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1 Laboratoire des Sciences et Techniques des Activités Physiques et Sportives de l'Université Paris-Sud, 91405 Orsay cedex, France; 2 Laboratoire de Physiologie, Faculté de Médecine, 94276 Kremlin-Bicêtre, France; and 3 Department of Physiology and Biophysics, University of Washington School of Medicine, Seattle, Washington 98195
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
FOOTNOTES
REFERENCES
ABSTRACT 
Papelier, Y., P. Escourrou, F. Helloco, and L. B. Rowell.
Muscle chemoreflex alters carotid sinus baroreflex response in
humans. J. Appl. Physiol. 82(2):
577-583, 1997.
The arterial baroreflex opposes pressor responses
to muscle ischemia (muscle chemoreflex). Our experiments sought to
quantify the unknown effects of muscle chemoreflex on carotid sinus
baroreflex (CSB) sensitivity. We generated CSB stimulus-response (S-R)
curves by pulsatile application (triggered by each electrocardiogram R
wave) of positive and negative neck pressure (from 60 to 
80 mmHg
in 20-mmHg steps of 20 s each) in seven normal young men. S-R curves
were obtained at rest (upright), during the last 3 min of upright cycle
ergometer exercise (150 W), and at the first minute of postexercise
recovery with leg circulation free (control). A second study repeated
the same procedures, except that leg circulation was occluded 20 s
before the end of exercise to elicit muscle chemoreflex, and occlusion
was maintained during recovery measurements (~3- to 4-min duration).
S-R curves for CSB were shifted upward and rightward (25 mmHg) to
higher arterial blood pressure (BP) by exercise and less so (10 mmHg) in recovery (free leg flow). Postexercise occlusion (muscle
chemoreflex) raised BP and shifted S-R curves above exercise curves.
CSB gain rose from 0.26 ± 0.06 (control) to 0.44 ± 0.08 (occlusion) during positive neck pressure application and
was reduced from 0.14 ± 0.04 to zero (0.04 ± 0.03) during negative neck pressure. Heart rate responses during
postexercise muscle chemoreflex were not significantly different from
control. Results reveal a nonlinear summation of CSB and muscle
chemoreflex effects on BP. BP-raising capability of muscle chemoreflex
enhances CSB responses to hypotension but overpowers baroreflex
opposition to hypertension.
arterial pressure; reflex sensitivity; autonomic nervous system; resetting; exercise
INTRODUCTION THE CAROTID SINUS BAROREFLEX response curve appears to
be reset or shifted to a higher operating pressure in response to
dynamic exercise in intact dogs (19, 36), rabbits (7), and humans (24,
26, 32), but sensitivity of the response is unaffected (34). The term
"resetting" refers to a shift in the baroreflex stimulus-response
(S-R) curve that relates carotid sinus transmural pressure to systemic
blood pressure (BP). The S-R curve is shifted rightward to a higher
carotid sinus pressure (CSP; 7, 26, 24). Such shifts are presumably
caused by a stimulus that alters the activity of central neurons of the
baroreflex arc (16, 20, 29, 30).
Rowell and O'Leary (29) proposed that the signal that resets the
arterial baroreflex during exercise is central command. An intact
baroreflex is necessary to raise BP at the onset of exercise (5, 19,
36). Central command appears to cause the initial rise in BP and
cardiac output by rapid vagal withdrawal (7, 12, 13), whereas any
contribution of sympathetic nervous activity (SNA) is delayed at least
10-15 s (37). Conversely, in moderate to severe exercise, the rise
in SNA contributes to the rise in BP and cardiac output. This
contribution becomes dominant after vagal withdrawal [e.g., above
a heart rate (HR) of ~100 beats/min in humans].
In addition to the arterial baroreflex, a muscle chemoreflex can also
raise HR (21), cardiac output (5, 39), and SNA (20). We do not know
whether or at what exercise intensity the muscle chemoreflex becomes
tonically active in humans (27). Sheriff et al. (33) showed that during
exercise the arterial baroreflex reduced the sensitivity of the muscle
chemoreflex, but the effect of the chemoreflex on the baroreflex has
not been defined. A possible effect of the muscle chemoreflex on the
arterial baroreflex could be a marked change in baroreflex sensitivity or gain. Depending on whether baroreceptors are stimulated or inhibited, the two reflexes could have opposing or additive effects on
systemic BP and SNA. If such were the case, then the previous findings
of constant slopes (sensitivity) for the carotid sinus baroreflex at
rest and across various work rates (19, 24, 26, 36) are not consistent
with a tonically active muscle chemoreflex during mild to heavy
exercise with unrestricted muscle perfusion.
