Arterial Baroreflex Sensitivity Research Articles

Arterial baroreflex sensitivity is a good predictor of inotropic responses to a phosphodiesterase inhibitor in human heart failure

Experimental study has shown that blunted arterial baroreflex function markedly attenuated inotropic responses to a phosphodiesterase inhibitor (PDEI) even in normal hearts. However, whether arterial baroreflex function is related to the inotropic responsiveness to a PDEI has not been clarified in human heart failure (HF). The goal of this study was to examine the relationship between inotropic responses to a PDEI and arterial baroreflex sensitivity in human HF. Twelve patients with HF were examined, and hemodynamic responses to milrinone (12.5, 25, and 50 microg/kg, intravenous injection) and arterial baroreflex sensitivity were assessed by pulse interval-left ventricular (LV) systolic pressure slope using nitroglycerin and phenylephrine. Milrinone (25 microg/kg) significantly increased LV dP/dt. Arterial baroreflex sensitivity was only one predictor of inotropic responses to milrinone by multivariate analysis; a strong positive correlation was also found between LV dP/dt and baroreflex sensitivity (y = 6.656X - 3.326, r = 0.93, p = 0.000). Inotropic effects of milrinone, a PDEI, correlated significantly with arterial baroreflex sensitivity, suggesting that the more baroreflex function was impaired, the more the inotropic effect of a PDEI was depressed in human HF.

Determinants of baroreflex function in juvenile end-stage renal disease

Arterial baroreflex sensitivity (BRS) is markedly reduced in middle-aged patients with end-stage renal disease (ESRD), due to the combined effects of aging, arterial stiffening, and autonomic neuropathy. Much less is known about the effects of ESRD on arterial baroreflex in juvenile patients. Therefore, we investigated baroreflex function and its relation to carotid artery elasticity and heart rate variability in children and young adults with ESRD. We studied 42 subjects (9-30 years): 14 patients on maintenance hemodialysis (HD), 14 renal transplant recipients (RT), and 14 healthy control subjects (C). Baroreflex function was determined by pharmacological (BRS) and spontaneous (sequence and spectral indices) techniques. Carotid artery elasticity was characterized by stiffness index beta. Heart rate variability was assessed using time and frequency domain measures. Data are expressed as mean+/-s.d. BRS was markedly reduced in HD as compared to C (10.0+/-4.2 vs 25.7+/-5.9 ms/mm Hg); spontaneous indices were reduced to similar extent. Carotid artery stiffness was approximately 50% higher in HD than in C and was inversely related to BRS. Heart rate variability was also compromised in HD, and was directly related to spontaneous indices. No significant differences existed in any of these variables between RT and C. Decreased baroreflex function in juvenile HD is partly due to loss of carotid artery elasticity and partly due to impaired heart rate variability. Renal transplantation may partly prevent impairment or improve compromised baroreflex function in young patients with ESRD.

Enhanced sympathetic outflow and decreased baroreflex sensitivity are associated with intermittent hypoxia-induced systemic hypertension in conscious rats

Long-term exposure to intermittent hypoxia (IH), such as that occurring in association with sleep apnea, may result in systemic hypertension; however, the time course changes in arterial pressure, autonomic functions, and baroreflex sensitivity are still unclear. We investigated the changes in cardiovascular neural regulations during the development of chronic IH-induced hypertension in rats. Sprague-Dawley rats were exposed to repetitive 1.25-min cycles (30 s of N2+45 s of 21% O2) of IH or room air (RA) for 6 h/day during light phase (10 AM-4 PM) for 30 days. Arterial pressure was measured daily using the telemetry system during RA breathing. The mean arterial pressure (MAP) and interpulse interval (PPI) signals were then used to assess the autonomic functions and spontaneous baroreflex sensitivity by auto- and cross-spectral analysis, respectively. Stable MAP, low-frequency power of MAP (BLF), and low-frequency power (LF)-to-high frequency power (HF) ratio of PPI (LF/HF) were significantly higher in IH-exposed rats, compared with those of RA-exposed rats. Elevation of the MAP, BLF, LF/HF, and minute ventilation started 5 days after IH exposure and lasted until the end of the 30-day observation period. Additionally, IH-exposed rats had significant lower slope of MAP-PPI linear regression (under a successively descending and ascending) and magnitude of MAP-PPI transfer function (at frequency ranges of 0.06-0.6 Hz or 0.6-2.4 Hz) after IH exposure for 17 days. However, RA-exposed rats did not exhibit these changes. The results of this study indicate that chronic IH-induced hypertension is associated with a facilitation of cardiovascular sympathetic outflow and inhibition of baroreflex sensitivity in conscious rats.

