Carotid-cardiac Baroreflex Research Articles

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.

Orthostatic intolerance and motion sickness after parabolic flight.

Because it is not clear that the induction of orthostatic intolerance in returning astronauts always requires prolonged exposure to microgravity, we investigated orthostatic tolerance and autonomic cardiovascular function in 16 healthy subjects before and after the brief micro- and hypergravity of parabolic flight. Concomitantly, we investigated the effect of parabolic flight-induced vomiting on orthostatic tolerance, R-wave-R-wave interval and arterial pressure power spectra, and carotid-cardiac baroreflex and Valsalva responses. After parabolic flight 1) 8 of 16 subjects could not tolerate 30 min of upright tilt (compared to 2 of 16 before flight); 2) 6 of 16 subjects vomited; 3) new intolerance to upright tilt was associated with exaggerated falls in total peripheral resistance, whereas vomiting was associated with increased R-wave-R-wave interval variability and carotid-cardiac baroreflex responsiveness; and 4) the proximate mode of new orthostatic failure differed in subjects who did and did not vomit, with vomiters experiencing comparatively isolated upright hypocapnia and cerebral vasoconstriction and nonvomiters experiencing signs and symptoms reminiscent of the clinical postural tachycardia syndrome. Results suggest, first, that syndromes of orthostatic intolerance resembling those developing after space flight can develop after a brief (i.e., 2-h) parabolic flight and, second, that recent vomiting can influence the results of tests of autonomic cardiovascular function commonly utilized in returning astronauts.

Carotid baroreflex responsiveness in heat-stressed humans.

The effects of whole body heating on human baroreflex function are relatively unknown. The purpose of this project was to identify whether whole body heating reduces the maximal slope of the carotid baroreflex. In 12 subjects, carotid-vasomotor and carotid-cardiac baroreflex responsiveness were assessed in normothermia and during whole body heating. Whole body heating increased sublingual temperature (from 36.4 +/- 0.1 to 37.4 +/- 0.1 degrees C, P < 0.01) and increased heart rate (from 59 +/- 3 to 83 +/- 3 beats/min, P < 0. 01), whereas mean arterial blood pressure (MAP) was slightly decreased (from 88 +/- 2 to 83 +/- 2 mmHg, P < 0.01). Carotid-vasomotor and carotid-cardiac responsiveness were assessed by identifying the maximal gain of MAP and heart rate to R wave-triggered changes in carotid sinus transmural pressure. Whole body heating significantly decreased the responsiveness of the carotid-vasomotor baroreflex (from -0.20 +/- 0.02 to -0.13 +/- 0.02 mmHg/mmHg, P < 0.01) without altering the responsiveness of the carotid-cardiac baroreflex (from -0.40 +/- 0.05 to -0.36 +/- 0.02 beats x min(-1) x mmHg(-1), P = 0.21). Carotid-vasomotor and carotid-cardiac baroreflex curves were shifted downward and upward, respectively, to accommodate the decrease in blood pressure and increase in heart rate that accompanied the heat stress. Moreover, the operating point of the carotid-cardiac baroreflex was shifted closer to threshold (P = 0.02) by the heat stress. Reduced carotid-vasomotor baroreflex responsiveness, coupled with a reduction in the functional reserve for the carotid baroreflex to increase heart rate during a hypotensive challenge, may contribute to increased susceptibility to orthostatic intolerance during a heat stress.

Baroreflex dysfunction induced by microgravity: potential relevance to postflight orthostatic intolerance.

