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The current U.S. extravehicular activity (EVA) suit is pressurized at 0.29 atm, which creates a risk of decompression sickness (DCS). If higher mobility is acquired, higher inner pressure is allowed. We previously demonstrated a wider range of motion (ROM) with lower muscle force using an elastic glove pressurized at 0.65 atm compared with a nonelastic glove pressurized at 0.29 atm, which simulated the current U.S. EVA suit. Pressurization at 0.65 atm is the lowest pressure that avoids DCS without prebreathing. For larger joints, other restraint parts are needed to depress ballooning of the elastic material during pressurization. In the present study, we developed hard restraint parts for the knee joint covering the elastic garment for the lower limb, and compared the ROM and flexion force between a dual and single axis during pressurization at 0.65 atm. The joint motion and force required during flexing action were recorded. During flexion, the ROM was significantly larger and the peak force was significantly lower with the dual-than single-axis part. Thus, a dual axis of hard restraint part has higher mobility than a single axis during pressurization without a risk of DCS.

Frequency-domain analyses of simultaneously recorded skin and muscle sympathetic nerve activities may yield unique information on otherwise obscure central processes governing human neural outflows. We used wavelet transform and wavelet phase coherence methods to analyse integrated skin and muscle sympathetic nerve activities and haemodynamic fluctuations, recorded from nine healthy supine young men. We tested two null hypotheses: (1) that human skin and muscle sympathetic nerve activities oscillate congruently; and (2) that whole-body heating affects these neural outflows and their haemodynamic consequences in similar ways. Measurements included peroneal nerve skin and tibial nerve muscle sympathetic activities; the electrocardiogram; finger photoplethysmographic arterial pressure; respiration (controlled at 0.25 Hz, and registered with a nasal thermistor); and skin temperature, sweating, and laser-Doppler skin blood flow. We made recordings at ∼27°C, for ∼20 min, and then during room temperature increases to ∼38°C, over 35 min. We analysed data with a wavelet transform, using the Morlet mother wavelet and wavelet phase coherence, to determine the frequencies and coherences of oscillations over time. At 27°C, skin and muscle nerve activities oscillated coherently, at ever-changing frequencies between 0.01 and the cardiac frequency (∼1 Hz). Heating significantly augmented oscillations of skin sympathetic nerve activity and skin blood flow, arterial pressure, and R-R intervals, over a wide range of low frequencies, and modestly reduced coordination between skin and muscle sympathetic oscillations. These results suggest that human skin and muscle sympathetic motoneurones are similarly entrained by external influences, including those of arterial baroreceptors, respiration, and other less well-defined brainstem oscillators. Our study provides strong support for the existence of multiple, time-varying central sympathetic neural oscillators in human subjects.

The present study examines the prevalence of subjective fatigue in young healthy males during 14 days of 6° head-down bed rest (HDBR) by using a multidimensional questionnaire. Forty-one subjects completed the Subjective Fatigue Scale questionnaire to assess the fatigue-related complaints and symptoms. The questionnaire is composed of three sections, with 10 items each. The sections measured drowsiness and dullness (Section 1), difficulty in concentration (Section 2), and the projection of physical disintegration (Section 3). The subjects answered simple questions between 1400 and 1700 on 6 measurement days before and during the HDBR period. The prevalence rate of low back pain was markedly high (80.5%) on the second day and more than 50% in the first half of the HDBR period, and any complaints related to either a lack of sleep or a deterioration in the quality of sleep continued until the end of the HDBR period. Our findings may be useful in developing preventive strategies against physical and mental fatigue associated with prolonged HDBR, horizontal bed rest, and microgravity environments.

