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Diminished forearm vasomotor response to central hypervolemic loading in aerobically fit individuals


Medicine & Science in Sports & Exercise: November 1996 - Volume 28 - Issue 11 - pp 1388-1395
Basic Sciences: Original Investigations

The aim of this study was to test the hypothesis that cardiopulmonary baroreflex control of forearm vascular resistance (FVR) during central hypervolemic loading was less sensitive in exercise trained high fit individuals (HF) compared to untrained average fit individuals (AF). Eight AF(age: 24 ± 1 yr and weight: 78.9 ± 1.7 kg) and eight HF (22± 1 yr 79.5 ± 2.4 kg) voluntarily participated in the investigation. Maximal aerobic power (determined on a treadmill), plasma volume and blood volume (Evans blue dilution method) were significantly greater in the HF than AF (60.8 ± 0.7 vs. 41.2 ± 1.9 ml·kg-1·min-1, 3.96 ± 0.17 vs 3.36 ± 0.08 l, and 6.33 ± 0.23 vs 5.28 ± 0.13 l). Baseline heart rate(HR), central venous pressure (CVP), mean arterial pressure (MAP, measured by an intraradial catheter or a Finapres finger cuff), forearm blood flow (FBF, plethysmography), and FVR, calculated from the ratio (MAP-CVP)/FBF, were not different between the HF and the AF. Lower body negative pressure (LBNP, -5,-10, -15, and -20 torr) and passive leg elevation (LE, 50 cm) combined with lower body positive pressure (LBPP, +5, +10, and +20 torr) were utilized to elicit central hypovolemia and hypervolemia, respectively. Range of CVP (from LBNP to LE+LBPP) was similar in the AF (from -3.9 to + 1.9 mm Hg) and HF (from-4.0 to +2.2 mm Hg). However, FVR/CVP was significantly less in the HF (-1.8± 0.1 unit·mm Hg-1) than AF (-3.4 ± 0.1 unit·mm Hg-1). The FVR decrease in response to increase in CVP was significantly diminished in the HF (-1.46 ± 0.45 unit·mm Hg-1) compared to the AF (-4.40 ± 0.97 unit·mm Hg-1), and during LBNP induced unloading the FVR/CVP of the HF (-2.01± 0.49 unit·mm Hg-1) was less (P < 0.08) than the AF (-3.28 ± 0.69 unit·mm Hg-1). We concluded that the cardiopulmonary baroreceptor mediated FVR reflex response was significantly less sensitive to changes in CVP in individuals who practice exercise training.

Department of Integrative Physiology and the Cardiovascular Research Institute, University of North Texas Health Science Center, Fort Worth, TX 76107

Submitted for publication April 1995.

Accepted for publication July 1996.

We appreciate Brian Foresman, D.O., for the clinical support, and Rita Welch-O'Connor, M.S., for the technical assistance during the investigation. We would also like to thank the reviewers for their time and effort contributed to strengthening our manuscript.

This study was supported by grants from AHA Texas Affiliate 93R-146, NIH HL45547, NIA AG14219, and NASA-NSCORT NAGW-3582.

Address for correspondence: Xiangrong Shi, Ph.D., Department of Integrative Physiology, University of North Texas, Health Science Center, 3500 Camp Bowie Boulevard, Fort Worth, TX 76107-2699.

Data from longitudinally (24,39) and cross-sectionally (25,31) designed studies indicate that exercise training appears to attenuate both arterial and cardiopulmonary baroreflex function. Mechanisms responsible for this training related diminished baroreflex sensitivity include an increase in arterial compliance(30), cardiac compliance (22) or both. In 1987, Mack et al. (25) evaluated the response of forearm vasomotor tone to nonhypotensive central hypovolemia and found that the increase in forearm vascular resistance (FVR) was significantly less in the exercise trained high fit individuals than the untrained average fit individuals during graded lower body negative pressure (LBNP) to -20 torr. Since there was no significant hypotension (i.e., stimulus) nor tachycardia(i.e., response) observed during steady-state low levels of LBNP(1,20,43), this attenuated FVR was assumed to be a result of an altered cardiopulmonary baroreflex function.

In contrast to central hypovolemia, the exercise training related alteration in cardiopulmonary baroreflex function has not been well defined during central hypervolemia. Giannattasio et al. (16) has reported that the reflex decrease in FVR was less during a 60° leg elevation induced increase in left ventricular end-diastolic volume in both runners and hammer throwers when compared to non-athletic subjects. However, there was a significantly higher forearm blood flow observed in their high fit subject group (16). It has been demonstrated that a high forearm blood flow may result in a different FVR response(23) probably due to a stimulated synthesis of the endothelium-derived relaxing factor nitric oxide (5). Therefore, the question remains as to whether endurance training attenuates the cardiopulmonary baroreceptor mediated FVR reflex response to central hypervolemia.

