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J Physiol (2003), 551.2, pp. 601-608
© Copyright 2003 The Physiological Society
DOI: 10.1113/jphysiol.2003.046029
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ABSTRACT |
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This investigation examined the interaction between carotid baroreflex (CBR) responsiveness during head-up tilt (HUT)-induced central hypovolaemia and aerobic fitness. Seven average fit (AF) individuals, with a mean maximal oxygen uptake (O2max) of 49 ± 1 (ml O2) kg-1min-1, and seven high fit (HF) individuals, with a
(Received 28 April 2003; accepted after revision 12 June 2003; first published online 17 June 2003)
Corresponding author S. Ogoh: Department of Integrative Physiology, University of North Texas Health Science Center, 3500 Camp Bowie Boulevard, Fort Worth, Texas 76107, USA. Email: sogoh{at}hsc.unt.edu
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INTRODUCTION |
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Endurance exercise training induces changes in cardiovascular structure and haemodynamic function, the most notable of which includes remodelling of the heart chambers (Levine et al. 1991a,b; Levine, 1993) and blood vessels (Snell et al. 1987; Cameron & Dart, 1994) associated with increases in the central blood volume (CBV, Sawka et al. 2000). While these morphological and functional changes confer some advantages to athletic performance, endurance-trained individuals are predisposed to orthostatic hypotension or intolerance with an early onset of symptoms of neurogenic syncope (Klein et al. 1969; Stegemann et al. 1974, 1975; Convertino, 1987; Raven & Pawelczyk, 1993). Orthostatic stress reduces the end-diastolic filling of the left ventricle causing a reduction in stroke volume (SV) and up to a 20 % fall in cardiac output (Harms et al. 1999). In a cross-sectional investigation, Levine (1993) suggested that orthostatic intolerance in endurance-trained athletes is a result of greater decreases in SV than in untrained subjects during the orthostatic challenge. In addition, he demonstrated that this functional characteristic of endurance-trained subjects was associated with the cardiac remodelling, increased CBV and increased cardiac compliance resulting in a steeper Frank-Starling cardiac function curve (Levine et al. 1991a,b).
In subjects without autonomic failure or cardiac dysfunction the neurally mediated reflexes, primarily the arterial baroreflexes (ABR), correct the decreases in mean arterial (MAP) and pulse pressure (PP) that occur during orthostasis (Van Lieshout et al. 2003). Evidence from both cross-sectional and longitudinal studies (Klein et al. 1977; Raven et al. 1984; Smith et al. 1988a,b; Stevens et al. 1992; Shi et al. 1993a,b; Raven et al. 1997; Smith et al. 2000) suggest that an attenuation of the ABR control of blood pressure is a contributing factor for the increased predisposition to orthostatic hypotension in endurance-trained subjects. More recently, Fadel et al. (2001) identified that the carotid baroreflex (CBR) control of vasomotion was compromised by endurance training, despite the fact that the CBR control of muscle sympathetic nerve activity was unchanged or augmented. In addition, endurance training attenuates the ABR control of renal sympathetic nerve activity in rabbits (DiCarlo & Bishop, 1990). The attenuation of the ABR control of the sympathetic activity to the kidneys was linked to increased inhibitory neural information emanating from the cardiopulmonary receptors resulting from the training-induced cardiac hypertrophy and changes in wall tension. These data suggest that endurance training results in an attenuation of baroreflex control of the vasculature.