Key points We studied healthy supine astronauts on Earth with electrocardiogram, non-invasive arterial pressure, respiratory carbon dioxide concentrations, breathing depth and sympathetic nerve recordings. The null hypotheses were that heart beat interval fluctuations at usual breathing frequencies are baroreflex mediated, that they persist during apnoea, and that autonomic responses to apnoea result from changes of chemoreceptor, baroreceptor or lung stretch receptor inputs. R-R interval fluctuations at usual breathing frequencies are unlikely to be baroreflex mediated, and disappear during apnoea. The subjects’ responses to apnoea could not be attributed to changes of central chemoreceptor activity (hypocapnia prevailed); altered arterial baroreceptor input (vagal baroreflex gain declined and muscle sympathetic nerve burst areas, frequencies and probabilities increased, even as arterial pressure climbed to new levels); or altered pulmonary stretch receptor activity (major breathing frequency and tidal volume changes did not alter vagal tone or sympathetic activity). Apnoea responses of healthy subjects may result from changes of central respiratory motoneurone activity. Abstract We studied eight healthy, supine astronauts on Earth, who followed a simple protocol: they breathed at fixed or random frequencies, hyperventilated and then stopped breathing, as a means to modulate and expose to view important, but obscure central neurophysiological mechanisms. Our recordings included the electrocardiogram, finger photoplethysmographic arterial pressure, tidal volume, respiratory carbon dioxide concentrations and peroneal nerve muscle sympathetic activity. Arterial pressure, vagal tone and muscle sympathetic outflow were comparable during spontaneous and controlled-frequency breathing. Compared with spontaneous, 0.1 and 0.05 Hz breathing, however, breathing at usual frequencies (∼0.25 Hz) lowered arterial baroreflex gain, and provoked smaller arterial pressure and R-R interval fluctuations, which were separated by intervals that were likely to be too short and variable to be attributed to baroreflex physiology. R-R interval fluctuations at usual breathing frequencies disappear during apnoea, and thus cannot provide evidence for the existence of a central respiratory oscillation. Apnoea sets in motion a continuous and ever changing reorganization of the relations among stimulatory and inhibitory inputs and autonomic outputs, which, in our study, could not be attributed to altered chemoreceptor, baroreceptor, or pulmonary stretch receptor activity. We suggest that responses of healthy subjects to apnoea are driven importantly, and possibly prepotently, by changes of central respiratory motoneurone activity. The companion article extends these observations and asks the question, Might terrestrial responses to our 20 min breathing protocol find expression as long-term neuroplasticity in serial measurements made over 20 days during and following space travel?

Although orthostatic hypotension is a common clinical syndrome after spaceflight and its ground-based simulation model, 6 degrees head-down bed rest (HDBR), the pathophysiology remains unclear. The authors' hypothesis that a decrease in sympathetic nerve activity is the major pathophysiology underlying orthostatic hypotension after HDBR was tested in a study involving 14-day HDBR in 22 healthy subjects who showed no orthostatic hypotension during 15-min 60 degrees head-up tilt test (HUT) at baseline. After HDBR, 10 of 22 subjects demonstrated orthostatic hypotension during 60 degrees HUT. In subjects with orthostatic hypotension, total activity of muscle sympathetic nerve activity (MSNA) increased less during the first minute of 60 degrees HUT after HDBR (314% of resting supine activity) than before HDBR (523% of resting supine activity, P < 0.05) despite HDBR-induced reduction in plasma volume (13% of plasma volume before HDBR). The postural increase in total MSNA continued during several more minutes of 60 degrees HUT while arterial pressure was maintained. Thereafter, however, total MSNA was paradoxically suppressed by 104% of the resting supine level at the last minute of HUT (P < 0.05 vs. earlier 60 degrees HUT periods). The suppression of total MSNA was accompanied by a 22 +/- 4-mmHg decrease in mean blood pressure (systolic blood pressure

Astronauts returning to Earth have reduced orthostatic tolerance and exercise capacity. Alterations in autonomic nervous system and neuromuscular function after spaceflight might contribute to this problem. In this study, we tested the hypothesis that exposure to microgravity impairs autonomic neural control of sympathetic outflow in response to peripheral afferent stimulation produced by handgrip and a cold pressor test in humans. We studied five astronauts approximately 72 and 23 days before, and on landing day after the 16 day Neurolab (STS-90) space shuttle mission, and four of the astronauts during flight (day 12 or 13). Heart rate, arterial pressure and peroneal muscle sympathetic nerve activity (MSNA) were recorded before and during static handgrip sustained to fatigue at 40 % of maximum voluntary contraction, followed by 2 min of circulatory arrest pre-, in- and post-flight. The cold pressor test was applied only before (five astronauts) and during flight (day 12 or 13, four astronauts). Mean (+/- S.E.M.) baseline heart rates and arterial pressures were similar among pre-, in- and post-flight measurements. At the same relative fatiguing force, the peak systolic pressure and mean arterial pressure during static handgrip were not different before, during and after spaceflight. The peak diastolic pressure tended to be higher post- than pre-flight (112 +/- 6 vs. 99 +/- 5 mmHg, P = 0.088). Contraction-induced rises in heart rate were similar pre-, in- and post-flight. MSNA was higher post-flight in all subjects before static handgrip (26 +/- 4 post- vs. 15 +/- 4 bursts min(-1) pre-flight, P = 0.017). Contraction-evoked peak MSNA responses were not different before, during, and after spaceflight (41 +/- 4, 38 +/- 5 and 46 +/- 6 bursts min(-1), all P > 0.05). MSNA during post-handgrip circulatory arrest was higher post- than pre- or in-flight (41 +/- 1 vs. 33 +/- 3 and 30 +/- 5 bursts min(-1), P = 0.038 and 0.036). Similarly, responses of MSNA and blood pressure to the cold pressor test were well maintained in-flight. We conclude that modulation of muscle sympathetic neural outflow by muscle metaboreceptors and skin nociceptors is preserved during short duration spaceflight.

