heart rate and carotid mean arterial pressure baroreflex function was augmented in microgravity compared with 1 g, suggesting that the vestibular system contributes to blood pressure regulation in humans on Earth.

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).

Carotid baroreflex control of heart rate is enhanced, while control of mean arterial pressure is preserved during whole body heat stress in young healthy men.

Whole body heat stress (WBH) results in numerous cardiovascular alterations that ultimately reduce orthostatic tolerance. While impaired carotid baroreflex (CBR) function during WBH has been reported as a potential reason for this decrement, study design considerations may limit interpretation of previous findings. We sought to test the hypothesis that CBR function is unaltered during WBH. CBR function was assessed in 10 healthy male subjects (age: 26 ± 3; height: 185 ± 7 cm; weight: 82 ± 10 kg; BMI: 24 ± 3 kg/m2; means ± SD) using 5-s trials of neck pressure (+45, +30, and +15 Torr) and neck suction (-20, -40, -60, and -80 Torr) during normothermia (NT) and passive WBH (Δ core temp ∼1°C). Analyses of stimulus response curves (four-parameter logistic model) for CBR control of heart rate (CBR-HR) and mean arterial pressure (CBR-MAP), as well as separate two-way ANOVA of the hypotensive and hypertensive stimuli (factor 1: thermal condition, factor 2: chamber pressure), were performed. For CBR-HR, maximal gain was increased during WBH (-0.73 ± 0.11) compared with NT (-0.39 ± 0.04, mean ± SE, P = 0.03). In addition, the CBR-HR responding range was increased during WBH (33 ± 5) compared with NT (19 ± 2 bpm, P = 0.03). Separate analysis of hypertensive stimulation revealed enhanced HR responses during WBH at -40, -60, and -80 Torr (condition × chamber pressure interaction, P = 0.049) compared with NT. For CBR-MAP, both logistic analysis and separate two-way ANOVA revealed no differences during WBH. Therefore, in response to passive WBH, CBR control of heart rate (enhanced) and arterial pressure (no change) is well preserved.

Carotid baroreflex control of heart rate is enhanced during whole‐body heat stress

Whole‐body heat stress (WBH) reduces orthostatic tolerance. While impaired carotid baroreflex (CBR) function during WBH has been reported, study design considerations may limit interpretation of previous findings. We sought to test the hypothesis that CBR function is unaltered during WBH. CBR function was assessed in ten subjects using 5‐sec trials of neck pressure (45, 30 and 15 Torr) and neck suction (−20, −40, −60 and − 80 Torr) during normothermia (NT) and passive WBH (Δ core temp ~1 °C). Analysis of stimulus response curves (4‐parameter logistic model) for CBR control of heart rate (CBR‐HR) and mean arterial pressure (CBR‐MAP), as well as separate 2‐way ANOVA of the hypo‐ and hypertensive stimuli (factor 1: thermal condition, factor 2: chamber pressure) were performed. For CBR‐HR, maximal gain was increased during WBH (−0.73±0.37) compared to NT (−0.39±0.11, p=0.03). In addition, the CBR‐HR responding range was increased during WBH (32±15) compared to NT (18±8 bpm, p=0.03). Separate analysis of hypertensive stimulation revealed enhanced HR responses during WBH at −40, −60 and −80 Torr (condition*chamber pressure interaction, p=0.049) compared to NT. For CBR‐MAP, both logistic analysis and separate 2‐way ANOVA revealed no differences during WBH. Therefore, despite marked orthostatic intolerance observed during WBH, CBR control of heart rate (enhanced) and arterial pressure (no change) is well‐preserved.

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.

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

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.

Carotid baroreflex control of heart rate and blood pressure in African Americans at rest and during exercise

African Americans (AA) are at an elevated risk for developing hypertension. Furthermore, previous studies have indicated exaggerated blood pressure responses to exercise among AA compared to Caucasian Americans (CA). However, little is known about baroreflex function in this racial group. The purpose of this study was to test the hypothesis that carotid baroreflex (CBR) control of heart rate (HR) and blood pressure is reduced in AA at rest and during exercise compared to CA. CBR control of HR and mean arterial blood pressure (MAP) was assessed in ten non-hypertensive men (5 AA and 5 CA, age 20–26 yr) using 5-sec trials of neck suction (NS, simulated hypertension) ranging from −20 to −80 Torr during rest and steady-state leg cycling (50% VO2MAX). At rest, the mean HR response to all trials of NS was attenuated in the AA group (AA, −10±4) compared to the CA group (−16±4 bpm), P<0.05. However, the mean MAP response to all trials of NS was not different between racial groups (AA, −6±2 vs CA, −7±2 mmHg). During steady-state exercise, no significant differences for the response to all trials of NS were found between racial groups for both HR (AA, −9±3 vs CA, −12±6 bpm) and MAP (AA, −6±1 vs CA, −8±2 mmHg). These findings suggest a potential difference in CBR control of the heart between AA and CA at rest, but that these differences may not be present during dynamic exercise. Support by NIH Grant R15HL096103

