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Am J Physiol Regul Integr Comp Physiol 276: R1434-R1442, 1999;
0363-6119/99 $5.00
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Vol. 276, Issue 5, R1434-R1442, May 1999

Upright posture reduces forearm blood flow early in exercise

J. Kevin Shoemaker1, Patrick M. McQuillan2, and Lawrence I. Sinoway1,3

Sections of 1 Cardiology and of 2 Anesthesiology, The Pennsylvania State University College of Medicine, The Milton S. Hershey Medical Center, Hershey 17033; and 3 Lebanon Veterans Affairs Medical Center, Lebanon, Pennsylvania 17042


    ABSTRACT
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

The hypothesis that upright posture could modulate forearm blood flow (FBF) early in exercise was tested in six subjects. Both single (2-s duration) and repeated (1-s work/2-s rest cadence for 12 contractions) handgrip contractions (12 kg) were performed in the supine and 70° head-up tilt (HUT) positions. The arm was maintained at heart level to diminish myogenic effects. Baseline brachial artery diameters were assessed at rest in each position. Brachial artery mean blood velocity (MBV; Doppler) and mean arterial pressure (MAP) (Finapres) were measured continuously to calculate FBF and vascular conductance. MAP was not changed with posture. Antecubital venous pressure (Pv) was reduced in HUT (4.55 ± 1.3 mmHg) compared with supine (11.3 ± 1.9 mmHg) (P < 0.01). For the repeated contractions, total excess FBF (TEF) was reduced in the HUT position compared with supine (P < 0.02). With the single contractions, peak FBF, peak vascular conductance, and TEF during 30 s after release of the contraction were reduced in the HUT position compared with supine (P < 0.01). Sympathetic blockade augmented the FBF response to a single contraction in HUT (P < 0.05) and tended to increase this response while supine (P = 0.08). However, sympathetic blockade did not attenuate the effect of HUT on peak FBF and TEF after the single contractions. Raising the arm above heart level while supine, to diminish Pv, resulted in FBF dynamics that were similar to those observed during HUT. Alternatively, lowering the arm while in HUT to restore Pv to supine levels restored the peak FBF and vascular conductance responses, but not TEF response, after a single contraction. It was concluded that upright posture diminishes the hyperemic response early in exercise. The data demonstrate that sympathetic constriction restrains the hyperemic response to a single contraction but does not modulate the postural reduction in postcontraction hyperemia. Therefore, the attenuated blood flow response in the HUT posture was largely related to factors associated with diminished venous pressures and not sympathetic vasoconstriction.

Doppler ultrasound; head-up tilt; sympathetic nervous system


    INTRODUCTION
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

THE RATE OF BLOOD FLOW adaptation at the onset of exercise has metabolic consequences later in the exercise period (10). Therefore, the control of blood flow dynamics has important implications for work performance. The rapid increase in forearm blood flow (FBF) at the onset of exercise (22, 24, 26) is due to the combined effects of the muscle pump (22) and a vasodilation that occurs within 2-4 s of the exercise onset (3, 30). Therefore, maneuvers that impact on either venous pressure (Pv) and/or vascular tone might alter the limb blood flow rate of adaptation at the onset of contractions.

At rest, limb blood flow is restrained by high levels of sympathetic vascular tone (12). Furthermore, sympathoexcitation can constrict skeletal muscle vasculature during steady-state contractions (1, 13, 14) and after ischemia (23, 28). Thus it is conceivable that the increase in sympathetic discharge to muscle vascular beds with upright posture (2, 19) might also impact on blood flow dynamics during the transition from rest to steady-state exercise.

