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Departments of Medicine and Cellular & Molecular Physiology, General Clinic Research Center, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Muscle sympathetic nerve
activity (MSNA) is altered by vestibular otolith stimulation. This
study examined interactive effects of the vestibular system and
baroreflexes on MSNA in humans. In study 1, MSNA was
measured during 4 min of lower body negative pressure (LBNP) at either
10 or 30 mmHg with subjects in prone posture. During the 3rd min of
LBNP, subjects lowered their head over the end of a table (head-down
rotation, HDR) to engage the otolith organs. The head was returned to
baseline upright position during the 4th min. LBNP increased MSNA above
baseline during both trials with greater increases during the 30-mmHg
trial. HDR increased MSNA further during the 3rd min of LBNP at 10
and 30 mmHg (
32% and 34%, respectively; P < 0.01). MSNA returned to pre-HDR levels during the 4th min of LBNP when
the head was returned upright. In study 2, MSNA was measured
during HDR, LBNP, and simultaneously performed HDR and LBNP. The sum of
MSNA responses during individual HDR and LBNP trials was not
significantly different from that observed during HDR and LBNP
performed together (131 ± 28 vs. 118 ± 47 units and
340 ± 77 vs. 380 ± 90 units for the 10 and 30
trials, respectively). These results demonstrate that vestibular
otolith stimulation can increase MSNA during unloading of the
cardiopulmonary and arterial baroreflexes. Also, the interaction between the vestibulosympathetic reflex and baroreflexes is
additive in humans. These studies indicate that the
vestibulosympathetic reflex may help defend against orthostatic
challenges in humans by increasing sympathetic outflow.
autonomic nervous system; baroreceptors; reflex; vestibulosympathetic reflex; otolith organs
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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IT WAS DEMONSTRATED by Doba and Reis (6) that bilateral transection of the vestibular nerves in paralyzed, anesthetized cats impaired reflex compensation for orthostatic hypotension produced by head-up tilt. This finding suggested that the vestibular system was involved in blood pressure regulation during postural changes. Subsequent animal studies showed that electrical stimulation of the vestibular nerve elicits changes in sympathetic nerve outflow (5, 10, 19, 32). A series of studies by Yates and co-workers (34, 38) has demonstrated the presence of a vestibulosympathetic reflex (VSR) in the cat. We have demonstrated in humans that head-down rotation (HDR) in the prone position elicits increases in muscle sympathetic nerve activity (MSNA) (9, 22-24, 28). Because other inputs (i.e., baroreflexes, central command, neck afferents, nonspecific receptors of the head, and visual inputs) during HDR have been systematically shown not to influence MSNA, responses observed with HDR have been attributed to the engagement of the VSR. Moreover, the otolith organs and not the semicircular canals appear to mediate this reflex in humans (24). This finding is in accordance with studies in the cat (39).
Because the VSR is triggered by changes in posture or gravitational forces acting on the vestibular apparatus, it has been postulated that this reflex is important in maintaining orthostasis. Likewise, the baroreflexes participate importantly in maintaining blood pressure with postural changes (7, 11). Therefore, the question as to how these two reflexes interact is important. The purpose of the present study was twofold: first, to determine whether vestibular otolith activation by HDR would augment MSNA during unloading of the baroreflexes, and second, to determine the nature of the interaction between the VSR and baroreflexes. It was hypothesized that activation of the VSR would further increase MSNA to help defend arterial pressure during baroreceptor unloading.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects
Twenty-one volunteers (10 men and 11 women) [age 28 ± 1 (mean ± SE) yr, height 168 ± 3 cm, weight 72 ± 2 kg] who were normotensive, nonsmokers, and not on medication were studied. After verbal explanation of the testing procedures was provided, written informed consent was obtained from all of the subjects. The experiments were approved by the Institutional Review Board at The Pennsylvania State University College of Medicine.Experimental Design
Study 1.