Previous studies have not addressed differences in ABR function of endurance-trained and average- or low-fit subjects during orthostatic stress. Levine et al. (1991a) investigated the relationship between CBR function and orthostatic intolerance during supine rest in endurance-trained subjects and suggested that CBR function was unrelated to fitness. However, a progressive increase in orthostatic stress (which unloads cardiopulmonary baroreceptors) increases CBR responsiveness (Pawelczyk & Raven, 1989; Cooper & Hainsworth, 2001, 2002). Pawelczyk & Raven (1989) investigated the interaction of both carotid and cardiopulmonary baroreceptor groups, demonstrating an augmentation of the carotid-cardiac (carotid-HR) and carotid-vasomotor (carotid-MAP) responsiveness during lower body negative pressure (LBNP)-induced reductions in central venous pressure (CVP). Cooper & Hainsworth (2001) reported that vascular resistance responses to changes in carotid transmural pressure were enhanced during LBNP, and suggest that the increase in baroreflex responsiveness would be protective against falls in blood pressure during prolonged orthostatic stress. In contrast, Cooper & Hainsworth (2002) did not document an increase in the baroreflex responsiveness of vasomotion during head-up tilt (HUT) in patients with posturally related syncope. Thus, it seems that an increase in ABR responsiveness resulting from cardiopulmonary baroreceptor unloading during orthostatic stress is a prerequisite for prolonged orthostatic tolerance. However, with the exception of data using LBNP to unload the cardiopulmonary baroreceptors (Raven & Pawelczyk, 1993), no investigation into the effects of endurance exercise training on the cardiopulmonary baroreceptor interaction with the CBR control of blood pressure during orthostasis has been reported. In addition, significant questions have been raised concerning the specificity of low pressures of LBNP in unloading the cardiopulmonary baroreceptors (Lacolley et al. 1992; Taylor et al. 1995). During HUT, the cardiopulmonary baroreceptors become progressively deactivated while the arterial baroreflex remains inactive despite the alterations in carotid arterial diameter up to 60 deg HUT (Lacolley et al. 1992). Hence, it remains unclear whether endurance exercise training affects the interaction between cardiopulmonary baroreceptors and arterial baroreflex function during orthostasis. Based upon findings from the application of LBNP (Raven & Pawelczyk, 1993), we hypothesized that the orthostatic intolerance in endurance-trained subjects was related to an attenuation of the increased CBR responsiveness that occurs during a progressive increase in orthostatic stress. Therefore we sought to examine whether endurance exercise training would alter carotid baroreflex responsiveness during progressive unloading of the cardiopulmonary baroreceptors induced by HUT.
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METHODS |
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Fourteen men (age 25 ± 1 years, height 182 ± 2 cm, and weight 74 ± 2 kg, mean ± S.E.M.) voluntarily participated in the investigation. Women were omitted from the investigation because their cardiac adaptations associated with endurance training are minimal (Levine et al. 1998; personal communication from Benjamin D. Levine). Each subject received a verbal and written explanation of objectives, techniques of measurement and risks and benefits associated with the investigation and provided written informed consent in accordance with the Helsinki Declaration for the use of human subjects in research as approved by the Ethics Committee of Copenhagen. The subjects were assigned to two distinct groups, average fit (AF) and high fit (HF), based upon their current history of endurance exercise training. The HF subjects had been performing regular aerobic training (> 20 h week-1) for over 2 years (i.e. three cyclists, two triathletes, two rowers) whereas AF subjects had not been performing a regular aerobic exercise (< 5 h week-1). Subsequent measurement of their maximal oxygen uptake (O2max) was obtained using a cycle ergometer. All subjects were asymptomatic for cardiovascular and respiratory disease, normotensive, and currently not taking prescription or over the counter medications. Prior to the experiments each subject was familiarized with the equipment and the experimental protocol. In addition, subjects were requested to abstain from caffeinated beverages, strenuous physical activity and alcohol for at least 24 h before testing.
Experimental protocol
On day 1 each subject performed maximal cycle exercise for the measurement of O2max. On day 2, separated by a minimum of one day, each subject was exposed to progressive HUT to 60 deg. After instrumentation, the subjects were placed supine on a tilt-table and fitted with a malleable lead neck collar for the application of neck pressure (NP) and neck suction (NS). After 10-15 min of rest the subjects were exposed to progressive HUT with 10 deg increments from -20 deg to +60 deg. Each stage was held for 8 min and CBR responsiveness was assessed during the last 3 min or each HUT stage. The subjects were supported by a bicycle saddle only (no footboard) to reduce leg muscle contraction. During HUT, the subjects were requested to abstain from leg movements in order to reduce the activity of the muscle pump.
Measurements
Exercise capacity. The O2max was assessed with an incremental protocol on a cycle ergometer (Monark 818e, Stockholm, Sweden). The workload was set at 60 W and was increased by 30 W every minute until the subjects could no longer maintain the pedalling frequency at 60 r.p.m. despite strong verbal encouragement. The subjects respired through a mouthpiece attached to a volume transducer while gases were continuously sampled for analysis of fractional concentrations of O2, CO2 and N2. The respiratory gas analysis system (CPX/D, Medical Graphics Corporation, MN, USA) was calibrated before each test using known standard gases.