Two methodological approaches have been used to assess the role of sympathetic constrictor tone on blood flow dynamics. First, the constricting effects of sympathetic tone can be removed. With this approach, local reductions in sympathetic discharge by sympathectomy (4, 17) or stellate ganglion blockade (12) resulted in increased blood flow at rest but little change during contractions. Furthermore, blocking systemic sympathetic outflow in dogs did not affect the rise in leg blood flow during the first 10 s of mild- to moderate-intensity exercise (22). Nonetheless, stellate ganglion blockade resulted in elevated exercise blood flow during heavier workloads (12). A second approach is to elevate sympathetic discharge and observe the blood flow response to exercise. With plethysmographic measures of forearm blood flow (FBF) made each minute, Joyner et al. (11) observed that the exercise hyperemic response was not different in the supine or upright postures. In contrast, brachial artery mean blood velocity (MBV) was reduced when moderate and heavy rhythmic contractions were performed during -60 mmHg lower body suction that did not alter mean arterial pressure (MAP) (25). In these earlier studies (11, 25) the effect of orthostatic stress on FBF was measured no earlier than 1 min of exercise when a substantial portion of the hyperemic adaptation to the increased metabolic rate may have been achieved (24, 26). Therefore, it is not clear if orthostatic stress and, by inference, augmented sympathetic outflow, alter the time course of FBF during the adaptation phase between rest and steady-state exercise conditions.

As indicated above, the muscle pump may also contribute to the large and rapid increase in FBF at the exercise onset. Because a major regulator of muscle pump capacity is venous volume/pressure (5, 18) the effect of posture on FBF dynamics may be dependent on the Pv. It is expected that the reduction in central venous pressure with upright posture would lead to reduced arm Pv and, therefore, reduced muscle pump capacity (5).

Therefore, the goals in this report were to investigate the effects of head-up tilt (HUT) on the early blood flow responses to muscle contractions and, if reduced by HUT, to determine if this effect was related to increased sympathetic tone or to diminished venous pressures. Doppler ultrasound measures of blood flow were used to allow continuous measures of limb perfusion after a single dynamic contraction and during the first 36 s of rhythmic exercise in each of the supine and 70° HUT postures.


    METHODS
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

Subjects

Ten healthy subjects (2 female, 8 male) volunteered for the study. The mean age of the subjects was 34.3 yr (ranging from 25 to 46 yr). Each volunteer provided signed consent to experimental procedures that had been approved by the Investigational Review Board at The Milton S. Hershey Medical Center.

Experimental Design

Effect of posture. In this study, the FBF response to both single contractions (n = 10) and 12 repeated contractions (n = 6) was assessed in each of the supine and HUT positions. As observed in our laboratory and by others (2), muscle sympathetic neural outflow in the peroneal nerve increases by two- to tenfold with upright posture. This increase in sympathetic discharge is directed to both leg and arm tissue (32). The HUT posture was maintained for ~5 min before any exercise was performed to allow stabilization of sympathetic outflow (7). In each position, the exercising limb was maintained at the level of the heart to diminish myogenic contributions to forearm vascular tone.

For the single contraction experiments, a 12-kg weight, which was fixed to a handgrip device by a cable and pulley mechanism, was lifted and lowered over 2 s. Continuous measures of heart rate (HR), blood pressure, and blood flow were obtained for 15 s before and 45 s after the contraction. Each subject performed three repeated single contractions in each posture.

On the same test day, six subjects also performed two or three repeated trials of rhythmic contractions after the single contraction protocol using the same exercise weight. Each trial consisted of 1 min of baseline and 12 contractions performed in a 1-s work/2-s rest cadence. Thus blood flow measures were obtained at baseline and for 36 s of exercise. This short duration of exercise was used to focus on the early exercise hyperemic response. Importantly, the duration of this exercise protocol was used to diminish the likelihood of possible exercise-induced increases in brachial artery diameter (24) so that changes in MBV would be proportional to changes in flow. At least 5 min of rest occurred between the repeated trials.

Follow-Up Experiments

Test of sympathetic contributions. Six subjects repeated the single contraction protocols before and after forearm sympathetic blockade. These studies were performed to investigate the role of increased sympathetic discharge with HUT in the posturally mediated reduction in exercise blood flow. These experiments were performed on the same test day as the single contraction protocol in four subjects and on a different test day in two others. Sympathetic blockade was accomplished by infusing bretylium tosylate (1 mg/kg) (Bier Block) into an elbow vein after sequential exsanguination of forearm blood volume and circulatory arrest (8). Circulatory arrest was applied using a compression cuff around the upper arm inflated to 250-300 mmHg. The circulatory arrest was maintained for 20 min. At least 60 min followed removal of circulatory arrest before the testing was resumed. In four individuals the change in forearm vascular resistance (FVR) during a cold pressor test (expressed as a percentage of baseline resistance) was measured before and after the Bier Block procedure to confirm adequate inhibition of sympathetic vasconstriction.

