Dynamic blood pressure control and middle cerebral artery mean blood velocity variability at rest and during exercise in humans.

AIMS: Cardiac failure and ischaemic heart disease patients receive standard of care cardiac beta(1)-adrenergic blockade medication. Such medication reduces cardiac output and cerebral blood flow. It is unknown whether the beta(1)-adrenergic blockade-induced reduction of cardiac output in the presence of an exercise-induced reduction in cardiac-arterial baroreflex gain affects cerebral blood flow variability. This study evaluated the influence of cardiac output variability on beat-to-beat middle cerebral artery mean blood velocity (MCA V(mean)) during exercise with and without cardiac beta(1)-adrenergic blockade. METHODS: Eight men (22 +/- 1 years; mean +/- SE) performed 15 min bouts of moderate (105 +/- 11 W) and heavy (162 +/- 8 W) intensity cycling before and after cardio-selective beta(1)-adrenergic blockade (0.15 mg kg(-1) metoprolol). The relationship between changes in cardiac output or mean arterial pressure (MAP) and MCA V(mean) as well as cardiac-arterial baroreflex gain were evaluated using transfer function analysis. RESULTS: Both exercise intensities decreased the low frequency (LF) transfer function gain between cardiac output and MCA V(mean) (P < 0.05) with no significant influence of beta(1)-blockade. In contrast, the LF transfer function gain between MAP and MCA V(mean) remained stable also with no significant influence of metoprolol (P > 0.05). The LF transfer function gain between MAP and HR, an index of cardiac-arterial baroreflex gain, decreased from rest to heavy exercise with and without beta(1)-blockade (P < 0.05). CONCLUSION: These findings suggest that the exercise intensity related reduction in cardiac-arterial baroreflex function at its operating point does not influence the dynamic control of MCA V(mean), even when the ability of exercise-induced increase in cardiac output is reduced by cardiac beta(1)-adrenergic blockade.

Standing up to the challenge of standing: a siphon does not support cerebral blood flow in humans.

Model studies have been advanced to suggest both that a siphon does and does not support cerebral blood flow in an upright position. If a siphon is established with the head raised, it would mean that internal jugular pressure reflects right atrium pressure minus the hydrostatic difference from the brain. This study measured spinal fluid pressure in the upright position, the pressure and the ultrasound-determined size of the internal jugular vein in the supine and sitting positions, and the internal jugular venous pressure during seated exercise. When the head was elevated approximately 25 cm above the level of the heart, internal jugular venous pressure decreased from 9.5 (SD 2.8) to 0.2 (SD 1.0) mmHg [n = 15; values are means (SD); P < 0.01]. Similarly, central venous pressure decreased from 6.2 (SD 1.8) to 0.6 (SD 2.6) mmHg (P < 0.05). No apparent lumen was detected in any of the 31 left or right internal veins imaged at 40 degrees head-up tilt, and submaximal (n = 7) and maximal exercise (n = 4) did not significantly affect internal jugular venous pressure. While seven subjects were sitting up, spinal fluid pressure at the lumbar level was 26 (SD 4) mmHg corresponding to 0.1 (SD 4.1) mmHg at the base of the brain. These results demonstrate that both for venous outflow from the brain and for spinal fluid, the prevailing pressure approaches zero at the base of the brain when humans are upright, which negates that a siphon supports cerebral blood flow.

Carotid baroreflex function during and following voluntary apnea in humans.

Muscle sympathetic nerve activity (MSNA) and arterial pressure increase concomitantly during apnea, suggesting a possible overriding of arterial baroreflex inhibitory input to sympathoregulatory centers by apnea-induced excitatory mechanisms. Apnea termination is accompanied by strong sympathoinhibition while arterial pressure remains elevated. Therefore, we hypothesized that the sensitivity of carotid baroreflex control of MSNA would decrease during apnea and return upon apnea termination. MSNA and heart rate responses to -60-Torr neck suction (NS) were evaluated during baseline and throughout apnea. Responses to +30-Torr neck pressure (NP) were evaluated during baseline and throughout 1 min postapnea. Apnea did not affect the sympathoinhibitory or bradycardic response to NS (P > 0.05); however, whereas the cardiac response to NP was maintained postapnea, the sympathoexcitatory response was reduced for 50 s (P < 0.05). These data demonstrate that the sensitivity of carotid baroreflex control of MSNA is not attenuated during apnea. We propose a transient rightward and upward resetting of the carotid baroreflex-MSNA function curve during apnea and that return of the function curve to, or more likely beyond, baseline (i.e., a downward and leftward shift) upon apnea termination may importantly contribute to the reduced sympathoexcitatory response to NP.

