Actu Physiol Scand 1990, 138, 145-153

Cardiovascular responses t o carotid sinus baroreceptor stimulation during moderate t o severe exercise in man S. S T R A N G E , L. B. ROWELL*, N. J. CHRISTENSENT and B. S A L T I N

August Krogh Institute, University of Copenhagen, Denmark, * Departments of Physiology and Biophysics and of Medicine (Cardiology), University of Washington, School of Medicine, Seattle, WA, USA, and Department of Internal Medicine and Endocrinology, Herlev University Hospital, Denmark

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STRANGE, S., ROWELL,L. B., CHRISTENSEN, N. J. & SALTIN,B. 1990. Cardiovascular response to carotid sinus baroreceptor stimulation during moderate to severe exercise in man. Actu Physiol Scand 138, 145-153, Received 9 August 1989, accepted 13 October 1989. ISSN 0001-6772. August Krogh Institute, University of Copenhagen, Denmark, Departments of Physiology and Biophysics and of Medicine (Cardiology), University of Washington, School of Medicine, Seattle, WA, USA, and Department of Internal Medicine and Endocrinology, Herlev University Hospital, Denmark. Our objective was to assess the importance of arterial baroreflexes in maintaining vasoconstriction in active muscle during moderate to severe exercise. Eight subjects exercised for 8-15 min, on a cycle ergometer at three levels (averages 94, 194, 261 W) requiring 40-88 7"of VO,max. Four times during each exercise level pulsatile negative pressure ( - 50 mmHg) was applied over the carotid sinuses for 30 s; suction was applied at each ECG R-wave for 250-400 ms. Before and during each neck suction, femoral venous blood flow (FVBF) was measured by constant infusion thermal dilution. At 94 W neck suction significantly reduced blood pressure (BP) (15 mmHg) and heart rate (HR) (7 beats min-'), and raised leg vascular conductance (LVC) ( I 1.4%) without changing FVBF. At 194 W, neck suction reduced BP (9 mmHg), HR (4 beats min-') and FVBF (5.1%, 240 ml min-'), and raised LVC (5.2%). At 261 W, LVC was unchanged by neck suction, but BP and FVBF both fell (9 mmHg and 650 ml min-' or 7.4 yo).We conclude that competing local vasodilation and sympathetic vasoconstriction control muscle blood flow during moderate exercise, and vasoconstrictor tone can be withdrawn by baroreceptor stimulation. High levels of vasoconstrictor outflow to muscle in severe exercise may not originate from baroreflexes.

Key words : blood pressure, leg blood flow, neck suction, noradrenaline, sympathetic nervous system, thermal dilution, vascular conductance.

I n this study we sought answers to two questions pertaining to the reflex control of muscle blood flow and arterial blood pressure during moderate to severe exercise in humans. O u r first question was whether the increased spillover of noradrenaline (NA) from active muscle (Savard et al. 1987) is accompanied by Correspondence : Seren Strange MD, August Krogh Institute, University of Copenhagen, 13 Universitetsparken, DK-2100 Copenhagen 0, Denmark.

vasoconstriction in these muscles that can be withdrawn by activating arterial baroreflexes. T h i s question has an important bearing on the issue of whether or not muscle blood flow during exercise is the resultant of competing metabolic vasodilation and neurogenic vasoconstriction. Several studies have focused on this, but there is substantial controversy among them (Shepherd 1983). I n dogs, whose capacity to supply all active muscles with blood exceeds that of humans by two- or threefold (Laughlin 1987), acute ablation of the sympathetic nerve supply to