The purpose of this investigation was to test the hypothesis that endurance exercise training reduces the cardiopulmonary baroreflex-FVR response to central hypervolemia. Cardiopulmonary baroreceptors were activated by 50-cm passive leg elevation and lower body positive pressure (LBPP) of +5, + 10, and+20 torr. The slope of the change in FVR in response to the change in central venous pressure during leg elevation and LBPP was considered as the index of the sensitivity (or gain) of the cardiopulmonary baroreflex and was compared between untrained average fit and exercise trained high fit individuals.

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Subjects. Eight healthy untrained average fit men and eight exercise trained high fit men voluntarily participated in this study (seeTable 1 for the physiological and demographic description of the subjects). Six of the high fit volunteers were trained long distance swimmers. Each subject received and signed an informed consent for the procedures outlined in the investigation. The protocol and the informed consent was approved by the Institutional Review Board of the University of North Texas Health Science Center at Fort Worth.

Procedure. All subjects were examined by our physician consultant. After having received approval for participation in the investigation, each subject performed a treadmill test to determine his maximal oxygen uptake (˙VO2max) during which the workload was gradually increased until the subject achieved volitional fatigue. Before the experimental test and 21 wk following the maximal exercise test, each subject was invited to the laboratory and was familiarized with the experimental protocol and measurements to be applied during the experiment. Prior to the familiarization session plasma volume (PV) was determined using the Evans blue dye dilution technique and calculated using a computer program introduced by Foldager and Blömqvist (14). Blood volume (BV) was calculated from peripheral venous micro hematocrit (Hct) and PV using the equation BV = PV/(1 - Hct).

The experimental test was conducted with the subject lying supine having the lower torso to the level of the iliac crest enclosed in a wooden box. The ambient condition was maintained at 25 ± 1°C temperature and 40-50% humidity. After 30 min of supine rest, the subject's baseline (control) heart rate (HR), arterial blood pressure (ABP) and central venous pressure (CVP) were recorded on a beat-to-beat basis for 5 min along with the measurement of forearm blood flow (FBF). After collection of the control data, -5 torr lower body negative pressure (LBNP) was applied. When the desired level of LBNP was achieved and stabilized (usually æ 1 min), the data (HR, ABP, CVP, and FBF) collection was resumed. Immediately after -5 torr, the LBNP was increased by -5 torr and was followed by a repeat of the data collection. This data collection protocol was repeated at each increase in -5 torr LBNP until -20 torr was achieved. After the completion of LBNP unloading procedure, the LBNP was released and the subjects were allowed to rest approximately 15 min. Following a repeat 5-min period of control data collection, a cardiopulmonary baroreceptor loading (increased central venous pressure) procedure was begun. Each subject passively elevated his legs 50 cm (feet above horizontal). Approximately 5 min after leg elevation (LE), HR, ABP, and CVP and FBF were collected for LE stage. Subsequently, lower body positive pressure (LBPP) of 5, 10, and 20 torr were applied in addition to the LE and the cardiovascular responses were measured at each stage of LBPP.

Measurements. During each experiment, the HR was monitored by standard lead II electrocardiogram. Arterial blood pressure was monitored by a Teflon catheter (Angiocath 20GA) inserted in the right radial artery or measured by a finger cuff using photoplethysmographic method (Finapres, Ohmeda). Our previous observations (37) demonstrated that by using appropriate measurement criteria the indirect arterial blood pressure was a reliable and valid measure of direct intra-arterial pressure. Central venous pressure was monitored by a double lumen catheter (Cook Critical Care) placed via each subject's median antecubital vein into the superior vena cava at the level between the 3rd-4th intercostal space confirmed under fluoroscopic observation (BV22, Philips, Eindhoven, The Netherlands). Both CVP and ABP catheters were connected through a sterile disposable pressure transducer (Cobe, Lake Wood, CO) interfaced with a pressure monitor (model Hewlett-Packard 78205D/7803B, or Tektronix 414). The zero reference pressure was set at the subject's mid-axillary line for both the CVP and ABP (direct and indirect) measures. Pressure transducers and monitors were calibrated before and after each experiment. During each experiment the HR, CVP, and ABP, i.e., mean arterial pressure (MAP), systolic and diastolic blood pressure, were acquired beat-to-beat via a customized data acquisition system interfaced with a minicomputer (Minc-23, Digital Equipment, Maynard, MA). Forearm blood flow was measured by venous occlusion plethysmography with a mercury-in-Silastic double-strain gauge. The subject's left arm was suspended with the wrist in a sling. The hand was occluded from the circulation by inflation of a wrist cuff to a pressure > 240 mm Hg for approximately 45 s before starting the measurement of the first FBF curve. Each FBF curve was recorded at 10-15 s of the venous cuff inflation with a pressure of 40 mm Hg. Five curves were recorded during each experimental condition and at least three curves were averaged for the measurement. Forearm vascular resistance(FVR) was calculated from the ratio of (MAP - CVP)/FBF.