Orthostatic intolerance is common when astronauts return to Earth: after brief spaceflight, up to two-thirds are unable to remain standing for 10 min. Previous research suggests that susceptible individuals are unable to increase their systemic vascular resistance and plasma noradrenaline concentrations above pre-flight upright levels. In this study, we tested the hypothesis that adaptation to the microgravity of space impairs sympathetic neural responses to upright posture on Earth. We studied six astronauts approximately 72 and 23 days before and on landing day after the 16 day Neurolab space shuttle mission. We measured heart rate, arterial pressure and cardiac output, and calculated stroke volume and total peripheral resistance, during supine rest and 10 min of 60 deg upright tilt. Muscle sympathetic nerve activity was recorded in five subjects, as a direct measure of sympathetic nervous system responses. As in previous studies, mean (+/- S.E.M.) stroke volume was lower (46 +/- 5 vs. 76 +/- 3 ml, P = 0.017) and heart rate was higher (93 +/- 1 vs. 74 +/- 4 beats min(-1), P = 0.002) during tilt after spaceflight than before spaceflight. Total peripheral resistance during tilt post flight was higher in some, but not all astronauts (1674 +/- 256 vs. 1372 +/- 62 dynes s cm(-5), P = 0.32). No crew member exhibited orthostatic hypotension or presyncopal symptoms during the 10 min of postflight tilting. Muscle sympathetic nerve activity was higher post flight in all subjects, in supine (27 +/- 4 vs. 17 +/- 2 bursts min(-1), P = 0.04) and tilted (46 +/- 4 vs. 38 +/- 3 bursts min(-1), P = 0.01) positions. A strong (r(2) = 0.91-1.00) linear correlation between left ventricular stroke volume and muscle sympathetic nerve activity suggested that sympathetic responses were appropriate for the haemodynamic challenge of upright tilt and were unaffected by spaceflight. We conclude that after 16 days of spaceflight, muscle sympathetic nerve responses to upright tilt are normal.

The present study was performed to test the hypothesis that calf venous capacitance would be reduced by mild gravitational stress through a vasomotor reflex in humans, and this response could be diminished with advancing age. Nine young (31 +/- 1 years, mean +/- SE) and 9 elderly (69 +/- 1 years) healthy males were exposed to a lower body negative pressure (LBNP) of 15 mmHg. Venous occlusion plethysmography was used to measure calf venous capacitance and calf blood flow. Muscle sympathetic nerve activity (MSNA) was recorded microneurographically from the tibial nerve along with cardiovascular variables. It was found that baseline MSNA was higher [21 +/- 4 (mean +/- SE) vs. 37 +/- 5 bursts x min(-1), young vs. elderly; p < 0.05] and calf venous capacitance was lower (1.71 +/- 0.12 vs. 1.44 +/- 0.10, ml x 100 ml(-1), young vs. elderly; p < 0.05) in the elderly group. At 15 mmHg-LBNP, heart rate and mean arterial pressure both remained unchanged, MSNA was enhanced, and calf blood flow was reduced in all subjects. Calf venous capacitance during LBNP decreased in the young, but did not change in the elderly. A significant negative correlation between percent changes in MSNA and percent changes in calf venous capacitance existed in the young group (y = 20.171x-11.863, r = 20.682; p = 0.0432), but disappeared in the elderly group. The ratio of percent changes in calf venous capacitance to percent changes in MSNA was markedly lower in the elderly (p < 0.01). In conclusion, these results substantiate our hypothesis that calf venous capacitance is reduced by mild LBNP through the vasomotor reflex, and this response is diminished in the elderly.

To test the hypothesis that leg vein filling and emptying functions could be impaired with advancing age, which would produce less blood volume redistribution toward the lower body and smaller sympathetic reflex response during mild gravitational stress, 9 young and 10 elderly healthy males were exposed to a lower body negative pressure (LBNP) of 15 mmHg. Venous occlusion plethysmography was used to determine the functions of the leg veins. We found that the baseline venous distensibility index (VDI) was lower (0.057 +/- 0.004 vs. 0.048 +/- 0.003 ml x 100 ml(-1) x mmHg(-1), young vs. elderly; p < 0.05), and half-emptying time (T(1/2)) was shorter (1.6 +/- 0.1 vs. 1.3 +/- 0.1 s, young vs. elderly; p < 0.05) in the elderly. At 15 mmHg-LBNP, VDI was decreased and T(1/2) was shortened significantly in the young group, but only slightly in the elderly group. Neither blood pressure nor heart rate changed significantly in either group. The reduction in peripheral venous pressure, which was recorded from the left antecubital vein at the cubital fossa, was less in the elderly, indicating a smaller decrease in central blood volume during LBNP; however, the enhancement of muscle sympathetic nerve activity was nearly the same as that in the young. We conclude that leg vein filling and emptying functions are impaired in elderly people, producing less blood pooling in the legs and smaller reduction in peripheral venous pressure during LBNP; the maintained sympathetic reflex response might be attributable to the well-preserved baroreflex function control of sympathetic outflow to the muscle in the elderly.