Microgravity imposes adaptive changes in the human body. This review focuses on the changes in baroreflex function produced by actual spaceflight, or by experimental models that simulate microgravity, e.g., bed rest. We will analyze separately studies involving baroreflexes arising from carotid sinus and aortic arch afferents ("high-pressure baroreceptors"), and cardiopulmonary afferents ("low-pressure receptors"). Studies from unrelated laboratories using different techniques have concluded that actual or simulated exposure to microgravity reduces baroreflex function arising from carotid sinus afferents ("carotic-cardiac baroreflex"). The techniques used to study the carotid-cardiac baroreflex, using neck suction and compression to simulate changes in blood pressure, have been extensively validated. In contrast, it is more difficult to selectively study aortic arch or cardiopulmonary baroreceptors. Nonetheless, studies that have examined these baroreceptors suggest that microgravity produces the opposite effect, ie, an increase in the gain of aortic arch and cardiopulmonary baroreflexes. Furthermore, most studies have focus on instantaneous changes in heart rate, which almost exclusively examines the vagal limb of the baroreflex. In comparison, there is limited information about the effect of microgravity on sympathetic function. A substantial proportion of subjects exposed to microgravity develop transient orthostatic intolerance. It has been proposed that alterations in baroreflex function play a role in the orthostatic intolerance induced by microgravity. The evidence in favor and against this hypothesis is reviewed.

Carotid baroreflex function during prolonged exercise.

The present investigation was designed to uncouple the hemodynamic physiological effects of thermoregulation from the effects of a progressively increasing central command activation during prolonged exercise. Subjects performed two 1-h bouts of leg cycling exercise with 1) no intervention and 2) continuous infusion of a dextran solution to maintain central venous pressure constant at the 10-min pressure. Volume infusion resulted in a significant reduction in the decrement in mean arterial pressure seen in the control exercise bout (6.7 +/- 1.8 vs. 11.6+/- 1.3 mmHg, respectively). However, indexes of central command such as heart rate and ratings of perceived exertion rose to a similar extent during both exercise conditions. In addition, the carotid-cardiac baroreflex stimulus-response relationship, as measured by using the neck pressure-neck suction technique, was reset from rest to 10 min of exercise and was further reset from 10 to 50 min of exercise in both exercise conditions, with the operating point being shifted toward the reflex threshold. We conclude that the progressive resetting of the carotid baroreflex and the shift of the reflex operating point render the carotid-cardiac reflex ineffectual in counteracting the continued decrement in mean arterial pressure that occurs during the prolonged exercise.

EFFECTS OF PARTIAL NEUROMUSCULAR BLOCKADE ON CAROTID BAROREFLEX FUNCTION DURING DYNAMIC EXERCISE IN HUMANS

1068 We evaluated the influence of central command on carotid-cardiac baroreflex function during steady state dynamic exercise. Five subjects (26±2 yrs) performed dynamic exercise at 20% V̇O2max for seven minutes. Each subject performed the exercise bout under two conditions: control and partial neuromuscular blockade using Norcuron (curare). Heart rate (HR; beats/min) and mean arterial pressure (MAP; mmHg) were measured throughout. Carotid baroreflex function (CBR) was recorded using a pulsed neck pressure/neck suction technique. Cardiac responses were used to model CBR curves. Threshold (TH), saturation (SAT), gain, range (RR) and minimum response (HRmin) were defined. Increased central command with curare significantly elevated MAP (117.6±5) and HR (112.8±6) from control MAP (92.3±5) and HR (98.5±6) during dynamic exercise (P<0.05). (Table)TableThe results indicate that the feed-forward efferent neural input from central command actively regulates the carotid baroreflex during low intensity dynamic exercise. Supported by Copenhagen Muscle Research Center

Association between aerobic capacity and carotid-cardiac baroreflex responsiveness in women.

The purpose of this study was to determine whether the positive correlation between carotid-cardiac baroreflex responsiveness and aerobic capacity (VO(2)max) that has been reported in men also occurs in women. Carotid-cardiac baroreflex responsiveness was tested in 40 healthy, normotensive women (age 18-35) using the variable neck pressure technique. Participants were subdivided into endurance-trained (ET; n = 11) and untrained (UT; n = 9) groups. No significant between-group difference was found in the range or gain of the carotid-cardiac baroreflex response despite a lower resting HR in the ET group. When participants were subdivided into high (HI; n = 13) and low (LO; n = 17) responders based on reflex RRI responses to CTP changes, no significant between-group differences were found in resting HR or VO(2)max levels. It was concluded that aerobic capacity (VO(2)max) is not a good predictor of cardiac-carotid baroreflex responsiveness in healthy women.