Statistics. Student's t-test was applied to determine the significance of the difference in the subjects' physical and physiologic variables between the AF and HF groups. Simple linear regression analysis was applied to calculate the slope of FVR to CVP as the cardiopulmonary baroreflex gain. Analysis of covariance (ANCOVA) was applied to determine the significant difference in the rate of change in cardiovascular response (i.e., increase in FVR per unit decrease in CVP) between the two fitness groups. Two-way analysis of variance (ANOVA) was applied to examine whether the different experimental stage (central hypovolemia or hypervolemia, factor I) and fitness level(factor II) significantly affected the cardiovascular responses. Significance level was set at P < 0.05.

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Table 2 summarizes the group mean data for the cardiovascular variables measured during rest, LBNP, LE, and LE + LBPP. There were no differences observed in the baseline variables between the two groups. The absence of a significant difference in baseline HR between the two fitness groups was primarily a result of the unusually low HR observed in the AF subject group in which seven of them had resting HR ≤ 59 bpm and one had a 45 bpm HR. However, the significantly greater ˙VO2max, total blood volumes, and plasma volumes of the HF group (see Table 1) indicated that the fitness difference was well established between the two groups.

During LBNP a significant decrease in CVP was observed at -10 torr in both fitness groups. The degree of central hypovolemia induced by -10 torr LBNP resulted in a significant increase in FVR without any detectable hypotension or tachycardia. In terms of unit increase in LBNP the decrease in CVP from baseline between the two fitness groups did not reach significance (ANCOVA,P > 0.05). At -20 torr LBNP pulse pressure was significantly narrowed in both AF and HF subjects associated with a small tachycardia(Table 2).

The 15 min of recovery from LBNP resulted in there being no difference in any baseline cardiovascular variable of either subject group, seeTable 2. Leg elevation (50 cm) alone induced a steady-state increase in CVP which was not statistically significant in either AF (+0.91 mm Hg) or HF (+0.83 mm Hg) subjects. Beginning at the LE plus 5 torr LBPP (LE+5 torr), the increases in CVP were observed to be significant in both AF (+1.33 mm Hg) and HF (+1.45 mm Hg) subject groups. CVP was progressively increased during LE +10 torr and LE +20 torr LBPP in AF (+1.56 and +1.90 mm Hg) and HF (+1.67 and +2.21 mm Hg) groups. Correspondingly, reflex decreases in FVR during LE and LE plus LBPP were observed. The decreased FVR was observed to be significant beginning at LE +5 torr in the AF subject group(-4.94 unit). In the HF subject group, however, the significant decrease in FVR was only observed at LE +20 torr (-2.89 unit), even though the rate of the change in CVP during LE and LE plus LBPP was not significantly different between the two groups of subjects. There was no significant change in HR during LE or LE plus LBPP in both subject groups, although SBP and PP in the HF subject group were seen to be significantly increased during LE +20 torr(+5.6 and +4.5 mm Hg).

Figure 1 illustrates that the ratio of change in FVR in terms of per unit change in CVP during LBNP up to -20 torr (central hypovolemic unloading of the cardiopulmonary baroreceptors) and LE plus LBPP up to 20 torr (central hypervolemic loading of the cardiopulmonary baroreceptors) was significantly (P < 0.001) diminished in the HF(-1.79 ± 0.12 unit·mm Hg-1) compared to the AF (-3.35± 0.08 unit·mm Hg-1) subjects. The slopes calculated after excluding the data points of -20 torr LBNP and LE+20 torr LBPP were still significantly (P < 0.001) different between the AF (-3.26± 0.10 unit·mm Hg-1) and the HF (1.75 ± 0.19 unit·mm Hg-1) groups, suggesting that the cardiopulmonary baroreceptor mediated FVR reflex response is significantly less sensitive in the HF subjects.