The purpose of study 1 (n = 12) was to
determine whether vestibular (otolith) activation increases MSNA during
unloading of the cardiopulmonary and arterial baroreflexes. Studies
were performed with the subjects in the prone position. The subjects
were positioned in a lower body negative pressure (LBNP) chamber such
that head was able to be maximally lowered without interference from
the end of the table. Each study began with the head in the baseline position for 3 min (Fig. 1). While in the
baseline position, the head was upright with the neck extended and the
chin supported. This position approximates gravitational orientation of
the head when an individual is in the upright posture
(28). After a 3-min baseline period, LBNP at 10 mmHg was
performed for 4 min. During the 3rd min of LBNP, the head was lowered
in the vertical plane maximally over the edge of the table (HDR). The
head was returned to the baseline position for the 4th min of LBNP.
After a 10-min rest period, the LBNP protocol was repeated at 30
mmHg. An investigator moved the head to all positions.
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Study 2.
The purpose of study 2 (n = 9) was to
determine the nature of the interaction between the VSR and
baroreflexes. The subjects performed three experimental trials in the
prone position as described previously. One trial examined responses to
HDR (i.e., vestibular activation of otolith organs) for 3 min. The
second trial examined responses to LBNP (i.e., baroreflex activation)
at 10 mmHg for 3 min. The third trial examined responses during
simultaneous activation of HDR and LBNP. The order of the three trials
was randomized with 20-min rest periods between trials. The three trials were then repeated with LBNP at 30 mmHg.
10 mmHg is
generally believed to have a primary effect on the cardiopulmonary baroreceptors, whereas the greater orthostatic stress elicited by 30
mmHg would engage both the cardiopulmonary and arterial baroreceptors
(13, 42). MSNA, mean arterial pressure (MAP), and heart
rate were measured during all trials. The ambient temperature of the
laboratory during these experiments ranged from 21 to 23°C.
Measurements
Multifiber recordings of MSNA were made by inserting a tungsten microelectrode into a peripheral nerve located behind or lateral to the right knee. A reference electrode was positioned subcutaneously 2-3 cm away from the recording electrode. To ensure that an adequate recording site for MSNA was obtained, we met previously described criteria (9). The nerve signal was amplified (50,000-90,000 times) and filtered with a bandwidth of 700-2,000 Hz. The filtered signal was rectified and integrated (time constant 0.1 s) to obtain a mean voltage display of the nerve activity. Sympathetic recordings that indicated possible electrode site shifts or electromyogram artifact during the experimental interventions were excluded.Continuous measurements of arterial blood pressure and heart rate were made by using a Finapres blood pressure monitoring unit (Ohmeda, Englewood, CO). The mean voltage neurogram, heart rate, and blood pressure tracing were collected (MacLab 8e; ADInstruments, Milford, MA) and routed to an on-line computer (Power Macintosh G3) for monitoring and data collection throughout the studies.
Data Analysis
MSNA was expressed as bursts per minute and total MSNA. Sympathetic bursts were identified from inspection of the mean voltage neurogram, and the sum of the area of those bursts per minute were measured by a computer program (Peaks; ADInstruments) and reported as total MSNA, expressed in arbitrary units.For study 1, an analysis of variance with repeated measures was used to determine the significance of LBNP on the dependent variables. A planned comparison was used to compare responses between the 2nd and 4th min of LBNP with those at the 3rd min of LBNP with HDR. In study 2, the change in MSNA from baseline for each trial was calculated. The sum of the change scores for HDR and LBNP performed separately was compared, with the use of a paired t-test, with the change score when HDR and LBNP were performed together. A significance level of P < 0.05 was used for all statistical tests. All values are means ± SE.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Study 1
HDR alone caused a significant increase in MSNA (6 ± 2 bursts/min and 81 ± 34 units) with no significant change in
heart rate or MAP. MSNA responses to the LBNP 10- and 30-mmHg
trials are shown in Fig. 2. There was no
difference in baseline MSNA between the 10- and 30-mmHg trials
(228 ± 50 and 236 ± 60 units, respectively). LBNP increased
MSNA during both trials but with greater increases during the 30-mmHg
trial. In both trials, HDR elicited an increase in MSNA during the 3rd
min of LBNP (125 ± 40 and 210 ± 50 units or 32%
and 34% for 10 and 30 mmHg, respectively) with a return in MSNA
to pre-HDR during the 4th min of LBNP when the head was returned to the
baseline (upright) position. Heart rate and MAP responses to the LBNP
trial are shown in Table 1. Heart rate
was not changed during the 10-mmHg trial but was significantly
increased during the 30-mmHg trial. MAP was not significantly changed
during LBNP in either trial. HDR during LBNP did not change heart rate
or MAP during either trial.