Syncope is defined as a transient loss of consciousness and postural tone, characterized by rapid onset, short duration, and spontaneous recovery, and the process of syncope progression is here described with two types of sympathetic change. Simultaneous recordings of microneurographically-recorded muscle sympathetic nerve activity (MSNA) and continuous and noninvasive blood pressure measurement has disclosed what is going on during the course of syncope progression. For vasovagal or neurally mediated syncope, three stages are identified in the course of syncope onset, oscillation, imbalance, and catastrophe phases. Vasovagal syncope is characterized by sympathoexcitation, followed by vagal overcoming via the Bezold-Jarisch reflex. Orthostatic syncope is caused by response failure or a lack of sympathetic nerve activity to the orthostatic challenge, followed by fluid shift and subsequent low cerebral perfusion. Four causes are considered for the compensatory failure that triggers orthostatic syncope: hypovolemia, increased pooling in the lower body, failure to activate sympathetic activity, and failure of vasoconstriction against sympathetic vasoconstrictive stimulation. Many pathophysiological conditions have been described from the perspectives of (1) exaggerated sympathoexcitation and (2) failure to activate the sympathetic nerve. We conclude that the sympathetic nervous system can control cardiovascular function, and its failure results in syncope; however, responses of the system obtained by microneurographically-recorded MSNA would determine the pathophysiology of the onset and progression of syncope, explaining the treatment effect that could be achieved by the analysis of this mechanism.

Muscle sympathetic nerve activity (MSNA) can be directly recorded from human peripheral nerves in situ using microneurography. MSNA plays an essential role to control systemic blood pressure against gravitational stress. MSNA was enhanced by changing posture against terrestrial gravity from lying to sitting, and from sitting to standing. This activity was enhanced by head-up tilt depending on the gravitational input from the head to the leg (+Gz) in the human body. Orthostatic hypotension occurred when MSNA response to gravitational stress was impaired both in high and low responders of this sympathetic outflow. Syncope was preceded and/or associated by a withdrawal of MSNA. MSNA was suppressed by short-term exposure to microgravity but was enhanced after long-term exposure to microgravity. Orthostatic intolerance after exposure to prolonged microgravity was associated with a reduction of increased MSNA response to gravitational stress. Aging influenced gravity-related responses of MSNA.

We studied three Russian cosmonauts to better understand how long-term exposure to microgravity affects autonomic cardiovascular control. We recorded the electrocardiogram, finger photoplethysmographic pressure, and respiratory flow before, during, and after two 9-mo missions to the Russian space station Mir. Measurements were made during four modes of breathing: 1) uncontrolled spontaneous breathing; 2) stepwise breathing at six different frequencies; 3) fixed-frequency breathing; and 4) random-frequency breathing. R wave-to-R wave (R-R) interval standard deviations decreased in all and respiratory frequency R-R interval spectral power decreased in two cosmonauts in space. Two weeks after the cosmonauts returned to Earth, R-R interval spectral power was decreased, and systolic pressure spectral power was increased in all. The transfer function between systolic pressures and R-R intervals was reduced in-flight, was reduced further the day after landing, and had not returned to preflight levels by 14 days after landing. Our results suggest that long-duration spaceflight reduces vagal-cardiac nerve traffic and decreases vagal baroreflex gain and that these changes may persist as long as 2 wk after return to Earth.

Astronauts usually work under much mental stress. However, it is unclear how and whether or not an exposure to microgravity affects physiological response to mental stress in humans. To examine effects of microgravity on vasomotor sympathetic and peripheral vasodilator responses to mental stress, we performed 10 min of mental arithmetic (MA) before and after 14 days of 6° head-down bed rest (HDBR), a ground-based simulation of spaceflight. Total muscle sympathetic nerve activity (MSNA, measured by microneurography) slightly increased during MA before HDBR, and this increase was augmented after HDBR. Calf blood flow (measured by venous occlusion plethysmography) increased and calf vascular resistance (calculated by dividing mean blood pressure by calf blood flow) decreased during MA before HDBR, but these responses were abolished after HDBR. Increases in heart rate and mean blood pressure during MA were not different between before and after HDBR. These findings suggest that HDBR augmented vasomotor sympathoexcitation but attenuated vasodilatation in the calf muscle in response to mental stress.