HUT. The subjects were instrumented with electrocardiogram electrodes (Q-10-25, Medicotest, Denmark). A cannula (1.1 mm i.d., 20G) was placed in the brachial artery of the non-dominant arm for measurement of the arterial pressure. Another cannula (1.4 mm i.d. 14G) was introduced into the superior vena cava via the left basilica vein for measurement of the CVP. Pressures were measured with Bentley transducers (Uden, The Netherlands) positioned at the level of the right atrium in the mid-axillary line, fastened to the subject, and connected to a pressure monitoring system (Dialogue 2000, Copenhagen, Denmark). Beat-to-beat data of cardiovascular variables were collected in a personal computer with customized acquisition software. Thoracic electrical impedance (TI) was measured using a 200 µA at 1.5 Hz monitor (C-guard, Danmeter, Odense, Denmark). Pairs of electrodes were placed on the right sternocleidomastoid muscle and the upper left ribs in the mid-clavicular line with an internal distance of 5 cm. This pattern of electrode placement has been used for evaluating changes in the CBV (Matzen et al. 1991; Perko et al. 1994). The outer two electrodes transmitted the current, while the inner two were sensing the voltage difference. Low frequency currents selectively detect extracellular fluid changes (Matzen et al. 1991; Cai et al. 2000a,b; 2002). The thoracic admittance (1/TI) was calculated as the index of CBV (Cai et al. 2000a,b; 2002). The SV was determined by a three-element model of arterial input impedance (Modelflow; Wesseling et al. 1993). Modelflow computes a flow wave from the arterial pressure wave that is integrated to obtain the SV of the heart. This methodology provides accurate estimates of changes in SV during HUT (Stok et al. 1993; Harms et al. 1999). However, since the Modelflow measure of SV has not been calibrated during HUT, SV was expressed as relative changes from its starting value at -20 deg (Remmen et al. 2002; Van Lieshout & Karemaker, 2003).
CBR responsiveness. The CBR control of HR and MAP was assessed using the rapid NP and NS protocol (Pawelczyk & Raven, 1989). After a normal expiration and breath-hold (at end-expiration), 12 consecutive pulses (ranges: +40 to -80 mmHg), each 500 ms in duration, were delivered to the carotid sinus precisely 50 ms after the R wave of the ECG, to elicit maximum baroreflex responses (Eckberg, 1977). Three trains of NP and NS were executed at each tilt stage with a minimum of 45 s between successive trials. Estimated changes in carotid sinus pressure (CSP) were calculated as MAP minus the neck chamber pressure. The CBR stimulus-response curve was defined as the nine-beat data period corresponding to the four positive-pressure pulses and five negative-pressure stimuli. The nine-beat HR and MAP responses that best represent the peak reflex response range were selected and aligned with the calculated CSP to complete the stimulus-response data set. The parameters of each curve were averaged to provide a mean curve at each tilt stage for each subject.
Data and statistical analysis
The carotid-HR and the carotid-MAP responses were evaluated by plotting the peak changes in HR and MAP against estimated CSP, respectively. Each CBR stimulus-response curve was fitted to the logistic model described by Kent et al. (1972). This function incorporates the equation:
HR or MAP = A1{1 + exp[A2(ECSP - A3)]}- 1 + A4,
where HR or MAP is the dependent variable, ECSP is the estimated carotid sinus pressure, A1 is the range of response of the dependent variable (maximum - minimum), A2 is the gain coefficient (i.e. slope), A3 is the carotid sinus pressure required to elicit equal pressor and depressor responses (centring point), and A4 is the minimum response of HR or MAP. Data were fitted to this model by a non-linear least-squares regression to predict a curve of 'best fit' to each set of raw data. The operating point is defined as the ECSP of the pre-stimulus HR or MAP value before the application of the NP and NS stimulus. The gain was calculated from the first derivative of the logistic function and the maximal gain (Gmax) was applied as the index of CBR responsiveness. Threshold (CSPthr), the point where no further increase in the dependent variable occurred despite reductions in ECSP and saturation (CSPsat), the point where no further decrease in the dependent variable occurred despite increases in ECSP, were calculated as the maximum and minimum second derivatives, respectively, of the logistic function curve. For calculation of CSPthr and CSPsat, we applied equations described by Chen & Chang (1991): CSPthr = -2.0/A2 + A3 and CSPsat = 2.0/A2 + A3. These calculations of CSPthr and CSPsat are the CSP at which MAP or HR are within 5 % of their maximal or minimal responses (Fig. 1).