The evidence for an action of a muscle chemoreflex in humans originates
from experiments on subjects in whom the limb circulation was occluded
(with thigh cuffs) during both exercise and postexercise recovery (2).
Systemic BP is then raised by a sympathetic- mediated rise in cardiac
output and by vasoconstriction. The goal of these experiments was to
test the hypothesis that the baroreflex and chemoreflex act in
summation on the control of BP. Our aim was to establish S-R curves for
the human carotid sinus baroreflex during seated rest, exercise, and
exercise recovery with normal free flow recovery and to compare these
curves with those obtained during exercise recovery with severe muscle
ischemia. The ischemia-induced muscle chemoreflex was generated by
total circulatory occlusion of the legs.
METHODS
6 ± 5 mmHg)
remained unchanged during exercise (6 ± 13 mmHg) up to 280 ± 40 W and during postexercise recovery. In addition, from
measurements recorded with the Finapres 2300 E during exercise,
Papelier et al. (24) found S-R curves similar to those found by Potts
et al. (26), who used invasive radial artery measurements. HR was
obtained from the electrocardiogram (ECG) by a Biotach amplifier
(Gould). All variables were recorded on a Gould ES 1000 recorder.
Neck chamber.
A lead neck chamber enclosed the front two- thirds of the neck,
extending from the mandible and the ear lobes to the sternum and
clavicle (8). One part of the chamber was connected by a solenoid valve
to a vacuum that could apply either pressure or suction. Chamber
pressure was measured by a Statham P23 ID transducer mounted on the
chamber. The ECG was monitored continuously (Siemens Mingograph) and
fed into a computer from which a routine detected the R wave and
triggered the opening of the valve with a 40-ms delay; the stimulus
duration was 400 ms at rest and during recovery and 200 ms at exercise.
Chamber pressure during the opening of the valve was changed from 60 to
80 mmHg by decrements of 20 mmHg. Each decrement of this
staircase of neck pressure stimulus was applied over a 20-s duration,
and measurements were achieved during steady-state response, that is,
in the interval of 15-20 s after start of the stimulus. This delay
permitted the completion of both rapid vagal and slow sympathetic
responses.
Exercise protocol.
On the day of the experiment, the subject came to the laboratory in the
morning after a light breakfast. The experimental protocol is
illustrated in Fig. 1. Subjects exercised
on an electrically braked cycle ergometer (Siemens). A carotid sinus
S-R curve was obtained while the subject was seated at rest on the
ergometer. Thereafter, subjects exercised for a first period at 150 W
for 7 min (control). Carotid sinus S-R curves were obtained before the
onset of exercise, during the last 3 min of exercise, and 1 min after
the end of exercise (recovery). Then they rested for 1 h. The second
bout of exercise conformed to the same protocol except that two
inflatable cuffs were taped to the thighs of the subject. Twenty
seconds before the end of exercise, thigh cuffs were inflated to
280-300 mmHg in <1 s to elicit muscle ischemia. Subjects were
instructed to keep cycling rate until the end of period. The cuffs
remained inflated for the 3- to 4-min postexercise occlusion; during
that time, the measurements for the final S-R curve were performed.
Data analysis. Measurements of HR and BP were averaged over the last respiratory cycle during each 20-s step of neck pressure and then plotted against corresponding CSP. CSP was computed by subtracting the recorded peak (pulsatile) neck pressure (algebraic value) from mean BP at the finger (corrected for the hydrostatic pressure difference between the level of the finger and that of the carotid sinus). The S-R curves for BP and HR from each subject were drawn by computing the linear regression (31) by the least squares method. Statistical analysis. A t-test was performed to compare the slopes of linear regressions of all BP and HR values during recovery without or with thigh cuffs inflated. To take into account the problem of the different prevailing pressures of the seven subjects, the slopes of the curves were computed as
MAP vs. CSP (with MAP = MAP minus prevailing pressure, and also for CSP). Because of the nonlinear shape of the S-R curve for BP during recovery with leg ischemia, we compared slopes of the right part of the curves (5 points
for each subject) referring to negative neck pressures (from zero neck
pressure to 80 mmHg) and slopes of the left part of the curves
(3 points) referring to positive neck pressures (from 20 to 60 mmHg).
In addition, a one-way analysis of variance with repeated mesurements
was performed to compare the slopes of S-R curves for BP between rest
and exercise.