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exercising hindlimbs was without effect on blood flow at any level of exercise (Donald et al. 1970), indicating that in this animal there is no tonic restraint of blood flow to the active muscles. In contrast, Vatner et al. (1970) found evidence for tonic vasoconstriction. Donald et al. (1970) and Thompson & Mohrman (1983) also showed that moderate electrical stimulation of the sympathetic nerves to the hindlimb caused similar percentage reductions in muscle blood flow at rest and the most severe exercise. Remensnyder et al. (1962) and Kjellmer ( I965), who performed similar experiments, concluded that the vascular response to maximal stimulation of the sympathetic nerves was markedly reduced with increasing exercise intensity (calculation of the conductance changes, however, does not support this view [Rowell 19891). I n humans, demands of skeletal muscle for blood flow appear to outstrip cardiac pumping capacity so that vasoconstriction is necessary to maintain arterial blood pressure (Clausen 1976, Secher et al. 1977, Klausen et al. 1982). Again, the marked spillover of NA from active muscles of humans during maximal exercise is thought to reflect this sympathetic control (Savard et al. I 989). Accordingly, our second question concerned the role of arterial baroreflexes in the control of muscle blood flow during exercise in humans. Several studies have shown that arterial baroreflexes exert as much control over blood pressure during mild to moderate exercise as at rest (Beveglrd & Shepherd 1966, Melcher & Donald 1981, Ludbrook 1983, Walgenbach & Donald 1983, Ebert 1986). I n dogs, stimulation of the carotid sinus nerves during moderate exercise causes release of sympathetic tone to the exercising limb and increases vascular conductance in the muscle vascular bed which is alreadj- metabolically vasodilated (Vatner et al.

1970). T h u s , the specific aim of our study was t o determine whether an increase in carotid sinus baroreceptor activity will increase the vascular conductance in contracting skeletal muscle in humans during moderate to severe exercise.

M A T E R I A L S AND METHODS SubJects. Seven men and one woman, aged 21-29 )ears, volunteered as subjects, and after being fully informed consented to participate. The study was approved by the Copenhagen Ethics Committee. All subjects were physically active students in good

health; one was a competitive triathlete. Their maximal oxygen uptakes ranged from 3.19 to 4.72 I min-' (average 4.28 1 min-') or from 46.3 to 68.5 mi kg-I min-' (average 57.1 ml kg-' min-'). Neck suction device. A lead neck suction chamber (see Eckberg et al. 1975) enclosed the front two-thirds of the neck, extending from the mandible and the earlobes to the sternum and the clavicles. An ordinary vacuum cleaner was connected through a solenoid valve to the front of the chamber. Chamber pressure was measured from a Statham Pz3-ID pressure transducer mounted on the chamber, and the signal was amplified (Simonsen and Weel Press 8041). The electrocardiogram (ECG) was monitored continuously (Simonsen and Weel Quadriscope 8034). An IBM PC/XT and a PASCAL routine detected the R-wave of the ECG and triggered the opening of the solenoid valve with a Io-ms delay. The stimulus duration was varied between 400 and zooms, depending on the heart rate. Chamber pressure could be changed from o to - 50 mmHg in j o ms. Beat-by-beat neck suction was performed for approximately 35 s to allow time for blood flow measurements and blood sampling. Leg bloodjlow. Leg blood flow was determined by a constant-infusion thermodilution technique as described by Andersen & Saltin (1985). Briefly, a soft Teflon catheter ( j F, 1 2 cm long) was percutaneously inserted in the right femoral vein with the tip advanced centrally to a location approximately 2 cm below the inguinal ligament. A thermistor probe (Edslab probe 94-030-z.gF) was inserted through the venous catheter and advanced 6 8 cm proximal to the catheter tip. Ice-cold saline was infused at a rate of 47.9 or 119 ml min-' for 2 e 3 0 s through four side-holes in the venous catheter and the temperature in the femoral venous blood was recorded continuously by an Edslab Cardiac Output Computer 9520. Blood flow measurements were obtained in pairs (control plus neck suction) and repeated four times at each work level. During neck suction, measurements were obtained after 1-15 s when heart rate and blood pressure were stable at the new level. Blood pressure and heart rate. A zo-gauge arterial catheter was percutaneously inserted in the right femoral artery and blood pressure was continuously recorded from a Medex Novatrans strain gauge pressure transducer. Mean blood pressure was determined from electronically filtered ( I Hz) pulsatile pressure (Simonsen and Weel Press 8041). Heart rate was continuously monitored from the ECG and Simonsen and Weel Quadriscope. All variables were recorded continuously on a Siemens-Elema Mingograf. Blood samples. Blood samples were taken simultaneously from the femoral artery and vein. Arterial samples were taken from the catheter used for blood pressure measurement. Haemoglobin content and oxygen saturation were measured by an OSM 11