Effect of arm position (Pv ). Further experiments were performed by five of the original ten subjects to more closely investigate the role of altered Pv in posturally mediated changes in exercise blood flow. While subjects were supine, the forearm was elevated ~10 cm above the heart to drain venous volume and produce a Pv that was similar between the supine and HUT positions. While the subjects were in HUT, the arm was also lowered below heart level to reproduce Pv levels observed while supine with the arm level to the heart. Brachial artery blood pressure with the different arm positions was measured by keeping the finger and hand from which blood pressure was recorded at the level of the Doppler probe.

Reproducibility and order effects. Five of the original ten subjects repeated the single handgrip contraction protocol on a separate test day to investigate the reproducibility of the postcontraction hyperemic response. In two of these subjects, the order of testing was reversed from the original study so that the HUT position was investigated first followed by the supine position.

Data acquisition. After assuming the supine position on a tilt table, each subject was instrumented for HR [electrocardiogram (ECG)], blood pressure (Finapres, Ohmeda, Madison, WI), and blood flow in the brachial artery of the right arm. Doppler flow velocity (Multigon model 500M, Multigon, Yonkers, NY) measures were made using a 4-MHz probe fixed to the skin so that the brachial artery was insonated at 45°. Brachial artery diameters obtained at rest at each level of posture were measured using 2-D Echo Doppler ultrasound with a 7.5-MHz probe (Interspec XL, Interspec, Conshohocken, PA).

Venous pressure in the antecubital fossa was obtained using a 1.25-in., 20-gauge catheter (Angiocath) inserted in a retrograde fashion into a vein draining the exercising muscle. This catheter was connected to a pressure transducer maintained at the level of the catheter tip. The measures of Pv were obtained to account for HUT-induced changes in the pressure gradient across the arm. The finger of the left hand from which arterial blood pressures were obtained was held at the level of the pulsed Doppler probe to obtain measures of MAP. Analog signals of the ECG, blood pressure, MBV, and Pv variables were sampled at 100 Hz.

Data Analysis

For each of the single and repeated contraction studies, beat-by-beat values for HR, FBF, and MAP were obtained by integrating the area of the signals between consecutive R waves of the ECG tracing. On the basis of prior evidence (24), it was assumed that the brachial artery diameter would not increase during the first 30-40 s of exercise. Therefore, FBF was calculated as the product of MBV and vessel cross-sectional area (pi r2; where r is the vessel radius) using the diameter measure made at rest and the MBV measures obtained during and following the exercise. Forearm blood flow was normalized to milliliters per minute.

Rest. In each of the supine and HUT positions, measures of HR, MAP, Pv, and FBF were averaged over 30-40 heart beats at rest to provide baseline data. FVR was calculated as FVR = (MAP - Pv)/FBF.

Single contractions. For each individual single contraction, beat-by-beat values for HR, MAP, and FBF were determined for 15 s before and for 30 s after the release of the contraction. The FBF response to the single contractions was analyzed by determining the total excess flow (TEF) volume over the 30-s postcontraction period. The TEF was assessed by summing the beat-by-beat flow volumes and subtracting the resting equivalent [baseline FBF (ml/beat) · number of heart beats in the 30-s period]. Also, the peak FBF and vascular conductance response was determined for each single trial over the 10 subjects. Peak vascular conductance was calculated as FBF/MAP on the assumption that postcapillary venuole pressure was reduced to zero for a brief period after the contraction. Although vascular resistance was calculated for rest conditions, conductance was used with exercise because this value is a more sensitive index of vascular tone in high-flow states (15). The data were averaged over the repeated trials to obtain a single data set for each subject. Subsequently, the beat-by-beat blood flow responses were time aligned and averaged over 1-s time windows to produce a single curve for each subject in each posture for time course presentation.

Rhythmic contractions. Beat-by-beat determination of HR, MAP, and FBF was made over 1 min of rest and the 36 s of exercise that included 12 contraction/relaxation cycles. The hyperemic response to the rhythmic contractions was analyzed in two ways. First, the TEF over 36 s was computed by summing the flow volumes for each heart beat and then subtracting the resting equivalent (baseline flow/beat · number of heart beats in the 36-s period). Second, the flow and vascular conductance responses at 15 and 36 s of the exercise test were compared in the two postures. Vascular conductance was calculated as FBF/MAP.