The carotid baroreflex is reset following prolonged exercise in humans

Alterations in the carotid baroreflex (CBR) control of arterial pressure may explain the reduction in arterial pressure and left ventricular (LV) function after prolonged exercise. We examined the CBR control of heart rate (HR) and mean arterial pressure (MAP), in addition to changes in LV function, pre- to post-exercise. Seven males (age, mean ± SEM; 29 ± 4 years) completed 4 h of ergometer rowing at a workload of 10-15% below the lactate threshold. The CBR control of HR and MAP was assessed via the rapid neck-suction/pressure protocol. LV systolic function was measured by echocardiography, where ejection fraction (EF), the ratio of systolic blood pressure to end systolic volume (SBP/ESV) and stroke volume (SV) were estimated. Following exercise MAP was reduced (12 ± 3%) and HR was elevated (35 ± 5%; P < 0.05). Furthermore, CBR control of MAP was relocated to the left on the stimulus-response curve (P < 0.05) demonstrating that the CBR operated around a lower arterial pressure. Concomitantly, LV systolic function was reduced, indicated by a decrease in EF (22 ± 2%), SBP/ESV (32 ± 14%) and SV (25 ± 5%, P < 0.05). The reduced EF and SBP/ESV were associated with the decreased MAP operating point (r² = 0.71 and r² = 0.47, respectively, P < 0.05). The CBR is reset after prolonged exercise to a lower prevailing arterial pressure. This resetting of the CBR may contribute to the reduction arterial pressure and LV function after exercise.

Sex Differences In Carotid Baroreflex Control Of Heart Rate At Rest And During Dynamic Exercise In Humans

Previous studies in animals have demonstrated that the arterial baroreflex control of heart rate (HR) was greater in female compared to male rodents. In contrast, equivocal results have been reported in humans with several studies reporting that young women, in fact, exhibit a reduced cardiac baroreflex sensitivity compared to young men. In addition, to date, no studies have examined differences in the baroreflex control of HR during exercise in young men and women. PURPOSE: To determine if the carotid baroreflex control of HR differs between young men and women at rest or during dynamic exercise. METHODS: Beat-to-beat HR and blood pressure were measured in nine young women (22±1 yr) and men (22±1 yr) at rest and during steady-state leg cycling at 50% HR reserve. All women were studied during the early follicular phase of the menstrual cycle (days 2-5). Five second pulses of neck suction (NS, -60 Torr) and neck pressure (NP, + 40 Torr) were applied to selectively load and unload the carotid baroreceptors, respectively. In addition, HR variability analyses were employed to investigate time and frequency domain indices of parasympathetic and sympathetic control of HR. RESULTS: At rest and during exercise, HR responses to NS were significantly greater in women than men (rest, D -16±3 women vs. D -8±1 men bpm, P = 0.002; exercise, D -17±3 women vs. D -6±1 men bpm, P = 0.004), whereas responses to NP were similar between groups (rest, D + 7±1 women vs. D + 5±1 men bpm, P = 0.222; exercise, D + 4±1 women vs. D + 2±1 men bpm, P = 0.096). In addition, there were no differences in HR variability measurements between women and men both at rest and during exercise. CONCLUSION: Carotid baroreflex mediated HR responses to a hypertensive challenge are greater in young women both at rest and during exercise. In contrast, the ability of the carotid-cardiac baroreflex to respond to a hypotensive challenge is similar between young women and men. Overall, these preliminary data suggest that sex differences in cardiac baroreflex responses are selective to hypertensive challenges both at rest and during exercise.