Arterial baroreflexes during exercise

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Fig. I. Record showing timing of neck suction (- 50 mmHg) with ECG. Suction was triggered on R-wave. Duration was fixed at a given work rate so as to accommodate changes in rate as shown. Note the increase in R-R interval and fall in femoral arterial blood pressure (electronically damped). to the laboratory at 08.00 h or 13.00h and at least 2 h after a light meal. Catheters were inserted, and after a 30-min rest period, subjects exercised on a cycle ergometer at three different work rates (60 cycles min-') which required approximately 40, 70 and 8506 of their maximal oxygen uptakes. The duration of exercise was 14-16 min at each level with a 15-min rest period after the second exercise period. The third exercise period was divided into two 8-min periods with 5 min of rest in between. The neck suction chamber was placed around the front two-thirds of the neck. At each work level, a negative pressure of - 50 mmHg was applied at each ventricular contraction (ECG R-wave) to superimpose changes in carotid sinus transmural pressure on the natural arterial pulse wave, as illustrated in Fig. I . After a 5-min warm-up period at each level, heart rate, arterial blood pressure, leg blood flow and arteriovenous oxygen difference were measured before and during each application of neck suction. All variables were measured in four sets - four with and

Hemoxymeter (Radiometer, Copenhagen, Denmark). Plasma lactate was measured by a Yellow Springs Lactate Analyzer 231,. Plasma catecholamines were measured by a single isotope-derivative assay (Christensen et al. 1980). Pulmonary oxygen uptake. Pulmonary oxygen uptake was measured by the Douglas bag method. A Tissot spirometer was used for volume measurements ; 0, and CO, content were measured with paramagnetic (Servomex) and infrared (Beckman LBL-11) systems respectively. Procedures

A subject's maximal oxygen uptake was determined approximately I week before the final experiment by establishing a plateau of oxygen uptake with increasing work rate on a cycle ergometer. The subjects were familiarized with all experimental procedures on one or two separate occasions before the final experiment. On the day of the final experiment, the subjects came

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Fig. 3. Pilot experiment (data from one subject). Neck suction was added to combined arm and leg exercise. Brachial arterial blood pressure declined from 120 to 40 mmI-ig due to compression of the subclavian arteries b!- the lower edge of the lead chamber. !our without neck suction during each exercise period. Wood samples were taken simultaneously from the femoral artery and vein after the last blood flow measurement at each work level (for typical protocol see Fig. 2); one pair was taken before and the other during application of neck suction. Pulmonary oxygen uptake was measured a t each work level. Culrrrkutrons. Leg vascular conductance was calculated from each of four sets of measurements of leg blood flow (four without and four with neck suction) di\-ided by each accompanying mean arterial pressure. Cptake of oxygen and release of lactate by the leg were calculated from the averages of the four flow measurements (with and without suction) and the single measurement of arterial and femoral venous oxygen and lactate concentration. for each condition. Srutistirs. For the statistical evaluation we used the non-parametric Wilcoxon's matched-pairs signedranks test. The level of significance was set at o.oj, one-tailed. ~

Cominrnts on methods

In pilot experiments neck suction at - 50 mmHg was applied during combined upright c y l e exercise and arm cranking (three subjects). When neck suction was applied, subjects experienced severe arm fatigue. We discovered that the suction interfered with sub&\-ian blood flow and markedl!- reduced brachial arterial pressure (lower edge of the lead chamber compressed the subclavian arteries behind the clavicles). Fig. 3 illustrates one case in which neck suction reduced brachial arterial mean pressure from 100to 40 mmHg. -1valid measurement of blood pressure required that Re used the femoral artery.

( I 5 mmHg) and an I I .4 "/b rise in leg vascular conductance at the lowest work rate. The effect of neck suction on these variables was reduced with increased severity of exercise; at the highest workload it had no effect on leg vascular conductance despite a 9 mmHg fall in mean arterial pressure.

Blood pressure Neck suction caused a reduction in blood pressure at all three levels of exercise (Fig. 4). The absolute reduction was most pronounced at the lowest work rate ( I S mmHg) and was the same (9 mmHg) at the second and third levels of exercise. Mean arterial blood pressure fell to a new stable level 1 0 - 1 2 s following onset of neck suction after a small initial undershoot which corresponded in time to the nadir of heart rate (Fig. 2).

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Fig. 4. Average (with SEM) arterial blood pressure during exercise at three levels before (control, 0-0) and during neck suction (NS, 0-0) in eight subjects ("denotes only six subjects at exercise level 2 ) . P values denote significant decrease in pressure with suction at all work rates.

