| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1 Human Cardiovascular Research Laboratory, Department of Kinesiology and Applied Physiology, University of Colorado at Boulder, Boulder 80309; and 2 Divisions of Cardiology and Geriatric Medicine, Department of Medicine, University of Colorado Health Sciences Center, Denver, Colorado 80262
 |
ABSTRACT |
|---|
 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Cardiovagal
baroreflex sensitivity (BRS) declines with advancing age in
humans, but the underlying mechanism has not been established. Using
two different approaches, we determined the relation between
age-associated decline in cardiovagal BRS and the compliance of an
artery in which arterial baroreceptors are located. First, we measured
carotid artery compliance (via the simultaneous application of
ultrasonography and arterial applanation tonometry) and cardiovagal BRS
(phase IV of the Valsalva maneuver) in 47 healthy sedentary men that
varied widely in age (19-76 yr). Cardiovagal BRS declined
progressively with age (r = 
0.69; P 
0.001) and was positively related to carotid artery compliance (r = 0.71; P 0.001). Stepwise
multiple-regression analysis revealed that carotid artery compliance
was the strongest independent physiological correlate of cardiovagal
BRS and that it explained 51% of the total variance. Second, we
studied 13 middle-aged and older previously sedentary men (age 56 ± 2 yr) before and after 13 wk of aerobic exercise intervention. Regular
exercise increased both cardiovagal BRS and carotid artery compliance
(P < 0.05) and the two events were strongly and
positively related (r = 0.72; P < 0.01). We conclude that reduced carotid artery compliance may play an
important mechanistic role in age-associated decrease in cardiovagal
BRS in healthy sedentary humans.
aging; baroreceptor; exercise training
| |
INTRODUCTION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
CARDIOVAGAL BAROREFLEX SENSITIVITY (BRS) is an important determinant of electrical stability in the heart (5, 12) and is a key mechanism for short-term (i.e., beat-to-beat) arterial blood pressure regulation in humans (18, 24). We and others (8, 14, 17, 19) have demonstrated that cardiovagal BRS declines with advancing age in humans; however, the underlying mechanism has not been established. A long-hypothesized possibility is that the age-associated decrease in compliance of the large elastic cardiothoracic arteries in which the arterial baroreceptors are embedded (carotid and ascending aorta) is responsible for the decline in cardiovagal BRS (23, 28). The vascular structure of the carotid sinus area determines the deformation of and strain on the arterial baroreceptors during acute changes in arterial blood pressure (10). In this context, the reduced compliance of the carotid artery with age (3, 28) would be expected to restrict the ability of its mechanically sensitive segments to transduce changes in intravascular pressure into the appropriate afferent nerve signals to the central nervous system. Currently, however, there is no direct experimental support for a relation between age-associated reductions in carotid artery compliance and cardiovagal BRS.
In the present study, we tested the hypothesis that the age-associated decline in cardiovagal BRS is related to reduced carotid artery compliance in healthy adult humans. To comprehensively address this issue, we used two approaches. First, we determined the relation between cardiovagal BRS and carotid artery compliance in a large population of healthy men that varied widely in age. Second, we used regular aerobic exercise, an intervention that partially reverses age-associated reductions in cardiovagal BRS (19), to determine if increases in cardiovagal BRS are accompanied by corresponding increases in carotid artery compliance.
| |
METHODS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Study Subjects
The study included 47 sedentary men (age 19-76 yr). All subjects were normotensive (blood pressure < 140/90 mmHg), nonobese (body mass index < 30 kg/m2), nonsmoking, and not taking any medications known to affect baseline autonomic/cardiovascular functions (e.g., heart rate or blood pressure). Additionally, all subjects had no apparent cardiovascular disease as assessed by a medical questionnaire. Subjects of age >40 yr were further evaluated by physical examination and resting and maximal treadmill exercise electrocardiograms (ECGs). For the exercise intervention, 13 men of age >50 yr were studied before and after 3 mo of regular aerobic exercise. The experimental protocol was approved by the Human Research Committee of the University of Colorado at Boulder. Written informed consent was obtained from all participants after the nature, purpose, and risks of the study were explained.Measurements
Subjects refrained from food and caffeine consumption for 4 h before the experimental protocol began.Cardiovagal BRS. Cardiovagal BRS was assessed using the Valsalva maneuver as recently explained (19). Described briefly, after 15 min of seated rest, subjects expired forcibly through a small mouthpiece for a 10-s period while maintaining an expiratory mouth pressure of 40 mmHg. Measurements of mouth pressure, R-R interval (measured via ECG), and beat-to-beat arterial blood pressure (Finapres; Ohmeda) were collected continuously (Windaq; Dataq Instruments) before, during, and after the maneuver. Subjects performed two trials separated by 5 min, during which time cardiovascular function returned to initial baseline values.
