Muscle sympathetic nerve activity during intense lower body negative pressure to presyncope in humans.
Activation of sympathetic efferent traffic is essential to maintaining adequate arterial pressures during reductions of central blood volume. Sympathetic baroreflex gain may be reduced, and muscle sympathetic firing characteristics altered with head-up tilt just before presyncope in humans. Volume redistributions with lower body negative pressure (LBNP) are similar to those that occur during haemorrhage, but limited data exist describing arterial pressure-muscle sympathetic nerve activity (MSNA) relationships during intense LBNP. Responses similar to those that occur in presyncopal subjects during head-up tilt may signal the beginnings of cardiovascular decompensation associated with haemorrhage. We therefore tested the hypotheses that intense LBNP disrupts MSNA firing characteristics and leads to a dissociation between arterial pressure and sympathetic traffic prior to presyncope. In 17 healthy volunteers (12 males and 5 females), we recorded ECG, finger photoplethysmographic arterial pressure and MSNA. Subjects were exposed to 5 min LBNP stages until the onset of presyncope. The LBNP level eliciting presyncope was denoted as 100% tolerance, and then data were assessed relative to this normalised maximal tolerance by expressing LBNP levels as 80, 60, 40, 20 and 0% (baseline) of maximal tolerance. Data were analysed in both time and frequency domains, and cross-spectral analyses were performed to determine the coherence, transfer function and phase angle between diastolic arterial pressure (DAP) and MSNA. DAP-MSNA coherence increased progressively and significantly up to 80% maximal tolerance. Transfer functions were unchanged, but phase angle shifted from positive to negative with application of LBNP. Sympathetic bursts fused in 10 subjects during high levels of LBNP (burst fusing may reflect modulation of central mechanisms, an artefact arising from our use of a 0.1 s time constant for integrating filtered nerve activity, or a combination of both). On average, arterial pressures and MSNA decreased significantly the final 20 s before presyncope (n = 17), but of this group, MSNA increased in seven subjects. No linear relationship was observed between the magnitude of DAP and MSNA changes before presyncope (r = 0.12). We report three primary findings: (1) progressive LBNP (and presumed progressive arterial baroreceptor unloading) increases cross-spectral coherence between arterial pressure and MSNA, but sympathetic baroreflex control is reduced before presyncope; (2) withdrawal of MSNA is not a prerequisite for presyncope despite significant decreases of arterial pressure; and (3) reductions of venous return, probably induced by intense LBNP, disrupt MSNA firing characteristics that manifest as fused integrated bursts before the onset of presyncope. Although fusing of integrated sympathetic bursts may reflect a true physiological compensation to severe reductions of venous return, duplication of this finding utilizing shorter time constants for integration of the nerve signal is required.
Cooke
William H
WH
Department of Health and Kinesiology, University of Texas at San Antonio, San Antonio, TX 78249, USA. william.cooke@utsa.edu
Rickards
Caroline A
CA
Ryan
Kathy L
KL
Kuusela
Tom A
TA
Convertino
Victor A
VA
D000328:Adult; D017704:Baroreflex; D001794:Blood Pressure; D004562:Electrocardiography; D005260:Female; D006470:Hemorrhage / Q000503:physiopathology; D006801:Humans; D008150:Lower Body Negative Pressure; D008297:Male; D009132:Muscles / Q000294:innervation* / Q000503:physiopathology; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D013575:Syncope / Q000503:physiopathology*
Circulation. 2000 Dec 5;102(23):2898-906
11104751
Am J Physiol Heart Circ Physiol. 2003 Feb;284(2):H584-97
12399256
J Auton Nerv Syst. 1982 Nov;6(3):293-302
7169499
J Physiol. 1994 Jan 15;474(2):331-8
8006818
Med Biol Eng Comput. 1985 Jul;23(4):352-8
4046655
Brain. 1985 Jun;108 ( Pt 2):423-38
4005530
Am J Physiol Heart Circ Physiol. 2005 Oct;289(4):H1758-69
15937091
Circulation. 2000 Feb 29;101(8):886-92
10694528
Auton Neurosci. 2004 Apr 30;111(2):127-34
15182742
Am J Physiol. 1974 Mar;226(3):724-30
4817426
J Physiol. 2006 Nov 1;576(Pt 3):947-58
16916904
Am J Physiol. 1951 Apr 1;165(1):158-66
14829585
J Physiol. 1978 Jan;274:621-37
625012
Eur Heart J. 1990 Dec;11 Suppl I:26-32
2092987
J Physiol. 1999 Jun 1;517 ( Pt 2):617-28
10332107
Am J Physiol Regul Integr Comp Physiol. 2003 Dec;285(6):R1504-13
12920060
J Appl Physiol (1985). 1987 Dec;63(6):2558-62
3436888
Physiol Rev. 1974 Jul;54(3):566-95
4601623
Auton Neurosci. 2002 Jan 10;95(1-2):141-5
11871780
J Physiol. 2001 Mar 15;531(Pt 3):861-9
11251065
Circulation. 1996 Mar 1;93(5):1043-65
8598068
J Neurol Sci. 1980 Sep;47(3):433-48
7420119
Auton Neurosci. 2007 Oct 30;136(1-2):43-51
17482525
Acta Physiol Scand. 1968 Sep-Oct;74(1):96-108
4235387
J Physiol. 1995 Feb 15;483 ( Pt 1):289-98
7776239
Clin Auton Res. 2002 Dec;12(6):483-6
12598954
Am J Physiol. 1987 Sep;253(3 Pt 2):H680-9
3631301
Am J Physiol Heart Circ Physiol. 2007 Mar;292(3):H1420-6
17085534
Am J Physiol. 1998 Apr;274(4):H1099-105
9575912
Am J Physiol. 1996 Oct;271(4 Pt 2):R837-47
8897972
Physiologist. 1987 Feb;30(1 Suppl):S62-3
3562628
J Clin Invest. 1992 Nov;90(5):1657-65
1430196
Am J Physiol Heart Circ Physiol. 2002 Feb;282(2):H773-83
11788429
Circulation. 1997 Oct 21;96(8):2509-13
9355886
Ann Intern Med. 1989 Sep 1;111(5):439-41
2764408
Muscle Nerve. 2007 Nov;36(5):595-614
17623856
Cardiovasc Eng. 2008 Mar;8(1):23-9
18041583
Acta Physiol Scand. 2003 Mar;177(3):359-65
12609007
J Auton Nerv Syst. 1982 Nov;6(3):287-91
7169498
J Physiol. 2009 Feb 15;587(Pt 4):713-9
19218620
Crit Care Med. 2008 Jun;36(6):1892-9
18496361
J Appl Physiol (1985). 2004 Apr;96(4):1249-61
15016789
Brain. 1986 Aug;109 ( Pt 4):695-715
3730811
Acta Physiol Scand. 1972 Feb;84(2):164-76
5015184
Am J Physiol Heart Circ Physiol. 2002 Jun;282(6):H2210-5
12003830
Circulation. 2004 Nov 2;110(18):2931-7
15505093