Interaction between central-peripheral chemoreflexes and cerebro-cardiovascular control

We investigated the interaction between hypoxia and hypercapnia on ventilation and on cerebro-cardio-vascular control. A group of 12 healthy subjects performed rebreathing tests to determine the ventilatory response to hypoxia, at different levels of carbon dioxide (CO(2)), and to normoxic hypercapnia. Oxygen saturation (SaO(2)), end-tidal CO(2) (et-CO(2)), minute ventilation, blood pressure, R-R interval and mid-cerebral artery flow velocity (MCFV) were continuously recorded. The hypoxic ventilatory response significantly increased under hypercapnia and decreased under hypocapnia (slopes L/min/% Sa O(2): -0.33 +/- 0.05, -0.74 +/- 0.02 and -1.59 +/- 0.3, p < 0.0001, in hypocapnia, normocapnia and hypercapnia, respectively). At similar degrees of ventilation, MCFV increased more markedly during normocapnic hypoxia than normoxic hypercapnia; the slopes linking MCFV to hypoxia remained unchanged at increasing levels of et-CO(2), whereas the regression lines were shifted upward. The R-R interval decreased more markedly during normocapnic hypoxia than normoxic hypercapnia and the arterial baroreflex sensitivity was decreased only by hypoxia. Cardiovascular responses to hypoxia were not affected by different levels of et-CO(2). We conclude that concomitant hypoxia and hypercapnia, while increasing ventilation synergistically, exert an additive effect on cerebral blood flow. Increased sympathetic activity (and reduced baroreflex sensitivity) is one of the mechanisms by which hypoxia stimulates cardiac sympathetic activity.

Noninvasive measurement of blood pressure variability: accuracy of the Finometer monitor and comparison with the Finapres device

To assess the accuracy of spectral indices of arterial pressure variability and baroreflex sensitivity obtained from beat-by-beat noninvasive blood pressure recordings by the Finometer device, we compared these measures with those obtained from intra-arterial recordings. The performance of the Finometer was also compared to the traditional Finapres device. In 19 cardiac disease patients, including myocardial infarction, heart failure and cardiac transplant, we estimated the power of systolic and diastolic pressures in the VLF (0.01–0.04 Hz), LF (0.04–0.15 Hz) and HF (0.15–0.45 Hz) bands and computed absolute and percentage errors relative to intra-arterial brachial pressure. We also computed the characteristic frequency of each band (i.e. the barycentric frequency of spectral components identified in the band). The variability of systolic pressure in the VLF and LF bands was markedly overestimated by both the Finometer and Finapres (p < 0.01), with percentage median errors of respectively 130% and 103% (Finometer), and 134% and 78% (Finapres). The HF power was substantially unchanged using the Finometer and reduced using the Finapres (−28%, p < 0.05). The limits of agreement between noninvasive and invasive spectral measurements were wide. Linear system analysis showed that most (>80%) of the power of noninvasive signals was linearly related to the power of the invasive signal. The characteristic frequency of each band was substantially preserved in both noninvasive signals. The results for diastolic pressure were similar, but the Finapres errors in the VLF and LF bands were lower. Baroreflex sensitivity was significantly underestimated by both devices (Finometer: −31%, Finapres: −24%). Despite previous studies having shown that brachial artery waveform reconstruction performed by the Finometer has improved the accuracy of blood pressure measurement compared to the Finapres device, measurement of blood pressure variability in cardiac disease patients provides worse results in most spectral parameters and a better accuracy only in the HF band of systolic pressure.