Data analysis was performed during phase IV of the Valsalva maneuver. Systolic blood pressure values were linearly regressed against corresponding (lag 1) R-R intervals on a beat-to-beat basis from the point at which the R-R interval began to lengthen, and continued to the point of maximal systolic blood pressure elevation. The slope from the R-R interval and the systolic blood pressure relation was used as a measure of cardiovagal BRS if the correlation coefficient exceeded r = 0.80. The correlation between cardiovagal BRS values obtained from this procedure and the Oxford technique is excellent (r = 0.91) (21). The average of the two trials was used for each subject.Carotid arterial compliance. Carotid arterial compliance was determined with subjects under supine resting conditions using ultrasound imaging with simultaneous arterial applanation tonometry as previously described (28). Carotid arterial diameters were measured from images obtained from a Toshiba SSH-140 ultrasound machine equipped with a high-resolution linear array transducer. Longitudinal images were obtained 1-2 cm proximal to the carotid bulb and were analyzed using image-analysis software on a PC computer after analog-to-digital conversion (DT-3152; Data Translations). Simultaneously the central arterial pressure waveforms were obtained noninvasively using a pencil-type probe containing a high-fidelity strain-gauge transducer (TCB-500; Millar Instruments) placed on the contralateral common carotid artery. These waveforms were calibrated to the mean arterial pressure from the periphery to account for variations in hold-down pressure (1).
Arterial blood pressure and heart rate at rest. Chronic resting arterial blood pressure was determined noninvasively over the brachial artery using a semiautomated device (Dinamap XL; Johnson and Johnson) after patients rested quietly for 15 min in a sitting position. The average of three consecutive measures is reported. Heart rate at rest was determined from the ECGs.
Body composition. Body composition was determined using dual-energy X-ray absorptiometry (Lunar Radiation).
Maximal oxygen consumption. Maximal oxygen consumption was measured using on-line open-circuit spirometry as we have previously described (27).
Exercise Intervention
Subjects performed home-based exercise for a 3-mo period as previously described (19). In brief, subjects were asked to walk or walk-jog most days of the week for a period of 40-45 min/day at an intensity of 60-85% of their individually determined maximal heart rates. Adherence to the exercise prescription was documented via the use of heart rate monitors and physical activity logs (19, 28).Statistical Analyses
Univariate correlation and regression analyses were performed to determine the relations between selected physiological variables. Partial correlation analysis was used to statistically remove the influence of one variable on the relation between two other variables. Forward-stepwise multiple-regression analyses were used to determine independent physiological correlates of the age-associated decline in cardiovagal BRS. To do so, only variables that had significant univariate correlations with cardiovagal BRS were entered in the model. A repeated-measures ANOVA was used to determine significant mean group changes in the intervention study. All data are reported as means ± SE. Statistical significance was set at P < 0.05.| |
RESULTS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Cross-sectional study.
Selected subject characteristics are presented in Table
1. Cardiovagal BRS declined progressively
with increasing subject age (r = 0.69;
P < 0.001; y = 0.32x + 26.95). Cardiovagal BRS was significantly related to carotid artery
compliance (r = 0.71; P < 0.001;
y = 10.46x 1.95; Fig.
1), percent body fat (r = 0.37; P < 0.01; y = 0.38x + 20.73), diastolic blood pressure
(r = 0.37; P < 0.01;
y = 0.28x + 30.56), heart rate at
rest (r = 0.52; P < 0.001;
y = 0.37x + 34.57), and maximal
oxygen consumption (r = 0.57; P < 0.001; y = 0.55x 8.13). Stepwise
multiple-regression analysis revealed that among these correlated
variables, carotid artery compliance was the strongest independent
physiological correlate of cardiovagal BRS as it explained 51% of the
variance. An additional 20% of the variance in cardiovagal BRS was
accounted for by heart rate at rest. No other variables entered in the
model. When the influence of carotid artery compliance was accounted for using a partial correlation analysis, the relation between cardiovagal BRS and age was markedly weakened (r = 0.38), as age explained only 14% of the interindividual variability
in cardiovagal BRS.
|
|
Intervention study.
