J. PIyeiol. (1977), 272, pp. 399-414 With 9 text-figuree Printed in Great Britain

399

POSTURAL EFFECTS ON MUSCLE NERVE SYMPATHETIC ACTIVITY IN MAN

BY DAVID BTJRKE,* GORAN SUNDLOF AND B. GUNNAR WALLIN From the Departments of Clinical Neurophysiology and Internal Medicine, Academic Ho8pital, University of Uppeala, Sweden

(Received 11 March 1977) SUMMARY

1. Pulse-synchronous bursts of multi-unit sympathetic activity (MSA) were recorded in peroneal muscle nerve fascicles in eight healthy subjects when lying, sitting and standing. The sympathetic activity was quantitated by counting the number of bursts in the mean voltage neurogram/ min. Postural changes were analysed by considering the total activity to be a product of the number of bursts in relation to the number of heart beats (burst incidence) and the heart rate. 2. In lying there were large interindividual differences in total activity, but for all subjects the activity increased when going from lying to sitting and from sitting to standing. With a few exceptions the increase between the lying and sitting postures was associated with an increase in both burst incidence and heart rate whereas between the sitting and standing postures there was an increase in heart rate but on the average no change in burst incidence. 3. When going from lying to sitting or from sitting to standing the magnitude of the change in burst incidence was inversely related to the initial burst incidence so that subjects with low initial values usually showed greater increases in burst incidence than subjects with high initial values. Some subjects with high initial values decreased their burst incidence. 4. With changes in postures there was an inverse linear relationship between the fraction of the change in MSA associated with a change in burst incidence and the fraction associated with a change in heart rate. An increase in total activity could be obtained by changing only burst incidence, by increasing heart rate without changing burst incidence, or by * C. J. Martin Travelling Fellow of the National Health and Medical Research Council of Australia.

400 D. BURKE, G. SUNDLOF AND B. G. WALLIN appropriate changes in both parameters. The slope of the regression line was -0*53 indicating that for adequate postural compensation fewer additional bursts were required when the compensatory response involved an increase in heart rate rather than an increase in only burst incidence. 5. It is suggested that an impairment of the ability to regulate heart rate will make subjects with high burst incidence in the lying position orthostatically more vulnerable than those with low burst incidence. 6. Shortly after standing up one subject developed bradyeardia and subsequently fainted. The nerve recording was maintained until the subject collapsed. During the initial bradycardia no sympathetic bursts occurred suggesting that the syncope was associated with an interruption of normal baroreflex feedback between blood pressure and sympathetic outflow. INTRODUCTION

Changes of body position from lying to sitting and from sitting to standing lead to widespread circulatory readjustments counteracting the tendency for blood to pool in the legs. The effectiveness of these adjustments, which involve a decrease in cardiac output, an increase in heart rate and an increase in total peripheral resistance, is such that mean arterial blood pressure is maintained approximately constant (Gauer & Thron, 1965). The increased total peripheral resistance seems to be due in part to an increased resistance in the vascular bed of skeletal muscle, as shown during both actual (Hildebrandt, 1960; Brigden, Howarth & Sharpey-Schaefer, 1950) and simulated orthostatic situations (see Wolthius, Bergman & Nicogossian, 1974). Since sympathetic ganglion blockade causes orthostatic hypotension it is clear that sympathetic mechanisms are responsible for some of the reflex adjustments. However, so far no direct studies of sympathetic nervous activity during sitting or standing have been made in man and consequently our understanding of these reflex mechanisms is still incomplete. In a recent investigation in recumbent man Sundl6f & Wallin (1977) found that the spontaneously occurring fluctuations in sympathetic vasoconstrictor outflow to muscle (MSA) occur synchronously in different extremities. They also found that each individual had a fairly constant and reproducible amount of MSA from day to day, but that there were marked differences between individuals. With this evidence for a generalized and individually constant muscle nerve 'sympathetic tone' in the recumbent position as background, the present experiments were undertaken to investigate the differences in MSA in the lying, sitting and standing positions.