Assessing the genetic background of arterial baroreflex sensitivity: a complex issue

Assessing the genetic background of arterial baroreflex sensitivity: a complex issue

Elevated myocardial repolarization lability and reduced arterial baroreflex sensitivity in subjects with high–normal blood pressure

Elevated myocardial repolarization lability and reduced arterial baroreflex sensitivity in subjects with high–normal blood pressure

Exercise Training Improves Baroreflex Sensitivity Associated With Oxidative Stress Reduction in Ovariectomized Rats

The protection from coronary events that young women have is sharply reduced at menopause. Oxidative stress and baroreflex sensitivity impairment of the circulation have been demonstrated to increase cardiovascular risk. On the other hand, exercise training has been indicated as a nonpharmacological treatment for many diseases. The aim of the present study was to test the hypothesis that exercise training can improve baroreflex sensitivity associated with reduction in oxidative stress in ovariectomized rats, an experimental model of menopause. Exercise training was performed on a treadmill for 8 weeks. Arterial pressure and baroreflex sensitivity, which were evaluated by tachycardic and bradycardic responses to changes in arterial pressure, were monitored. Oxidative stress was evaluated by chemiluminescence and superoxide dismutase and catalase antioxidant enzyme activities. Exercise training reduced resting mean arterial pressure (112+/-2 vs 122+/-3 mm Hg in the sedentary group) and heart rate (325+/-4 vs 356+/-12 bpm in the sedentary group) and also improved baroreflex sensitivity (tachycardic response, 63% and bradycardic response, 58%). Myocardium (25%) and gastrocnemius muscle (48%) chemiluminescence were reduced, and myocardial superoxide dismutase (44%) and gastrocnemius catalase (97%) activities were enhanced in trained rats in comparison with sedentary rats. Myocardium chemiluminescence was positively correlated with systolic arterial pressure (r=0.6) and inversely correlated with baroreflex sensitivity (tachycardic response, r=-0.8 and bradycardic response, r=-0.7). These results indicate that exercise training in ovariectomized rats improves resting hemodynamic status and reflex control of the circulation, probably associated with oxidative stress reduction, suggesting a homeostatic role for exercise training in reducing cardiovascular risk in postmenopausal women.

Slow Breathing Improves Arterial Baroreflex Sensitivity and Decreases Blood Pressure in Essential Hypertension

Sympathetic hyperactivity and parasympathetic withdrawal may cause and sustain hypertension. This autonomic imbalance is in turn related to a reduced or reset arterial baroreflex sensitivity and chemoreflex-induced hyperventilation. Slow breathing at 6 breaths/min increases baroreflex sensitivity and reduces sympathetic activity and chemoreflex activation, suggesting a potentially beneficial effect in hypertension. We tested whether slow breathing was capable of modifying blood pressure in hypertensive and control subjects and improving baroreflex sensitivity. Continuous noninvasive blood pressure, RR interval, respiration, and end-tidal CO2 (CO2-et) were monitored in 20 subjects with essential hypertension (56.4+/-1.9 years) and in 26 controls (52.3+/-1.4 years) in sitting position during spontaneous breathing and controlled breathing at slower (6/min) and faster (15/min) breathing rate. Baroreflex sensitivity was measured by autoregressive spectral analysis and "alpha angle" method. Slow breathing decreased systolic and diastolic pressures in hypertensive subjects (from 149.7+/-3.7 to 141.1+/-4 mm Hg, P<0.05; and from 82.7+/-3 to 77.8+/-3.7 mm Hg, P<0.01, respectively). Controlled breathing (15/min) decreased systolic (to 142.8+/-3.9 mm Hg; P<0.05) but not diastolic blood pressure and decreased RR interval (P<0.05) without altering the baroreflex. Similar findings were seen in controls for RR interval. Slow breathing increased baroreflex sensitivity in hypertensives (from 5.8+/-0.7 to 10.3+/-2.0 ms/mm Hg; P<0.01) and controls (from 10.9+/-1.0 to 16.0+/-1.5 ms/mm Hg; P<0.001) without inducing hyperventilation. During spontaneous breathing, hypertensive subjects showed lower CO2 and faster breathing rate, suggesting hyperventilation and reduced baroreflex sensitivity (P<0.001 versus controls). Slow breathing reduces blood pressure and enhances baroreflex sensitivity in hypertensive patients. These effects appear potentially beneficial in the management of hypertension.