The purpose of this study was to evaluate the ability of touch to discriminate fine-surface textures and to suggest possible mechanisms of the discriminations. Two experiments were performed. In experiment 1, aluminum-oxide abrasive papers were adopted as stimuli, and psychometric functions and difference thresholds were determined in fine-surface-texture discrimination tasks. The grit values of abrasive papers were 400, 600, 1200, 2000, 3000, 4000, and 8000; corresponding average particle sizes were 40, 30, 12, 9, 5, 3, and 1 micron, respectively. Ten subjects participated in experiment 1. The difference thresholds obtained in experiment 1 were between 2.4 and 3.3 microns. In experiment 2, the tasks were discriminations of ridge height. The cross sections of the etched ridges were rectangular and the ridge heights were 6.3, 7.0, 8.6, 10.8, 12.3, 18.5, and 25.0 microns. Six subjects participated in experiment 2. The difference thresholds in experiment 2 were between 0.95 and 2.0 microns. It was reasoned, based on the Weber fraction values calculated from the difference thresholds and on the limit of neural information-processing ability of humans, that the subjects discriminate fine roughness only from the amplitude information presented in surface unevenness.

We previously showed that caloric vestibular stimulation elicits increases in sympathetic outflow to muscle (MSNA) in humans. The present study was conducted to determine the effect of this stimulation on sympathetic outflow to skin (SSNA). The SSNA in the tibial and peroneal nerves and nystagmus was recorded in nine subjects when the external meatus was irrigated with 50 ml of cold (10 degrees C) or warm (44 degrees C) water. During nystagmus, the SSNA in tibial and peroneal nerves decreased to 50 +/- 4% (with baseline value set as 100%) and 61 +/- 4%, respectively. The degree of SSNA suppression in both nerves was proportional to the maximum slow-phase velocity of nystagmus. After nystagmus, the SSNA increased to 166 +/- 7 and 168 +/- 6%, respectively, and the degree of motion sickness symptoms was correlated with this SSNA increase. These results suggest that the SSNA response differs from the MSNA response during caloric vestibular stimulation and that the SSNA response elicited in the initial period of caloric vestibular stimulation is different from that observed during the period of motion sickness symptoms.

Muscle sympathetic nerve activity (MSNA) was measured directly along with blood pressure at rest in 69 healthy women (20–79 yr old) and 76 age-matched healthy men (16–80 yr old). All were nonobese and normotensive. In the women and men the MSNA was positively correlated with age (women: y = 0.788 x − 5.418, r = 0.846, P < 0.0001; men: y = 0.452 x + 12.565, r = 0.751, P < 0.0001). The regression intercept of y was significantly lower ( P < 0.0001) in the women than in the men, and the regression slope was significantly steeper ( P < 0.0001) in the women. The MSNA was lower in women than in men among those

To evaluate the response of vasomotor sympathetic nerve activity to lower body positive pressure (LBPP), muscle sympathetic nerve activity (MSNA) was microneurographically recorded from the tibial nerve in 10 healthy young men, along with hemodynamic variables and echocardiogram, during exposure to incremental LBPP at 10, 20, and 30 mmHg in the supine position. MSNA was suppressed to a similar extent (27%) at 10- and 20-mmHg LBPP. However, at 30-mmHg LBPP, MSNA tended to increase but was still nearly at the control value. Mean arterial pressure was elevated (11%), total peripheral resistance markedly increased (36%), and stroke volume and cardiac output tended to decrease at 30-mmHg LBPP. Heart rate remained unchanged throughout the procedures. Left atrial dimension significantly increased during 10- and 30-mmHg LBPP, indicating an increased cardiac filling. These results suggest that the inhibitory effect of the cardiopulmonary baroreflex on MSNA at 10- and 20-mmHg LBPP could be counteracted by the sympathoexcitatory effect of the intramuscular pressure-sensitive mechanoreflex at 30-mmHg LBPP. However, the increment of total peripheral resistance at 30-mmHg LBPP may not depend exclusively on this small enhancement of MSNA.