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Figure 1. A schematic representation of the baroreflex function curve The centring point (CP) is the carotid sinus pressure required to elicit equal pressor and depressor responses. The operating point (OP) is the carotid sinus pressure at which the pre-stimulus HR or MAP was located. The gain curve was calculated from the first derivative of the logistic function, and the maximal gain (Gmax) was located at the centring point and applied as the index of CBR responsiveness. CSPthr is the carotid sinus transmural pressure at the threshold of the reflex, and CSPsat is the carotid sinus transmural pressure at the saturation of the reflex. The difference between CSPthr and CSPsat is the operating range of the reflex. | ||
A two-way analysis of variance (ANOVA) with repeated measures was employed to determine significant differences at different tilt angles in HF and AF. A Student-Newman-Keuls test was employed post hoc when main effects were significant. In addition, Student's t test was used for fitness comparisons. Statistical significance was set at P < 0.05. Linear regression analysis was applied to calculate the slope of Gmax to 
thoracic admittance. Analyses were conducted using SigmaStat (SPSS Inc., Chicago, IL, USA). These parameters were averaged and presented as group means.
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RESULTS |
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By design, the group mean O2max of HF subjects was greater than that of the AF subjects (Table 1). There were no significant group differences in physiological characteristics in the supine position.
Cardiovascular response to HUT
The progressive increase in HUT markedly decreased the thoracic admittance from -20 to +60 deg, an index of the change in CBV (P < 0.001), but there was no significant difference in the thoracic admittance between AF and HF subjects (Fig. 2C). The CVP also decreased in both AF and HF subjects during HUT, P < 0.001 (Fig. 2A). With the reduction in CVP and thoracic admittance during HUT, a decrease in SV (P < 0.001) was observed (Fig. 2B). The change in SV from -20 deg to +60 deg HUT was not different between AF and HF subjects (AF, SV = -31.8 ± 4.4 %; HF, SV = -36.4 ± 2.6 %, P = 0.191), whereas the change in CVP was different (AF, CVP = -7.6 ± 0.7 mmHg; HF, CVP = -12.6 ± 0.7 mmHg, P < 0.001). Tachycardia was also observed in AF and HF subjects at 30 deg to 60 deg (P < 0.01, Fig. 2F). These increases in HR compensated for the decreases in SV and thereby cardiac output (Ÿ) was constant throughout the HUT. There were no changes in systolic blood pressure (SBP). However, MAP (Fig. 2D) and diastolic blood pressure (DBP) were increased (P < 0.001). Thus, pulse pressure (PP) was decreased similarly (P < 0.001) in AF and HF subjects at 40 deg to 60 deg (Fig. 2E).
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Figure 2. Changes in cardiovascular variables during head-up-tilt (HUT) for average (AF, Values are means ± S.E.M. CVP, central venous pressure; SV, stroke volume; S, siemens; MAP, mean arterial pressure; PP, pulse pressure; HR, heart rate; bpm, beats min-1. * Different from supine, P < 0.05. † Difference between groups, P < 0.05. | ||
The mean group data relating CVP to thoracic admittance (1/TI), or CBV, illustrate the pressure-volume relationship of the right heart (Fig. 3). The data were fitted to an exponential function which best described the relationship between CVP and thoracic admittance. The HF subjects had larger absolute and relative changes in CVP over an equivalent range of thoracic admittance. These data indicate that the right heart of the HF subjects was larger, more compliant, and more distensible than that of the AF subjects.