RESULTS
At the onset of pulsatile neck suction, mean BP and, to a smaller
extent, HR decreased. Both reached a steady state 10-15 s after
the onset of stimulus (Fig. 2).
80
mmHg. This record shows nonlinear decrease in mean arterial pressure
(MAP) (i.e., when muscle chemoreflex is elicited by leg occlusion) in
relationship with decreasing neck collar pressure. bpm, beats/min.
Figure 3 shows the relationship between MAP
and CSP during the control period
(A) and test period with leg
occlusion (B). During the control
period, the S-R curve was shifted upward and rightward by 27 mmHg
during exercise and returned back close to the resting curve and values
during recovery. There was no significant effect of the exercise bout
on the slope of the S-R curve. For the test period (Fig.
3B), resting and exercise curves
were similar to control. Muscle chemoreflex stimulation by postexercise
leg occlusion induced an upward shift of the prevailing pressure
compared with the free flow recovery. This shift is even greater than
the shift previously elicited by exercise bout. In addition, the shape of the S-R curve is broadly altered. The slope of the positive neck
pressures side (left side) of the S-R curve appears to be significantly
steeper. In contrast, with negative neck pressures, the slope of the
right side of the S-R curve was significantly reduced to become not
significantly different from zero. Moreover, the slopes of the two
entire curves are significantly different: the recovery S-R curve is
flatter with leg occlusion than during free-flow recovery.
), exercise (
), and recovery (
) without leg occlusion
(control). Blood pressure S-R curve during control period was shifted
by 25 mmHg during exercise and returned to resting curve during normal
recovery. B: S-R curves obtained from
test period (with leg occlusion at end-exercise and during recovery).
Postexercise leg occlusion raised blood pressure, shifted S-R steeper
with positive neck pressures, and resulted in slope of S-R curve close
to zero with negative neck pressures. Dashed lines, movement of
prevailing pressure point.
Table 1 shows the changes in prevailing BP and HR, and the values of slopes (± SD) of linear regressions for mean BP and HR, during recovery without and with thigh cuffs inflated. Figure 4 represents these significant changes in the curve for MAP.
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Figure 5 shows the relationship between HR
and CSP during control period (A)
and test period with leg occlusion
(B). During exercise, changing CSP
had little effect on the slope of the response curve, which was not
significantly different from the resting curve. During recovery of
control period, the baroreflex response curve returned back to the
values observed at rest. For the test period, muscle chemoreflex
stimulation by leg occlusion does not induce a significant upward shift
of recovery curve compared with control recovery (91 ± 18 vs. 84 ± 16.7 beats/min), and the slope remained unchanged (0.18 ± 0.025 vs. 0.16 ± 0.021 beats · min
1 · mmHg1).
), exercise (), and recovery ()
without leg occlusion (control). B:
curves obtained from test period (with leg occlusion). HR responses to
carotid sinus stimulation were not significantly different between
recovery without or with leg occlusion. Dashed lines, movement of prevailing heart rate point.
DISCUSSION
The primary finding from this study is that the activation of the muscle chemoreflex, by producing severe muscle ischemia, markedly changed the shape of the carotid sinus S-R curve. Figure 3 reveals a nonlinear summation of the effects of arterial baroreflex and muscle chemoreflex on arterial pressure and thus presumably on SNA as well. When carotid sinus transmural pressure was lowered below the prevailing BP (that is below its presumed operating point), each rise in systemic BP with each increment in positive neck pressure was progressively more pronounced. The slope (or sensitivity) of the function curve was significantly increased (Table 1). This upward shift of the function curve could be attributed to the additive effects of the vasoconstriction caused by reduced carotid sinus transmural pressure (i.e., similar to carotid sinus hypotension) and to the vasoconstriction caused by muscle ischemia. When carotid sinus transmural pressure was raised above prevailing BP by application of negative pressure to the neck, the reduction in systemic BP previously seen during both rest and exercise was virtually abolished. The slope of the function curve over a range of CSP above the operating point for the reflex was not significantly different from zero. This upward shift of the function curve could be attributed to two opposing effects on SNA. The reductions in SNA and in systemic BP normally induced by carotid sinus hypertension were overcome here by the augmentation in SNA caused by muscle ischemia (i.e., the muscle chemoreflex).