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Study 2
The change in MSNA for the three trials and the sum of the HDR and LBNP trials are shown in Fig. 3. HDR performed alone increased MSNA for each trial. Likewise, LBNP performed alone at10 and 30 mmHg increased MSNA, with significantly greater
increases during the 30-mmHg trial. Simultaneous HDR and LBNP
increased MSNA by 118 ± 47 and 380 ± 90 units for the
10- and 30-mmHg trials, respectively. These increases in MSNA were
comparable to the sum of the changes in MSNA during the HDR and LBNP
trials performed alone (131 ± 28 units and 340 ± 77 units for the 10- and 30-mmHg trials, respectively). An original
recording of MSNA from one subject during the three trials is presented
in Fig. 4.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The principal findings from these studies are that HDR during LBNP increases MSNA and that there is an additive interaction between the baroreflexes and VSR. These results indicate that the vestibular system may assist in defending against orthostatic challenges in humans by elevating MSNA.
It has been postulated from animal studies that the VSR contributes to orthostasis (34, 37). Doba and Reis (6) were the first to clearly demonstrate that the vestibular system has a role in cardiovascular responses to postural changes. They found that bilateral transection of the vestibular nerve impaired reflex compensation of arterial pressure following head-up tilt in anesthetized, paralyzed cats. The initial reduction in arterial pressure was greater with tilt, and the ensuing reflex increase in arterial pressure was blunted after transection of the vestibular nerve. Recently, these findings have been replicated in conscious, awake cats (12).
The current study tested the concept that the VSR contributes to
orthostasis in humans. LBNP was used to elicit an orthostatic challenge, and HDR was used to activate the otolith organs and the VSR
in humans. During LBNP, MSNA increased during both 10- and 30-mmHg
trials, and HDR elicited further increases in MSNA during LBNP. These
findings indicate that the VSR can increase MSNA during an orthostatic
challenge in humans. The VSR occurred despite elevated MSNA elicited by
the unloading of the baroreflexes. Thus the VSR can strongly influence
sympathetic outflow to skeletal muscle.
The absolute mean increase in MSNA tended to be greater with HDR during
LBNP performed at 30 mmHg. For this reason, and because of the lack
of data on the possible neural interaction between the baroreflexes and
the VSR in both animals and humans, we sought to determine the
interaction of these two reflexes on MSNA in study 2. The
results indicate that the interaction of the baroreflexes and the VSR
is additive. Thus these findings suggest that little or no central
integration exists between these two reflexes and that output of both
reflexes on MSNA works independently of each other in humans. This
concept is supported by the work of Yates and co-workers (29, 30,
35, 40, 41), who have shown that the VSR and baroreflex neural
circuitry is very distinct in the cat. They have reported that the
baroreceptor and vestibular reflex pathways remain separate until they
synapse on the presympathetic neurons in the rostral ventrolateral
medulla. However, electrical stimulation of the vestibular nerve has
been demonstrated to activate a few neurons in the nucleus tractus
solitarii, which is the first central synapse of the baroreflex
(36).
Although these two cardiovascular reflexes do not appear to interact centrally to modify sympathetic outflow during an orthostatic challenge, they certainly complement each other. It might be speculated that, during movement or a change in posture, the VSR acts immediately to defend against a possible hypotension episode before a drop in arterial pressure is sensed by the baroreceptors. Thus the VSR feed-forward property would aid in the stabilization of arterial pressure before the baroreflexes are engaged.
Although LBNP did not result in hypotension, the finding that both
heart rate and MSNA increased with LBNP indicates that the baroreflexes
were engaged. Moreover, the findings that heart rate was increased in
the 30- and not the 10-mmHg trial and that MSNA was significantly
greater during the 30-mmHg trial support the notion that the arterial
baroreflex, in addition to the cardiopulmonary reflex, was engaged
during this trial (13, 17, 42). Thus the experimental
interventions should have permitted us to test our question of whether
an interaction existed between the VSR and baroreflexes with regard to
MSNA. However, the conclusions from this study are limited to the
unloading of the baroreflexes because responses to baroreceptor loading
were not examined. In the cat, elevation of arterial pressure
attenuates sympathetic outflow elicited by electrical stimulation of
the vestibular nerve (14).