RESETTING OF THE CAROTID ARTERIAL BAROREFLEX DURING PROLONGED EXERCISE - EFFECT ON CARDIOVASCULAR DRIFT

1207 Eight healthy subjects performed two one hour bouts of leg cycling exercise at 65% of maximal oxygen uptake (VO2max) with a) no intervention and b) continuous infusion of a dextran solution to maintain central venous pressure. Volume infusion resulted in a significant reduction in the decrement in stroke volume (SV) and mean arterial pressure (MAP), i.e. cardiovascular drift, seen in the control exercise bout. However, indices of central command such as heart rate (HR), VO2, and ratings of perceived exertion (RPE) rose to a similar extent during both exercise conditions. In addition, the carotid-cardiac baroreflex (CBR) stimulus-response relationship, as measured using the neck pressure/neck suction technique, was reset from 10 to 50 minutes of exercise in both exercise conditions with the operating point being significantly shifted toward the reflex threshold and no significant difference in reflex gain. Therefore, as cardiovascular drift becomes manifest, progressive resetting of the CBR (which we suggest occurs due to increases in central command) renders the baroreflex ineffectual in counteracting the decrement in MAP. The table below represents percent change from 10 to 50 minutes of exercise. CP indicates CBR centering point. (mean±SE, *indicates significant difference; p<0.05)Table

Interaction of Semicircular Canal Stimulation with Carotid Baroreceptor Reflex Control of Heart Rate

The carotid-cardiac baroreflex contributes to the prediction of orthostatic tolerance; experimental attenuation of the reflex response leads to orthostatic hypotension in humans and animals. Anecdotal observations indicate that rotational head movements about the vertical axis of the body can also induce orthostatic bradycardia and hypotension through increased parasympathetic activity. We therefore measured the chronotropic response to carotid baroreceptor stimulation in 12 men during varying conditions of vestibulo-oculomotor stimulation to test the hypothesis that stimulation of the semicircular canals associated with head movements in the yaw plane inhibits cardioacceleration through a vagally mediated baroreflex. Carotid-cardiac baroreflex response was assessed by plotting R-R intervals (ms) at each of 8 neck pressure steps with their respective carotid distending pressures (mmHg). Calculated baroreflex gain (maximal slope of the stimulus-response relationship) was measured under 4 experimental conditions: 1) sinusoidal whole-body yaw rotation of the subject in the dark without visual fixation (combined vestibular-oculomotor stimulation); 2) yaw oscillation of the subject while tracking a small head-fixed light moving with the subject (vestibular stimulation without eye movements); 3) subject stationary while fixating on a small light oscillating in yaw at the same frequency, peak acceleration, and velocity as the chair (eye movements without vestibular stimulation); and 4) subject stationary in the dark (no eye or head motion). Head motion alone and with eye movement reduced baseline baroreflex responsiveness to the same stimulus by 30%. Inhibition of cardioacceleration during rotational head movements may have significant impact on functional performance in aerospace environments, particularly in high-performance aircraft pilots during high angular acceleration in aerial combat maneuvers or in astronauts upon return from spaceflight who already have attenuated baroreflex functions.

Effects of vestibular and oculomotor stimulation on responsiveness of the carotid-cardiac baroreflex.