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Figure 3. Pressure volume curves of the right heart using central venous pressure (CVP) and thoracic admittance (1/TI) in average (AF, For the HF subjects, the mean pressure-volume curve was expressed as CVP = -5.62 + (1.04 | ||
CBR responsiveness during HUT
There appeared to be little change in the shape of either the HR or MAP stimulus-response curves in AF and HF subjects despite the reduction in CBV elicited during stepwise tilt. In addition, there was no change in the relationships between the operating point (OP) and the centring point (CP) of both the carotid-HR and the carotid-MAP baroreflex curves of the AF and HF subjects. However, a gradual increase in the carotid-HR baroreflex Gmax and the carotid-MAP baroreflex Gmax occurred during HUT (Fig 4A and B). Compared with HF subjects, the Gmax of both carotid-HR and carotid-MAP baroreflex of the AF increased markedly more than for the HF subjects during HUT. The average of the individual's slope of regression between Gmax and thoracic admittance of the AF group was greater than the HF group in both carotid-HR (AF; 0.56 ± 0.34 vs. HF; 0.06 ± 0.04 beats min-1 mmHg-1 (S . 10-3)-1, P = 0.07) and carotid-MAP (AF; 0.07 ± 0.02 vs. HF; 0.02 ± 0.01 beats min-1 mmHg-1 (S . 10-3)-1, P = 0.05).
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DISCUSSION |
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The findings of the present investigation provide new information concerning the relationship between chronic physical activity-induced increases in aerobic fitness and the attenuated responsiveness (Gmax) of the carotid baroreflex during an orthostatic challenge. Specifically the AF subjects had marked increases in Gmax of the carotid-HR and carotid-MAP baroreflexes during progressive unloading of the cardiopulmonary baroreceptor induced by HUT. In contrast, the increase in Gmax of the carotid-HR and carotid-MAP baroreflexes of the HF subjects was markedly attenuated.
The data of the present investigation indicate that the HF group had an increased right ventricular compliance and a larger thoracic admittance, an index of CBV, and a larger CVP compared to the AF group (Fig. 2 and Fig. 3). The HF group had a greater decrease in CVP than the AF group with the same change in thoracic admittance during HUT from -20 deg-1 to +60 deg, confirming the increased compliance of the right heart of the HF compared to the AF subjects (Fig. 3). These findings suggest that the morphological and functional adaptations identified in the left heart in response to endurance training (Levine et al. 1991a,b) also occur in the right heart. Consequently, the decrease in SV that occurs for a given decrease in CBV during HUT was greater for the HF compared to AF subjects. However, the changes in Ÿ, HR, PP and arterial pressure during HUT were similar between the HF and AF groups (Fig. 2).
During HUT, the fall in PP of the HF subjects compared to the AF subjects, even in the presence of an increased MAP, would be expected to increase the responsiveness of the carotid baroreflex (Seagard et al. 1992, 1993). The presence of the type I afferent fibres within the carotid sinus is probably the reason that the CBR is more responsive than the aortic baroreceptors to changes in pulsatile pressure (James & Daly, 1970). In addition, during LBNP-induced unloading of the cardiopulmonary baroreceptors the CBR responsiveness (Gmax) was increased (Pawelczyk & Raven, 1989). However, despite the haemodynamic changes that occurred during the HUT being more likely to increase the CBR responsiveness of the HF than the AF subjects because of the HF subjects' more marked decrease in PP, the data suggest otherwise. The linear relationship between the increased carotid-HR and carotid-MAP baroreflexes' responsiveness (Gmax) and changes in thoracic admittance during HUT was less for HF than AF subjects (Fig. 4). These findings suggest that the carotid-cardiac and carotid-vasomotor baroreflex responsiveness of the HF subjects was attenuated during HUT.
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Figure 4. Maximum gain of carotid-cardiac (A) and carotid-vasomotor (B) baroreflexes of average (AF, For the HF subjects maximum gain of the carotid-cardiac and carotid-vasomotor baroreflexes were Gmax = 0.07 | ||
One possible explanation for these findings involves the greater afferent neural information emanating from the cardiopulmonary baroreceptors resulting in greater inhibition of the arterial baroreflex within the nucleus tractus solitarii (NTS). DiCarlo and Bishop (1988, 1990) showed in rabbits a greater inhibition of the arterial-renal sympathetic nerve activity reflex by using lignocaine (lidocaine) injected into the pericardial sac before and after training. They suggested that the exercise training-induced cardiac hypertrophy and the concomitant increases in wall stress were the source of the increased cardiopulmonary baroreceptor stimulation and subsequent inhibition of the renal sympathetic nerve activity reflex. A similar finding was observed in a cross-sectional comparison of HF, AF and low fit human subjects during a LBNP-induced reduction in CVP (Raven & Pawelczyk, 1993). Both AF and low fit subjects had an increase in Gmax of both the carotid-HR and the carotid-MAP baroreflexes during LBNP, whereas the Gmax in the HF subjects was unchanged (Raven & Pawelczyk, 1993).