It is possible that the beneficial effect of the augmented MSNA elicited by HDR will only be observed during frank hypotension. It has been reported that HDR during head-up tilt increased total peripheral resistance and arterial pressure in subjects with neurogenic orthostatic hypotension (3). Our previous studies have clearly shown that increases in MSNA elicited by HDR mediate increases in vascular resistance (9, 22, 23, 28). Thus, together, these studies support the concept that the VSR elicits physiologically important increases in MSNA and total peripheral resistance when orthostasis is being seriously challenged.
The VSR may have clinical importance in a number of physiological states. Orthostatic intolerance affects an estimated 500,000 Americans (25). The mechanism for this condition, which can lead to presyncopal symptoms and syncope, is not entirely clear. It is possible that alterations in the VSR in these patients contribute to this syndrome. Additionally, increased incidence of orthostatic intolerance or postural hypotension is observed in the elderly (16, 27). Because morphological changes to the otolith organs have been observed to occur with aging (1, 2, 15, 21), it is possible that the VSR is altered in the elderly and predisposes them to orthostatic hypotension. Moreover, orthostatic intolerance has been identified as an independent predictor of mortality in elderly men (18). Similarly, astronauts frequently experience orthostatic intolerance after spaceflight (4, 31). As with aging, exposure to microgravity has been shown to elicit changes to the otolith organs and thereby may affect the VSR and contribute to postspaceflight orthostatic intolerance (8, 26, 33). Future studies are needed to specifically address these hypotheses.
What evidence supports the concept that the activation of MSNA by HDR is mediated by the VSR? Unlike options in animals, lesioning the vestibular nerve is not a viable option in healthy humans. Therefore, we have conducted a series of studies to address this crucial question (9, 22-24, 28). These studies have eliminated a number of nonlabyrinthine mechanisms that could have elicited MSNA increases with HDR. The mechanisms excluded were change in visual inputs (28), unloading of the cardiopulmonary and arterial baroreflexes (28), activation of neck muscle afferents (22), engagement of central command (22-24), and input from nonspecific receptors located in the head that are activated by increases in cerebral pressure (9). Because the subject's body is stationary during the maneuver, activation of possible extravestibular gravitational receptors is eliminated (20). Additionally, MSNA increases are graded to the degree of HDR, and MSNA fails to increase when head-down neck extension is performed in the supine posture (9). Head-down neck extension in the supine posture would stimulate the otolith organs in the opposite manner compared with HDR in the prone position. Finally, we have shown that natural stimulation of the horizontal semicircular canals in humans does not activate MSNA in humans (24), which is in agreement with findings in animal studies (39). Therefore, the cumulative evidence strongly suggests that HDR activates MSNA via the VSR.
In summary, HDR elicited further increases in MSNA during unloading of the cardiopulmonary and arterial baroreflexes. The interaction between the VSR and baroreflexes were found to be additive for MSNA. The results indicate that the VSR may help defend orthostatic challenges in humans by increasing sympathetic outflow to skeletal muscle.
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ACKNOWLEDGEMENTS |
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This project was supported by National Heart, Lung, and Blood Institute Grant HL-58503 and National Aeronautics and Space Administration Grant NAG 9-1034. Additional support came from a National Institutes of Health-sponsored General Clinical Research Center with National Center for Research Resources Grant M01 RR-10732.
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FOOTNOTES |
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Address for reprint requests and other correspondence: C. A. Ray, Penn State College of Medicine (Cardiology), Milton S. Hershey Medical Center, Div. of Cardiology H047, 500 Univ. Dr., Hershey, PA 17033-2390 (E-mail: caray{at}psu.edu).
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. Section 1734 solely to indicate this fact.
Received 6 March 2000; accepted in final form 23 June 2000.