POSTURAL EFFECTS ON SYMPATHETIC ACTIVITY

401

METHODS Material. Neural recordings were made in twenty-three experimental sessions on eight healthy volunteers, aged 23-56 years, all of whom gave informed consent to the experimental procedure. With the exception of one recording during lying made from the right median nerve at the elbow level, all recordings were obtained from muscle nerve fascicles of the peroneal nerve at the fibular head. On seven subjects recordings were made in the lying, sitting and standing positions, and on one subject during lying and sitting only. In one experiment neural recordings were made in all three positions, in eleven experiments in two positions, and in eleven experiments in one position (lying). On four subjects recordings during lying were performed 2-4 times and on four subjects recordings during sitting were performed twice. The interval between experiments on any one subject ranged from two weeks to several months. Micro-electrode8, recording technique and display systems have recently been described in detail (Sundlof & Wallin, 1977). In brief, neural recordings were made with insulated tungsten micro-electrodes with a tip diameter of 1-5 jam. After amplification the neural activity was fed through an RC-integrating network (time constant 0-05 or 0-1 see) to obtain a mean voltage neurogram. Both the original neural record and mean voltage neurogram were stored together with other variables (see below) on an 8-channel FM tape recorder. For analysis the experimental data were displayed on an ink-jet recorder (Mingograf 800, Siemens-Elma Ltd) with a paper speed of 3-5 mm/sec. The records were divided into analysis periods comprising approximately 3 min each (range 2-4 min) and the amount of neural activity was determined from the chart by counting the number of pulse-synchronous sympathetic bursts in the mean voltage record for each analysis period. E.c.g. was recorded by surface electrodes on the chest. Respiratory movements were recorded by a strain gauge strapped around the chest with a rubber band. Intra-a-terial blood pressure (B.P.) and central venous pressure (C VP) were monitored in two experiments in each of which neural activity was recorded in the lying and sitting positions. The arterial catheter was introduced into the left brachial artery and placed with the tip in the axilla. The venous catheter was introduced into the left medial cubital vein and the tip positioned in the right atrium. The pressures were monitored by EMT 35 and EMT 33 pressure transducers, respectively, coupled to EMT 31 electromanometers (Siemens-Elema Ltd). Experimental procedure. Subjects were in a comfortable recumbent position, were sitting upright, or were standing. In most experiments during sitting the leg from which recordings were obtained was held with the knee joint semi-extended and the foot resting on a pillow 10-20 cm above the floor level. This posture stabilized the peroneal nerve and was essential if the recording site was to be maintained during transition from sitting to standing. The other knee joint was kept at 900, with the sole of the foot against the floor. When standing, subjects were instructed to bear the body-weight mainly on the free leg and were encouraged to lean backwards against a support since this minimized muscle contraction in the legs. The micro-electrode was inserted manually through the intact skin and guided into a muscle nerve fascicle by electric stimuli delivered through the electrode. Small electrode adjustments were then made until a recording site was found in which spontaneously occurring pulsatile bursts of multi-unit sympathetic activity could be recorded. Details of the identification procedure and evidence that the impulses derive from sympathetic vasoconstrictor fibres have been summarized by Sundlof & Wallin (1977). When a recording site with good signal-to-noise ratio for

402

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D. BURKE, G. SUNDLOF AND B. G. WALLIN

sympathetic impulses was found, the activity at rest was recorded for subsequent quantitative determinations. At the start of an experiment the subject had usually been in the initial posture (lying or sitting) for 30 min or more before recordings were made. Most changes of posture required the interruption of recording. A new recording site was found usually within 2-15 min but in three cases searching for approximately 60 min was necessary, and in three cases a stable recording site was maintained during the transition from sitting to standing. In some experiments during lying manoeuvres such as fist clenching, mental stress and the Valsalva manoeuvre were performed. The first 20 sec after each manoeuvre were not included in quantitative determinations of the number of sympathetic bursts at rest. During sitting and standing, the Valsalva manoeuvre was performed occasionally. Lying