Vagal heart rate responses to chronic beta‐blockade in human heart failure relate to cardiac norepinephrine spillover

We have documented a pre-junctional beta-2 adrenoceptor mediated reduction in cardiac norepinephrine spillover (CNES) in heart failure patients receiving chronic beta-blockade. Our present objective was to ascertain the consequence of this decrease for vagal heart rate (HR) regulation by determining CNES, arterial baroreflex sensitivity for HR (BRS) and arterial baroreflex modulation of muscle sympathetic nerve activity (MSNA) before and upon 4 months of beta-blockade with either carvedilol or metoprolol. In 19 heart failure patients in sinus rhythm (age: 55+/-2 [mean+/-S.E.]; ejection fraction: 20+/-2%), beta-blockade increased BRS from 4.8+/-0.9 to 7.9+/-1.3 ms/mm Hg (P<0.005) but had no effect on arterial baroreflex modulation of MSNA. Changes in CNES and BRS were inversely related (r=-0.52; n=16, P<0.05). Chronic beta-blockade in heart failure augments reflex vagal control of HR at an efferent site of interaction involving blockade of cardiac sympathetic pre-junctional beta-2 adrenoceptors that facilitate NE release.

Reduced α‐adrenoceptor responsiveness and enhanced baroreflex sensitivity in Cry‐deficient mice lacking a biological clock

To reveal the role of clock genes in generating the circadian rhythm of baroreflexes, we continuously measured mean arterial pressure and baroreflex sensitivity in free-moving normal wild-type mice, and in Cry-deficient mice which lack a circadian rhythm, in constant darkness for 24 h. In wild-type mice the mean arterial pressure was higher at night than during the day, and was accompanied by a significantly enhanced baroreflex sensitivity of -13.6 +/- 0.8 at night compared with -9.7 +/- 0.7 beats min(-1) mmHg(-1) during the day (P < 0.001). On the other hand, diurnal changes in arterial pressure disappeared in Cry-deficient mice with remarkably enhanced baroreflex sensitivity compared with wild-type mice (P < 0.001): -21.9 +/- 1.6 at night and -23.1 +/- 2.1 beats min(-1) mmHg(-1) during the day. Moreover, the mean arterial pressure response to 10 microg kg(-1) of phenylephrine, an alpha1-adrenoceptor agonist, was severely suppressed in Cry-deficient mice regardless of time, while that for the wild-type mice was 10.1 +/- 1.9 mmHg in the night, significantly lower than 22.0 +/- 3.5 mmHg in the day (P < 0.01). These results suggest that CRY genes are involved in generating the circadian rhythm of baroreflex sensitivity, partially by regulating alpha(1)-adrenoceptor-mediated vasoconstriction in peripheral vessels.

Nocturnal hemodialysis increases arterial baroreflex sensitivity and compliance and normalizes blood pressure of hypertensive patients with end-stage renal disease

Impaired neural control of heart rate, elevated arterial stiffness, and hypertension place patients with end-stage renal disease (ESRD) at increased risk of cardiovascular mortality. Nocturnal hemodialysis (6 x 8 hours/week), a more intense program than conventional hemodialysis (3 x 4 hours/week), lowers blood pressure and restores brachial dilator responses to hyperemia and nitrates. We hypothesized that nocturnal hemodialysis would increase arterial baroreflex sensitivity for heart rate of hypertensive ESRD patients by an afferent vascular mechanism. Ten consecutive hypertensive ESRD patients (age 42 +/- 4) (mean +/- SEM) receiving conventional hemodialysis were studied before and 2 months after conversion to nocturnal hemodialysis. Regression slopes relating RR interval responses to rises or falls in systolic blood pressure were averaged to derive spontaneous baroreflex sensitivity for heart rate for each patient, and the stroke volume/pulse pressure ratio was used to estimate total arterial compliance. Dialysis dose (Kt/V per session) increased from 1.2 +/- 0.05 to 2.1 +/- 0.1 (P < 0.05). Despite withdrawal of antihypertensive medications (from 2.9 to 0.1 drugs/patient), nocturnal hemodialysis lowered systolic blood pressure (from 143 +/- 4 to 120 +/- 6 mm Hg) (P= 0.001). Both baroreflex sensitivity (from 4.76 +/- 1.1 msec/mm Hg to 6.91 +/- 1.1 msec/mm Hg) (P= 0.04) and total arterial compliance (from 0.98 +/- 0.13 mL/mm Hg to 1.43 +/- 0.2 mL/mm Hg) (P= 0.02) were higher following conversion to nocturnal hemodialysis. Increases in baroreflex sensitivity correlated with increases in stroke volume/pulse pressure (r= 0.845, P= 0.002). These findings are consistent with the concept that nocturnal hemodialysis increases baroreflex sensitivity via greater afferent baroreceptor responsiveness to pulsatile pressure. A more favorable risk profile, due to enhanced baroreflex regulation of the circulation and vascular compliance, may translate into lower cardiovascular event rates in ESRD patients receiving nocturnal hemodialysis.