Potential limitations of the study. It was not possible to superpose the two reflexes during exercise because the 3-4 min of total occlusion needed to complete the S-R curve would cause severe discomfort. Alternatively, partial occlusion to reduce rather than arrest blood flow would cause severe venous congestion and probable damage to venous valves. Investigating the muscle chemoreflex during recovery allows one to isolate it from any effects of muscle mechanoreflex or central command, although the interaction of the two reflexes during exercise cannot be evaluated. However, as much as the chemoreflex per se markedly altered the baroreflex slope, whereas neither exercise nor recovery per se did so, interaction of these two reflexes during exercise would probably reveal the same effects on baroreflex slope (i.e., sensitivity). Pain. The issue of pain as a possible contribution to pressor responses to ischemia has been dealt with repeatedly (1, 11, 28). Alam and Smirk (1) showed that pain was not involved in the BP reflex ischemic response in man. Furthermore, Freund et al. (11) showed that BP response remained similar after withdrawal of painful sensations by gradual sensory nerve blockade in humans. In the present study, we eliminated or greatly minimized discomfort by proper packing and securing of cuff placement, as described previously (28). Competition between aortic and carotid sinus baroreceptors is always a concern as discussed previously (24, 34). If the superimposability of the S-R curves for these two baroreflexes [found in dogs by Angell-James and de Burgh Daly (4)] applies to humans, then the aortic reflex should reduce carotid sinus reflex sensitivity to the same degree across conditions. Thus comparisons would be valid. Transmission of neck chamber pressure was reviewed by Eckberg and Sleight (9). Some have found complete transmission in both dogs and humans, whereas one group observed transmission of positive and negative pressure to be reduced by 14 and 36%, respectively, at the sinus (18). Whichever findings apply, comparisons of curves are valid because transmission defects should be the same across conditions (24). Hemodynamic effect of the occlusion. Mechanical effects of occlusion on BP observed at rest are commonly <10 mmHg (6, 28, 38). Bonde-Petersen et al. (6) showed an increase of 6 mmHg MAP at rest, after 1-min leg occlusion, and 9 mmHg after 3 min. Williamson et al. (38), using a similar design, found an increase of ~3 mmHg MAP (from ~83 to 86 mmHg) with only thigh cuff inflation and no significant alteration of total peripheral resistance. Therefore, in the present study, the rise in BP cannot be explained by the reduction in vascular conductance due to the occlusion of the circulation of the both legs. Again, Wyss et al. (39) showed in dogs that the rise in BP is attributable to a rise in cardiac output and to a fall in vascular conductance resulting mostly from active vasoconstriction and only partly from passive mechanical effect of leg circulation occlusion. Conversely, during exercise and recovery, purely mechanical effects per se would be large (without a baroreflex) and could easily reach 250-300 mmHg, depending on leg blood flow (6, 27). However BP is maintained during postexercise occlusion at a particular level by combined responses of chemoreflex and baroreflex (i.e., by variable combination of elevated cardiac output and/or vasoconstriction outflow) (27). The purely mechanical effect of occlusion during recovery subsequent to mild exercise with sensory blockade (no chemoreflex) was very small relative to the unblocked reflex pressor response [see Figs. 1, 2, 3, 4 in Freund et al. (11)]. Perhaps the most serious limitation would be applications of neck pressure during a non-steady-state response to the muscle chemoreflex. The protocol for producing the chemoreflex was the same as used in several previous studies (6, 10, 11, 28) during which BP also remained virtually constant during 3 min of postexercise occlusion. Interaction between baroreflex and chemoreflex on BP. The effects of muscle chemoreflex activation on the carotid S-R curve have not been described previously. The only direct evidence concerning the interaction between these two reflexes was obtained from dogs in which sinoaortic denervation eliminated baroreflex opposition to the rise in systemic BP generated by the chemoreflex (33). The slope or sensitivity of the muscle chemoreflex increased by a factor of 2.25 after denervation of the arterial baroreceptors. Thus the baroreflex could reduce the pressor response to muscle ischemia by 60%. However, these results provided no evidence concerning how the muscle chemoreflex might affect the strength of the baroreflex. The sensitivity of the carotid sinus reflex during exercise, as found previously (19, 24, 26, 36), was not significantly different from the sensitivity at rest. The same was true during recovery without occlusion. Because occlusion during exercise raised BP by increasing SNA and altering cardiac output and vasoconstriction outflow (39), it would be expected to have the same effects on the carotid sinus S-R curve during exercise as it does during postexercise occlusion. That is, in