Sitting

Standing

5 sec Fig. 1. Differences between mean voltage records of MSA in lying, sitting and standing postures obtained from the same subject, during one experimental session. Traces are from above: respiratory movements (as in subsequent Figures inspiration upwards); mean voltage MSA (time constant 0.05 sec); e.c.g.; instantaneous heart rate. RESULTS

As illustrated in Fig. 1 the general character of the MSA during sitting and standing was similar to that during lying: the sympathetic impulses were grouped in pulse-synchronous bursts with a short pause in the activity between bursts even when the pulse rate was high. When lying the bursts often occurred irregularly without distinct grouping but when sitting or standing fairly long sequences of bursts separated by silent periods were common (see also Fig. 7). Quantitatively there were increases in the total amount of MSA when going from lying to sitting and from sitting to standing. This is illustrated both by the records shown in Fig. 1 and by the quantitative summary of all data from one subject shown in Fig. 2. In each posture the total amount of activity (expressed as bursts/min) was fairly constant from one 3 min analysis period to the next and, in general, the differences between

403

POSTURAL EFFECTS ON SYMPATHETIC ACTIVITY Lying

Standing

Sitting

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1 3 5 7 Fig. 2. Changes in MSA between lying, sitting and standing postures in one subject. Each point represents the number of burstslmin (*) or bursts/100 heart beats (0) during a 3 min analysis period. Data obtained from two experiments, one comprising lying, the other sitting and standing 1 3 5 7

1 3 57

postures.

Bursts/1 00 heart beats

Bursts/min

Heart rate/min

120 F

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80 F

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Fig. 3. Collected data on changes of burst incidence, heart rate and total MSA between lying (A), sitting (B) and standing (C) postures for all subjects. For each subject neural activity and heart rate are given as mean values of all analysis periods in each posture. Filled circles connected by thick lines represent averages for the whole material.

404 D. BURKE, G. SUNDL5F AND B. G. WALLIN postures were clear with little or no overlap. To analyse the differences in more detail it proved useful to consider the total amount of activity as a product of (a) the burst incidence, i.e. the number of bursts relative to the number of heart beats, and (b) the hear rate. Fig. 3 summarizes the differences between the three parameters in each posture for all recordings in all subjects. For each individual, neural activity and heart rate are given as mean values of all analysis periods in a certain posture. When lying there were large differences in burst incidence between subjects, the range being from 10 to 83 bursts/100 heart beats. In most subjects, when going from lying to sitting the increase in total activity was associated with both an increase in burst incidence and an increase in heart rate. The magnitude of the change in burst incidence was, however, inversely correlated to the initial burst incidence (r = -0.76) and for the two subjects with the highest initial values the incidence actually decreased, the data from one of these subjects being seen in Fig. 2. The net result of these changes was that when sitting the burst incidence ranged from 42 to 84 bursts/100 heart beats, so that the differences between subjects were reduced. Most subjects increased their heart rate between lying and sitting. The sole exception decreased her heart rate from 86 to 76 but this was accompanied by a marked increase in burst incidence (from 10 to 42/min). The increase in sympathetic activity between sitting and standing mainly reflected an increase in heart rate and on the average there was no change in burst incidence. For most subjects the increase in heart rate between sitting and standing was greater than that between lying and sitting. The most pronounced increase in heart rate between sitting and standing (from 90 to 131 beats/min) was seen in a subject who at the same time decreased his burst incidence from 66 to 51 bursts/100 heart beats (same subject as in Fig. 1). The differences in heart rate and in burst incidence between the lying and sitting positions and between the sitting and standing positions were inversely related. A consequence of this can be illustrated by considering the total MSA change between two postures to be composed of two components, one calculated from the change in burst incidence (assuming heart rate unchanged) and one from the change in heart rate (assuming burst incidence unchanged). Such calculations were made on the data from those experiments in which one or more changes of posture were made during the experiments and the results are shown in Fig. 4. The relationship thus derived fits a linear regression line of slope - 0-53 (r = -0.81). Thus, on changing posture, an adequate increase in total MSA could be obtained without increasing heart rate (changing only burst incidence) or by increasing heart rate in parallel with sympathetic outflow (no change in burst incidence), but in most cases burst incidence and