All 13 middle-aged and older men completed the exercise intervention.
On average, subjects completed 44 ± 3 min of exercise per
session, 5.5 ± 0.4 exercise sessions per week, and 14 ± 1 wk of exercise at an intensity of 72 ± 2% of individually
determined maximal heart rate. There were no significant changes in
body mass, body fat percentage, blood pressure, heart rate at rest, or
maximal oxygen consumption. However, heart rate and ratings of
perceived exertion at a standardized submaximal workload of 
70% of
the initial (baseline) maximal oxygen consumption decreased (P < 0.01), and treadmill time to exhaustion improved
by 20% (P < 0.001; see Table
2).
|
2) ± 0.09 to (1.38 × 102) ± 0.12 mm2/mmHg; P < 0.05]; see Fig. 2B. There was a strong and positive relation between the changes in carotid arterial compliance and cardiovagal BRS (r = 0.72; P < 0.01;
see Fig. 2C). The increase in carotid arterial compliance
explained >50% of the variability associated with the improvement in
cardiovagal BRS. No other variable was related to the changes in
cardiovagal BRS.
|
| |
DISCUSSION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
The primary new findings from the present study are as follows. First, among healthy sedentary men that vary widely in age, cardiovagal BRS is most strongly related to carotid artery compliance. Second, improvements in cardiovagal BRS with exercise intervention are strongly and positively related to the corresponding increases in carotid artery compliance in previously sedentary middle-aged and older men. Taken together, these findings indicate that reduced carotid artery compliance may play an important mechanistic role in the age-associated reduction in cardiovagal BRS in sedentary humans.
At least six lines of experimental evidence from the present study support an independent association between age-related changes in cardiovagal BRS and carotid artery compliance in healthy sedentary men. First, our univariate correlation analyses revealed that carotid artery compliance was strongly and positively related to cardiovagal BRS in a population varying widely in age (r = 0.71). Second, when the influence of carotid artery compliance was accounted for using partial correlation analysis, the relation between cardiovagal BRS and age was dramatically weakened, with age explaining only a very small (14%) portion of the variance in cardiovagal BRS. Third, stepwise multiple-regression analysis revealed that carotid artery compliance was the primary independent physiological determinant of the age-associated decline in cardiovagal BRS, as it explained 51% of the interindividual variance. Fourth, when the influence of age was removed via partial correlation analysis, the strength of the relation between cardiovagal BRS and carotid arterial compliance remained highly significant (r = 0.44). Fifth, when carotid arterial compliance was removed from the cardiovagal BRS-age relation using analysis of covariance, there was no longer a significant association between cardiovagal BRS and age. Finally, the increase in cardiovagal BRS in response to an aerobic exercise intervention was strongly related to corresponding increases in carotid artery compliance. Taken together, these results indicate that decreased carotid arterial compliance may be an important mechanism underlying age-related reductions in cardiovagal BRS. Additionally, our present findings also suggest that cardiovagal BRS-arterial compliance association is not simply due to colinearity with age.
We should emphasize that in general only ~50% of the interindividual variance in cardiovagal BRS was explained by carotid artery compliance in the present study protocols. It is possible that given the normal measurement error with these two variables, our correlation may have underestimated the true strength of the relation; that is, carotid artery compliance may have explained more of the decline in cardiovagal BRS with age than is indicated by our correlation-based analyses. Other mechanisms, however, also may have contributed to the remaining variability. For example, age-associated reductions in muscarinic receptor density in the sinoatrial node (9, 22) might result in less lengthening of the R-R interval in response to the same reflex increase in cardiac vagal nerve activity. Moreover, changes in the central nervous system integration of the baroreflex could alter afferent-efferent coupling and contribute to the decline in cardiovagal BRS with age. We know of no specific experimental evidence supporting this mechanism, but it remains a possibility.