Figure 2 summarizes the individual gains (FVR/CVP) and the group mean gains during LBNP (starting from the baseline, -5, -10, -15, and -20 torr) induced central hypovolemia and during LE plus LBPP (starting from the baseline, LE, LE+5, LE+10, LE+20 torr) induced central hypervolemia, respectively. During both unloading and loading, the cardiopulmonary baroreceptor mediated forearm vasomotor responses were substantially diminished in the HF (-2.01 ± 0.49 and -1.46 ± 0.45 unit·mm Hg-1) compared to the AF (-3.28 ± 0.69 and -4.40± 0.97 unit·mm Hg-1) subjects. Furthermore, the same conclusion still holds when the slopes are calculated after excluding the data points of -20 torr LBNP during unloading (in the HF vs. AF: -1.86 ± 0.48 vs -2.81 ± 0.65 unit·mm Hg-1, P < 0.13 one-tailed t-test) and without LE+20 torr LBPP during loading (-1.21± 0.53 vs. -5.29 ± 1.62 unit·mm Hg-1, P< 0.04).

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The major finding of the present investigation was that within a similar range of decreases and increases in CVP the forearm vasomotor reflex responses were significantly less in the exercise trained high fit (HF) subjects than the untrained average fit (AF) subjects. Our data confirmed previous reports(24,25) that the sensitivity of the cardiopulmonary baroreceptor mediated FVR reflex response was diminished in the HF compared to the AF subjects during LBNP induced central hypovolemia. Furthermore, the present investigation demonstrated that the cardiopulmonary baroreceptor mediated forearm vasodilator response to graded central hypervolemia was significantly less in the HF than the AF subjects.

Though the majority of the published data support the notion that exercise training results in a diminution of the cardiopulmonary baroreflex sensitivity during LBNP induced central hypovolemia, Takeshita et al.(40) have reported that the cardiopulmonary baroreflex control of FVR response induced by -10 torr LBNP was significantly augmented in football athletes compared to non-athletes and Jingu et al.(19) subsequently found that the cardiopulmonary baroreceptor mediated forearm vaso-constriction during -10 torr LBNP was significantly greater after than before cycling exercise training with 3 d·wk-1 for 4 months in a group of subjects aged from 36 to 67 yr old. The age difference of Jingu et al.'s subjects may not be a factor in this difference in response as Seals and Chase (34) have demonstrated in a group of subjects aged 45-68 yr old that the increases in FVR were significantly diminished following exercise training. The reason for the discrepancy between the data of Takeshita et al. (40) and Jingu et al. (19) with the previous findings of an exercise training induced attenuation of the cardiopulmonary baroreflex sensitivity (16,21,24,25,34) is unclear. One possible difference is the fact that the trained group of subjects were not sufficiently trained.

The data concerning the effect of exercise training on the cardiopulmonary baroreflex function during central hypervolemia is scarce. Giarmattasio et al.(16) demonstrated that a reflex forearm vasodilation mediated by the cardiopulmonary baroreceptors during a 60° leg elevation was significantly less in trained than untrained subjects. Our data from the present investigation are in agreement with this previous finding in that we found that exercise training appeared to diminish the cardiopulmonary baroreflex sensitivity in response to central hypervolemia.

Cardiopulmonary baroreceptors are located within the venoatrial junctions(9,12), atria (3,28), ventricles (2), and pulmonary arteries(6,9), and are subserved primarily by the afferent vagus limb (4,26,27,28), which constantly exert a tonic restraint on the cardiovascular center. When the cardiopulmonary baroreceptors are stimulated by central hypervolemia or increasing CVP, this tonic restraint is enhanced and peripheral vasodilation occurs (2,3,6,9,11,32). This vasodilation is mediated via a sympathoinhibition of efferent nerve traffic and helps maintain the systemic arterial pressure constant and prevent the disturbance of the arterial baroreceptors. When the cardiopulmonary baroreceptor mediated reflex vasodilation is unable to accommodate the increase in central volume and thus does not maintain a systemic arterial pressure constant, the arterial baroreceptors (within the aortic arch and carotid sinus) will be stimulated and a further vasodilation will occur which is mediated by the arterial baroreflex. Passive leg elevation (LE, +50 cm) combined with lower body positive pressure (LBPP) resulted in CVP being significantly increased in both subject groups, suggesting a central hypervolemia. This increase in CVP was associated with peripheral vasodilation indicated by the decrease in FVR, see Figure 1. Since there was no systemic hypertension observed in the AF subjects, this decrease in FVR during LE+LBPP was presumed to be a result of a reflex activation of the cardiopulmonary baroreceptors. This cardiopulmonary baroreceptor mediated reflex peripheral vasodilation, maintained cardiovascular homeostasis (i.e., systemic normotension) in response to the central hypervolemia. However, in the HF subjects we observed a systemic hypertension during LE plus 20 torr LBPP induced central hypervolemia, which cannot be attributed to the LBPP activated intramuscular mechanoreceptors (36). This systemic hypertension suggested that the decrease in FVR of the HF group during LE + LBPP induced central hypervolemia, may have been a result of both cardiopulmonary and arterial baroreceptor mediated activation, and further indicates an attenuated cardiopulmonary baroreflex sensitivity.