POSTURAL EFFECTS ON SYMPATHETIC ACTIVITY 405 heart rate changed in appropriate proportions. The slope of the relationship indicates that if there was no change in heart rate a greater number of additional sympathetic bursts was required to maintain adequate orthostasis. The decreases in burst incidence and heart rate which were mentioned in the preceding paragraph as exceptions to the general trend may be satisfactorily explained by this inverse relationship. Change in MSA (heart rate) 40 Bursts/min

30 0 0 0 0.

Change in MSA*

(bustncdene)-20

10

-10

40

Bursts/mmn

-10

-20

Fig. 4. Relationship between the fraction of the total MSA change associated with a change in burst incidence and the fraction associated with a change in heart rate for those experiments in which one or more postural changes were made. Filled circles represent changes between lying and sitting and open circles between sitting and standing postures.

No attempt was made to compare the absolute strength of sympathetic bursts in different postures because the precise record locations within the fascicles were not identical. However, since an increase in the impulse frequency within each burst might show up as an increase in the proportion of large to small bursts, the relative distribution of bur8t amplitude in the mean voltage neurograms were measured for each posture. No consistent differences were found between the shapes of the amplitude spectra for the three postures, lying, sitting and standin. For the subject with the highest heart rate when standing and the greatest difference in heart rate between the lying and st Anding postures, bsrst duration tended to be shorter when stands than when lying. However, in the other subjects, no differences in burst duration were found in the different postures, confirming that significant differences in burst duration

D. BURKE, G. SUNDLOF AND B. G. WALLIN 406 are found only when there are large variations in heart rate (Wallin, Delius & Sundlof, 1974). MSA in relation to blood pressure and central venous pressure. Qualitatively, the relationship between the fluctuations in B.P. and the occurrence of sympathetic bursts was similar in lying and sitting, i.e. the bursts Sitting

Lying

125 mmHg

+10 mmHg

-10 .

1 20/min

5 sec Fig. 5. Experimental records showing relationships between mean voltage MSA (second traces) and intra-arterial B.P. (third traces) and CVP (fourth traces) in sitting and lying postures in the same experiment. Upper and lowest traces show respiratory movements and instantaneous heart rate, respectively. In the lying posture there is an intermittent movement artifact on the CVP trace associated with respiration.

tended to occur during reductions in B.P. and disappear as B.P. increased. As illustrated in Fig. 5, the differences in neural pattern commonly seen between the recumbent and upright postures were related to the fact that in sitting (and presumably also in standing) the oscillations in B.P. tended to be larger and slower than when lying. In contrast to the intimate correlation between variations in B.P. and nerve activity, inspection of the records revealed no relationship between the fluctuations in CVP (most of which were related to respiration) and the occurrence of sympathetic bursts

(cf. Fig. 5).

In one subject both diastolic and mean B.P. were slightly higher when sitting than when lying but in the other subject arterial pressures were unchanged. In both cases CVP was reduced by 10-20 mm Hg. The findings are illustrated in Fig. 5 by experimental records from one subject

POSTURAL EFFECTS ON SYMPATHETIC ACTIVITY 407 and in Fig. 6 by all the experimental data from the other subject in whom pressure recordings were made. The transition from sitting to standing. In three subjects it was possible to maintain the recording position during the transition from sitting to standing. The manoeuvre was associated with similar changes in MSA and pulse rate in two of the subjects, as illustrated in Fig. 7. The process of