both conditions, the reductions in SNA and in systemic BP caused by carotid sinus hypertension (neck suction) would be opposed by the augmentation of SNA and BP caused by muscle ischemia. If this is so, then the constancy of baroreflex slope from rest to heavy exercise [up to 70-75% of maximal O2 uptake (24)] suggests that the sympathetic responses to carotid sinus hypertension and hypotension are not being opposed by an active muscle chemoreflex. It is particularly unlikely that the muscle chemoreflex would exert such an effect during mild to moderate exercise, because the gain of the muscle chemoreflex [effect of a change in femoral BP on systemic BP corrected for the mechanical effects of occlusion (39)] is two times greater than the gain of the carotid sinus reflex (the effect of a change in CSP on systemic BP) when the latter is nonoperative (33). Thus, the muscle chemoreflex could readily reduce baroreflex gain to zero when their effects on BP are opposed. Similarly, it could double carotid sinus effects of BP when both reflexes function to raise BP. We saw carotid sinus gain rise from 0.26 to 0.44 during occlusion. The implication is that the muscle chemoreflex is not tonically active. If this is correct, then we might expect small reductions in muscle perfusion during heavy exercise to alter baroreflex sensitivity. Chemoreflex and baroreflex effects on HR. HR was less affected than systemic BP by the manipulation of CSP during exercise. During recovery from exercise with or without ischemia, the slopes of the function curves were the same. The apparent lack of a significant effect of the muscle chemoreflex on HR is a consistent finding (20, 21) that is attributed to a differential effect of the muscle chemoreflex on sympathetic activation of the heart vs. the blood vessels. However, with parasympathetic blockade (atropine), both systemic BP and HR remained elevated during postexercise ischemia in dogs, whereas
-blockade reduced this tachycardia (21). Thus, during
postexercise ischemia, the muscle chemoreflex-induced rise in SNA to
the heart is maintained. But the sudden restoration of vagal activity
at the cessation of exercise obscures the effects of the sustained
cardiac sympathetic activation (21). Sympathetic activation of sinus
node activity is normally overpowered by the dominance of vagal control
(17). This lack of effect of muscle chemoreflex stimulation on the
slope of S-R curve for HR is consistent with the fact that, at the end of exercise, central command acting on cardiovascular system rapidly decreases because of the suspension of somatomotor activation.
Importance of muscle chemoreflex in exercise.
Any suggestion that the muscle chemoreflex does not alter the
baroreflex sensitivity during exercise (i.e., under free-flow conditions) warrants caution, even if the slope of the S-R curve remains constant across multiple work rates. The muscle chemoreflex is
a flow-sensitive pressure-raising reflex that can also partially restore blood flow to muscle when its flow is reduced below a critical
threshold at which oxygen transport to muscle becomes inadequate (22,
39). The reflex does not appear to be tonically active under free-flow
conditions. This partial restoration of muscle blood flow requires an
increase in cardiac output (6, 39). Otherwise, if exercise is severe
and the ability to raise cardiac output is limited, the muscle
chemoreflex simply overpowers the baroreflex and drives up BP by
vasoconstricting active muscle mass, which in these conditions
represents ~80% or more of total vascular conductance. Because
cardiac output cannot increase and because vasoconstriction to other
major vascular beds is close to maximum, the muscle chemoreflex cannot
raise total blood flow in this setting. Possibly the recently
discovered differences in 
-adrenoreceptor sensitivity to
norepinephrine and metabolites of oxidative and glycolytic muscle
fibers (3, 23, 35) optimize the intramuscular distribution of blood
flow when the chemoreflex is activated. On the other hand, whenever the
total mass of active muscle and the rise in total vascular conductance
overwhelm cardiac pumping capacity, any decline in BP could be more
easily reversed by the additive actions of the muscle chemoreflex and
the arterial baroreflex.
In conclusion, our results show that muscle chemoreflex reduced the
sensitivity of the carotid sinus S-R curve to zero with carotid sinus
hypertension and raised this sensitivity with carotid sinus
hypotension. These results do not allow us to draw a conclusion on the
effect of muscle chemoreflex on carotid sinus baroreflex during
exercise, but they put forward a hypothesis that can be easily tested
in nonhuman species.
ACKNOWLEDGEMENTS
This research was supported by Université Paris-Sud (Contrat interdisciplinaire no. 89-09) and Institut de Recherches Internationales Servier. L. B. Rowell was supported by National Heart, Lung, and Blood Institute Grant HL-16910.
FOOTNOTES
Address for reprint requests: Y. Papelier, S.T.A.P.S. de l'Université Paris-Sud, bât. 335, Centre Scientifique, 91405 Orsay cedex, France.
Received 17 July 1995; accepted in final form 21 October 1996.
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