The mechanism responsible for the training induced decrease in cardiopulmonary baroreflex sensitivity has not been defined. However, it has been postulated that the diminished cardiopulmonary baroreflex sensitivity observed in the HF subjects may be associated with the exercise training induced cardiac hypertrophy (16). Consequently, a remodeling of the properties of the cardiac tissues as well as a change in cardiopulmonary mechano-receptor function may occur. Convertino et al.(7) reported that 10-wk cycling exercise training significantly increased CVP which was linearly related to a 9% increase in total blood volume along with a 20% of increase in ˙VO2max. Giarmattasio et al. (16) previously observed normal healthy subjects, runners and hammer throwers and found that there was an inverse association of septal wall thickness with reflex change in FVR(P < 0.05). DiCarlo and Bishop (10) demonstrated using rabbits that an 8-wk endurance exercise training program enhanced cardiac afferent inhibition on the arterial baroreceptor mediated renal sympathetic nerve activity. When the enhanced tonic inhibitory influence of the trained rabbits was removed by the intrapericardiac injection of procainamide the training related difference in cardiac afferent inhibition disappeared (10). However, the underlying mechanism of this physiologic adaptation associated with a change in cardiopulmonary baroreceptor function following exercise training is different from that observed in patients with hypertension induced cardiac hypertrophy(18) or congestive heart failure(13) whose cardiopulmonary baroreflex sensitivity is also diminished. The pathologic hypertrophy associated with hypertension or heart failure is usually accompanied by a reduction of cardiac compliance(29), and appears to impair the responsiveness of the cardiopulmonary baroreflex to a change in pressure, i.e., with a given pressure less stretch is transmitted to the loci where the cardiopulmonary baroreceptors are located. In contrast, the exercise training related physiologic hypertrophy is found to be associated with an increase in cardiac compliance (22). Consequently, the diminished sensitivity of the cardiopulmonary baroreflex observed in the HF subjects may result from the fact that a given pressure transforms into less strain around the cardiopulmonary baroreceptors.

In the present investigation, the HF subject group had a total blood volume 1.05 l greater than that of the AF subject group (Table 1), whereas the CVP was similar in the two groups (Table 2), indicating a greater total vascular capacitance associated with exercise training. However, Convertino et al. (7) have previously reported an +1.8 mm Hg elevation of CVP (from 9.5 ± 0.5 to 11.3 ± 0.6 mm Hg) in a group of 14 subjects following 10 wk of upright cycling exercise training. These authors indicated that a higher CVP was associated with an exercise training induced hypervolemia without alteration in total effective venous capacitance (7). The discrepancy between the present and previous data may be related to the difference in the length of exercise training between cross-sectionally and longitudinally designed studies, in addition to the fact that most of our subjects were swimmers who were trained in the supine position. Nonetheless, there is an implication of an increase in the compliance in the subjects following 10 wk of training in Convertino et al.'s study (7). If one calculates the change in CVP in relation to the change in total blood volume based on total effective venous compliance 2.3 ml·mm Hg-1·-1 (11) or 2.7 ml·mm Hg-1·kg-1 (15) in humans, the predicted elevation of CVP would be greater (i.e., +2.5 or +2.1 mm Hg) than that observed (an 1.8 mm Hg increase) as a result of the increase in total blood volume +5.7 ml·kg-1 body weight (i.e., increased from 64.8± 2.2 to 70.51 ± 2.9 ml·kg-1) following 10 wk of exercise training (7). We hypothesize that the difference between the predicted and observed CVP would become greater with a further extended exercise training induced hypervolemia.