New insights into differential baroreflex control of heart rate in humans.

Recent data indicate that bilateral carotid sinus denervation in patients results in a chronic impairment in the rapid reflex control of blood pressure during orthostasis. These findings are inconsistent with previous human experimental investigations indicating a minimal role for the carotid baroreceptor-cardiac reflex in blood pressure control. Therefore, we reexamined arterial baroreflex [carotid (CBR) and aortic baroreflex (ABR)] control of heart rate (HR) using newly developed methodologies. In 10 healthy men, 27 +/- 1 yr old, an abrupt decrease in mean arterial pressure (MAP) was induced nonpharmacologically by releasing a unilateral arterial thigh cuff (300 Torr) after 9 min of resting leg ischemia under two conditions: 1) ABR and CBR deactivation (control) and 2) ABR deactivation. Under control conditions, cuff release decreased MAP by 13 +/- 1 mmHg, whereas HR increased 11 +/- 2 beats/min. During ABR deactivation, neck suction was gradually applied to maintain carotid sinus transmural pressure during the initial 20 s after cuff release (suction). This attenuated the increase in HR (6 +/- 1 beats/min) and caused a greater decrease in MAP (18 +/- 2 mmHg, P < 0.05). Furthermore, estimated cardiac baroreflex responsiveness (DeltaHR/DeltaMAP) was significantly reduced during suction compared with control conditions. These findings suggest that the carotid baroreceptors contribute more importantly to the reflex control of HR than previously reported in healthy individuals.

Role of central command in carotid baroreflex resetting in humans during static exercise.

The purpose of the experiments was to examine the role of central command in the exercise-induced resetting of the carotid baroreflex. Eight subjects performed 30 % maximal voluntary contraction (MVC) static knee extension and flexion with manipulation of central command (CC) by patellar tendon vibration (PTV). The same subjects also performed static knee extension and flexion exercise without PTV at a force development that elicited the same ratings of perceived exertion (RPE) as those observed during exercise with PTV in order to assess involvement of the exercise pressor reflex. Carotid baroreflex (CBR) function curves were modelled from the heart rate (HR) and mean arterial pressure (MAP) responses to rapid changes in neck pressure and suction during steady state static exercise. Knee extension exercise with PTV (decreased CC activation) reset the CBR-HR and CBR-MAP to a lower operating pressure (P < 0.05) and knee flexion exercise with PTV (increased CC activation) reset the CBR-HR and CBR-MAP to a higher operating pressure (P < 0.05). Comparison between knee extension and flexion exercise at the same RPE with and without PTV found no difference in the resetting of the CBR-HR function curves (P > 0.05) suggesting the response was determined primarily by CC activation. However, the CBR-MAP function curves were reset to operating pressures determined by both exercise pressor reflex (EPR) and central command activation. Thus the physiological response to exercise requires CC activation to reset the carotid-cardiac reflex but requires either CC or EPR to reset the carotid-vasomotor reflex.

Intraoperative treatment strategy to reduce the incidence of postcardiopulmonary bypass atrial fibrillation.

PURPOSE: Postcardiopulmonary bypass atrial fibrillation remains a constant complication associated with coronary revascularization, the incidence of which occurs from 20% to 35%. Previous studies have addressed this problem in the postoperative setting utilizing pharmacological agents, but the results have been variable. The purpose of this study was to evaluate a novel intraoperative strategy to reduce the incidence of postcardiopulmonary bypass atrial fibrillation. We theorized that leukocyte depletion by filtration with the addition of aprotinin would reduce the systemic inflammatory effects of bypass and reduce the incidence of atrial fibrillation. METHODS: One hundred and twenty-two patients participated in this randomized study. Only isolated primary coronary revascularization procedures on cardiopulmonary bypass were included. The control group (n=55) received standard moderate hypothermic blood cardioplegia cardiopulmonary bypass. The treatment group (n=65) received similar cardiopulmonary bypass with the addition of strategic leukocyte depletion with Pall Biomedical Products (East Hills, NY) leukodepletion filters and full-dose aprotinin. RESULTS: The intraoperative addition of leukocyte depletion by filtration with aprotinin reduced the incidence of postcardiopulmonary bypass atrial fibrillation by 72%. The incidence.of atrial fibrillation in the control group was 27% (15 of 55). In contrast, the occurrence of atrial fibrillation in the treated group was only 7.6% (5 of 65) (p<0.025). CONCLUSIONS: This novel intraoperative treatment strategy of both mechanical (leukocyte filtration) and pharmacological (aprotinin) intervention appears to markedly reduce the incidence of postcardiopulmonary bypass atrial fibrillation. To our knowledge, this is the first study to combine these two treatment strategies. A previous study has noted a decline in atrial fibrillation with aprotinin in the animal model, but not to the extent observed in our study. The beneficial effects of the reduction of atrial fibrillation include reduced risk of emboli formation and the incidence of ischemia in the heart, lung and brain. In addition, a decrease in length of hospital stay, recovery time and overall cost occurred.