P1

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-20 Fig. 6. Collected data on the relationship between diastolic B.P., CVP and MSA in lying and sitting postures in one experiment. Each point represents average diastolic B.P. (0) and total MSA (0) during a 3 min analysis period. The CVP is given as the average maximum, minimum and mean values for each posture.

standing up lasted approximately 10 sec and a few seconds before stable stance was achieved a sequence of strong pulse-synchronous bursts, lasting 8-10 sec, was initiated. This burst sequence was followed by a pause of approximately the same duration after which ensued the pattern of sympathetic activity appropriate to the new posture. As in Fig. 7 no significant differences in burst strength were seen between sitting and standing. This finding must be interpreted with caution, however, since it is difficult to exclude a minor change in recording site during the standing up manoeuvre. In both cases heart rate increased to a higher level, either during the standing up manoeuvre or slightly after stable stance had been achieved. In the third case, the act of standing up initiated a sequence of four pulse-synchronous bursts during the last part of the manoeuvre. I18

P HY

272

D. BURKE, G. SUNDLOF AND B. G. WALLIN 408 However, instead of increasing as in the other subjects, pulse rate decreased, the subject became syncopal and fainted. The events are illustrated in Fig. 8. The left part of the Figure shows the sympathetic activity when sitting

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Fig. 7. Experimental record showing the changes in MSA (second trace) and instantaneous heart rate (lowest trace) during the act of standing up (indicated by horizontal bar). Upper trace respiratory movements and third trace e.c.g. Sitting Standing

*

. ... * ..

1360/mm

2 sec Fig. 8. Experimental records showing mean voltage MSA and heart rate during fainting reaction. Left part obtained in sitting 2-3 min before standing up, right part in standing, starting just when stable stance had been achieved and ending with subject collapsing (arrow). Records photographed from oscilloscope on AC mode. Traces as in Fig. 7.

2-3 min before standing. The sequence on the right begins when the subject had just stood up with the last part of the initial burst sequence. A further sympathetic burst occurred as the pulse rate decreased, and at the

409 POSTURAL EFFECTS ON SYMPATHETIC ACTIVITY arrow the subject collapsed. During the brief sequence when standing a unitary neural discharge was apparent in the background. Although the electrode position probably changed slowly before the collapse, the activity of the same unit could be recorded throughout the whole sequence suggesting that any change in recording site must have been small and insufficient to prevent the recording of sympathetic bursts, should they have occurred. Furthermore, a sudden prolongation of the interval between successive heart beats such as is seen in the figure would normally have provoked an unusually strong sympathetic discharge (Wallin et al. 1974). In view of these considerations, it seems reasonable to conclude that the fainting reaction was associated with a cessation of sympathetic outflow to the vascular bed of skeletal muscle. TABiE 1. Average amount of sympathetic activity in repeated recordings when sitting

Subject H.J.

Expt no.

Bursts/100 heart beats

Bursts/min

I 59 4 47-4 II 58.9 39.0 I S.A.* 70*1 62*4 I 64*0 61*2 II 63.3 52*2 KEH I 89*7 62*4 II 78*0 63*6 I A.S. 56*5 41*4 56-9 II 38*4 * In experiment I recordings when sitting were made both before and after

standing.

Reproducibility. The incidence of sympathetic bursts is highly reproducible in the same individuals when lying (Sundlof & Wallin, 1977). Four subjects from the material of Sundlof & Wallin participated in the present investigation and the additional recordings when lying provided values for burst incidence comparable to previous data for the same subjects. Repeated recordings were performed on four subjects when sitting. Table 1 summarizes the mean values for the neural activity in these recordings, each of which lasted 6-17 min. The differences between recordings on the same subject were again quite small, the greatest difference in burst incidence being 11D7 bursts/100 heart beats, and in total activity being 10'2 bursts/min. In order to minimize factors likely to produce inconsistencies within and between recordings, care was taken to ensure that subjects were as x8-2