1 Skin sympathetic nerve activity (SSNA) was recorded in seven male subjects from the peroneal nerve by microneurography, and the temporal correspondence of spontaneously occurring SSNA bursts with vasodilatation and sweating responses on the dorsal foot was studied during a mild body heating at rest. 2 Some SSNA bursts were followed by a sweat expulsion with a latency of 2.4 ± 0.4 s, and some bursts by a transient vasodilatation with a latency of 2.2 ± 0.4 s (means ± s.d.). SSNA bursts followed both by a sweat expulsion and by a vasodilatation response (Type 1), those followed only by a sweat expulsion (Type 2) and those followed only by a vasodilatation response (Type 3) were 70 %, 10 % and 1 % of the total bursts examined, respectively. 3 For Type 1 bursts, there was a significant, but weak linear relationship among the burst amplitude, the amplitude of the corresponding vasodilatation and the amplitude of the corresponding sweat expulsion. 4 It was concluded that SSNA contains vasodilatory activity which is synchronous with sudomotor nerve activity. The results suggest that such vasodilatory activity contributes to sustaining the sweat gland function by supplying sufficient blood.

To assess autonomic dysfunction, skin sympathetic nerve activity (SSNA) of four patients with Guillain-Barré syndrome was microneurographically studied in the acute and remission phase. Autonomic symptoms such as sinus tachycardia, palmar hyperhidrosis, hypertension, and orthostatic hypotension were present in the acute phase, but all subsided during remission. Basal resting SSNA and the responses to various physical and mental stimuli were all increased in the acute phase and returned almost to normal during remission. Rate of response in sweat rate and blood flow against SSNA were kept proportionally constant during both the acute and remission phases. These findings suggest that some autonomic nerve symptoms of Guillain-Barré syndrome, particularly during the acute phase, are due to increased SSNA.

The gravity-dependency and age-dependency of noradrenergic vasoconstrictor outflow to skeletal muscle (muscle sympathetic nerve activity ; MSNA) in humans was analyzed by applying microneurography technique. The basal level of MSNA in the horizontally supine position increased with aging without significant changes in arterial baroreflex sensitivity. MSNA responded to +Gz load by head-up tilt and to simulated microgravity by thermoneutral head-out immersion with increasing and decreasing the activity, respectively. These gravity-related responses of MSNA were age-dependent, being reduced by aging. Simultaneously monitored hemodynamic responses to +Gz load and to simulated microgravity were also age-dependent, being reduced by aging. The gravity-dependent and also age-dependent changes in the noradrenergic vasoconstrictor outflow to muscle seem to be related to the mechanisms controlling the gravity-dependent fluid shift in the human body.

In order to analyze sympathetic nerve discharges as an entity, not as the decomposed parts, a non-linear mathematical analyzing technique including chaos and fractal theory was utilized in healthy normal subjects. Muscle sympathetic nerve activity (MSNA) was recorded using the microneurography technique during supine position and tilt up position. MSNA was integrated by the integrator and analyzed in the computer system using the non-linear mathematical analyzing technique. Time series data of the sympathetic nerve discharges were quantified in R-R interval time series data and analyzed with the Lorenz plot. Fractal dimension analysis of the MSNA was performed by the changing coarse graining level (box-counting method). Both during supine position and tilt up, MSNA showed the characteristics of fractals. After the tilt up of the bed, MSNA tone was increased and the fractal dimensions of both R-R interval and MSNA were increased. Our results suggest that MSNA tone contributed to the increases of the fractal dimension.

マイクロニューログラフィによリヒトの交感神経活動電位の直接的な記録が可能となり,現在,我が国を含む世界各国の研究者によって本法が応用され,ヒトの交感神経機能に関する多くの知見が報告されている.本稿ではヒトで記録できる交感神経活動のうち骨格筋の血管を支配し循環調節に重要な役割を担う筋交感神経活動の記録法と,本法を用いた研究の成績の概要について述べる.

We examined the effect of mental stress on muscle sympathetic nerve activity (MSNA) by microneurographically measuring the MSNA of the tibial nerve while subjects read aloud. A delayed auditory feedback task (DAF) was employed with a delay interval of 200 ms and these performances were compared to those in the absence of DAF in five healthy men (28 +/- 2 years). The mean blood pressure was significantly elevated during reading both in the presence of DAF and in its absence, and the pressor response was more exaggerated in the presence of DAF than its absence. MSNA and plasma norepinephrine levels were significantly increased during reading in the presence of DAF but not in its absence, whereas heart rate was mildly increased at the same extent during reading in both the presence and absence of DAF. The results suggest that mental stress produces elevation in blood pressure and mediates the activation of sympathetic nerve activity.

In order to assess age-related changes in sympathetic nerve activity controlling blood pressure, we recorded muscle sympathetic nerve activity, blood pressure, and heart rate during head-up tilt in 10 healthy elderly (69–75 years) and 16 healthy young (19–23 years) subjects. The elderly had significantly lower responsiveness of muscle sympathetic nerve activity to postural change than did the young subjects. In the elderly, marked rise in blood pressure without increase in muscle sympathetic nerve activity was observed in nearly upright position during head-up tilt, whereas this phenomenon was not observed in the young. We conclude that neural control function of blood pressure during head-up tilt in the elderly differs from that in the young, which may be due to age-related change in baroreflex function.