Haemodynamic changes during neck pressure and suction in seated and supine positions.

We sought to quantify the contribution of cardiac output (Q) and total vascular conductance (TVC) to carotid baroreflex-mediated changes in mean arterial pressure (MAP) in the upright seated and supine positions. Acute changes in carotid sinus transmural pressure were evoked using brief 5 s pulses of neck pressure and neck suction (NP/NS) via a simplified paired neck chamber that was developed to enable beat-to-beat measurements of stroke volume using pulse-doppler ultrasound. Percentage contributions of Q and TVC were achieved by calculating the predicted change in MAP during carotid baroreflex stimulation if only the individual changes in Q or TVC occurred and all other parameters remained at control values. All NP and NS stimuli from +40 to -80 Torr (+5.33 to -10.67 kPa) induced significant changes in Q and TVC in both the upright seated and supine positions (P < 0.001). Cardiopulmonary baroreceptor loading with the supine position appeared to cause a greater reliance on carotid baroreflex-mediated changes in Q. Nevertheless, in both the seated and supine positions the changes in MAP were primarily mediated by alterations in TVC (percentage contribution of TVC at the time-of-peak MAP, seated 95 +/- 13, supine 76 +/- 17 %). These data indicate that alterations in vasomotor activity are the primary means by which the carotid baroreflex regulates blood pressure during acute changes in carotid sinus transmural pressure.

Brain activation by central command during actual and imagined handgrip under hypnosis.

The purpose was to compare patterns of brain activation during imagined handgrip exercise and identify cerebral cortical structures participating in "central" cardiovascular regulation. Subjects screened for hypnotizability, five with higher (HH) and four with lower hypnotizability (LH) scores, were tested under two conditions involving 3 min of 1) static handgrip exercise (HG) at 30% of maximal voluntary contraction (MVC) and 2) imagined HG (I-HG) at 30% MVC. Force (kg), forearm integrated electromyography, rating of perceived exertion, heart rate (HR), mean blood pressure (MBP), and differences in regional cerebral blood flow distributions were compared using an ANOVA. During HG, both groups showed similar increases in HR (+13 +/- 5 beats/min) and MBP (+17 +/- 3 mmHg) after 3 min. However, during I-HG, only the HH group showed increases in HR (+10 +/- 2 beats/min; P < 0.05) and MBP (+12 +/- 2 mmHg; P < 0.05). There were no significant increases or differences in force or integrated electromyographic activity between groups during I-HG. The rating of perceived exertion was significantly increased for the HH group during I-HG, but not for the LH group. In comparison of regional cerebral blood flow, the LH showed significantly lower activity in the anterior cingulate (-6 +/- 2%) and insular cortexes (-9 +/- 4%) during I-HG. These findings suggest that cardiovascular responses elicited during imagined exercise involve central activation of insular and anterior cingulate cortexes, independent of muscle afferent feedback; these structures appear to have key roles in the central modulation of cardiovascular responses.

Increases in intramuscular pressure raise arterial blood pressure during dynamic exercise.

This investigation was designed to determine the role of intramuscular pressure-sensitive mechanoreceptors and chemically sensitive metaboreceptors in affecting the blood pressure response to dynamic exercise in humans. Sixteen subjects performed incremental (20 W/min) cycle exercise to fatigue under four conditions: control, exercise with thigh cuff occlusion of 90 Torr (Cuff occlusion), exercise with lower body positive pressure (LBPP) of 45 Torr, and a combination of thigh cuff occlusion and LBPP (combination). Indexes of central command (heart rate, oxygen uptake, ratings of perceived exertion, and electromyographic activity), cardiac output, stroke volume, and total peripheral resistance were not significantly different between the four conditions. Mechanical stimulation during LBPP and combination conditions resulted in significant elevations in intramuscular pressure and mean arterial pressure from control at rest and throughout the incremental exercise protocol (P < 0.05). Conversely, there existed no significant changes in mean arterial pressure when the metaboreflex was stimulated by cuff occlusion. These findings suggest that under normal conditions the mechanoreflex is tonically active and is the primary mediator of exercise pressor reflex-induced alterations in arterial blood pressure during submaximal dynamic exercise in humans.