Autonomic nervous system influence on arterial baroreflex control of heart rate during exercise in humans

A combination of sympathoexcitation and vagal withdrawal increases heart rate (HR) during exercise, however, their specific contribution to arterial baroreflex sensitivity remains unclear. Eight subjects performed 25 min bouts of exercise at a HR of 90, 120, and 150 beats min-1, respectively, with and without metoprolol (0.16 +/- 0.01 mg kg(-1); mean +/- S.E.M.) or glycopyrrolate (12.6 +/- 1.6 microg kg-1). Carotid baroreflex (CBR) function was determined using 5 s pulses of neck pressure (NP) and neck suction (NS) from +40 to -80 Torr, while transfer function gain (GTF) was calculated to assess the linear dynamic relationship between mean arterial pressure and HR. Spontaneous baroreflex sensitivity (SBR) was evaluated as the slope of sequences of three consecutive beats in which systolic blood pressure and the R-R interval of the ECG either increased or decreased, in a linear fashion. The beta-1 adrenergic blockade decreased and vagal cardiac blockade increased HR both at rest and during exercise (P < 0.05). The gain at the operating point of the modelled reflex function curve (GOP) obtained using NP and NS decreased with workload independent of beta-1 adrenergic blockade. In contrast, vagal blockade decreased GOP from -0.40 +/- 0.04 to -0.06 +/- 0.01 beats min-1 mmHg-1 at rest (P < 0.05). Furthermore, as workload increased both GOP and SBR, and GOP and GTF were correlated (P < 0.001), suggesting that the two dynamic methods applied to evaluate arterial baroreflex (ABR) function provide the same information as the modelled GOP. These findings suggest that during exercise the reduction of arterial baroreceptor reflex sensitivity at the operating point was a result of vagal withdrawal rather than an increase in sympathetic activity.

Baroreflex sensitivity normalization after cardiac resynchronization therapy

Neurohormonal activation is a key factor in the development and progression of chronic heart failure. Abnormalities in arterial baroreceptors has long been hypothesized to play an important pathogenic role by reducing the restraining influence on efferent autonomic neural activity to the cardiovascular system eventually leading to sympathetic hyperactivity and parasympathetic withdrawal. The arterial baroreflex sensitivity is tested by estimating the extent of change in heart rate following spontaneous, or pharmacologically induced systemic arterial blood pressure alterations and has been proposed as a valid index of the cardiovascular system capability to reflexly increase parasympathetic activity. In the clinical setting the methodology most extensively used relies on intravenous administration of phenylephrine, a pure alpha-agonist drug that activates arterial baroreceptors and leads to a reflex bradycardia, which can be measured as pulse interval prolongation: baroreflex sensitivity is quantified in ms of pulse interval prolongation for each mm Hg of arterial pressure increase elicited by the drug. In patients with chronic heart failure alterations in baroreceptor have been shown to provide information on the risk of death [ [1] Mortara A. La Rovere M.T. Pinna G.D. et al. Arterial baroreflex modulation of heart rate in chronic heart failure: clinical and hemodynamic correlates and prognostic implications. Circulation. 1997; 96: 3450-3458 Crossref PubMed Scopus (401) Google Scholar ]. Although optimization of medical treatment partially restores autonomic imbalance [ [2] Marin-Neto J.A. Pintya A.O. Gallo Jr., L. Maciel B.C. Abnormal baroreflex control of heart rate in decompensated congestive heart failure and reversal after compensation. Am J Cardiol. 1991; 67: 604-610 Abstract Full Text PDF PubMed Scopus (41) Google Scholar ], even with optimal pharmacotherapy a number of patients remain symptomatic. In this setting, a novel approach is cardiac resynchronization therapy, an intervention that, reducing the mechanical ventricular dissynchrony, has been shown to favorably impact on morbidity and functional capacity, as demonstrated by reduced hospitalization rate, improved quality of life, left ventricular ejection fraction, New York Heart Association class, mean distance walked in 6 min [ 3 Cazeau S. Leclercq C. Lavergne T. et al. MUSTIC Study InvestigatorsEffects of multisite biventricular pacing in patients with heart failure and intraventricular conduction delay. N Engl J Med. 2001; 344: 873-880 Crossref PubMed Scopus (2516) Google Scholar , 4 Abraham W.T. Fisher W.G. Smith A.L. et al. MIRACLE Study GroupCardiac resynchronization in chronic heart failure. N Engl J Med. 2002; 346: 845-853 Google Scholar ]. Recent data indicate that cardiac resynchronization therapy can also improve heart rate variability [ [5] Adamson P.B. Kleckner K.J. VanHout W.L. Srinivasan S. Abraham W.T. Cardiac resynchronization therapy improves heart rate variability in patients with symptomatic heart failure. Circulation. 2003; 108: 266-269 Crossref PubMed Scopus (130) Google Scholar ], a marker of autonomic nervous system activity. However, the effect of cardiac resynchronization therapy on the reflex control of the heart has not been yet investigated.