Twelve healthy men underwent measurement of their carotid-cardiac baroreflex response during varying conditions of vestibulo-oculomotor stimulation to test the hypothesis that vestibular and/or oculomotor stimulation associated with head movements in the yaw plane inhibit baroreflex control of heart rate. We assessed the carotid-cardiac baroreflex response by plotting R-R intervals (in milliseconds) at each of eight neck pressure steps with their respective carotid distending pressures (in millimeters mercury). Baroreflex sensitivity was measured under four experimental conditions: 1) sinusoidal whole body yaw rotation of the subject in the dark without visual fixation (combined vestibular-oculomotor stimulation); 2) yaw oscillation of the subject while tracking a small head-fixed light moving with the subject (vestibular stimulation without eye movements); 3) subject stationary while fixating on a small light oscillating in yaw at the same frequency, peak acceleration, and velocity as the chair (eye movements without vestibular stimulation); and 4) subject stationary in the dark (no eye or head motion). Head motion alone reduced baseline baroreflex responsiveness by 30% from 3.8 +/- 0.5 to 2.6 +/- 0.5 ms/mmHg. Eye motion alone also reduced the baroreflex response by 13% (0.5 ms/mmHg) to 3.3 +/- 0.5 ms/mmHg. During head motion, the effect of eye motion was negligible (2.7 +/- 0.4 ms/mmHg). These results suggest that vestibular stimulation associated with head movements in yaw inhibits vagally mediated baroreflex control of heart rate, whereas oculomotor stimulation is less of a factor and only in the absence of vestibular stimulation.

Slowing of carotid-cardiac baroreflex with standing and with isometric and dynamic muscle activity.

We hypothesized that the carotid-cardiac baroreflex becomes slowed in conditions with increased sympathetic activity. Changes in heart rate (HR) and blood pressure in response to 10-s trains of 50-mmHg pulses of neck suction (NS) were studied in six male subjects during supine rest, upright rest, isometric arm exercise at 30% of maximum voluntary contraction, and dynamic leg exercise at 100 W in the sitting position. Estimated mean carotid distending pressure increased by approximately 20 mmHg with 50-mmHg, QRS-triggered, pulsatile NS. Repeated NS sequences were performed in each condition. The amplitude of the bradycardic response was highly variable among the subjects and did not differ significantly between conditions, mean values ranging from 0.3 to 0.6 beats.min-1.mmHg-1. In supine rest, the full bradycardic response appeared within < 1 s, i.e., during or immediately after the R-R interval of the first NS pulse. In the other conditions it took significantly longer, 2-3 s or three to seven R-R intervals, for the full HR responses to develop. Our results support the notion that the carotid-cardiac baroreflex in humans becomes slowed under conditions of concurrent sympathetic stimulation.

Influence of apnea on cardiovascular responses to neck suction during exercise.

Short-lasting neck suction (NS) is a common method to assess the carotid-cardiac baroreflex, and NS is usually applied during apnea to avoid breath-synchronous variations of heart rate (HR) and blood pressure. We hypothesized that the apnea might provoke cardiovascular effects that could confound the HR and blood pressure responses to NS. HR and blood pressure responses to 10-s trains of 50-mmHg pulses of NS were studied in six male subjects during supine rest, upright rest, isometric arm exercise at 30% of maximal voluntary contraction, and dynamic leg exercise at 100 W in the sitting position. Repeated NS sequences were performed during apnea preceded by a relaxed expiration to functional residual capacity and during eupnea. Initial HR responses to NS were similar during eupnea and apnea in all conditions. However, during isometric and dynamic exercise, recordings made under eupneic and apneic conditions differed during the second half of the NS period. During apneic isometric arm contraction, the elevation of mean carotid distending pressure (MCDP) (arterial pressure at carotid level minus NS pressure) was maintained at a 25-35% higher level than during eupneic isometric exercise over the last half of the NS period. In dynamic exercise, mean arterial pressure and MCDP started to increase after 3-5 s of apneic NS, whereas they were maintained during eupnea. One to three seconds later, HR started to drop markedly in apneic subjects, reaching values 20 beats/min lower than those in eupneic subjects at the end of the NS. We conclude that cardiovascular effects of apnea may appear after only 8 s of apnea in dynamic exercise and therefore could confound responses to NS.

Application of acute maximal exercise to protect orthostatic tolerance after simulated microgravity.