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
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D. J. Dyckman, K. D. Monahan, and C. A. Ray Effect of baroreflex loading on the responsiveness of the vestibulosympathetic reflex in humans J Appl Physiol, September 1, 2007; 103(3): 1001 - 1006. [Abstract] [Full Text] [PDF]
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A. Kitano, J. K. Shoemaker, M. Ichinose, H. Wada, and T. Nishiyasu Comparison of cardiovascular responses between lower body negative pressure and head-up tilt J Appl Physiol, June 1, 2005; 98(6): 2081 - 2086. [Abstract] [Full Text] [PDF]
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R. L. Mori, L. A. Cotter, H. E. Arendt, C. J. Olsheski, and B. J. Yates Effects of bilateral vestibular nucleus lesions on cardiovascular regulation in conscious cats J Appl Physiol, February 1, 2005; 98(2): 526 - 533. [Abstract] [Full Text] [PDF]
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T. E. Wilson and C. A. Ray Effect of thermal stress on the vestibulosympathetic reflexes in humans J Appl Physiol, October 1, 2004; 97(4): 1367 - 1370. [Abstract] [Full Text] [PDF]
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T. E. Wilson, N. T. Kuipers, E. A. McHugh, and C. A. Ray Vestibular activation does not influence skin sympathetic nerve responses during whole body heating J Appl Physiol, August 1, 2004; 97(2): 540 - 544. [Abstract] [Full Text] [PDF]
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 B. Xue, K. Skala, T. A. Jones, and M. Hay Diminished baroreflex control of heart rate responses in otoconia-deficient C57BL/6JEi head tilt mice Am J Physiol Heart Circ Physiol, August 1, 2004; 287(2): H741 - H747. [Abstract] [Full Text] [PDF]
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D. E. Watenpaugh, G. A. Breit, T. M. Buckley, R. E. Ballard, G. Murthy, and A. R. Hargens Human cutaneous vascular responses to whole-body tilting, Gz centrifugation, and LBNP J Appl Physiol, June 1, 2004; 96(6): 2153 - 2160. [Abstract] [Full Text] [PDF]
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W. H. Cooke, J. R. Carter, and T. A. Kuusela Human cerebrovascular and autonomic rhythms during vestibular activation Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2004; 286(5): R838 - R843. [Abstract] [Full Text] [PDF]
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B. J. Yates The vestibular system and cardiovascular responses to altered gravity Am J Physiol Regulatory Integrative Comp Physiol, January 1, 2004; 286(1): R22 - R22. [Full Text] [PDF]
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T. M. Gotoh, N. Fujiki, T. Matsuda, S. Gao, and H. Morita Roles of baroreflex and vestibulosympathetic reflex in controlling arterial blood pressure during gravitational stress in conscious rats Am J Physiol Regulatory Integrative Comp Physiol, January 1, 2004; 286(1): R25 - R30. [Abstract] [Full Text]
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K. D. Monahan and C. A. Ray Vestibulosympathetic reflex during orthostatic challenge in aging humans Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2002; 283(5): R1027 - R1032. [Abstract] [Full Text] [PDF]
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J. R. Carter, C. A. Ray, and W. H. Cooke Vestibulosympathetic reflex during mental stress J Appl Physiol, October 1, 2002; 93(4): 1260 - 1264. [Abstract] [Full Text] [PDF]
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K. D. Monahan and C. A. Ray Interactive effect of hypoxia and otolith organ engagement on cardiovascular regulation in humans J Appl Physiol, August 1, 2002; 93(2): 576 - 580. [Abstract] [Full Text] [PDF]
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 N. H. Barmack, P. Errico, A. Ferraresi, H. Fushiki, V. E. Pettorossi, and V. Yakhnitsa Cerebellar Nodulectomy Impairs Spatial Memory of Vestibular and Optokinetic Stimulation in Rabbits J Neurophysiol, February 1, 2002; 87(2): 962 - 975. [Abstract] [Full Text] [PDF]
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 C. A. Ray and K. D. Monahan Aging Attenuates the Vestibulosympathetic Reflex in Humans Circulation, February 26, 2002; 105(8): 956 - 961. [Abstract] [Full Text] [PDF]
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Significantly different from 2nd and 4th minute of LBNP
(P < 0.05).