A semi-automatic computerized method to measure baroreflex-mediated heart rate responses that reduces interobserver variability

Arterial baroreflex sensitivity estimated by pharmacological impulse stimuli depends on intrinsic signal variability and usually a subjective choice of blood pressure (BP) and heart rate (HR) values. We propose a semi-automatic method to estimate cardiovascular reflex sensitivity to bolus infusions of phenylephrine and nitroprusside. Beat-to-beat BP and HR time series for male Wistar rats (N = 13) were obtained from the digitized signal (sample frequency = 2 kHz) and analyzed by the proposed method (PRM) developed in Matlab language. In the PRM, time series were low-pass filtered with zero-phase distortion (3rd order Butterworth used in the forward and reverse direction) and presented graphically, and parameters were selected interactively. Differences between basal mean values and peak BP (deltaBP) and HR (deltaHR) values after drug infusions were used to calculate baroreflex sensitivity indexes, defined as the deltaHR/deltaBP ratio. The PRM was compared to the method traditionally (TDM) employed by seven independent observers using files for reflex bradycardia (N = 43) and tachycardia (N = 61). Agreement was assessed by Bland and Altman plots. Dispersion among users, measured as the standard deviation, was higher for TDM for reflex bradycardia (0.60 +/- 0.46 vs 0.21 +/- 0.26 bpm/mmHg for PRM, P < 0.001) and tachycardia (0.83 +/- 0.62 vs 0.28 +/- 0.28 bpm/mmHg for PRM, P < 0.001). The advantage of the present method is related to its objectivity, since the routine automatically calculates the desired parameters according to previous software instructions. This is an objective, robust and easy-to-use tool for cardiovascular reflex studies.

Viscerosensory-cardiovascular reflexes: altered baroreflex sensitivity in irritable bowel syndrome

Animal studies have demonstrated that visceral afferent stimulation alters autonomic cardiovascular reflexes. This mechanism might play an important role in the pathophysiology of conditions associated with visceral hypersensitivity, such as irritable bowel syndrome (IBS). As such, studies in humans are lacking, we measured viscerosensory-cardiovascular reflex interactions in IBS patients and healthy controls. Systolic blood pressure (SBP), heart rate (HR), and arterial baroreflex sensitivity (BRS) were studied in 87 IBS patients and 36 healthy controls under baseline conditions and during mild (15 mmHg) and intense (35 mmHg) visceral stimulation by rectal balloon distension. BRS was computed from continuous ECG and arterial blood pressure signals (Finapres-method) during 5-min periods of 15-min metronome respiration. Baseline SBP and HR were not different between patients and controls. In both groups, SBP increased similarly during rectal stimulation, whereas HR decreased during mild and increased intense stimulation. BRS was significantly higher in patients compared with controls at baseline (7.9 +/- 5.4 vs. 5.7 +/- 3.7 ms/mmHg, P = 0.03) and increased significantly in both groups during mild stimulation. This increase persisted in controls during intense stimulation, but BRS returned to baseline in patients. BRS was not significantly different between groups during rectal distension. This study demonstrates the presence of a viscerosensory-cardiovascular reflex in healthy individuals and in IBS patients. The increased BRS in IBS patients at baseline may either be a training-effect (frequent challenging of the reflex) or reflects altered viscerosensory processing at the nucleus tractus solitarii.