Statistics. Unless indicated otherwise, the hyperemic responses to single contractions in the supine and HUT postures were compared with supine values using a two-tailed paired t-test. The effect of posture on FBF and vascular conductance responses at selected times during the rhythmic exercise trials was assessed by a repeated measures two-way ANOVA with a mixed-effects linear model. Significant differences in the ANOVA procedure were further analyzed using Tukey's post hoc test. These tests were performed using the SAS statistical software (SAS Institute, Cary, NC). The level of statistical significance for all tests was P < 0.05. All values are means ± SE.


    RESULTS
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

Rest

Brachial artery diameter at rest was not different between the supine (4.2 ± 0.4 mm) and HUT (4.2 ± 0.4 mm) positions. HR was increased in the HUT position relative to supine (P < 0.0001), but MAP was not altered (Table 1). Baseline FBF was not different between the supine and HUT postures. Compared with the supine position, baseline Pv was reduced in the HUT posture (P < 0.01). Visual inspection of the MBV waveforms (Fig. 1) indicates that HUT was associated with slightly reduced peak systolic velocity at rest and a greater magnitude of negative deflection immediately after the systolic pulse wave. These changes suggest an increase in FVR with HUT. However, examination of the relationship between MAP and FBF at rest did not demonstrate an increase in FVR on assumption of the upright posture (Table 1).

                              
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  		Table 1.   Forearm hemodynamics at rest in supine and 70° HUT postures



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  		Fig. 1.   Continuous tracings of mean blood velocity response from 1 subject after single contractions performed in supine (A) and 70° head-up tilt (HUT; B) postures. Peak magnitude and duration of hyperemic response was reduced in upright posture.

Single Contractions

The hyperemic response to a single strong contraction was greater in the supine compared with the HUT position. A representative response of this effect for a single trial performed by one individual is shown in Fig. 1. The averaged response over 10 individuals for each condition is shown in Fig. 2. The peak FBF and vascular conductance, as well as the TEF during 30 s after the single contractions (TEF30), were reduced in the HUT position compared with the supine trials (P < 0.004) (Table 2).


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  		Fig. 2.   Mean hyperemic response to a 2-s duration dynamic contraction in supine and 70° HUT postures. Forearm blood flow (FBF) increased rapidly after a single contraction and returned to baseline levels by ~30 s after release of contraction. Peak magnitude and duration of hyperemic response were reduced in upright posture. Values are mean of 3 trials performed by 10 subjects in each condition. Data points represent mean response aligned in 1-s time bins. Dotted line at time 0 denotes muscle relaxation after 2-s dynamic contraction.


                              
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  		Table 2.   Forearm hyperemic responses to a single contraction in supine and 70° HUT postures

Sympathetic Blockade

Compared with the control trial (53 ± 28 ml/min), FBF at rest was increased after the Bier Block procedure (120 ± 73 ml/min; P < 0.05). The percentage increase in FVR after 90 s of a cold pressor test was reduced from 43 ± 10% in the control trial to 9.7 ± 4.0% after sympathetic blockade (P < 0.05). These data verified successful attenuation of sympathetic constrictor effects on forearm vasculature.

The time course of the increase in blood flow to the single contractions before and after sympathetic blockade is shown for each posture in Fig. 3. The blockade procedure did not modulate the posturally mediated reduction to peak FBF, peak vascular conductance, or TEF responses after the single contractions (Table 3). Sympathetic blockade also did not alter the effect of posture on the duration of the postcontraction hyperemic duration (i.e., the period between the release of the contraction and the time when FBF returned to baseline levels) (Table 3). Sympathetic blockade prolonged the hyperemic response to a single contraction in the supine posture (Table 3). Importantly, the increase in FBF between baseline and the peak response (Delta FBF) was augmented in the HUT posture (P < 0.05) and tended to increase in the supine position (P < 0.08) after sympathetic blockade (Fig. 4). The magnitude of blockade effect on the Delta FBF was similar in both postures (~35 ml/min).