An alteration of the cardiopulmonary baroreflex function has been reported to be present in as short a time as 3 wk (25). This period of time appears to be less than that required for the attainment of the training induced changes in cardiac morphology. Therefore, there must be other mechanisms involved in the training related diminution of the cardiopulmonary baroreflex sensitivity, in addition to the increases in cardiac chamber size and compliance as observed following prolonged exercise training regimes. Previously, Thompson et al. (41) reported that an increase in plasma volume 333 ml by ingestion of a flavored isotonic saline at a volume equal to 2% of lean body mass significantly attenuated the FVR reflex response to graded LBNP in their AF subjects, though neither arterial blood pressure nor arterial (carotid) baroreflex function was affected. These data implied that the diminished cardiopulmonary baroreceptor mediated FVR reflex response in the HF may be related to a training induced hypervolemia that could be observed within a few days of continuous exercise training(8,25). These data appeared to be consistent with the report by Mack et al. (23), who compared the effect of the increases in CVP elicited by -6° head-down tilt and rapid volume expansion (8 ml·kg-1) with 5% human serum albumin solution on the cardiopulmonary baroreflex function and found that volume expansion, not head-down tilt, significantly decreased the FVR reflex response of the AF subjects. Since both volume expansion and head-down tilt significantly offset the operational point of the cardiopulmonary baroreflex to a higher prevailing CVP, the different FVR response to the LBNP-induced central hypovolemia could not be attributed to the receptors or their afferent traffic to the cardiovascular control center. Especially as it has recently been shown that after 8-12 wk of daily spontaneous running no change in the stimulus-response relationship of single-fiber cardiopulmonary vagal afferent response to elevation of left atrial pressure in rats (33) occurred, even though the training effect (i.e., resting bradycardia and cardiac hypertrophy) was manifest. Therefore, peripheral adaptations, i.e., the end-organ, or the change in central integration, may be responsible for the difference between the volume loading and head-down tilt cardiopulmonary baroreflex response. Interestingly, Mack et al. (24) observed that volume expansion, not head down tilt, significantly increased baseline forearm blood flow. A volume expansion induced higher blood flow would stimulate the synthesis of the endothelium-derived relaxing factor nitric oxide (5) which could attenuate the peripheral vasoconstrictor response. However, Calver et al. (5) demonstrated that the decrease in forearm blood flow in response to the infusion of norepinephrine via the brachial artery was greater at a higher flow rate. Therefore, if the higher blood flow was associated with the greater blood volume observed in the HF subjects, an augmented rather than a diminished FVR response in the HF group during LBNP elicited sympathoexcitation should have occurred. In the present study, neither forearm blood flow nor FVR was significantly different between the two fitness groups(Table 2), although blood volume and plasma volume were significantly greater in the HF than AF subject group (Table 1).

Another possible mechanism by which the cardiopulmonary baroreflex may be affected involves the volume-regulatory hormones such as atrial natriuretic factor (42) or vasopressin (35). However, in both a cross-sectional comparison (38) and a longitudinal comparison (7,8) it has been found that exercise training does not have a significant effect on these volume regulatory hormones, although there is a significant hypervolemia observed in the trained subjects. These data imply that there is a resetting of volume receptors associated with the functional (i.e., compliance) and/or morphologic(i.e., hypertrophy) changes in the loci of the cardiopulmonary baroreceptors following exercise training. In summary, the data of the present investigation and those of previous reports suggest that an alteration of the integration of afferent signals to the cardiovascular center may explain the exercise training induced diminution of the cardiopulmonary baroreflex sensitivity.

One major limitation of this study was that the changes in CVP may or may not adequately reflect the changes in the stimuli of the cardiopulmonary baroreceptors, since the volume induced deformation of cardiopulmonary region may be a more important index of the perturbation of the cardiopulmonary baroreceptors. However, it has been demonstrated that exercise training results in an increase in cardiac compliance (22) and/or total effective peripheral compliance (see above discussion). Thus, there would be a greater volume change, probably a greater deformation in the loci of the cardiopulmonary baroreceptors, in terms of per unit CVP change in the HF. In the present investigation, there was no difference in the change in CVP between the AF and HF subjects throughout the experimental protocol and thus the change in volume could be greater in the HF who could have a greater compliance. Subsequently, the ratio of the changes in FVR to volume in the HF group would be even smaller compared with the slope of FVR/CVP. Therefore, we contend that the conclusion drawn from the present investigation was not misrepresented by the gain calculated from the slope of FVR/CVP.

In summary, the data of the present investigation demonstrated that during central hypervolemic loading of the cardiopulmonary baroreceptors the forearm vasodilation was significantly reduced in the exercise trained HF subjects. This finding was consistent with the training related decrease in cardiopulmonary baroreflex sensitivity observed during LBNP induced central hypovolemia reported previously and confirmed in the present investigation. The underlying mechanisms responsible for the exercise training induced diminution of the cardiopulmonary baroreflex may be initiated from an alteration of the central integration with the afferent signals followed by the functional and morphologic adaptations occurring in the loci of the cardiopulmonary baroreceptors.