Effect of muscle metaboreflex activation on carotid-cardiac baroreflex function in humans

Whether the activation of metabolically sensitive skeletal muscle afferents (i.e., muscle metaboreflex) influences cardiac baroreflex responsiveness remains incompletely understood. A potential explanation for contrasting findings of previous reports may be related to differences in the magnitude of muscle metaboreflex activation utilized. Therefore, the present study was designed to investigate the influence of graded intensities of muscle metaboreflex activation on cardiac baroreflex function. In eight healthy subjects (24 +/- 1 yr), the graded isolation of the muscle metaboreflex was achieved by post-exercise ischemia (PEI) following moderate- (PEI-M) and high- (PEI-H) intensity isometric handgrip performed at 35% and 45% maximum voluntary contraction, respectively. Beat-to-beat heart rate (HR) and blood pressure were measured continuously. Rapid pulse trains of neck pressure and neck suction (+40 to -80 Torr) were applied to derive carotid baroreflex stimulus-response curves. Mean blood pressure increased significantly from rest during PEI-M (+13 +/- 3 mmHg) and was further augmented during PEI-H (+26 +/- 4 mmHg), indicating graded metaboreflex activation. However, the operating point gain and maximal gain (-0.51 +/- 0.09, -0.48 +/- 0.13, and -0.49 +/- 0.12 beats.min(-1).mmHg(-1) for rest; PEI-M and PEI-H) of the carotid-cardiac baroreflex function curve were unchanged from rest during PEI-M and PEI-H (P > 0.05 vs. rest). Furthermore, the carotid-cardiac baroreflex function curve was progressively reset rightward from rest to PEI-M to PEI-H, with no upward resetting. These findings suggest that the muscle metaboreflex contributes to the resetting of the carotid baroreflex control of HR; however, it would appear not to influence carotid-cardiac baroreflex responsiveness in humans, even with high-intensity activation during PEI.

The carotid baroreflex is reset following prolonged exercise in humans

Alterations in the carotid baroreflex (CBR) control of arterial pressure may explain the reduction in arterial pressure and left ventricular (LV) function observed after prolonged exercise. We examined the CBR control of heart rate (HR) and mean arterial pressure (MAP), in addition to changes in LV function, pre‐ to post exercise. Seven males (age, 29 ± 7 yrs) completed 4 h of ergometer rowing at a workload 10–15% below lactate threshold. CBR control of HR and MAP was assessed before and after exercise via the rapid neck suction/pressure method. LV systolic function was assessed by echocardiography, where ejection fraction (EF), systolic pressure/volume ratio (SBP/ESV) and stroke volume (SV) were estimated. After exercise MAP was reduced (12 ± 3%) and HR was elevated (35 ± 5%; P&lt;0.05), indicating a relocation of the CBR operating point. Furthermore, the CBR operating pressure was relocated to the left on the HR and MAP stimulus‐response curve (P&lt;0.05) demonstrating that the CBR operated at a lower arterial pressure. Concomitantly, EF (22 ± 2%), SBP/ESV (32 ± 14%) and SV (25 ± 5%, P&lt;0.05) were reduced after exercise. The reduced EF and SBP/ESV were associated with the decreased MAP operating point (r2=0.71 and r2=0.47, P&lt;0.05). In conclusion, the CBR is reset to a lower prevailing arterial pressure after prolonged exercise, which may contribute to the reduction arterial pressure and LV function observed.

Exercise intensity influences cardiac baroreflex function at the onset of isometric exercise in humans

We sought to examine the influence of exercise intensity on carotid baroreflex (CBR) control of heart rate (HR) and mean arterial pressure (MAP) at the onset of exercise in humans. To accomplish this, eight subjects performed multiple 1-min bouts of isometric handgrip (HG) exercise at 15, 30, 45 and 60% maximal voluntary contraction (MVC), while breathing to a metronome set at eupneic frequency. Neck suction (NS) of -60 Torr was applied for 5 s at end expiration to stimulate the CBR at rest, at the onset of HG (<1 s), and after approximately 40 s of HG. Beat-to-beat measurements of HR and MAP were recorded throughout. Cardiac responses to NS at onset of 15% (-12 +/- 2 beats/min) and 30% (-10 +/- 2 beats/min) MVC HG were similar to rest (-10 +/- 1 beats/min). However, HR responses to NS were reduced at the onset of 45% and 60% MVC HG (-6 +/- 2 and -4 +/- 1 beats/min, respectively; P < 0.001). In contrast to HR, MAP responses to NS were not different from rest at exercise onset. Furthermore, both HR and MAP responses to NS applied at approximately 40s of HG were similar to rest. In summary, CBR control of HR was transiently blunted at the immediate onset of high-intensity HG, whereas MAP responses were preserved demonstrating differential baroreflex control of HR and blood pressure at exercise onset. Collectively, these results suggest that carotid-cardiac baroreflex control is dynamically modulated throughout isometric exercise in humans, whereas carotid baroreflex regulation of blood pressure is well-maintained.