It has been shown that the degree of vibrotactile adaptation is smaller on the middle finger tip than on the palm, and that it is greater when measured with a small contactor than with a large contactor. We produced a mathematical model to illustrate these phenomena. All experimental results could be simulated with the model on the basis of the following hypotheses: (1) that the accumulated discharge density of mechanoreceptive units depended on the site of stimulation and the size of the contactor; (2) that the discharge threshold of a mechanoreceptive unit was higher in post-adaptation than in pre-adaptation; (3) that the slope of stimulus-discharge function was gentler in post-adaptation than in pre-adaptation

Many earlier human studies have reported that increasing the tilt angle of head-up tilt (HUT) results in greater muscle sympathetic nerve activity (MSNA) response, indicating the amplitude dependence of sympathetic activation in response to orthostatic stress. However, little is known about whether and how the inclining speed of HUT influences the MSNA response to HUT, independent of the magnitude of HUT. Twelve healthy subjects participated in passive 30 degrees HUT tests at inclining speeds of 1 degrees (control), 0.1 degrees (slow), and 0.0167 degrees (very slow) per second. We recorded MSNA (tibial nerve) by microneurography and assessed nonstationary time-dependent changes of R-R interval variability using a complex demodulation technique. MSNA averaged over every 10 degrees tilt angle increased during inclination from 0 degrees to 30 degrees , with smaller increases in the slow and very slow tests than in the control test. Although a 3-min MSNA overshoot after reaching 30 degrees HUT was observed in the control test, no overshoot was detected in the slow and very slow tests. In contrast with MSNA, increases in heart rate during the inclination and after reaching 30 degrees were similar in these tests, probably because when compared with the control test, greater increases in plasma epinephrine counteracted smaller autonomic responses in the very slow test. These results indicate that slower HUT results in lower activation of MSNA, suggesting that HUT-induced sympathetic activation depends partially on the speed of inclination during HUT in humans.

A 54-year-old man complained of burning pain, warm skin and erythema in his extremities. A diagnosis of primary erythromelalgia was made. Microneurography was used to clarify the role of skin sympathetic nerve activity in the pathophysiology of primary erythromelalgia. The patient showed normal skin sympathetic nerve activity but no vasoconstriction response. Aspirin activated the skin sympathetic nerve activity and improved vasoconstriction producing symptomatic relief. These results suggest that the lack of vasoconstriction following vasoconstrictor activity of the skin sympathetic nerves results in increased skin blood flow and burning pain.

There have so far been few reports on the static regulations of cerebral and systemic circulation during prolonged head-down bed rest (HDBR). Our aim was to investigate the time course changes in static cerebral and systemic circulation during 14 days of 6 degrees HDBR.Sixteen subjects participated in the HDBR study. The systolic, mean, and diastolic cerebral blood flow velocities (CBFVs) of the middle cerebral artery were measured using a transcranial Doppler technique. Cerebrovascular bed resistance indices, i.e., resistance index (RI), pulsatility index (PI), and estimated regional cerebrovascular resistance (CVRest) were calculated. The systemic cardiovascular functions, i.e, heart rate (HR), mean arterial pressure (MAP), left ventricular ejection time (LVET), stroke volume (SV), cardiac output (CO), and total peripheral resistance (TPR) were measured or calculated.All CBFVs consistently showed significant decreases from the 2nd day to the last day of the HDBR. The RI and PI showed a rising tendency throughout the HDBR. The CVRest showed significantly higher levels in the later half of the HDBR. The HR and MAP did not change during the HDBR.The adaptive process of cerebral circulation triggered by HDBR begins very early and leads to a new equilibrium within few days after the onset of HDBR. The alteration of static cerebral circulation with prolonged HDBR, i.e., lowered CBFVs and somewhat higher cerebrovascular bed resistance implies a reduction in the cerebral circulation, but it does not necessarily imply the impaired regulation of cerebral circulation.