Previous studies investigating the association between arterial compliance and BRS have produced inconsistent results. Lage and colleagues (16) examined the relation in normotensive and hypertensive individuals and found that arterial compliance correlated poorly with BRS. It is possible, however, that methodological limitations precluded demonstration of a significant relation between these events in that study. In particular, steady-state infusions of phenylephrine hydrochloride and sodium nitroprusside were used to alter arterial blood pressure. Sustained alterations in arterial pressure by these vasoactive drugs can result in rapid baroreflex resetting (25) and might affect arterial compliance via changes in smooth muscle tone. In fact, BRS determined via the "gold standard" bolus drug-infusion technique does not correlate with that obtained via steady-state drug infusion (26). Rather, the present results are more consistent with those of Bonyhay and colleagues (6), who demonstrated that carotid artery distensibility was strongly associated with cardiovagal BRS in a small group of young adults. In the present investigation, we used the combination of: 1) a much larger study sample varying widely in age, and 2) a more definitive intervention-based experimental approach that purposely evoked changes in cardiovagal BRS in an attempt to dissociate BRS and carotid artery compliance. We found that cardiovagal BRS and carotid artery compliance remained consistently and significantly associated within both of these study designs.
Our findings have potentially important physiological and clinical implications. The present results indicate that interventions that increase the compliance of the large elastic arteries in the cardiothoracic circulation may be effective in attenuating the reduction in cardiovagal BRS with age (19). Reductions in cardiovagal BRS are associated with potentially adverse changes in blood pressure control including an increase in arterial blood pressure variability (15, 31), which is an independent risk factor for cardiovascular disease (29). Moreover, low cardiovagal BRS is associated with myocardial electrical instability and increased susceptibility to ventricular fibrillation and cardiac sudden death, particularly in the presence of preexisting myocardial ischemia (5). The prevalence of both high arterial blood pressure variability (15, 31) and cardiac sudden death (13) increases markedly with advancing age. Thus interventions that increase central arterial compliance might be used in the prevention of such age-associated cardiovascular disorders. In this context, arterial compliance can be modified by various lifestyle (e.g., regular exercise and dietary sodium restriction) and pharmacological interventions (2, 20, 28).
The mechanisms by which regular aerobic exercise improves arterial compliance are not clear. Structural changes in the arterial wall are believed to occur over years. Thus it is unlikely that short-term regular aerobic exercise increased arterial compliance by this mechanism. It is possible to speculate, however, that the increased mechanical distending pressure during the exercise bouts "stretched" the collagen fibers and modified age-related cross linking within them, and thereby increased arterial compliance (11). Additionally, arterial compliance can be altered over a short time period by modulating the sympathetic-adrenergic tone of smooth muscle cells in the arterial wall (4, 7). It is therefore possible that regular exercise increased arterial compliance by reducing the chronic restraint exerted by sympathetic-adrenergic tone either directly or by enhancing the sympathoinhibitory effect of nitric oxide (30).
There are at least two important limitations associated with the present study: 1) because our data are based solely on correlation analyses, we cannot determine cause and effect between cardiovagal BRS and carotid arterial compliance with age; and 2) arterial compliance was measured under basal resting conditions, whereas cardiovagal BRS was determined during a blood-pressure-perturbing maneuver. It is likely that the stimulus-response characteristics of the arterial baroreceptors are different under these two conditions and thus could influence the results of our study.
In conclusion, the results of the present study indicate that reduced carotid artery compliance may be an important mechanism underlying age-associated reductions in cardiovagal BRS.
| |
ACKNOWLEDGEMENTS |
|---|
The authors thank Yoli Casas, Teresa Wilson, Jayne Semmler, and Linda Shapiro for technical assistance in the present study.
| |
FOOTNOTES |
|---|
This study was supported by National Institutes of Health Grants AG-00847 (to H. Tanaka), AG-06537, AG-13038, and AG-16071 (to D. R. Seals).
Address for reprint requests and other correspondence: H. Tanaka, Dept. of Kinesiology and Applied Physiology, Univ. of Colorado at Boulder, Boulder, CO 80309-0354 (E-mail: tanakah{at}colorado.edu).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 30 November 2000; accepted in final form 7 February 2001.
| |
REFERENCES |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
1.
Armentano, R,
Megnien JL,
Simon A,
Bellenfant F,
Barra J,
and
Levenson J.
Effects of hypertension on viscoelasticity of carotid and femoral arteries in humans.
Hypertension
26:
48-54,
1995
2.
Avolio, AP,
Clyde KM,
Beard TC,
Cooke HM,
Ho KK,
and
O'Rourke MF.