We tested the hypothesis that one bout of maximal exercise performed at the conclusion of prolonged simulated microgravity would improve blood pressure stability during an orthostatic challenge. Heart rate (HR), mean arterial blood pressure (MAP), norepinephrine (NE), epinephrine (E), arginine vasopressin (AVP), plasma renin activity (PRA), atrial natriuretic peptide (ANP), cardiac output (Q), forearm vascular resistance (FVR), and changes in leg volume were measured during lower body negative pressure (LBNP) to presyncope in seven subjects immediately prior to reambulation from 16 days of 6 degrees head-down tilt (HDT) under two experimental conditions: 1) after maximal supine cycle ergometry performed 24 h before returning to the upright posture (exercise) and 2) without exercise (control). After HDT, the reduction of LBNP tolerance time from pre-HDT levels was greater (P = 0.041) in the control condition (-2.0 +/- 0.2 min) compared with the exercise condition (-0.4 +/- 0.2 min). At presyncope after HDT, FVR and NE were higher (P < 0.05) after exercise compared with control, whereas MAP, HR, E, AVP, PRA, ANP, and leg volume were similar in both conditions. Plasma volume (PV) and carotid-cardiac baroreflex sensitivity were reduced after control HDT, but were restored by the exercise treatment. Maintenance of orthostatic tolerance by application of acute intense exercise after 16 days of simulated microgravity was associated with greater circulating levels of NE, vasoconstriction, Q, baroreflex sensitivity, and PV.

Bradycardia during baroreflex stimulation and active or passive stressor tasks: cardiorespiratory fitness and hostility.

We examined whether the resting bradycardia associated with cardiorespiratory fitness extends to lowered heart rate (HR) and mean arterial pressure during novel passive or active laboratory stressors and to a longer heart period during stimulation of the carotid-cardiac vagal baroreflex, independently of the Type A behavior pattern (TABP) and hostility. Forty-four normotensive Caucasian men (18-35 years of age) completed the Structured Interview for TABP, the Cook-Medley Hostility Scale, and a peak oxygen uptake (Vo2peak) test. Vo2peak was inversely related to HR prior to, during, and after each stressor and was positively related to heart period during baroreflex testing. Hostility was inversely related to heart period during baroreflex testing. TABP had no effects. Our findings indicate that cardiorespiratory fitness and low hostility are independently associated with a bradycardia during stimulation of the carotid-cardiac baroreflex, consistent with a possible enhancement of cardiac vagal tone.

Augmented baroreflex heart rate gain after moderate-intensity, dynamic exercise.

The occurrence of a sustained vasodilation and hypotension after acute, dynamic exercise suggests that exercise may alter arterial baroreflex mechanisms. Therefore, we assessed systemic hemodynamics, baroreflex regulation of heart rate, and cardiac vagal tone after 60 min of cycling at 60% peak oxygen consumption in 12 healthy, untrained men and women (ages 21-28 yr). We derived sigmoidal carotid-cardiac baroreflex relations by measurement of R-R interval changes induced by ramped, stepwise, R-wave-triggered changes in external neck pressure from 40 to -65 mmHg. We estimated tonic cardiac vagal control with power spectral analysis of R-R interval variability in the respiratory frequency band (0.2-0.3 Hz) during frequency- and tidal volume-controlled breathing. Both mean arterial pressure and total peripheral resistance were reduced postexercise [pressure: from 86 +/- 2 (mean +/- SE) to 81 +/- 2 mmHg; resistance: from 23 +/- 2 to 16 +/- 1 units; both P < 0.05]. Cardiac output was increased postexercise (from 3.9 +/- 0.3 to 5.5 +/- 0.5 l/min, P < 0.05). Both slope and range of the carotid-cardiac baroreflex relation were increased postexercise (slope: from 4.7 +/- 0.7 to 6.1 +/- 0.9 ms/mmHg; range: from 186 +/- 23 to 238 +/- 30 ms, P < 0.05). Respiratory R-R interval variability (cardiac vagal tone) was not changed at any time after exercise, whereas heart rate and plasma norepinephrine levels were elevated. Thus moderate-intensity, dynamic exercise increases heart rate and cardiac output, reduces peripheral vascular resistance, and augments baroreflex responsiveness. Our data suggest that augmented baroreflex heart rate gain restrains rather than contributes to postexercise hypotension, which appears to be mediated predominately by vasodilation.

