Effects of short-term and prolonged bed rest on the vestibulosympathetic reflex

Abstract

Dyckman DJ, Sauder CL, Ray CA. Effects of short-term and prolonged bed rest on the vestibulosympathetic reflex. Am J Physiol Heart Circ Physiol 302: H368 -H374, 2012. First published October 21, 2011 doi:10.1152/ajpheart.00193.2011.-The mechanism(s) for post-bed rest (BR) orthostatic intolerance is equivocal. The vestibulosympathetic reflex contributes to postural blood pressure regulation. It was hypothesized that muscle sympathetic nerve responses to otolith stimulation would be attenuated by prolonged head-down BR. Arterial blood pressure, heart rate, muscle sympathetic nerve activity (MSNA), and peripheral vascular conductance were measured during head-down rotation (HDR; otolith organ stimulation) in the prone posture before and after short-duration (24 h; n ϭ 22) and prolonged (36 Ϯ 1 day; n ϭ 8) BR. Head-up tilt at 80°was performed to assess orthostatic tolerance. After short-duration BR, MSNA responses to HDR were preserved (⌬5 Ϯ 1 bursts/min, ⌬53 Ϯ 13% burst frequency, ⌬65 Ϯ 13% total activity; P Ͻ 0.001). After prolonged BR, MSNA responses to HDR were attenuated ϳ50%. MSNA increased by ⌬8 Ϯ 2 vs. ⌬3 Ϯ 2 bursts/min and ⌬83 Ϯ 12 vs. ⌬34 Ϯ 22% total activity during HDR before and after prolonged BR, respectively. Moreover, these results were observed in three subjects tested again after 75 Ϯ 1 days of BR. This reduction in MSNA responses to otolith organ stimulation at 5 wk occurred with reductions in head-up tilt duration. These results indicate that prolonged BR (ϳ5 wk) unlike short-term BR (24 h) attenuates the vestibulosympathetic reflex and possibly contributes to orthostatic intolerance following BR in humans. These results suggest a novel mechanism in the development of orthostatic intolerance in humans. blood pressure; autonomic nervous system; muscle sympathetic nerve activity; hypotension ORTHOSTATIC INTOLERANCE (OI) is the inability to maintain blood pressure and cerebral perfusion while in the upright position. Moreover, the failure to maintain blood pressure in the upright posture is associated with increased mortality (26). Head-down bed rest (BR) is used to simulate microgravity and physical deconditioning and to elicit OI (13). Mechanisms believed to contribute to the development of OI with BR include: impaired vagal baroreflex responses (5), an inadequate increase in sympathetic discharge (18, 42), cardiac atrophy (24), an inability to increase peripheral vascular resistance (3, 25), and hypovolemia (29). Studies indicate that alterations in sympathetic nerve activity contribute to the development of OI (13,18,25,42). Hypotensive episodes during head-up tilt appear to be closely related to lack of increased muscle sympathetic nerve activity (MSNA) (25). MSNA is attenuated during tilt following 14 days of BR in subjects that experienced OI (42). Despite considerable research on this topic, the mechanisms for OI have been an enigma. One possible mechanism for the development of OI after BR that has not been examined is an alteration of the vestibulosympathetic reflex (VSR).Data exist demon...

Sex differences in blood pressure control during 6° head-down tilt bed rest

“…We found an increase in sympathetic activity when measured by LF SBP, no main effect of bed rest on catecholamines, and no change in the response of either measurement to the drug doses with bed rest. Baseline sympathetic activity or the response to an orthostatic stimulus have been reported to decrease (11,20,57), not change (15,17,52,57), or increase with bed rest (40,52). The differences in these findings may be due to different study lengths, stimulus during the measurement, or methodology, where the particular method could be measuring muscle nerve activity, sympathetic tone, or cardiac sympathetic activity.…”

Postural Tachycardia Syndrome: A Heterogeneous and Multifactorial Disorder

“…29,30 These findings indicate the presence of physical deconditioning, which may be an important factor in the development of orthostatic symptoms, regardless of the underlying pathophysiology. 30,31 Bed rest or deconditioning also decreases the gain of the vasoconstrictor baroreceptor reflex 32,33 and the vestibulosympathetic reflex, 34 which could also predispose patients to orthostatic intolerance. However, there is evidence that bed rest or deconditioning does not primarily affect the reflex control of muscle sympathetic nerve activity.…”

Syncope in an Athlete

“…These patients exhibit greater and more persistent tachycardia when upright, reduced left ventricular mass, reduced stroke volume, and reduced peak oxygen uptake during and after exercise compared with control subjects (3,12,26). The phenomenon of deconditioning also decreases the response to the vasoconstrictor baroreceptor reflex (3,4,17) and vestibulosympathetic reflex (3,6). Our patient was a highly competitive and active division I athlete making this subtype highly unlikely.…”

“…Abnormal processing of sensory information, including somatic hypervigilance and behavioral amplification, can contribute also to persistence of symptoms, including those symptoms not triggered by orthostatic stress, such as fibromyalgia, visceral pain, and chronic dizziness. Although it is common for POTS patients to have a noticeable drop in blood pressure upon standing, some patients have no change or may even experience an increase in blood pressure upon standing (6,21). Because of the presence of multiple comorbidities not directly related to the presenting orthostases (chronic fatigue, sleep disturbances, and myofascial pain) (3), as well as the pathophysiologic heterogeneity of orthostatic intolerance, these patients are difficult to recognize and pose a particular challenge in management (3).…”