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exercise levels. Flow was significantly reduced at levels 2 and 3 (* n = 6, as in Fig. 4). (b) Average leg vascular conductance was significantly increased at levels I and 2 . 0-0, control; n--o, NS, - 50 mmHg.

Leg blood Jow and vascular conductance Neck suction increased leg conductance by II.4 % at the lowest work rate, but had no significant effect On leg flow (Fig. 5). At levels 2 and 3, neck suction flow but indecreased leg creased leg conductance Only at the second level (Fig. 5 ) .

Heart rate The fall in heart rate in response to neck suction diminished with increasing work rate (Fig. 6). The change in heart rate after onset of neck suction followed the characteristic pattern illustrated in Figs. I and 2 . T h e RR interval was longest after the fourth second of suction and reached a new stable level within 10-12 s. The heart rate values in Fig. 6 are mean values taken from the period 1-20 s after the onset of neck suction.

Leg blood flow, a-v oxygen difference, and calculated oxygen uptake increased in proportion to the exercise intensity (Table I ) . That portion of the two legs to which blood flow was measured (gluteal muscles were not included) consumed 74, 68 and 70% Of the pulmonary Oxygen uptake at exercise levels '-3 respectively* Neck suction caused a small decrease in leg oxygen uptake at the highest work rate (99 ml min-' or 7y0, see Table I ) .

Noradrenaline and lactate Arterial noradrenaline and lactate increased along with work intensity (Table I ) , Femoral venous values for noradrenaline were similar to arterial values (not shown). Femoral venous concentrations of lactate revealed rates of lactate release that increased from 0.2 to 0.7 mmol min-' with increasing work rate. Neck suction significantly (P < 0.025) increased lactate release from 0.7 to 1.9 mmol min-' at the highest work rate. DISCUSSION The primary question raised in this study was whether carotid sinus hypertension during nearmaximal exercise would cause a much greater fall in blood pressure than that seen at the lower exercise levels. If high rates of noradrenaline spillover from muscle at or near maximal exercise reflect an action of the arterial baroreflex to

S.Strange et al.

150 Table

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maintain blood pressure, then a release of this vasoconstriction by carotid sinus hypertension should have major effects on muscle vascular conductance. This reasoning assumes that a second powerful pressure-raising reflex, the muscle chemoreflex, and also the aortic baroreflex do not successfully oppose the release of vasoconstriction as discussed below. Activation of the carotid sinus reflex caused a significant increase in leg vascular conductance when the exercise required 40-7ooo of VO,max (levels I and 2). At the highest work rate, which required 81-9joh of VO?max (average 88',,), carotid sinus stimulation significantly decreased the arterial blood pressure, but did not change vascular conductance of the exercising leg. The increase in leg vascular conductance was 0.00j 1 min-' mmHg-' or I I .40,0 at level I (409, of 6'0, max). The cardiac output at this level should have been close to 14.5I min-' during control conditions and 13.6 1 min-' during neck suction (correcting cardiac output for the fall in heart rate by assuming that stroke volume remains constant). With a mean blood pressure of 1 1 3 mmHg during control conditions and 98 mmHg during neck suction, the increase in total vascular conductance during neck suction amounts to 0.01I 1 m i n ~ mmHg-'. Thus, almost

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all of the increase in total vascular conductance during neck suction would appear to have occurred in the two exercising legs at this level. At the second work level (69'),b of VO,max) the increase in leg vascular conductance was 0.003 1 min-' mmHg-' or 5.296. With an assumed cardiac output of 20.4 1 min-' similar calculations (as above) reveal that only about two-thirds of the increase in total vascular conductance during neck suction could have occurred in the exercising legs. At the highest work level, the rise in total vascular conductance, which lowered blood pressure by 9 mmHg, could not have occurred in the legs; their vascular conductance did not change. What haemodynamic changes are responsible for the hypotension induced by neck suction in resting subjects ? This stimulus reduces total peripheral resistance (Ernsting & Perry 1957, Bjurstedt et al. 197j), whereas direct electrical stimulation of the sinus nerve lowers both cardiac output and total peripheral resistance (Epstein et a / . 1969, Farrehi 1972). The large rise in conductance of the vascular bed supplied by the external iliac artery (Tyden et al. 1979) and the fall in directly recorded muscle sympathetic activity during carotid sinus stimulation (Rbth et ul. 1981) point to the importance of muscle in

