scholarly journals Attenuated sympathetic nerve responses after 24 hours of bed rest

2002 ◽  
Vol 282 (6) ◽  
pp. H2210-H2215 ◽  
Author(s):  
Mazhar H. Khan ◽  
Allen R. Kunselman ◽  
Urs A. Leuenberger ◽  
William R. Davidson ◽  
Chester A. Ray ◽  
...  

Bed rest reduces orthostatic tolerance. Despite decades of study, the cause of this phenomenon remains unclear. In this report we examined hemodynamic and sympathetic nerve responses to graded lower body negative pressure (LBNP) before and after 24 h of bed rest. LBNP allows for baroreceptor disengagement in a graded fashion. We measured heart rate (HR), cardiac output (HR × stroke volume obtained by echo Doppler), and muscle sympathetic nerve activity (MSNA) during a progressive and graded LBNP paradigm. Negative pressure was increased by 10 mmHg every 3 min until presyncope or completion of −60 mmHg. After bed rest, LBNP tolerance was reduced in 11 of 13 subjects ( P < .023), HR was greater ( P< .002), cardiac output was unchanged, and the ability to augment MSNA at high levels of LBNP was reduced (rate of rise for 30- to 60-mmHg LBNP before bed rest 0.073 bursts · min−1 · mmHg−1; after bed rest 0.035 bursts · min−1 · mmHg−1; P < 0.016). These findings suggest that 24 h of bed rest reduces sympathetic nerve responses to LBNP.

2009 ◽  
Vol 587 (20) ◽  
pp. 4987-4999 ◽  
Author(s):  
William H. Cooke ◽  
Caroline A. Rickards ◽  
Kathy L. Ryan ◽  
Tom A. Kuusela ◽  
Victor A. Convertino

2001 ◽  
Vol 280 (5) ◽  
pp. H2230-H2239 ◽  
Author(s):  
James A. Pawelczyk ◽  
Julie H. Zuckerman ◽  
C. Gunnar Blomqvist ◽  
Benjamin D. Levine

Cardiovascular deconditioning reduces orthostatic tolerance. To determine whether changes in autonomic function might produce this effect, we developed stimulus-response curves relating limb vascular resistance, muscle sympathetic nerve activity (MSNA), and pulmonary capillary wedge pressure (PCWP) with seven subjects before and after 18 days of −6° head-down bed rest. Both lower body negative pressure (LBNP; −15 and −30 mmHg) and rapid saline infusion (15 and 30 ml/kg body wt) were used to produce a wide variation in PCWP. Orthostatic tolerance was assessed with graded LBNP to presyncope. Bed rest reduced LBNP tolerance from 23.9 ± 2.1 to 21.2 ± 1.5 min, respectively (means ± SE, P= 0.02). The MSNA-PCWP relationship was unchanged after bed rest, though at any stage of the LBNP protocol PCWP was lower, and MSNA was greater. Thus bed rest deconditioning produced hypovolemia, causing a shift in operating point on the stimulus-response curve. The relationship between limb vascular resistance and MSNA was not significantly altered after bed rest. We conclude that bed rest deconditioning does not alter reflex control of MSNA, but may produce orthostatic intolerance through a combination of hypovolemia and cardiac atrophy.


2004 ◽  
Vol 286 (1) ◽  
pp. R151-R157 ◽  
Author(s):  
Atsunori Kamiya ◽  
Daisaku Michikami ◽  
Satoshi Iwase ◽  
Junichiro Hayano ◽  
Toru Kawada ◽  
...  

Space-flight and its ground-based simulation model, 6° head-down bed rest (HDBR), cause cardiovascular deconditioning in humans. Because sympathetic vasoconstriction plays a very important role in circulation, we examined whether HDBR impairs α-adrenergic vascular responsiveness to sympathetic nerve activity. We subjected eight healthy volunteers to 14 days of HDBR and before and after HDBR measured calf muscle sympathetic nerve activity (MSNA; microneurography) and calf blood flow (venous occlusion plethysmography) during sympathoexcitatory stimulation (rhythmic handgrip exercise). HDBR did not change the increase in total MSNA ( P = 0.97) or the decrease in calf vascular conductance ( P = 0.32) during exercise, but it did augment the increase in calf vascular resistance ( P = 0.0011). HDBR augmented the transduction gain from total MSNA into calf vascular resistance, assessed as the least squares linear regression slope of vascular resistance on total MSNA (0.05 ± 0.02 before HDBR, 0.20 ± 0.06 U·min-1·burst-1after HDBR, P = 0.0075), but did not change the transduction gain into calf vascular conductance ( P = 0.41). Our data indicate that α-adrenergic vascular responsiveness to sympathetic nerve activity is preserved in the supine position after HDBR in humans.


2000 ◽  
Vol 278 (2) ◽  
pp. R445-R452 ◽  
Author(s):  
Atsunori Kamiya ◽  
Satoshi Iwase ◽  
Hiroki Kitazawa ◽  
Tadaaki Mano ◽  
Olga L. Vinogradova ◽  
...  