Post‐exercise palpation of pulse rates: its applicability to habitual exercisers

Despite the increased popularity of heart rate (HR) monitors, endurance-trained adults as well as habitual exercisers often use pulse rate palpation to periodically monitor exercise intensity. However, due to the rapid recovery of HR following exercise bouts, post-exercise palpation of pulse rates may underestimate exercise HR. To test this hypothesis, we studied 20 young physically active adults performing two sets of exercise for 5 min at 70% and 85% of maximal HR on the treadmill; one with carotid and another with radial pulse count. Post-exercise palpation of pulse rate was lower (P < 0.01) than the actual HR during exercise, underestimating exercise HR by 20-27 bpm (beats per min). Even when ECG tracings of HR were analyzed immediately after exercise (0-15 s), a significant underestimation of exercise HR (7-9 bpm) still persisted (P < 0.05). Following exercise, pulse rate obtained by carotid palpation at both intensities and radial palpation at the lower intensity was no different from the corresponding HR measured with ECG. In the radial artery trial at the higher exercise intensity, pulse rate following exercise was lower (10 bpm; P < 0.05) than ECG-derived HR. Arterial stiffness, which is closely associated with arterial baroreflex sensitivity, was not significantly related to the changes in HR with carotid palpation. We concluded that post-exercise pulse palpations may not be appropriate as an indicator of exercise intensity in habitual exercisers.

Arterial Stiffness And Baroreflex Sensitivity Following Acute Resistance Versus Aerobic Exercise

PURPOSE The primary focus of this study was to examine arterial stiffness (AS) and baroreflex sensitivity (BRS) after an acute bout of aerobic exercise (AE) compared to resistance exercise (RE). A secondary aim of this investigation was to test the hypothesis that acute alterations in AS stemming from AE versus RE may be related to differential changes in peripheral sympathetic vasomotor tone (SVMT). METHODS AS, BRS, and SVMT were assessed before and 20-min after a bout of AE (30-min cycling at 65% of VO2peak) and RE (3 sets of 10 reps; total body regimen) in 13 male participants (25 ± 0.7 yrs). Pulse wave velocity (PWV) was used to measure central (carotid-femoral) and peripheral (femoral-anterior tibialis) AS. BRS was derived via the sequence technique. For assessment of SVMT, continuous beat-to-beat systolic arterial pressures (SAPLF) were spectrally decomposed using Fast Fourier transforms and power spectra within the low-frequency bandwidth of 0.04–0.15 Hz were considered representative of SVMT. Data were analyzed using an ANOVA with repeated measures. RESULTS SAP, DAP, and MAP did not change from rest to the 20-min recovery following AE and RE. A mode-by-time interaction (P <0.001) was detected for central PWV, due to a significant increase in PWV (4.8 ± 0.30 to 5.8 ± 0.31 m/s; P <0.05) following RE and a significant decrease in PWV (5.3 ± 0.16 to 4.8 ± 0.25 m/s) following AE (P <0.05). A mode-by-time interaction was also detected for peripheral PWV (p <0.05) due to a significant decrease in peripheral PWV following AE (8.9 ± 0.25 to 8.3 ± 0.25 m/s; P <0.05) with no change in RE (8.7 ± 0.33 to 9.0 ± 0.31 m/s). BRS was significantly lower following RE (25.1 ± 4.2 to 12.7 ± 2.2 ms/mmHg) compared with AE(27.2 ± 3.1 to 21.9 ± 3.0 ms/mmHg; P <0.004). SAPLF increased significantly after AE (8.0 ± 1.1 to 11.9 ± 1.7 ms2, p < 0.05) and RE (8.8 ± 1.9 to 14.9 ± 3.2 ms2, p < 0.05), but there was no interaction. CONCLUSIONS Acute AE and RE differentially affect arterial and autonomic function. AE decreased both central and peripheral AS, while RE significantly increased central AS. BRS was reduced after both bouts of exercise, but significantly greater reductions were seen following RE. Alterations in AS following AE compared to RE appear not to be mediated by differences in SVMT.