Arterial baroreflexes during exercise the hypotensive response. During mild (45 W) exercise neck suction ( - 50 mmHg) lowered blood pressure (14-15.6yo)mainly by reducing cardiac output; at a higher work rate (135 W), more than half of the fall in pressure was attributable to the rise in total vascular conductance (906) (Bevegird & Shepherd 1966). It is not known in which vascular regions conductance rose. If skin blood flow were a significant fraction of total leg blood flow and if vasoconstrictor tone to the skin were increased, then a significant portion of the rise in leg vascular conductance could have occurred in skin. If so, the effects of neck suction in our study should be greatest at the highest work rates at which the thermal drive to raise skin blood flow and the vasoconstrictor drive that opposes it are greatest (Rowell 1983, Johnson 1986). Our findings do not support this idea. Inasmuch as most results favour the view that carotid sinus hypertension will withdraw sympathetic vasoconstrictor tone to active muscle, the question is why this effect and the fall in blood pressure was not greatest at the highest work rate when noradrenaline spillover from the active muscles is greatest (Savard et al. 1989). Three possible explanations are as follows : ( I ) Our highest level of exercise, which required on average 88% of voz max, may not have been high enough to encroach upon cardiac pumping capacity. If so, then baroreflex adjustments would not be required to maintain blood pressure. ( 2 ) Carotid sinus hypertension is more effectively buffered by the aortic baroreceptors as the intensity of exercise increases toward maximal. (3) Other pressure-raising reflexes compete with the carotid sinus reflex and prevent the expected fall in blood pressure. First, it is not clear what intensity of submaximal exercise is required to encroach upon cardiac pumping ability. It is clear that once maximal cardiac output and oxygen uptake are reached, additional vasodilation of active muscle would require vasoconstriction somewhere in order to prevent a fall in blood pressure. This vasoconstriction would be expected to occur in active muscles because they have most of the vascular conductance. If this severity of exercise was reached in our study, one would expect stimulation of the carotid sinus baroreceptors to release vasoconstriction in active muscles and to elicit a substantial fall in blood pressure.

I 5I

I t is not certain that previous experiments which were designed to overload the heart actually achieved their goal. When Secher et al. (1977) superimposed heavy arm exercise on severe leg exercise, the addition of the arms led to vasoconstriction and decreased blood flow in the exercising legs despite the fact that the combined loads required only 71-83% of VO,max (lower than predicted from either arm exercise or leg exercise levels alone). Furthermore, the restriction in leg blood flow during combined arm and leg exercise occurred at submaximal work rates and well before maximal cardiac output was attained. The cause of this vasoconstriction is unknown. There was no fall in blood pressure, thus no reason to expect that baroreflexes would elicit the vasoconstriction. A possible explanation for these results is that arm exercise by itself triggers much greater sympathetic outflow than occurs during equivalent levels of leg exercise (Bevegird et al. 1966). That is, the additional vasoconstrictor drive originates from the arms (muscle chemoreflex?) and not the arterial baroreceptors. Parenthetically, the fact that arms release much more lactate than legs at a given work rate supports the idea of a chemoreflex originating from the arms, in that this reflex appears to be triggered by H+ and lactate within the muscles (Sheriff et al. 1987, Victor et al. 1988, Sinoway et al. 1989). A second possible explanation for the smaller blood pressure response to neck suction at the high work rates could be that opposition from the aortic baroreceptors is stronger owing to their possibly greater sensitivity at higher blood pressure. The response to neck suction is always opposed by the aortic baroreflex, but if the normal operating point of the aortic baroreceptors were substantially higher than that of the carotid sinuses (as concluded by Donald & Edis [1971]) then effects of carotid sinus stimulation would become less as pressures rose at the highest levels of exercise. Angell-James & Daly (1971) found the same operating points for the carotid sinus and aortic baroreceptors over a wide range of pulsatile pressures (in contrast to Donald & Edis [1971], who used non-pulsatile pressure). If these results apply to humans we cannot explain why, based on baroreflex sensitivity, the effect of neck suction is less at the highest work rate than at the lowest. A third possible explanation for our finding is that a flow-sensitive, pressure-raising reflex from active muscle (muscle chemoreflexes) may op-