D. BURKE, G. SUNDLOF AND B. G. WALLIN 410 comfortable as possible in each position. Nevertheless, in two experiments, one during lying and one during sitting, burst strength and burst incidence, although initially stable, gradually and progressively increased. The increase in sympathetic activity was associated with increasingly severe discomfort such that the prevailing posture ultimately became intolerable. Fig. 9 illustrates the change in nerve activity for one of the subjects. Such changes have not been seen with acute mental stress or mild degrees of discomfort (Delius, Hagbarth, Hongell & Wallin, 1972) and it may be relevant that the subject illustrated in Fig. 9 was the one who fainted shortly afterwards on standing up (cf. Fig. 8). B

A

3,

,. _________________________

,.,..........................

....

1 20/min 60

5 sec Fig. 9. Increase in sympathetic activity associated with severe discomfort in sitting subject. Records in A obtained early in the experiment when subject was comfortable, records in B approximately 9 min later shortly before discomfort became intolerable. Traces as in Fig. 7. Same subject as in Fig. 8.

DISCUSSION

The present results confirm previous indirect evidence from haemodynamic studies that the outflow of sympathetic vasoconstrictor impulses to the vascular bed of skeletal muscle is higher in upright postures than in lying (Gauer & Thron, 1965). Although the sympathetic activity during sitting and standing was recorded only in peroneal nerves the results probably apply to upper limb nerves as well, since Sundl6f & Wallin (1977) recently showed that during lying there was a high degree of similarity between sympathetic discharges in upper and lower extremities. It is most unlikely that the recorded changes in number of bursts between different postures were artifacts due to differences in the quality of the recording positions in the nerve. At rest in the lying posture Sundl6f & Wallin (1977) found the burst incidence to be individually constant

411 POSTURAL EFFECTS ON SYMPATHETIC ACTIVITY in different recording sites and on different occasions, and they suggested that sympathetic neurones in muscle nerves are subjected to a fairly homogeneous central drive. The situation is probably reasonably similar when subjects are at rest in upright postures and one would therefore not expect burst incidence figures to be affected significantly by minor differences in recording sites. Certainly, the data obtained in the repeated recordings in the sitting posture were quite reproducible (Table 1). The pulse synchrony in the MSA is to a large extent a baroreflex effect brought about by each systolic pressure wave inhibiting the outflow of sympathetic impulses. The bursts themselves correspond to the diastoles when the baroreceptor inhibition is less marked (Adrian, Bronk & Phillips, 1932; Weidinger & Leschhorn, 1964; Green & Heffron, 1968). Since the MSA has this pulse-synchronous character both in the horizontal and upright postures, the total activity may be increased by three mechanisms: an increase in the number of bursts relative to the number of heart beats; an increase in heart rate; and an increase in the average number of impulses/burst. Positive evidence was found for only the first two mechanisms but the third mechanism cannot be excluded since the present recording technique is not suitable for comparing burst amplitudes in different electrode positions. Postural compensating mechanisms. When lying a wide range of burst incidence, from 10 to 83 bursts/100 heart beats, was seen in different subjects and in another study incidences of less than 10 and more than 90 were reported (Sundi6f & Wallin, 1977). The reason for these differences is not known. However, under physiological conditions the baroreflexly controlled vascular bed of skeletal muscle is an important organ for buffering transient B.P. changes and the wide scatter raises the question by which mechanisms subjects at the low end of the range decrease and subjects at the high end increase their MSA when demand for such changes arise. In this context it should be remembered that sitting and standing, rather than lying, probably should be regarded as the resting 'physiological' postures (cf. Gauer & Thron, 1965) and it is in these postures that the demand for efficient baroreflex compensation will be most pronounced. Since in the present investigation the minimal burst incidence in sitting was 42 bursts/100 heart beats all subjects would be able to decrease their MSA in this posture. On the other hand, for those subjects with a high burst incidence the data suggest that their ability to increase the MSA is associated with their ability to increase heart rate. The effectiveness of the mechanism was clearly demonstrated in those subjects who, when changing posture had a decreased burst incidence, yet still produced a higher level of MSA associated with an increase in heart rate. Consequently, in addition to being important for adjusting cardiac output the