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1. Abboud, F. M., D. L. Eckberg, U. J. Johannsen, and A. L. Mark. Carotid and cardiopulmonary baroreceptor control of splanchnic and forearm vascular resistance during venous pooling in man. J. Physiol. 286:173-184, 1979.
2. Aviado, D. M. Jr., T. H. Lt, B. Calesnick, and R. Bill, Jr. Cardiovascular adjustments to pressure changes in left ventricle and peripheral arteries. Fed. Proc. 10:7, 1951.
3. Aviado, D. M. Jr., T. H. Li, W. Kalow, M. Hess, and G. Turnbull. Chemo- and presso-reflexes from perfused heart and lungs of dogs.Fed. Proc. 9:255, 1950.
4. Aviado, D. M. Jr. and C. F. Schmidt. Reflexes from stretch receptors in blood vessels, heart and lungs. Physiol. Rev. 35:247-300, 1955.
5. Calver, A., J. Collier, D. Green, and P. Vallance. Effect of acute plasma volume expansion on peripheral arteriolar tone in healthy subjects. Clin. Sci. 83:541-547, 1992.
6. Churchill, E. D., and O. Cope. The rapid shallow breathing resulting from pulmonary congestion and edema. J. Exp. Med. 49:531-537, 1929.
7. Convertino, V. A., G. W. Mack, and E. R. Nadel. Elevated central venous pressure: a consequence of exercise training-induced hypervolemia? Am. J. Physiol. 260:R273-R277, 1991.
8. Convertino, V. A., P. J. Brock, L. C. Keil, E. M. Bernauer, and J. E. Greenleaf. Exercise training-induced hypervolemia: role of plasma albumin, renin, and vasopressin. J. Appl. Physiol. 48:657-664. 1980.
9. Daly, I. De B., G. Ludany, A. Todd, and E. G. Verney. Sensory receptors in the pulmonary vascular bed. Q. J. Exp. Physiol. 27:123-146, 1937.
10. Dicarlo, S. E. and V. S. Bishop. Exercise training enhances cardiac afferent inhibition of baroreflex function. Am. J. Physiol. 258:H212-H220, 1990.
11. Echt. M., J. Duweling, O. H. Gauer, and L. Lange. Effective compliance of the total vascular bed and the intrathoracic compartment derived from changes in central venous pressure induced by volume changes in man. Circ. Res. 34:61-68, 1974.
12. Edis, A. J., D. E. Donald, and J. T. Shepherd. Cardiovascular reflexes from stretch of pulmonary vein-atrial junctions in the dog. Circ. Res. 27:1091-1100, 1970.
13. Fergson, D. W., F. M. Abboud, and A. L. Mark. Selective impairment-of baroreflex mediated vasoconstrictor responses in patients with ventricular dysfunction. Circulation. 69:451460, 1984.
14. Foldager, N. and C. G. Blomqvist. Repeated plasma volume determination with the Evans blue dye dilution technique: the method and a computer program. Comput. Biol. Med. 21:3541, 1991.
15. Gauer, O. H., J. P. Henry, and H. O. Sieker. Changes in central venous pressure after moderate hemorrhage and transfusion in man.Circ. Res. 4:79-84, 1956.
16. Giarmattasio, C., G. Servalle, G. B. Bolla, et al. Cardiopulmonary receptor reflexes in normotensive athletes with cardiac hypertrophy. Circulation. 82:1222-1229, 1990.
17. Grassi. G., C. Giannattasio. G. Seravalle, G. Osculati, F. Valagussa. A. Zanchetti, and G. Mancia. Cardiopulmonary receptor and arterial baroreceptor reflexes after acute myocardial infarction. Am. J. Cardiol. 69:873-878, 1992.
18. Grassi, G., C. Giannattasio, J. Cleroux, C. Cuspidi, L. Sampieri, G. Bolla, and G. Mancia. Cardiopulmonary reflex before and after regression of left ventricular hypertrophy in essential hypertension.Hypertension 12:227-237, 1988.
19. Jingu, S., A. Takeshita, T. Imaizumi, M. Nakamura, M. Shindo, and H. Tanaka. Exercise training augments cardiopulmonary baroreflex control of forearm vascular resistance in middle-aged subjects.Circulation?/Author: Is journal as meant?52:162-168, 1988.
20. Johnson, J. M., L. B. Rowell, M. Niederberger, and M. M. Eisman. Human splanchnic and forearm vasoconstrictor responses to reductions of right atrial and aortic pressures. Circ. Res. 34:515-524. 1974.
21. Kouame, N., A. Nadeau, Y. Lacouriere, and J. Cleroux. Effects of different training intensities on the cardiopulmonary baroreflex control of forearm vascular resistance in hypertensive subjects. Hypertension 25:391-398, 1995.