Vagal cardiac function and arterial blood pressure stability.

This study was designed to investigate the importance of vagal cardiac modulation in arterial blood pressure (ABP) stability before and after glycopyrrolate or atropine treatment. Changes in R-R interval (RRI) and ABP were assessed in 10 healthy young (age, 22 +/- 1.8 yr) volunteers during graded lower body negative pressure (LBNP) before and after muscarinic cholinergic (MC) blockade. Transient hypertension was induced by phenylephrine (1 microg/kg body wt), whereas systemic hypotension was induced by bilateral thigh cuff deflation after a 3-min suprasystolic occlusion. Power spectral densities of systolic [systolic blood pressure (SBP)] and diastolic ABP variability were examined. Both antimuscarinic agents elicited tachycardia similarly without significantly affecting baseline ABP. The increase in SBP after phenylephrine injection (+14 +/- 2 mmHg) was significantly augmented with atropine (+26 +/- 2 mmHg) or glycopyrrolate (+27 +/- 3 mmHg) and associated with a diminished reflex bradycardia. The decrease in SBP after cuff deflation (-9.2 +/- 1.2 mmHg) was significantly greater after atropine (-15 +/- 1 mmHg) or glycopyrrolate (-14 +/- 1 mmHg), with abolished reflex tachycardia. LBNP significantly decreased both SBP and RRI. However, after antimuscarinic agents, the reduction in SBP was greater (P < 0.05) and was associated with less tachycardia. Antimuscarinic agents reduced (P < 0.05) the low-frequency (LF; 0.04-0.12 Hz) power of ABP variability at rest. The LF SBP oscillation was significantly augmented during LBNP, which was accentuated (P < 0.05) after antimuscarinic agents and was correlated (r = -0.79) with the decrease in SBP. We conclude that antimuscarinic agents compromised ABP stability by diminishing baroreflex sensitivity, reflecting the importance of vagal cardiac function in hemodynamic homeostasis. The difference between atropine and glycopyrrolate was not significant.

Comparison of aortic and carotid baroreflex stimulus-response characteristics in humans.

In order to characterize the stimulus-response relationships of the arterial, aortic, and carotid baroreflexes in mediating cardiac chronotropic function, we measured heart rate (HR) responses elicited by acute changes in mean arterial pressure (MAP) and carotid sinus pressure (CSP) in 11 healthy individuals. Arterial (aortic + carotid) baroreflex control of HR was quantified using ramped changes in MAP induced by bolus injection of phenylephrine (PE) and sodium nitroprusside (SN). To assess aortic-cardiac responses, neck pressure (NP) and suction (NS) were applied during PE and SN administration, respectively, to counter alterations in CSP thereby isolating the aortic baroreflex. Graded levels of NP and NS were delivered to the carotid sinus using a customized neck collar device to assess the carotid-cardiac baroreflex, independent of drug infusion. The operating characteristics of each reflex were determined from the logistic function of the elicited HR response to the induced change in MAP. The arterial pressures at which the threshold was located on the stimulus-response curves determined for the arterial, aortic and carotid baroreflexes were not significantly different (72+/-4, 67+/-3, and 72+/-4 mm Hg, respectively, P > 0.05). Similarly, the MAP at which the saturation of the reflex responses were elicited did not differ among the baroreflex arcs examined (98+/-3, 99+/-2, and 102+/-3 mm Hg, respectively). These data suggest that the baroreceptor populations studied operate over the same range of arterial pressures. This finding indicates each baroreflex functions as both an important anti-hypotensive and anti-hypertensive mechanism. In addition, this investigation describes a model of aortic baroreflex function in normal healthy humans, which may prove useful in identifying the origin of baroreflex dysfunction in disease- and training-induced conditions.

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.

Effects of partial neuromuscular blockade on carotid baroreflex function during exercise in humans.