To examine how long-lasting microgravity simulated by 6° head-down bed rest (HDBR) induces changes in the baroreflex control of muscle sympathetic nerve activity (MSNA) at rest and changes in responses of MSNA to orthostasis, six healthy male volunteers (range 26–42 yr) participated in Valsalva maneuver and head-up tilt (HUT) tests before and after 120 days of HDBR. MSNA was measured directly using a microneurographic technique. After long-term HDBR, resting supine MSNA and heart rate were augmented. The baroreflex slopes for MSNA during Valsalva maneuver (in supine position) and during 60° HUT test, determined by least-squares linear regression analysis, were significantly steeper after than before HDBR, whereas the baroreflex slopes for R-R interval were significantly flatter after HDBR. The increase in MSNA from supine to 60° HUT was not different between before and after HDBR, but mean blood pressure decreased in 60° HUT after HDBR. In conclusion, the baroreflex control of MSNA was augmented, whereas the same reflex control of R-R interval was attenuated after 120 days of HDBR.


2002 ◽  
Vol 282 (1) ◽  
pp. R38-R45 ◽  
Author(s):  
Katsuya Yamauchi ◽  
Yuka Tsutsui ◽  
Yutaka Endo ◽  
Sueko Sagawa ◽  
Fumio Yamazaki ◽  
...  

The present study was designed to test the hypothesis that sympathetic nerve activity is attenuated in a hyperbaric environment. Response of muscle sympathetic nerve activity (MSNA) to central circulatory hypovolemic stress, lower body negative pressure (LBNP), was measured in nine men at normal and at 3 atm pressures. The stress consisted of 4 min each of control and LBNP at −20 and −40 mmHg. In addition to MSNA, heart rate, stroke volume (SV), forearm blood flow (FBF), and volume of the lower leg were recorded. A reduction of baseline HR occurred with increased forearm vascular resistance at 3 atm abs. The baseline MSNA decreased during hyperbaria. MSNA increased progressively with increasing LBNP in both atmospheric pressures, and the change from the baseline (ΔMSNA) was similar in both conditions. Changes in SV, FBF, and volume of the lower legs in response to LBNP were not statistically different during exposure to 2 atm pressures. The present study suggests that hyperbaria attenuates sympathetic nerve activity; however, its responsiveness to hypovolemic stress was not affected by hyperbaric exposure.


2004 ◽  
Vol 96 (6) ◽  
pp. 2103-2108 ◽  
Author(s):  
Jian Cui ◽  
Thad E. Wilson ◽  
Craig G. Crandall

The purpose of this project was to test the hypothesis that increases in muscle sympathetic nerve activity (MSNA) during an orthostatic challenge is attenuated in heat-stressed individuals. To accomplish this objective, MSNA was measured during graded lower body negative pressure (LBNP) in nine subjects under normothermic and heat-stressed conditions. Progressive LBNP was applied at -3, -6, -9, -12, -15, -18, -21, and -40 mmHg for 2 min per stage. Whole body heating caused significant increases in sublingual temperature, skin blood flow, sweat rate, heart rate, and MSNA (all P < 0.05) but not in mean arterial blood pressure ( P > 0.05). Progressive LBNP induced significant increases in MSNA in both thermal conditions. However, during the heat stress trial, increases in MSNA at LBNP levels higher than -9 mmHg were greater compared with during the same LBNP levels in normothermia (all P < 0.05). These data suggest that the increase in MSNA to orthostatic stress is not attenuated but rather accentuated in heat-stressed humans.


1989 ◽  
Vol 66 (6) ◽  
pp. 2778-2781 ◽  
Author(s):  
R. F. Rea ◽  
B. G. Wallin

Nonhypotensive lower body negative pressure (LBNP) is reported to decrease forearm but not calf blood flow as measured by strain-gauge plethysmography. This suggests that unloading of cardiopulmonary receptors increases sympathetic outflow to arm but not to leg. To test this hypothesis we measured muscle sympathetic nerve activity (MSA) in the arm (radial nerve) and leg (peroneal nerve) simultaneously during LBNP. In eight healthy subjects, we measured heart rate, blood pressure, and radial and peroneal MSA during LBNP at 10 and 20 mmHg. There was no difference between radial and peroneal MSA at rest, and there were successive parallel increases of MSA in both nerves during LBNP at 10 and 20 mmHg. These data indicate that there are nearly identical increases of sympathetic outflow to the arm and leg during mild to moderate degrees of orthostatic stress.


2004 ◽  
Vol 287 (5) ◽  
pp. H2147-H2153 ◽  
Author(s):  
Masashi Ichinose ◽  
Mitsuru Saito ◽  
Takeshi Ogawa ◽  
Keiji Hayashi ◽  
Narihiko Kondo ◽  
...  

We tested the hypothesis that orthostatic stress would modulate the arterial baroreflex (ABR)-mediated beat-by-beat control of muscle sympathetic nerve activity (MSNA) in humans. In 12 healthy subjects, ABR control of MSNA (burst incidence, burst strength, and total activity) was evaluated by analysis of the relation between beat-by-beat spontaneous variations in diastolic blood pressure (DAP) and MSNA during supine rest (CON) and at two levels of lower body negative pressure (LBNP: −15 and −35 mmHg). At −15 mmHg LBNP, the relation between burst incidence (bursts per 100 heartbeats) and DAP showed an upward shift from that observed during CON, but the further shift seen at −35 mmHg LBNP was only marginal. The relation between burst strength and DAP was shifted upward at −15 mmHg LBNP (vs. CON) and further shifted upward at −35 mmHg LBNP. At −15 mmHg LBNP, the relation between total activity and DAP was shifted upward from that obtained during CON and further shifted upward at −35 mmHg LBNP. These results suggest that ABR control of MSNA is modulated during orthostatic stress and that the modulation is different between a mild (nonhypotensive) and a moderate (hypotensive) level of orthostatic stress.


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