D. BURKE, G. SUNDLOIF AND B. G. WALLIN 412 present study suggests that heart rate variations also contribute in a significant way to the variations of muscle 'sympathetic tone'. This raises the possibility that subjects with high burst incidence in lying may well be orthostatically more vulnerable than those with low burst incidence should drugs or disease impair their ability to regulate heart rate, as occurs with age, hypertension and intrinsic heart disease (Gribbin, Pickering, Sleight & Peto, 1971; Eckberg, Drabinsky & Braunwald, 1971), and with the use of ,-adrenergic blocking agents. When changing posture, the relationship between the component of the change in total MSA due to a change in burst incidence and that related to a parallel change in heart rate had a slope of - 053 (Fig. 4), a value which suggests that the two mechanisms are not equally effective. For what was adequate postural compensation in each case, fewer additional bursts were required if these were associated with an increase in heart rate rather than with an increase in only burst incidence. The explanation of this phenomenon probably lies in the fact that, when heart rate and sympathetic outflow change in parallel, the two factors on which blood pressure depends, namely cardiac output and peripheral resistance, will alter. In contrast, changes in burst incidence in the absence of a change in heart rate can affect blood pressure only through the peripheral resistance. Underlying reflex mechanisms. In the present experiments there were only small changes in arterial B.P. recorded at the heart level on going from lying to sitting, and it is generally agreed that systolic pressure usually changes little but that diastolic pressure may increase 5-10 mm Hg between recumbent and upright postures (Mayerson, 1959; Gauer & Thron, 1965). Since, on assumption of upright postures, the arterial baroreceptors in the carotid sinuses are elevated some 20-25 cm above heart level, the small changes in pressure at heart level will result in a pressure reduction at the level of the carotid sinus receptors. The fall in pressure at receptor level will be maximal on going from lying to sitting, but there will be little further change on going from sitting to standing. On the other hand, the CVP decreases on going from lying to sitting and would probably decrease even further on going from sitting to standing. It seems reasonable to conclude that the stimulus producing the observed changes in total sympathetic activity may result from the combined action of high and low pressure receptors when going from lying to sitting, but that when going from sitting to standing the major stimulus probably comes from low pressure receptors. Evidence that both types of receptors may affect MSA has been seen in human experiments involving carotid sinus nerve stimulation (Wallin, Sundlof & Delius, 1975) and lower body suction (Sundlof & Wallin, 1976).

POSTURAL EFFECTS ON SYMPATHETIC ACTIVITY 413 The finding that postural stimuli, which appear qualitatively similar, cause different responses in different subjects indicates that adequate haemodynamic compensation is achieved by a complex interaction of a number of reflex mechanisms affecting both the level of MSA and the balance between the sympathetic and parasympathetic influences on the heart. Clearly when several reflex mechanisms are involved in a compensatory response, it may be misleading to evaluate the efficacy of the response by studying one reflex mechanism in isolation. The fainting reaction. In syncopal reactions blood pressure and heart rate are known to fall before the loss of consciousness (Brigden et al. 1950; Murray, Thompson, Bowers & Albright, 1968) and, as far as can be judged, the same events occurred in the subject who fainted in the present study. Since arterial baroreflex mechanisms exert a powerful control over the outflow of MSA (Wallin et al. 1974, 1975) a fall in B.P. and heart rate would normally lead to an increased MSA. The finding that the fainting reaction was associated with an absence of MSA therefore suggests that in part the syncope was due to an interruption of the normal feed-back between B.P. and sympathetic outflow. The investigation was supported by the Swedish Medical Research Council grant no. B76-04X-3546-05C. REFERENCES