1. This investigation was designed to determine the contribution of central command to the resetting of the carotid baroreflex during static and dynamic exercise in humans. 2. Thirteen 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 partial neuromuscular blockade (to increase central command influence) using Norcuron (curare). Carotid baroreflex function was determined at rest and during steady-state exercise using a rapid neck pressure/neck suction technique. Whole-body Norcuron was repeatedly administered to effectively reduce hand-grip strength by approximately 50 % of control. 3. Partial neuromuscular blockade increased heart rate, mean arterial pressure, perceived exertion, lactate concentration and plasma noradrenaline concentration during both static and dynamic exercise when compared to control (P < 0.05). No effect was seen at rest. Carotid baroreflex resetting was augmented from control static and dynamic exercise by partial neuromuscular blockade without alterations in gain (P < 0.05). In addition, the operating point of the reflex was relocated away from the centring point (i.e. closer to threshold) during exercise by partial neuromuscular blockade (P < 0.05). 4. These findings suggest that central command actively resets the carotid baroreflex during dynamic and static exercise.

Arterial baroreflex control of sympathetic nerve activity during acute hypotension: effect of fitness.

We examined arterial baroreflex control of muscle sympathetic nerve activity (MSNA) during abrupt decreases in mean arterial pressure (MAP) and evaluated whether endurance training alters baroreflex function. Acute hypotension was induced nonpharmacologically in 14 healthy subjects, of which 7 were of high fitness (HF) and 7 were of average fitness (AF), by releasing a unilateral arterial thigh cuff after 9 min of resting ischemia under two conditions: control, which used aortic and carotid baroreflex (ABR and CBR, respectively) deactivation; and suction, which used ABR deactivation alone. The application of neck suction to counteract changes in carotid sinus transmural pressure during cuff release significantly attenuated the MSNA response (which increased 134 +/- 32 U/14 s) compared with control (which increased 195 +/- 43 U/14 s) and caused a greater decrease in MAP (19 +/- 2 vs. 15 +/- 2 mmHg; P < 0.05). Furthermore, during both trials, the HF subjects exhibited a greater decrease in MAP compared with AF subjects despite an augmented baroreflex control of MSNA. These data indicate that the CBR contributes importantly to the MSNA response during acute systemic hypotension. Additionally, we suggest that an impaired control of vascular reactivity hinders blood pressure regulation in HF subjects.

Anatomical and functional characteristics of carotid sinus stimulation in humans.

Transmission characteristics of pneumatic pressure to the carotid sinus were evaluated in 19 subjects at rest and during exercise. Either a percutaneous fluid-filled (n = 12) or balloon-tipped catheter (n = 7) was placed at the carotid bifurcation to record internal transmission of external neck pressure/neck suction (NP/NS). Sustained, 5-s pulses, and rapid ramping pulse protocols (+40 to -80 Torr) were recorded. Transmission of pressure stimuli was less with the fluid-filled catheter compared with that of the balloon-tipped catheter (65% vs. 82% negative pressure, 83% vs. 89% positive pressure; P < 0.05). Anatomical location of the carotid sinus averaged 3.2 cm (left) and 3.6 cm (right) from the gonion of the mandible with a range of 0-7.5 cm. Transmission was not altered by exercise or Valsalva maneuver, but did vary depending on the position of the carotid sinus locus beneath the sealed chamber. These data indicate that transmission of external NP/NS was higher than previously recorded in humans, and anatomical variation of carotid sinus location and equipment design can affect transmission results.

Neural blockade during exercise augments central command's contribution to carotid baroreflex resetting.

This investigation was designed to determine central command's role on carotid baroreflex (CBR) resetting during exercise. Nine volunteer subjects performed static and rhythmic handgrip exercise at 30 and 40% maximal voluntary contraction (MVC), respectively, before and after partial axillary neural blockade. Stimulus-response curves were developed using the neck pressure-neck suction technique and a rapid pulse train protocol (+40 to -80 Torr). Regional anesthesia resulted in a significant reduction in MVC. Heart rate (HR) and ratings of perceived exertion (RPE) were used as indexes of central command and were elevated during exercise at control force intensity after induced muscle weakness. The CBR function curves were reset vertically with a minimal lateral shift during control exercise and exhibited a further parallel resetting during exercise with neural blockade. The operating point was progressively reset to coincide with the centering point of the CBR curve. These data suggest that central command was a primary mechanism in the resetting of the CBR during exercise. However, it appeared that central command modulated the carotid-cardiac reflex proportionately more than the carotid-vasomotor reflex.

Hypnotic manipulation of effort sense during dynamic exercise: cardiovascular responses and brain activation.