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  		Fig. 3.   Mean hyperemic response to a 2-s duration dynamic contraction in supine and 70° HUT postures before and after forearm sympathetic blockade (Bier Block). Sympathetic blockade augmented FBF response in each posture but did not modulate postural reduction of postcontraction hyperemia. Values are mean of 3 trials performed by 6 subjects in each condition. Data points represent mean response aligned in 1-s time bins.


                              
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  		Table 3.   Effect of forearm sympathetic blockade on hyperemic responses after a single contraction



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  		Fig. 4.   Increase in Delta FBF between baseline levels and peak response observed after a 2-s dynamic contraction (12 kg) was greater after sympathetic blockade of forearm (Bier Block), particularly in 70° HUT position. * Significantly greater than control (CTL) trial (P < 0.05).

Effect of Arm Position

While subjects were supine, raising the arm above the heart to reduce venous volume attenuated the peak vascular conductance (VC) and FBF response as well as the TEF30 after a single contraction to levels that were comparable to HUT with the arm held level with the heart (Fig. 5). While subjects were in HUT, lowering the arm to increase venous volume restored the peak VC and FBF response to levels that were similar to the supine, arm level condition (Fig. 5); however, TEF30 was only partially restored with this maneuver because of a greater duration of postcontraction hyperemia while subject was supine with the arm level versus all other conditions.


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  		Fig. 5.   Effect of arm position and posture on FBF response to a single contraction lasting 2 s performed in supine and 70° HUT positions. Peak FBF (A), vascular conductance (VC; B), and total excess flow (TEF) during 30 s after contraction (TEF30; C) were reduced when venous volume was reduced by elevating arm while supine or by HUT posture. Peak FBF and VC during HUT were restored to levels observed during supine when exercising limb was lowered below heart level; however, TEF30 was not restored by this maneuver. Values are mean of 3 trials performed by 5 subjects in each condition. * Significant difference between connected bars (P < 0.05).

Reproducibility and Order Effects

The postural effect on TEF over 30 s and the peak FBF response were reproducible, and the order of testing did not interfere with the results (Table 4).

                              
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  		Table 4.   Reproducibility of peak FBF and TEF30 after a single contraction in supine and 70° HUT position

Rhythmic Contractions

The analysis of rhythmic contraction responses was based on a total of 17 repeated trials in the supine position and 16 trials in the HUT position for the six subjects. At 15 s after the onset of contractions, neither FBF nor vascular conductance were altered by HUT (Fig. 6). However, by 36 s both FBF and vascular conductance were less in the HUT trials compared with the supine trials (P < 0.05) (Fig. 6). Compared with supine (77 ± 7 ml), TEF volume during 36 s of exercise, a measure that accounts for changes in HR with HUT, was reduced in the HUT position (55 ± 4 ml; P < 0.02) (Fig. 7).


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  		Fig. 6.   Postural effects on FBF (A) and VC (B) during 12 repeated handgrip contractions. Statistical comparisons were made at 15 and 36 s of exercise. * Significantly different from supine (P < 0.05). Dotted line indicates onset of contractions. Data points represent mean response over the contraction/relaxation cycle (3 s) for 17 repeated trials in supine and 16 trials in HUT positions.



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  		Fig. 7.   TEF above baseline during 12 repeated contractions in supine and HUT postures. * Significantly different from supine (P < 0.05).


    DISCUSSION
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

In the current study, continuous measures of FBF were made with single and repeated contractions to investigate the effect of elevated sympathetic discharge on the time course of hyperemia at the onset of exercise. The main finding was that the peak and total forearm hyperemic responses early in exercise were diminished when either single or 12 repeated contractions were performed at 70° of HUT compared with supine. Subsequent experiments indicated that sympathetic constrictor tone restrains FBF at the onset of contractions. However, HUT diminished both the magnitude and duration of the postcontraction hyperemia both before and after sympathetic blockade. Altering arm positions in either posture demonstrated that the peak FBF and vascular conductance responses to a single strong contraction were sensitive to Pv. Therefore, there are three main conclusions from the current study. First, upright exercise can attenuate the blood flow dynamic response at the onset of exercise. Second, sympathetic constrictor tone appears to modulate the magnitude of the postcontraction blood flow response, particularly in the upright posture. Third, a major contributor to the postural effect is independent of sympathetic discharge and is linked to changes in venous pressure or volume. These results suggest that the postural reduction in blood flow at the onset of exercise was largely due to the diminution of muscle pump functional capacity.