ADROAN, E. D., BRONK, D. W. & PRImPs, G. (1932). Discharges in mammalian sympathetic nerves. J. Phy8iol. 74, 115-133. BRIGDEN, W., HOWARTE, S. & SHARPEY-SCHAEFER, E. P. (1950). Postural changes in the peripheral blood-flow of normal subjects with observations on vasovagal fainting reactions as a result of tilting, the lordotic posture, pregnancy and spinal anaesthesia. Clin. Sci. 9, 79-91. DELus, W., HAGBA9TE, K.-E., HONGELL, A. & WAEIm, B. G. (1972). Manoeuvres affecting sympathetic outflow in human muscle nerves. Acta phyaiol. 8cand. 84, 82-94. EcrBnamd, D. L., DRABINSKY, M. & BRAuNWALD, E. (1971). Defective cardiac parasympathetic control in patients with heart disease. New Engl. J. Med. 285, 877-883. GAuER, 0. H. & TiRON, H. L. (1965). Postural changes in the circulation. In Handbook of Physiology, section II, vol. 3, ed. HAMILTON, W. F. & Dow, P., pp. 24092439. Washington, D.C.: American Physiological Society. GREEN, J. H. & HEFFRON, P. F. (1968). Studies upon the relationship between baroreceptor and sympathetic activity. Q. JZ Physiol. 53, 23-32. GxRBBIN, B., PICKERING, T. G., SLEIGHT, P. & PETO, R. (1971). Effect of age and high blood pressure on baroreflex sensitivity in man. Circulation Res. 29, 424431. HIT.DEBRNDT, G. (1960). Die Durchblutung der menschlichen Wadenmuskulatur bei orthostatischer Belastung. Plugers Arch. ge8. Physiol. 272, 6-7. MAYERSON, H. S. (1959). Arterial pressure and its control. In Cardiology, vol. 1, Normal heart and vessels, part 2, cardiovascular functions, ed. LuiSADA, A. A., pp. 124-131. New York: McGraw-Hill.

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MURaY, R. H., THOMPsON, L. J., Bowers, J. A. & ALBRIGKT, C. D. (1968). Hemodynamic effects of graded hypovolemia and vasodepressor syncope induced by lower body negative pressure. Am. HeartJ. 76, 799-811. SUNDLWF, G. & WALLIN, B. G. (1976). The effect of lower body negative pressure on muscle nerve sympathetic activity in man. VIIth European Congre88 of Cardiology, Amsterdam. Abstract, Book I, p. 159. SUNDLOP, G. & WALLN, B. G. (1977). The variability of muscle nerve sympathetic activity in resting recumbent man. J. Physiol. 272, 383-397. WALLIN, B. G., DELIUS, W. & SUNDLOF, G. (1974). Human muscle nerve sympathetic activity in cardiac arrhythmias. Scand. J. clin. Lab. Invest. 34, 293-300. WALiN, B. G., SUNDLOF, G. & DELIuS, W. (1975). The effect of carotid sinus nerve stimulation on muscle and skin nerve sympathetic activity in man. Pflugerm Arch. ge8. Phy8iol. 358, 101-110. WEIDINGER, H. & LESCHHORN, V. (1964). Sympathische Tonisierung und rhythmische Blutdrucksschwankungen. Z. Krei8laufforsch. 53, 985-1002. WOLTHIUs, R. A., BERGMAN, S. A. & NIcOGOSSLkN, A. E. (1974). Physiological effects of locally applied reduced pressure in man. Physiol. Rev. 54, 566-595.

Postural effects on muscle nerve sympathetic activity in man.

J. PIyeiol. (1977), 272, pp. 399-414 With 9 text-figuree Printed in Great Britain 399 POSTURAL EFFECTS ON MUSCLE NERVE SYMPATHETIC ACTIVITY IN MAN...
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