Effect of dynamic exercise on human carotid-cardiac baroreflex latency

We compared the beat-to-beat responses of heart rate (HR) after brief activation of carotid baroreceptors in resting humans with the responses obtained during mild-to-moderate levels of dynamic exercise [25 and 50% of peak O2 uptake (VO2peak)] to investigate the effect of exercise on baroreflex latency. Carotid baroreceptors were activated by a pressure pulse (5 s) of neck suction (NS, -80 Torr) and neck pressure (NP, +40 Torr) during held expiration. At rest the peak change in HR to NS/NP occurred during the first several heartbeats (1st-3rd beat), whereas during mild and moderate exercise peak HR responses occurred near the end of the NS/NP pulse (6th-8th beat). In contrast, time (s) to the peak change in HR was not different between rest and exercise (P > 0.05). Reflex tachycadia to NP progressively decreased during exercise (17 +/- 3, 10 +/- 1, and 4 +/- 1% of control, rest vs. 25% VO2peak, vs. 50% VO2peak, respectively, P < 0.05), and a strong positive correlation was found between the magnitude of the reflex tachycardia and a measure of HR variability (cardiac vagal tone index, r = 0.74, P < 0.0001). Reflex bradycardia to NS gradually increased during exercise (13 +/- 2, 17 +/- 2, and 18 +/- 2% of control, rest vs. 25% VO2peak, vs. 50% VO2peak, respectively, P = 0.10) and was negatively correlated with cardiac vagal tone (r = 0.42, P < 0.06).(ABSTRACT TRUNCATED AT 250 WORDS)

Carotid–cardiac baroreflex and training status: significance of initial responsiveness

The aim of this study was to demonstrate that within a population of healthy men (n = 15) of varying levels of aerobic fitness (VO2max = 36-74 mL.kg-1.min-1), (i) there are high and low responders with respect to carotid-cardiac baroreflex responsiveness, despite similar baseline heart rates (HRs) both at rest and during dynamic exercise, and (ii) there is a weak association between this responsiveness and training status (VO2max) because of a large overlap in the responses between trained (endurance, ET) and untrained (UT) individuals. Baroreflex function curves were derived during supine rest for each subject by applying varying pressures around the neck in a beat-to-beat ramp (for 12 beats) of +40 to -60 mmHg (1 mmHg = 133.3 Pa). Subjects were divided into low (n = 8) and high (n = 7) responders on the basis of the magnitude of the maximal dynamic R-R interval (RRI) range of the baroreflex curve. Both bradycardic (percent slowing) and tachycardic (percent acceleration) components of the baroreflex curve, and peak sinus node responses (HR, RRI) to continuous neck suction (-60 mmHg) at rest and during exercise (cycling, 45% VO2max) were greater in high compared with low responders (p < 0.05), as assessed using both HR and RRI scales.(ABSTRACT TRUNCATED AT 250 WORDS)

Autonomic responses of women with parental hypertension. Effects of physical activity and fitness.

We studied the moderating effects of cardiorespiratory fitness and physical activity on heart rate and blood pressure responses to psychophysiological stressors and the carotid-cardiac baroreflex in young normotensive women with a parental history of hypertension (n = 31). Testing occurred during the follicular menstrual phase. Subjects were divided into high versus moderate (46.6 +/- 6.5 versus 35.9 +/- 1.9 mL.kg-1.min-1) VO2peak and high versus moderate (1217.7 +/- 98.4 versus 1015.5 +/- 49.4 J.kg-1.wk-1) physical activity groups. The groups did not differ in heart rate or blood pressure responses to mental arithmetic or the cold-face test. However, the highly fit women had longer maximal R-R intervals compared with the moderately fit women when the carotid-cardiac baroreflex was stimulated by negative pressures applied to the neck during resting conditions (P < .01). The carotid-cardiac baroreflex was attenuated during mental arithmetic compared with rest in both the moderately fit and moderately active women but not in the highly fit and highly active groups. We find no evidence that aerobic fitness reduces sympathetic responses to laboratory stressors in young women with parental hypertension. Our findings are consistent with greater parasympathetic tone during sympathetic challenge for the highly fit and highly active subjects. Clarification of autonomic balance during carotid baroreflex stimulation at rest and during sympathetic challenge after exercise training would provide important information regarding mechanisms that regulate cardiovascular responses to autonomic challenge in women at risk for hypertension.