Cardiac and vasomotor components of the carotid baroreflex control of arterial blood pressure during isometric exercise in humans

We sought to examine the importance of the cardiac component of the carotid baroreflex (CBR) in control of blood pressure during isometric exercise. Nine subjects performed 4 min of ischaemic isometric calf exercise at 20% of maximum voluntary contraction. Trials were repeated with beta1-adrenergic blockade (metoprolol, 0.15 +/- 0.003 mg kg(-1)) or parasympathetic blockade (glycopyrrolate, 13.6 +/- 1.5 microg kg(-1)). CBR function was determined using rapid pulses of neck pressure and neck suction from +40 to -80 mmHg, while heart rate (HR), mean arterial pressure (MAP) and changes in stroke volume (SV, Modelflow method) were measured. Metoprolol decreased and glycopyrrolate increased HR and cardiac output both at rest and during exercise (P < 0.05), while resting and exercising blood pressure were unchanged. Glycopyrrolate reduced the maximal gain (G(max)) ofthe CBR-HR function curve (-0.58 +/- 0.10 to -0.06 +/- 0.01 beats min(-1) mmHg(-1), P < 0.05), but had no effect on the G(max) of the CBR-MAP function curve. During isometric exercise the CBR-HR curve was shifted upward and rightward in the metoprolol and no drug conditions, while the control of HR was significantly attenuated with glycopyrrolate (P < 0.05). Regardless of drug administration isometric exercise produced an upward and rightward resetting of the CBR control of MAP with no change in G(max). Thus, despite marked reductions in CBR control of HR following parasympathetic blockade, CBR control of blood pressure was well maintained. These data suggest that alterations in vasomotor tone are the primary mechanism by which the CBR modulates blood pressure during low intensity isometric 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.

The interaction of central command and the exercise pressor reflex in mediating baroreflex resetting during exercise in humans

Central command and the exercise pressor reflex can independently reset the carotid baroreflex (CBR) during exercise. The present investigation assessed the interactive relationship between these two neural mechanisms in mediating baroreflex resetting during exercise. Six men performed static leg exercise at 20% maximal voluntary contraction under four conditions: control, no perturbation; neuromuscular blockade (NMB) induced by administration of the neuromuscular blocking agent Norcuron (central command activation); MAST, application of medical antishock trousers inflated to 100 mmHg (exercise pressor reflex activation); and Combo, NMB plus MAST (concomitant central command and exercise pressor reflex activation). With regard to CBR control of heart rate (HR), both NMB and Combo conditions resulted in a further resetting of the carotid-cardiac stimulus-response curve compared to control conditions, suggesting that CBR-HR resetting is predominately mediated by central command. In contrast, it appears that CBR control of blood pressure can be mediated by signals from either central command or the exercise pressor reflex, since both NMB and MAST conditions equally augmented the resetting of the carotid-vasomotor stimulus-response curve. With regard to the regulation of both HR and blood pressure, the extent of CBR resetting was greater during the Combo condition than during overactivation of either central command or the exercise pressor reflex alone. Therefore, we suggest that central command and the exercise pressor reflex interact such that signals from one input facilitate signals from the other, resulting in an enhanced resetting of the baroreflex during exercise.

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.

Effects of exercise pressor reflex activation on carotid baroreflex function during exercise in humans.