The second possible explanation may be an endurance training-mediated decrease in the transduction of the sympathetic neural signal at the vascular bed. Fadel et al. (2001) identified in HF subjects a reduced vascular responsiveness during acute hypotension regardless of an augmented muscle sympathetic nerve activity resulting from arterial baroreflex unloading. However, the data of the present investigation identify arterial normotension increasing to hypertension with a concomitant decrease in pulse pressure during HUT, suggesting that the primary increase in sympathetic nerve activity and vasoconstriction results from the more profound effects of cardiopulmonary unloading. Subsequently, the CBR reflex responses during HUT occur on a background of increased sympathetic neural activity. Importantly, the CBR-MAP reflex response is indicative of CBR control of vasomotion, while the CBR-HR reflex response reflects the CBR control of cardiac output (Ogoh et al. 2002). Furthermore, the CBR-vasomotor response contributes more than 80-95 % of the CBR-mediated changes in MAP (Ogoh et al. 2002). In the present investigation, the linear relationship between Gmax of the carotid-vasomotor reflex or the carotid-cardiac reflex with thoracic admittance (CBV) during HUT was four to five times greater in the AF compared to the HF (Fig. 4). These findings suggest that (1) the increased neural inhibition emanates from the training-induced cardiac hypertrophy; and (2) the attenuated vasomotor response to a given sympathetic activity of the endurance exercise-trained individuals may be responsible for the reduced CBR responsiveness.
Some potential limitations in interpreting the results of the present investigation include the following. (1) The use of CVP as an index of right cardiac filling and the use of thoracic admittance as an index of changes in central blood volume in developing the right heart pressure-volume relationship (Fig. 3). However, because the right heart CVP-thoracic admittance relationship and their fitness differences were similar to the left heart pressure-volume (left ventricular end-diastolic pressure (LVEDP) vs. left ventricular end-diastolic volume (LVEDV)) relationship and fitness differences identified by Levine et al. (1991a,b), we suggest that the differences in right heart compliance were related to the differences in fitness between the HF and AF groups. (2) Lacolley et al. (1992) and Taylor et al. (1995) identified that the use of low pressures (0-20 Torr) of LBNP produced changes in ascending and descending aortic and carotid sinus diameters such that selective unloading of the cardiopulmonary (CP) baroreceptor was not attainable. Hence, the results of previous investigations (Zoller et al. 1972; Johnson et al. 1974; Victor & Mark, 1985; Pawelczyk & Raven, 1989) of the CBR-CP baroreflex interaction were confounded by proportionally different but simultaneous disengagement of the arterial and CP baroreceptors. Lacolley et al. (1992) found similar effects of LBNP and HUT on carotid arterial diameter. However, the aortic area or carotid diameter was not consistently decreased in a progressive manner and there were no significant changes in effector baroreflex responses (HR or vasoconstriction) until a LBNP of -20 Torr or a HUT at 60 deg was achieved. The present investigation suggests that when the cardiopulmonary baroreceptors are unloaded during HUT, an augmentation of the CBR occurs independent of carotid baroreceptor disengagement. This interaction appears to be more functional in the AF than in the HF subjects.
In summary, we have examined the effect of endurance training on the interaction between cardiopulmonary baroreceptoers and the carotid baroreflex responsiveness during HUT-induced changes in CBV. The data indicate that unloading of cardiopulmonary baroreceptors increased carotid baroreflex responsiveness markedly in AF subjects, while the carotid baroreflex responsiveness of the HF subjects was only moderately affected. These findings provide an explanation for the increased incidence of orthostatic hypotension and intolerance in endurance-trained athletes.
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Acknowledgements
The authors appreciate the time and effort expended by the volunteer subjects. We thank Keiko Ogoh B.S. for her technical assistance and Lisa Marquez for her assistance in preparing the document. This study was supported in part by NIH Grant no. HL-045547 and by the Danish National Research Foundation (504-14).
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) and high fit (HF, 
) subjects
10-12)e0.149TI (r = 0.97) and for the AF subjects, the mean pressure-volume curve was expressed as CVP = -7.37 + (9.36