Improved arterial distensibility in normotensive subjects on a low sodium diet.
Arteriosclerosis
6:
166-169,
1986
3.
Avolio, AP,
Deng FQ,
Li WQ,
Luo YF,
Huang ZD,
Xing LF,
and
O'Rourke MF.
Effects of aging on arterial distensibility in populations with high and low prevalence of hypertension: comparison between urban and rural communities in China.
Circulation
71:
202-210,
1985
4.
Barenbrock, M,
Spieker C,
Witta J,
Evers S,
Hoeks APG,
Rahn KH,
and
Zidek W.
Reduced distensibility of the common carotid artery in patients treated with ergotamine.
Hypertension
28:
115-119,
1996
5.
Billman, GE,
Schwartz PJ,
and
Stone HL.
Baroreceptor reflex control of heart rate: a predictor of sudden cardiac death.
Circulation
66:
874-879,
1982
6.
Bonyhay, I,
Jokkel G,
and
Kollai M.
Relation between baroreflex sensitivity and carotid artery elasticity in healthy humans.
Am J Physiol Heart Circ Physiol
271:
H1139-H1144,
1996
7.
Boutouyrie, P,
Locolley P,
Girerd X,
Beck L,
Safar M,
and
Laurent S.
Sympathetic activation decreases medium-sized arterial compliance in humans.
Am J Physiol Heart Circ Physiol
267:
H1368-H1376,
1994
8.
Bristow, JD,
Gribbin B,
Honour AJ,
Pickering TG,
and
Sleight P.
Diminished baroreflex sensitivity in high blood pressure and ageing man.
J Physiol (Lond)
202:
45P-46P,
1969.
9.
Brodde, OE,
Konschak U,
Becker K,
Ruter F,
Poller U,
Jakubetz J,
Radke J,
and
Zerkowski HR.
Cardiac muscarinic receptors decrease with age.
J Clin Invest
101:
471-478,
1998[ISI][Medline].
10.
Brown, AM.
Receptors under pressure: an update on baroreceptors.
Circ Res
46:
1-10,
1980
11.
Bruel, A,
Ortoft G,
and
Oxlund H.
Inhibition of cross-links in collagen is associated with reduced stiffness of the aorta in young rats.
Atherosclerosis
140:
135-145,
1998[ISI][Medline].
12.
Cerati, D,
and
Schwartz PJ.
Single cardiac vagal fiber activity, acute myocardial ischemia, and risk for sudden death.
Circ Res
69:
1389-1401,
1991
13.
Gilman, JK,
Jalal S,
and
Naccarelli GV.
Predicting and preventing sudden death from cardiac causes.
Circulation
90:
1083-1092,
1994
14.
Gribbin, B,
Pickering TG,
Sleight P,
and
Peto R.
Effect of age and high blood pressure on baroreflex sensitivity in man.
Circ Res
29:
424-431,
1971
15.
Imai, Y,
Aihara A,
Ohkubo T,
Nagai K,
Tsuji I,
Minami N,
Satoh H,
and
Hisamichi S.
Factors that affect blood pressure variability: a community-based study in Ohasama, Japan.
Am J Hypertens
10:
1281-1289,
1997[ISI][Medline].
16.
Lage, SG,
Polak JP,
O'Leary DH,
and
Creager MA.
Relationship of arterial compliance to baroreflex function in hypertensive patients.
Am J Physiol Heart Circ Physiol
265:
H232-H237,
1993
17.
Laitinen, T,
Hartikainen J,
Vanninen E,
Niskanen L,
Geelen G,
and
Lansimies E.
Age and gender dependency of baroreflex sensitivity in healthy subjects.
J Appl Physiol
84:
576-583,
1998
18.
Mancia, G,
Parati G,
Pomidossi G,
Casadei R,
Rienzo MD,
and
Zanchetti A.
Arterial baroreflexes and blood pressure and heart rate variabilities in humans.
Hypertension
8:
147-153,
1986
19.
Monahan, KD,
Dinenno FA,
Tanaka H,
Clevenger CM,
DeSouza CA,
and
Seals DR.
Regular aerobic exercise modulates age-associated declines in cardiovagal baroreflex sensitivity in healthy men.
J Physiol (Lond)
529:
263-271,
2000
20.
O'Rourke, M.