The purpose of this investigation was to hypnotically manipulate effort sense during dynamic exercise and determine whether cerebral cortical structures previously implicated in the central modulation of cardiovascular responses were activated. Six healthy volunteers (4 women, 2 men) screened for high hypnotizability were studied on 3 separate days during constant-load exercise under three hypnotic conditions involving cycling on a 1) perceived level grade, 2) perceived downhill grade, and 3) perceived uphill grade. Ratings of perceived exertion (RPE), heart rate (HR), blood pressure (BP), and regional cerebral blood flow (rCBF) distributions for several sites were compared across conditions using an analysis of variance. The suggestion of downhill cycling decreased both the RPE [from 13 +/- 2 to 11 +/- 2 (SD) units; P < 0.05] and rCBF in the left insular cortex and anterior cingulate cortex, but it did not alter exercise HR or BP responses. Perceived uphill cycling elicited significant increases in RPE (from 13 +/- 2 to 14 +/- 1 units), HR (+16 beats/min), mean BP (+7 mmHg), right insular activation (+7.7 +/- 4%), and right thalamus activation (+9.2 +/- 5%). There were no differences in rCBF for leg sensorimotor regions across conditions. These findings show that an increase in effort sense during constant-load exercise can activate both insular and thalamic regions and elevate cardiovascular responses but that decreases in effort sense do not reduce cardiovascular responses below the level required to sustain metabolic needs.

Carotid baroreflex regulation of sympathetic nerve activity during dynamic exercise in humans.

We sought to determine whether carotid baroreflex (CBR) control of muscle sympathetic nerve activity (MSNA) was altered during dynamic exercise. In five men and three women, 23.8 +/- 0.7 (SE) yr of age, CBR function was evaluated at rest and during 20 min of arm cycling at 50% peak O(2) uptake using 5-s periods of neck pressure and neck suction. From rest to steady-state arm cycling, mean arterial pressure (MAP) was significantly increased from 90.0 +/- 2.7 to 118.7 +/- 3.6 mmHg and MSNA burst frequency (microneurography at the peroneal nerve) was elevated by 51 +/- 14% (P < 0.01). However, despite the marked increases in MAP and MSNA during exercise, CBR-Delta%MSNA responses elicited by the application of various levels of neck pressure and neck suction ranging from +45 to -80 Torr were not significantly different from those at rest. Furthermore, estimated baroreflex sensitivity for the control of MSNA at rest was the same as during exercise (P = 0.74) across the range of neck chamber pressures. Thus CBR control of sympathetic nerve activity appears to be preserved during moderate-intensity dynamic exercise.

Differential baroreflex control of heart rate in sedentary and aerobically fit individuals.

PURPOSE: We compared arterial, aortic, and carotid-cardiac baroreflex sensitivity in eight average fit (maximal oxygen uptake, VO2max = 42.2+/-1.9 mL x kg(-1) x min(-1)) and eight high fit (VO2max = 61.9+/-2.2 mL x kg(-1) x min(-1)) healthy young adults. METHODS: Arterial and aortic (ABR) baroreflex functions were assessed utilizing hypo- and hyper-tensive challenges induced by graded bolus injections of sodium nitroprusside (SN) and phenylephrine (PE), respectively. Carotid baroreflex (CBR) sensitivity was determined using ramped 5-s pulses of both pressure and suction delivered to the carotid sinus via a neck chamber collar, independent of drug administration. RESULTS: During vasoactive drug injection, mean arterial pressure (MAP) was similarly altered in average fit (AF) and high fit (HF) groups. However, the heart rate (HR) response range of the arterial baroreflex was significantly attenuated (P < 0.05) in HF (31+/-4 beats x min(-1)) compared with AF individuals (46+/-4 beats x min(-1)). When sustained neck suction and pressure were applied to counteract altered carotid sinus pressure during SN and PE administration, isolating the ABR response, the response range remained diminished (P < 0.05) in the HF population (24+/-3 beats x min(-1)) compared with the AF group (41+/-4 beats x min(-1)). During CBR perturbation, the HF (14+/-1 beats-min(-1)) and AF (16+/-1 beats-min(-1)) response ranges were similar. The arterial baroreflex response range was significantly less than the simple sum of the CBR and ABR (HF, 38+/-3 beats x min(-1) and AF, 57+/-4 beats x min(-1)) in both fitness groups. CONCLUSIONS: These data confirm that reductions in arterial-cardiac reflex sensitivity are mediated by diminished ABR function. More importantly, these data suggest that the integrative relationship between the ABR and CBR contributing to arterial baroreflex control of HR is inhibitory in nature and not altered by exercise training.