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pose the fall in blood pressure. T h e chemoreflexes have essentially the same strength as the arterial baroreflexes. When both reflexes are intact, muscle chemoreflexes can correct about two-thirds of any deficit in muscle perfusion (Sheriff et al. 1989) ; arterial baroreflexes achieve a similar degree of correction for changes in arterial pressure (Walgenbach & Donald 1983, Sheriff et al. 1989). T h e two reflexes oppose each other ; the strength of the muscle chemoreflexes increased by nearly 2.5-fold when all arterial baroreflexes were eliminated by sinoaortic denervation in dogs (Sheriff et al. 1989). O u r findings might be explained by the competition between these reflexes. Activation of the carotid sinus reflex during severe exercise ( 8 1 ~ 9 5 ?Po2 ~ max) reduced leg blood flow by 650 ml min-'. T h i s passive flow reduction of 7 % was accompanied by a fall (7 yo)in uptake of oxygen and a rise (0.7 to 1.9 mmol min-') in lactate release by the leg. T h e fall in blood flow and particularly the rise in' muscle lactate (see Victor el al. 1988, Sheriff et al. 1989, Sinoway et al. 1989) could activate the muscle chemoreflex, which is normally attenuated about 60 yo by arterial baroreflexes (Sheriff et al. 1989). Without this opposition of the baroreflex by the muscle chemoreflex arterial pressure might have fallen far more than 9 mmHg. Furthermore, the muscle chemoreflex may have prevented any reduction in the high rates of sympathetic outflow to muscle that appear to typify such high levels of exercise (Savard et al. 1989). We found that arterial and femoral venous of noradrenaline reached concentrations 2.3 ng ml-', indicating high levels of sympathetic activity at the third level of exercise. W e observed no fall in plasma noradrenaline concentration during neck suction; however, the 15-20 s between onset of suction and withdrawal of blood might not have provided enough time to observe any change. Finally, our findings of an increase in leg vascular conductance during neck suction at the lowest work rate (4076 vo2 max) supports the view that muscle blood flow during exercise is the resultant of competing metabolic vasodilation and sympathetic vasoconstriction, as originally postulated for humans by Strandell & Shepherd (1967). O u r findings also suggest that the high levels of sympathetic activity during severe exercise may not originate mainly from arterial baroreflexes.

This research was supported by grants from the Danish Heart Association and the USPHS National Heart, Lung and Blood Institute (grant no. H L 16910). S. Strange received support from the Danish Medical Research Council. L. B. Rowell received support from the Danish Research Academy.

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BEVEGKRD, B.S. & SHEPHERD, J.T. 1966. Circulatory effects of stimulating the carotid arterial stretch receptors in man at rest and during exercise. f Clin Invest 45(1), 132-142.

BJURSTEDT, H.G., ROSENHAMER, G. & T Y D ~ NG. , 1975.Cardiovascular responses to changes in carotid sinus transmural pressure in man. Acta Physiol Stand 94, 497-505. BATH, E., LINDBLAD, L.E. & WALLIN,G.B. 1981. Effects of dynamic and static neck suction on muscle nerve sympathetic activity, heart rate and blood pressure. 3 Physiol311, 551-564. BEVEG~RD, S., FREYSCHUSS, U. & STRANDELL, T. 1966. Circulatory adaptation to arm and leg exercise in supine and sitting position. 3 Appl Physiol 21, 37-46.

N.J., VESTERGAARD, P., SBRENSEN, T . & RAFAELSEN, O.J. 1980. Cerebrospinal fluid adrenaline and noradrenaline in depressed patients. Acta Psychiat Scand 6 1 , 178-182. CLAUSEN,J.P. 1976. Circulatory adjustments to dynamic exercise and effect of physical training in normal subjects and patients with coronary artery disease. Prog Cardiovasc Dis 28, 459-495. DONALD,D.E. & EDIS, A.J. 1971. Comparison of aortic and carotid baroreflexes in the dog. 3Physiol 215,521-538. D.A. DONALD,D.E., ROWLANDS, D.J. & FERGUSON, 1970. Similarity of blood flow in the normal and the sympathectomized dog hind limb during graded exercise. Circ Res 26, 185-199. EBERT,T.J. I 986. Baroreflex responsiveness is maintained during isometric exercise in humans. 3Appl

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Cardiovascular responses to carotid sinus baroreceptor stimulation during moderate to severe exercise in man.

Our objective was to assess the importance of arterial baroreflexes in maintaining vasoconstriction in active muscle during moderate to severe exercis...
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