1. This investigation was designed to determine the contribution of the exercise pressor reflex to the resetting of the carotid baroreflex during exercise. 2. Ten subjects performed 3.5 min of static one-legged exercise (20 % maximal voluntary contraction) and 7 min dynamic cycling (20 % maximal oxygen uptake) under two conditions: control (no intervention) and with the application of medical anti-shock (MAS) trousers inflated to 100 mmHg (to activate the exercise pressor reflex). Carotid baroreflex function was determined at rest and during exercise using a rapid neck pressure/neck suction technique. 3. During exercise, the application of MAS trousers (MAS condition) increased mean arterial pressure (MAP), plasma noradrenaline concentration (dynamic exercise only) and perceived exertion (dynamic exercise only) when compared to control (P < 0.05). No effect of the MAS condition was evident at rest. The MAS condition had no effect on heart rate (HR), plasma lactate and adrenaline concentrations or oxygen uptake at rest and during exercise. The carotid baroreflex stimulus-response curve was reset upward on the response arm and rightward to a higher operating pressure by control exercise without alterations in gain. Activation of the exercise pressor reflex by MAS trousers further reset carotid baroreflex control of MAP, as indicated by the upward and rightward relocation of the curve. However, carotid baroreflex control of HR was only shifted rightward to higher operating pressures by MAS trousers. The sensitivity of the carotid baroreflex was unaltered by exercise pressor reflex activation. 4. These findings suggest that during dynamic and static exercise the exercise pressor reflex is capable of actively resetting carotid baroreflex control of mean arterial pressure; however, it would appear only to modulate carotid baroreflex control of heart rate.

Cardiopulmonary baroreceptors modulate carotid baroreflex control of heart rate during dynamic exercise in humans.

Numerous studies have reported that, at rest, maximal carotid baroreflex gain is modulated by cardiopulmonary baroreceptors. The purpose of this study was to measure the maximal gain for carotid baroreflex control of heart rate (HR) and blood pressure [mean arterial pressure (MAP)] during dynamic exercise alone and when exercise was accompanied by two levels of cardiopulmonary baroreceptor unloading. Lower body negative pressure (LBNP) produced similar reductions in central venous pressure (CVP) at rest and during exercise. Baroreflex gain for HR at rest was not affected by low-level LBNP but was significantly increased by high-level LBNP [-0.31 +/- 0.05 to -0.57 +/- 0.23 beats.min-1.mmHg-1 carotid sinus pressure (CSP), no LBNP vs. high-level LBNP, P < 0.05]. Exercise combined with low- and high-level LBNP resulted in reflex HR gains (-0.83 +/- 0.44 and -0.83 +/- 0.17 beats.min-1.mmHg-1 CSP, low- vs. high-level LBNP, P < 0.05) that were significantly greater than the algebraic sum of the HR gain measured during exercise and LBNP alone. Neither exercise nor the two levels of LBNP significantly altered baroreflex gain for MAP. The slope relating HR gain to CVP at rest was significant (0.07 +/- 0.02 beats.min-1.mmHg CSP-1.mmHg CVP-1, P < 0.01) and increased 114% during exercise (P < 0.05). A similar analysis of MAP gain found no difference in slope between rest and exercise (P > 0.05). Together these data indicate 1) a tonic inhibitory interaction between cardiopulmonary baroreceptors and carotid baroreflex control of HR during exercise, and 2) a nonlinear relationship between deactivation of cardiopulmonary baroreceptors and changes in carotid baroreflex gain. This interaction may improve overall cardiovascular regulation when central blood volume and/or CVP is reduced, as has been reported during prolonged exercise in the heat.

Carotid baroreflex responsiveness to lower body positive pressure-induced increases in central venous pressure

Lower body positive pressure (LBPP) was applied at 4 and 30 Torr to increase central venous pressure (CVP). CVP increased with LBPP (r = 0.55, P < 0.01), and the increases were significant at 4 and 30 Torr (7.4 and 7.8 mmHg) from the control (6.0 mmHg). During LBPP cardiac output increased, which was significantly related to the increase in CVP (r = 0.63, P < 0.01). The carotid baroreflex was elicited by trains of neck pressure and suction from 40 to -65 Torr. The carotid-cardiac and carotid-vasomotor baroreflex responses were assessed by determining the maximal gains of heart rate (HR) interval and intraradial mean arterial pressure (MAP) to changes in carotid sinus pressure using a logistic model. The carotid-cardiac and carotid-vasomotor baroreflex gains were negatively related to LBPP, and at 30 Torr, both gains (5.6 ms/mmHg and -0.14 mmHg/mmHg) were significantly smaller than the control (12.4 ms/mmHg and -0.24 mmHg/mmHg). The decreases in carotid-cardiac and carotid-vasomotor baroreflex sensitivity during LBPP were primarily associated with the increases in CVP (r = -0.52, P < 0.01, and r = -0.74, P < 0.01, respectively). These data suggest that the increases in CVP and/or central blood volume diminish the sensitivity of the carotid baroreflex control of HR and MAP by enhancing the tonic inhibitory influence from the cardiopulmonary baroreceptors.