Exp Brain Res (2006) 174: 701–711
DOI 10.1007/s00221-006-0515-6
RESEARCH ARTICLE
Leah R. Bent · Philip S. Bolton · Vaughan G. MaceWeld
Modulation of muscle sympathetic bursts by sinusoidal galvanic
vestibular stimulation in human subjects
Received: 29 November 2005 / Accepted: 19 April 2006 / Published online: 24 May 2006
© Springer-Verlag 2006
Abstract There is controversy as to whether the vestib-
ulosympathetic reXexes demonstrated in experimental
animals actually exist in human subjects. While head-
down neck Xexion and oV-vertical axis rotation can
increase muscle sympathetic nerve activity (MSNA) in
awake subjects, we recently showed that bipolar galvanic
vestibular stimulation (GVS) does not. However, it is
possible that our stimuli (2 mA, 1 s)—although capable
of causing strong postural and occulomotor responses—
were too brief. To address this issue we activated vestibular
aVerents using continuous sinusoidal (0.5–0.8 Hz, 60–100
cycles, §2 mA) bipolar binaural GVS in 11 seated sub-
jects. Sinusoidal GVS evoked robust vestibular illusions
of “rocking in a boat” or “swinging from side to side.”
Cross-correlation analysis revealed a cyclic modulation
of MSNA ranging from 31 to 86% across subjects
(mean § SE 58 § 5%), with total MSNA increasing by
156 § 19% (P = 0.001). Furthermore, we documented
de novo synthesis of sympathetic bursts that were cou-
pled to the sinusoidal input, such that two bursts—rather
than the obligatory single burst—could be generated
within a cardiac interval. This demonstrates that the
human vestibular apparatus exerts a potent facilitatory
inXuence on MSNA that potentially operates indepen-
dently of the baroreceptor system.
Keywords Vestibulosympathetic · Posture · Autonomic ·
Cardiovascular · Orthostatic hypotension
Introduction
The sympathetic nervous system, through its actions on
the heart and blood vessels, is a major operator in the
ongoing control of blood pressure. Muscle sympathetic
(vasoconstrictor) nerve activity, which occurs as bursts
of impulses time-locked to the cardiac cycle, is generated
when the arterial baroreceptors are unloaded during the
diastolic phase of the blood pressure cycle; the peak of
the burst corresponds to the onset of inhibition when the
baroreceptors are loaded during systole. It is known that
bilateral anaesthetic block of the glossopharyngeal and
vagus nerves, which interrupts aVerents from the arterial
baroreceptors, abolishes the normal cardiac rhythmicity
of muscle sympathetic neurones (Fagius et al. 1985).
Unitary recordings from individual muscle vasoconstric-
tor neurones indicate that they exhibit a tight coupling to
the cardiac cycle, but that they are also modulated by the
respiratory cycle (MaceWeld et al. 2002). While it is
known that baroreceptor, chemoreceptor, and pulmo-
nary aVerents project (via the solitary tract nucleus) to
the rostroventrolateral medulla (RVLM)—the primary
source of sympathetic motor output—there are other
inputs to the brainstem that can inXuence, and poten-
tially entrain, sympathetic neurones. One such source is
the vestibular apparatus, which is known to project to
the RVLM (Yates et al. 1991, 1993): sympathetic nerve
activity can be modiWed by electrical or natural stimula-
tion of vestibular aVerents in the cat (Yates and Miller
1994; Kerman et al. 2000), and bilateral section of these
aVerents in the cat attenuates the cardiovascular
responses to changes in posture (Doba and Reis 1974;
Jian et al. 1999).
Given the existence of anatomical substrates for ves-
tibulosympathetic reXexes, and evidence of their physio-
logical operation in experimental animals (Woodring
L. R. Bent
Department of Human Health and Nutritional Sciences,
University of Guelph, Guelph, ON, Canada N1G 2W1
P. S. Bolton
School of Biomedical Science, Faculty of Health,
University of Newcastle, Callaghan, NSW, 2287, Australia
V. G. MaceWeld (&)
Prince of Wales Medical Research Institute,
University of New South Wales, Barker St, Randwick, Sydney,
NSW, 2031, Australia
E-mail: vg.maceWeld@unsw.edu.au
Fax: +61-2-93991082