It is noteworthy that the postural effect was observed after the single contraction test but not until several contractions had been performed in the rhythmic contraction protocol. These seemingly inconsistent effects may be due to the inhibitory effect of a muscle contraction on limb perfusion (see Fig. 1). In the single contraction test, 2-4 s elapsed between the release of the contraction and the peak response. Although the peak flow response between rhythmic contractions occurs rapidly, the ensuing contraction and blood flow constriction occurred after only 2 s of relaxation so that the total hyperemic response to that contraction may not have been realized.

Rest

Venous pressure was reduced ~6-7 mmHg on going from the supine to the HUT postures. This magnitude of reduction in Pv is in agreement with the expected reduction in central venous pressure during orthostatic stress (16).

MAP was not different in the two postures. In contrast to earlier studies (11), we did not observe a reduction in baseline FBF, or an increase in FVR, during HUT. A possible explanation for this discrepancy may be differences in methods used to measure FBF. The studies that have observed reductions in FBF with upright posture used venous occlusion plethysmography (11). Although Doppler and plethysmographic measures of FBF have been highly correlated under some conditions (29, 31), there are limitations with each method that may impact on the ability to detect changes in FBF with upright posture. The limitations of Doppler ultrasound for arterial blood flow measures include uncertainty of insonation angles and possible probe position changes during the two postures. Our echo Doppler imaging to determine brachial artery dimensions also confirmed that, at the elbow, this vessel runs parallel to the skin. In addition, the elbow joint was maintained in the extended position and the probe placement and angle were not different in the two postures. Therefore, any errors in blood flow determination should have been similar between the supine and HUT measures. Inflation of the arm cuff for strain-gauge plethysmography measures of FBF impedes arterial inflow, resulting in an underestimation of total FBF when compared with Doppler ultrasound measures (9, 29); this effect has been observed both at rest and during conditions of high flow. Whether the magnitude of reduction in arterial inflow, or the compliance of the forearm, is different during upright posture when sympathetic outflow is elevated and venous volumes are diminished, is not known.

A second factor that may explain the differences in measured effects of posture on FBF to a resting forearm is the inclusion or exclusion of hand blood flow. In contrast to the earlier study (11), hand blood flow was not excluded from our measures of FBF at rest. If most of the increase in sympathetic nerve activity with the upright posture was directed to the muscle of the forearm rather than the hand, then the inclusion of hand blood flow may obscure the ability to observe a reduction in muscle blood flow at rest. However, the increased blood flow after a contraction would be directed to the forearm muscle, and sympathetic restraint of the hyperemic response might become more apparent.

Exercise

On the basis of observations of FBF during upright posture (11) and after stellate ganglion blockade studies (12), it has been argued that altered sympathetic discharge does not affect the adaptation of FBF at exercise onset in humans (11, 12). However, these earlier studies did not measure flow during the first 1 min of contractions when nearly all of the adaptation to exercise occurs (11, 24). Thus an interesting observation of the current study was that the contraction-induced increase in FBF above baseline was greater after sympathetic blockade. These data demonstrate that sympathetic vasoconstriction does blunt the rapid increase in FBF after a single contraction.

However, sympathetic blockade did not eliminate the postural reduction in postcontraction blood flow. Specifically, the postural reduction in TEF was not different before (-40 ± 9%) and after (-43 ± 11%) sympathetic blockade. Therefore, posture attenuated the peak and total blood flow response to exercise by a mechanism that was unrelated to sympathetic tone.

It is unlikely that different metabolic vasodilatory stimuli can account for the observed differences in postcontraction blood flow because the exercise challenge was identical in both postures. The diminished flow response during HUT may slow the washout of vasoactive muscle ions and metabolites and thereby alter the exercise hyperemia. However, if this effect were important, then a prolongation of the hyperemic period would be expected, but this was not observed (see Fig. 2).

A substantial portion of the early and rapid increase in limb blood flow with exercise may be due to the reduction in postcapillary venous volume and pressure immediately after a contraction and the consequent increase in perfusion pressure across the vascular bed (i.e., the muscle pump) (5, 22, 30). Therefore, the muscle pump may be more effective with a higher Pv, because this would increase the volume of blood that can be discharged from the compliant veins during a contraction. Accurate determination of potential of the muscle pump to contribute to the reduction in postcontraction hyperemia with HUT requires knowledge of postcapillary venuole pressures before and after the contraction. These pressures are not known. Nonetheless, the hyperemic responses to the varied arm positions in the current study support the concept that the magnitude of venous pressure before a contraction is an important modulator of postcontraction FBF.