Autonomic functions and orthostatic responses 24 h after acute intense exercise in paraplegic subjects

We tested the hypothesis that a bout of graded exercise designed to elicit maximal effort would increase the sensitivity of autonomically mediated baroreflexes and enhance blood pressure (BP) stability in subjects prone to postural hypotension. Therefore, we measured heart rate (HR), BP, forearm vascular resistance (FVR), and vasoactive hormone responses before and during 15 min of 70 degrees head-up tilt (HUT) in 10 paraplegic subjects (21-65 yr) on two occasions: 1) 24 h after maximal arm-crank exercise (postexercise) and 2) without exercise (control). During HUT, HR increased 30 beats/min in both postexercise and control, but the reduction in systolic BP (SBP) during control (-12.0 +/- 4.6 mmHg) was larger (P = 0.017) than that during HUT after exercise (-0.3 +/- 4.3 mmHg). The postexercise increase in FVR from supine to HUT of 17.0 +/- 2.4 to 24.8 +/- 3.2 peripheral resistance units (PRU) was greater (P = 0.042) than the increase observed during control (18.3 +/- 3.7 to 19.5 +/- 3.1 PRU). The gain of the carotid-cardiac baroreflex was also increased (P = 0.049) after exercise. Responses in norepinephrine, vasopressin, and plasma renin-angiotensin induced by HUT were similar for control and postexercise, and there was no difference in either leg compliance or plasma volume between the two conditions. Additionally, HR and SBP responses to phases II and IV of the Valsalva maneuver, indexes of integrated baroreflex sensitivity, were increased (P < 0.05) after maximal exercise compared with control. Thus acute intense exercise eliminated orthostatic hypotension in paraplegics, was associated with increased FVR and baroreflex sensitivity, and was independent of blood volume changes.

Unilateral carotid-cardiac baroreflex responses in exercise trained and untrained men.

To determine effects of aerobic exercise training on individual contributions of the right and left carotid sinus baroreflex control of the cardiac interval, heart rate [expressed as R-R Interval (RRI)] and mean arterial pressure (MAP) responses were elicited by pulsed trains of neck suction and pressure in exercise trained (ET = 8) and untrained (UT = 8) men. ET subjects had a greater (mean +/- SD) maximal oxygen uptake (VO2max) than UT subjects (ET = 64.5 +/- 2.4 ml.kg.min-1 vs UT = 39.8 +/- 3.7 ml.kg.min-1; P < 0.001). A neck collar device was modified for delivery of suction and pressure pulses to only one side of the neck. Carotid-cardiac gains for right, left, and bilateral baroreflexes were determined from the logistic function of RRI responses to changes in estimated carotid sinus pressure (ECSP). There were no significant differences in the maximal gains for bilateral (ET = 6.4 +/- 1.8 vs UT = 5.9 +/- 1.3 ms.mm Hg-1 ECSP), right sided (ET = 5.3 +/- 1.2 vs UT = 4.5 +/- 1.2 ms.mm Hg-1 ECSP) or left sided (ET = 3.3 +/- 1.8 vs UT = 3.6 +/- 1.8 ms.mm Hg-1 ECSP) responses between groups and both groups demonstrated an inhibitory summation of reflexes. We suggest that right and left carotid-cardiac responses, as well as the summation of these reflexes, are quantitatively similar in exercise trained and untrained subjects.