Arterial stiffness, systolic blood pressure, and logical treatment of arterial hypertension.
Hypertension
15:
339-347,
1990
21.
Palmero, HA,
Caeiro TF,
Iosa DJ,
and
Bas J.
Baroreceptor reflex sensitivity index derived from phase 4 of the Valsalva maneuver.
Hypertension
3:
134-137,
1981
22.
Poller, U,
Nedelka G,
Radke J,
Ponicke K,
and
Brodde OE.
Age-dependent changes in cardiac muscarinic receptor function in healthy volunteers.
J Am Coll Cardiol
29:
187-193,
1997[Abstract].
23.
Rowe, JW.
Clinical consequences of age-related impairments in vascular compliance.
Am J Cardiol
60:
68G-71G,
1987[Medline].
24.
Sagawa, K.
Baroreflex control of systemic arterial pressure and vascular bed.
In: Handbook of Physiology. The Cardiovascular System: Peripheral Circulation and Organ Blood Flow. Bethesda, MD: Am. Physiol. Soc, 1983, sect. 2, vol. III, pt. 2, chapt. 14, p. 453-496.
25.
Smith, ML,
Beightol LA,
Fritsch-Yelle JM,
Ellenbogen KA,
Porter TR,
and
Eckberg DL.
Valsalva's maneuver revisited: a quantitative method yielding insight into human autonomic control.
Am J Physiol Heart Circ Physiol
271:
H1240-H1249,
1996
26.
Sullebarger, JT,
Liang CS,
Woolf PD,
Willick AE,
and
Richeson JF.
Comparison of phenylephrine bolus and infusion methods in baroreflex measurements.
J Appl Physiol
69:
962-967,
1990
27.
Tanaka, H,
DeSouza CA,
Jones PP,
Stevenson ET,
Davy KP,
and
Seals DR.
Greater rate of decline in maximal aerobic capacity with age in physically active vs. sedentary healthy women.
J Appl Physiol
83:
1947-1953,
1997
28.
Tanaka, H,
Dinenno FA,
Monahan KD,
Clevenger CM,
DeSouza CA,
and
Seals DR.
Aging, habitual exercise, and dynamic arterial compliance.
Circulation
102:
1270-1275,
2000
29.
Tsuji, H,
Venditti FJ,
Manders ES,
Evans JC,
Larson MG,
and
Feldman CL.
Reduced heart rate variability and mortality risk in an elderly cohort. The Framingham Heart Study.
Circulation
90:
878-883,
1994
30.
Zanzinger, J.
Role of nitric oxide in the neural control of cardiovascular function.
Cardiovasc Res
43:
639-649,
1999
31.
Zito, M,
Parati G,
Omboni S,
Cervone C,
Ulian L,
D'Aviero M,
Abate G,
and
Mancia G.
Effect of ageing on blood pressure variability.
J Hypertens
9:
S328-S329,
1991.
This article has been cited by other articles:
|
|
 |
|
  R. A. I. Lucas, J. D. Cotter, S. Morrison, and P. N. Ainslie The effects of ageing and passive heating on cardiorespiratory and cerebrovascular responses to orthostatic stress in humans Exp Physiol, October 1, 2008; 93(10): 1104 - 1117. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Leone, P. Ducimetiere, J. Gariepy, D. Courbon, C. Tzourio, J.-F. Dartigues, K. Ritchie, A. Alperovitch, P. Amouyel, M. E. Safar, et al. Distension of the Carotid Artery and Risk of Coronary Events: The Three-City Study Arterioscler. Thromb. Vasc. Biol., July 1, 2008; 28(7): 1392 - 1397. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 X. Shi, F. A. Schaller, N. Tierney, P. Chanthavong, S. Chen, P. B. Raven, and M. L. Smith Physically Active Lifestyle Enhances Vagal-Cardiac Function but Not Central Autonomic Neural Interaction in Elderly Humans Experimental Biology and Medicine, February 1, 2008; 233(2): 209 - 218. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. D. Monahan Effect of aging on baroreflex function in humans Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2007; 293(1): R3 - R12. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. P. Fisher, S. Ogoh, A. Ahmed, M. R. Aro, D. Gute, and P. J. Fadel Influence of age on cardiac baroreflex function during dynamic exercise in humans Am J Physiol Heart Circ Physiol, July 1, 2007; 293(1): H777 - H783. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Moller, J. S. Iversen, J. H. Henriksen, and F. Bendtsen Reduced baroreflex sensitivity in alcoholic cirrhosis: relations to hemodynamics and humoral systems Am J Physiol Heart Circ Physiol, June 1, 2007; 292(6): H2966 - H2972. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. C. Laterza, L. D.N.J. de Matos, I. C. Trombetta, A. M.W. Braga, F. Roveda, M. J.N.N. Alves, E. M. Krieger, C. E. Negrao, and M. U.P.B. Rondon Exercise Training Restores Baroreflex Sensitivity in Never-Treated Hypertensive Patients Hypertension, June 1, 2007; 49(6): 1298 - 1306. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. D. Steinback, D. D. O'Leary, J. Bakker, A. D. Cechetto, H. M. Ladak, and J. K. Shoemaker Carotid distensibility, baroreflex sensitivity, and orthostatic stress J Appl Physiol, July 1, 2005; 99(1): 64 - 70. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. E. DeVan, M. M. Anton, J. N. Cook, D. B. Neidre, M. Y. Cortez-Cooper, and H. Tanaka Acute effects of resistance exercise on arterial compliance J Appl Physiol, June 1, 2005; 98(6): 2287 - 2291. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. E. Hunt and W. B. Farquhar Nonlinearities and asymmetries of the human cardiovagal baroreflex Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2005; 288(5): R1339 - R1346. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. N. Thrasher Baroreceptors, baroreceptor unloading, and the long-term control of blood pressure Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2005; 288(4): R819 - R827. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Laitinen, L. Niskanen, G. Geelen, E. Lansimies, and J. Hartikainen Age dependency of cardiovascular autonomic responses to head-up tilt in healthy subjects J Appl Physiol, June 1, 2004; 96(6): 2333 - 2340. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. D. Monahan, I. Eskurza, and D. R. Seals Ascorbic acid increases cardiovagal baroreflex sensitivity in healthy older men Am J Physiol Heart Circ Physiol, June 1, 2004; 286(6): H2113 - H2117. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Scremin and W. L. Kenney Aging and the skin blood flow response to the unloading of baroreceptors during heat and cold stress J Appl Physiol, March 1, 2004; 96(3): 1019 - 1025. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. P. van Orshoven, P. L. Oey, L. J. van Schelven, J. M. M. Roelofs, P. A. F. Jansen, and L. M. A. Akkermans Effect of gastric distension on cardiovascular parameters: gastrovascular reflex is attenuated in the elderly J. Physiol., March 1, 2004; 555(2): 573 - 583. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Sharabi, R. Dendi, C. Holmes, and D. S. Goldstein Baroreflex Failure as a Late Sequela of Neck Irradiation Hypertension, July 1, 2003; 42(1): 110 - 116. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Miyachi, A. J. Donato, K. Yamamoto, K. Takahashi, P. E. Gates, K. L. Moreau, and H. Tanaka Greater Age-Related Reductions in Central Arterial Compliance in Resistance-Trained Men Hypertension, January 1, 2003; 41(1): 130 - 135. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. A. Lanfranchi and V. K Somers Arterial baroreflex function and cardiovascular variability: interactions and implications Am J Physiol Regulatory Integrative Comp Physiol, October 1, 2002; 283(4): R815 - R826. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. A. Kingwell, J. D. Cameron, A. M. Dart, K. D. Monahan, H. Tanaka, F. A. Dinenno, and D. R. Seals Large Artery Stiffness and Baroreflex Function Response Circulation, February 26, 2002; 105 (8): e56 - e56. [Full Text] [PDF]
|
|
|
|
|
|
M. F. O'Rourke, W. W. Nichols, B. E. Hunt, W. B. Farquhar, and J. A. Taylor Does Reduced Vascular Stiffening Fully Explain Preserved Cardiovagal Baroreflex Function in Older Physically Active Men? Response Circulation, January 15, 2002; 105 (2): e11 - e11. [Full Text] [PDF]
|
|
|
|
|
|
K. D. Monahan, H. Tanaka, F. A. Dinenno, and D. R. Seals Central Arterial Compliance Is Associated With Age- and Habitual Exercise-Related Differences in Cardiovagal Baroreflex Sensitivity Circulation, October 2, 2001; 104(14): 1627 - 1632. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