While these arm position experiments suggest that the observed postural effects on FBF are related to Pv, the nature of this relationship is unclear. If it is assumed that postcapillary pressure was reduced to similar levels after each contraction (27), then MAP becomes the driving force for FBF. However, MAP was similar in both positions and cannot explain the postural reduction in FBF early in exercise. In addition, restoring venous pressure while in HUT did not restore the TEF due to a prolonged hyperemic response while supine. On the basis of the current data, we speculate that conditions in the muscle before contraction that affect venous refill dynamics may determine the effectiveness of the muscle pump and the duration of the postcontraction hyperemia. Venous refill dynamics are dependent on the initial pressure and volume of the capacitance vessels, which, in turn, will be dependent on limb position and/or venous smooth muscle tone. Although the capacitance vessels of skeletal muscle are only sparsely innervated by adrenergic neurons (6), indirect evidence in human subjects is suggestive of moderate reflex sympathetic control over forearm venous tone (21). If so, then increased sympathetic tone of the capacitance vessels could reduce venous volume at a given pressure in addition to passive reductions in forearm venous volume with HUT (20). Under these conditions venous refill time after a contraction would be attenuated compared with the supine condition, producing a smaller muscle pump potential than could be predicted on the basis of Pv only. This effect may account for the ability to normalize the peak but not the duration of the postcontraction FBF response by lowering the arm while in HUT, inasmuch as this maneuver would increase Pv but not necessarily venous volume. Furthermore, elevating the forearm above the heart while in the supine posture would produce a passive reduction in baseline venous volume and pressure. This situation would also diminish venous refill time after a contraction, producing a shorter hyperemic period similar to that observed while in HUT despite large differences in sympathetic tone.

In summary, continuous measures of FBF by Doppler ultrasound after single contractions and during rhythmic contractions showed that the FBF response at the onset of exercise was attenuated in the upright posture compared with supine posture. In addition, the postcontraction hyperemia was augmented after sympathetic blockade, particularly in the HUT posture. Therefore, sympathetic tone restrained the magnitude of the FBF response after the single contractions protocol. However, sympathetic blockade did not reduce the posturally mediated reduction in postcontraction blood flow. Importantly, reducing forearm Pv while in the supine posture produced postcontraction flow responses that were similar to the HUT condition. Also, increasing forearm Pv while in HUT posture to levels that were observed during the supine posture restored the peak FBF response to a single contraction but the TEF remained diminished because of the abbreviated duration of hyperemia. Therefore, it was concluded that HUT does diminish the blood flow response at the onset of exercise by a mechanism that was unrelated to sympathetic vasoconstriction. We speculate that postural adjustments to forearm venous volume and pressure diminished the functional capacity of the muscle pump because of reductions in venous refill time.


    ACKNOWLEDGEMENTS

The nursing care supplied by the staff of the Penn State General Clinical Research Center at The Milton S. Hershey Medical Center was appreciated.


    FOOTNOTES

This work was supported National Institute of Aging Grant R01-AG12227 (to L. I. Sinoway), Veterans Administration Merit Review Award (to L. I. Sinoway), and National Institute of Health-sponsored General Clinical Research Center with Division of Research Resources Grant M01-RR10732. J. K. Shoemaker was supported by a Natural Sciences and Engineering Research Council of Canada postdoctoral fellowship.

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. §1734 solely to indicate this fact.

Address for reprint requests and other correspondence: J. K. Shoemaker, Section of Cardiology, MC H047, The Pennsylvania State Univ., The Milton S. Hershey Medical Center, PO Box 850, Hershey, PA 17033 (E-mail: kshoemak{at}gcrc.hmc.psghs.edu).

Received 13 July 1998; accepted in final form 2 February 1999.


    REFERENCES
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

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Am J Physiol Regul Integr Compar Physiol 276(5):R1434-R1442
0002-9513/99 $5.00 Copyright © 1999 the American Physiological Society


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