22. Levine, B. D., L. D. Lane, J. C. Buckey, D. B. Friedman, and C. G. Blomqvist. Left ventricular pressure-volume and Frank-Starling relations in endurance athletes. Implications for orthostatic tolerance and exercise performance. Circulation 84:1016 1023, 1991.
23. Mack, G. W., B. M. Quigley, T. Nishiyasu, X. Shi, and E. R. Nadel. Cardiopulmonary baroreflex control of forearm vascular resistance after acute blood volume expansion. Aviat. Space Environ. Med. 62:938-943, 1991.
24. Mack, G. W., C. A. Thompson, D. F. Doerr, E. R. Nadel, and V. A. Convertino. Diminished baroreflex control of forearm vascular resistance following training. Med. Sci. Sports Exerc. 23:1367-1374, 1991.
25. Mack, G. W., X. Shi, H. Nose, A. Tripathi, and E. R. Nadel. Diminished baroreflex control of forearm vascular resistance in physically fit humans. J. Appl. Physiol. 63:105-110, 1987.
26. Mancia, G., R. R. Lorenz, and J. T. Shepherd. Reflex control of circulation by heart and lungs. In: Cardiovascular Physiology, 2, Vol. 9., A. C. Guyton and A. W. Cowley, Eds. Baltimore: University Park Press, 1976, pp. 111-144.
27. Oberg, B. and S. White. Circulatory effects of interruption and stimulation of cardiac vagal afferents. Acta Physiol. Scand. 80:383-394, 1970.
28. Paintal, A. S. Vagal sensory receptors and their reflex effects. Physiol. Rev. 53:159-227, 1973.
29. Pearson, A. C., A. J. Latovitz, D. Mrosek, G. A. Williams, and H. L. Kennedy. Assessment of diastolic function in normal and hypertrophied hearts: caparison of Doppler echocardiography and M-mode echocardiography. Am. Heart J. 113:1417-1425, 1987.
30. Potts, J. T., T. Hatanka, and A. A. Shoukas. Increased arterial compliance alters carotid baroreceptor reflex control of cardiac output. FASEB J. 8:A262, 1994.
31. Raven, P. B., D. Rohm-Young, and C. G. Blomqvist. Physical fitness and cardiovascular response to lower body negative pressure. J. Appl. Physiol. 56:138-144, 1984.
32. Roddie, I. C., J. T. Shepherd, and R. F. Whelan. Reflex changes in vasoconstrictor tone in human skeletal muscle in response to stimulation of receptors in a low-pressure area of the intrathoracic vascular bed. J. Physiol. (Lond.) 139:369-376, 1957.
33. Scislo, T., S. Dicarlo, and H. L. Collins. Daily spontaneous running did not alter vagal afferent reactivity. Am. J. Physiol. 265:H1564-H1570, 1993.
34. Seals, D. R., and P. B. Chase. Influence of physical training on heart rate variability and baroreflex circulatory control. J. Appl. Physiol. 66:1886-1895, 1989.
35. Share, L. Role of vasopressin in cardiovascular regulation. Physiol. Rev. 68:1248-1284, 1988.
36. Shi, X., C. G. Crandall, and P. B. Raven. Hemodynamic responses to graded lower body positive pressure. Am. J. Physiol. 265:H69-H73, 1993.
37. Shi, X., J. M. Andresen, J. T. Potts, B. H. Foresman, S. A. Stern, and P. B. Raven. Aortic baroreflex control of heart rate during hypertensive stimuli: effect of fitness. J. Appl. Physiol. 74:1555-1562, 1993.
38. Shi, X., W. G. Squires, J. W. Williamson, C. G. Crandall, J. Chen, L. P. Krock, and P. B. Raven. Aerobic fitness: I. Response of volume regulating hormones to head-down tilt. Med. Sci. Sports Exerc. 24:991-998, 1992.
39. Stevens, G. H. J., B. H. Foresman, X. Shi, S. A. Stern, and P. B. Raven. Reduction in LBNP tolerance following prolonged endurance exercise training. Med. Sci. Sports Exerc. 25:713-721, 1993.
40. Takeshita, A., S. Jingu, T. Imaizumi, Y. Kunihiko, S. Koyanagi, and M. Nakamura. Augmented cardiopulmonary baroreflex control of forearm vascular resistance in young athletes. Circ. Res. 59:43-48, 1986.
41. Thompson, C., D. L. Tatro, D. A. Ludwig, and V. A. Convertino. Baroreflex responses to acute changes in blood volume in humans. Am. J. Physiol. 259:R792-R798, 1990.
42. Volpe, M., N. Deluca, G. Lembo, et al. Influence of atrial natriuretic factor on forearm reflex vasoconstriction induced by cardiopulmonary or arterial receptor unloading. J. Hypertens. 5(Suppl. 5):S63-S65, 1987.
43. Zoller, R. P., A. L. Mark, R. M. Abboud, P. G. Schmid, and D. D. Heistad. The role of low pressure baroreceptors in reflex vasoconstrictor responses in man. J. Clin. Invest. 51:2967-2972, 1972.


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