Sympathoexcitation by central ANG II: Roles for AT1 receptor upregulation and NAD(P)H oxidase in RVLM

Chronic heart failure is often associated with sympathoexcitation and blunted arterial baroreflex function. These phenomena have been causally linked to elevated central ANG II mechanisms. Recent studies have shown that NAD(P)H oxidase-derived reactive oxygen species (ROS) are important mediators of ANG II signaling and therefore might play an essential role in these interactions. The aims of this study were to determine whether central subchronic infusion of ANG II in normal animals has effects on O2- production and expression of NAD(P)H oxidase subunits as well as ANG II type 1 (AT1) receptors in the rostral ventrolateral medulla (RVLM). Twenty-four male New Zealand White rabbits were divided into four groups and separately received a subchronic intracerebroventricular infusion of saline alone, ANG II alone, ANG II with losartan, and losartan alone for 1 wk. On day 7 of intracerebroventricular infusion, mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) values were recorded, and arterial baroreflex sensitivity was evaluated while animals were in the conscious state. We found that ANG II significantly increased baseline RSNA (161.9%; P < 0.05), mRNA and protein expression of AT1 receptors (mRNA, 66.7%; P < 0.05; protein, 85.1%; P < 0.05), NAD(P)H oxidase subunits (mRNA, 120.0-200.0%; P < 0.05; protein, 90.9-197.0%; P < 0.05), and O2- production (83.2%; P < 0.05) in the RVLM. In addition, impaired baroreflex control of HR (Gain(max) reduced by 48.2%; P < 0.05) and RSNA (Gain(max) reduced by 53.6%; P < 0.05) by ANG II was completely abolished by losartan. Losartan significantly decreased baseline RSNA (-49.5%; P < 0.05) and increased baroreflex control of HR (Gain(max) increased by 64.8%; P < 0.05) and RSNA (Gain(max) increased by 67.9%; P < 0.05), but had no significant effects on mRNA and protein expression of AT1 receptor and NAD(P)H oxidase subunits and O2- production in the RVLM. These data suggest that in normal rabbits, NAD(P)H oxidase-derived ROS play an important role in the modulation of sympathetic activity and arterial baroreflex function by subchronic central treatment of exogenous ANG II via AT1 receptors.

The Contribution Of The Sympathetic And Parasympathetic Systems To Cardiac-arterial Baroreflex Sensitivity During Dynamic Exercise

During exercise, an alteration in the balance between the two divisions of the autonomic nervous system (sympathetic activation and vagal withdrawal) increases HR. However, the contribution of the sympathetic or vagal system to cardiac-arterial baroreflex sensitvity remains unclear. PURPOSE The purpose of this study was to examine the effects of sympathetic and parasympathetic activity to the heart at rest and during exercise on the cardiac-arterial baroreflex sensitivity. METHODS Eight subjects performed 20 min bouts of exercise at a steady-state heart rate (HR) of 90 (EX90), 120 (EX120), and 150 (EX150) beats/min with and without metoprolol (0.2 mg/kg) or glycopyrrolate (0.04 mg/kg). Systolic blood pressure (SBP), mean arterial pressure (MAP) and pulse interval (RRI) were continuously measured. Arterial baroreflex sensitivity (BRS) was evaluated by analyzing the slopes of spontaneously occurring sequences of three or more consecutive beats in which systolic blood pressure and pulse interval of the following beat either increased or decreased, in the same direction, in a linear fashion. RESULTS β-1 adrenagic blockade decreased (p < 0.05) and vagal cardiac blockade increased HR (p < 0.05) at rest and during the three exercise workloads. Without blockade, BRS gradually decreased with increasing exercise workload. While there was no significant difference in BRS with and without β-1 adrenagic blockade at rest and during exercise, vagal cardiac blockade decreased BRS from 26.0 ± 4.8 to 3.2 ± 0.4 ms/mmHg at rest (p < 0.05). However, during EX150 there was no difference in BRS with and without cardiac vagal blockade (1.8 ± 0.4 vs. 1.4 ± 0.3 ms/mmHg, P > 0.05). CONCLUSION This finding suggests that during exercise the reduction of cardiac-arterial baroreflex sensitivity occurs by vagal withdrawal and this reduction is not influenced by the exercise induced increase in sympathetic activity.