Although spaceflight and bed rest are known to cause muscular atrophy in the antigravity muscles of the legs, the changes in sympathetic and cardiovascular responses to exercises using the atrophied muscles remain unknown. We hypothesized that bed rest would augment sympathetic responses to isometric exercise using antigravity leg muscles in humans. Ten healthy male volunteers were subjected to 14-day 6° head-down bed rest. Before and after bed rest, they performed isometric exercises using leg (plantar flexion) and forearm (handgrip) muscles, followed by 2-min postexercise muscle ischemia (PEMI) that continues to stimulate the muscle metaboreflex. These exercises were sustained to fatigue. We measured muscle sympathetic nerve activity (MSNA) in the contralateral resting leg by microneurography. In both pre- and post-bed-rest exercise tests, exercise intensities were set at 30 and 70% of the maximum voluntary force measured before bed rest. Bed rest attenuated the increase in MSNA in response to fatiguing plantar flexion by ∼70% at both exercise intensities (both P < 0.05 vs. before bed rest) and reduced the maximal voluntary force of plantar flexion by 15%. In contrast, bed rest did not alter the increase in MSNA response to fatiguing handgrip and had no effects on the maximal voluntary force of handgrip. Although PEMI sustained MSNA activation before bed rest in all trials, bed rest entirely eliminated the PEMI-induced increase in MSNA in leg exercises but partially attenuated it in forearm exercises. These results do not support our hypothesis but indicate that bed rest causes a reduction in isometric exercise-induced sympathetic activation in (probably atrophied) antigravity leg muscles.

We investigated the effect of head-down bed rest (HDBR) for 14 days on thermoregulatory sweating and cutaneous vasodilation in humans. Fluid intake was ad libitum during HDBR. We induced whole body heating by increasing skin temperature for 1 h with a water-perfused blanket through which hot water (42 degrees C) was circulated. The experimental room was air-conditioned (27 degrees C, 30-40% relative humidity). We measured skin blood flow (chest and forearm), skin temperatures (chest, upper arm, forearm, thigh, and calf), and tympanic temperature. We also measured sweat rate by the ventilated capsule method in which the skin area for measurement was drained by dry air conditioned at 27 degrees C under similar skin temperatures in both trials. We calculated cutaneous vascular conductance (CVC) from the ratio of skin blood flow to mean blood pressure. From tympanic temperature-sweat rate and -CVC relationships, we assessed the threshold temperature and sensitivity as the slope response of variables to a given change in tympanic temperature. HDBR increased the threshold temperature for sweating by 0.31 degrees C at the chest and 0.32 degrees C at the forearm, whereas it reduced sensitivity by 40% at the chest and 31% at the forearm. HDBR increased the threshold temperature for cutaneous vasodilation, whereas it decreased sensitivity. HDBR reduced plasma volume by 11%, whereas it did not change plasma osmolarity. The increase in the threshold temperature for sweating correlated with that for cutaneous vasodilation. In conclusion, HDBR attenuated thermoregulatory sweating and cutaneous vasodilation by increasing the threshold temperature and decreasing sensitivity. HDBR increased the threshold temperature for sweating and cutaneous vasodilation by similar magnitudes, whereas it decreased their sensitivity by different magnitudes.

When astronauts return to Earth and stand, their heart rates may speed inordinately, their blood pressures may fall, and some may experience frank syncope. We studied brief autonomic and haemodynamic transients provoked by graded Valsalva manoeuvres in astronauts on Earth and in space, and tested the hypothesis that exposure to microgravity impairs sympathetic as well as vagal baroreflex responses. We recorded the electrocardiogram, finger photoplethysmographic arterial pressure, respiration and peroneal nerve muscle sympathetic activity in four healthy male astronauts (aged 38–44 years) before, during and after the 16 day Neurolab space shuttle mission. Astronauts performed two 15 s Valsalva manoeuvres at each pressure, 15 and 30 mmHg, in random order. Although no astronaut experienced presyncope after the mission, microgravity provoked major changes. For example, the average systolic pressure reduction during 30 mmHg straining was 27 mmHg pre-flight and 49 mmHg in flight. Increases in muscle sympathetic nerve activity during straining were also much greater in space than on Earth. For example, mean normalized sympathetic activity increased 445 % during 30 mmHg straining on earth and 792 % in space. However, sympathetic baroreflex gain, taken as the integrated sympathetic response divided by the maximum diastolic pressure reduction during straining, was the same in space and on Earth. In contrast, vagal baroreflex gain, particularly during arterial pressure reductions, was diminished in space. This and earlier research suggest that exposure of healthy humans to microgravity augments arterial pressure and sympathetic responses to Valsalva straining and differentially reduces vagal, but not sympathetic baroreflex gain.

To examine effects of static exercise on the arterial baroreflex control of vascular sympathetic nerve activity, 22 healthy male volunteers performed 2 min of static handgrip exercise at 30% of maximal voluntary force, followed by postexercise circulatory arrest (PE-CA). Microneurographic recording of muscle sympathetic nerve activity (MSNA) was made with simultaneous recording of arterial pressure (Portapres). The relationship between MSNA and diastolic arterial pressure was calculated for each condition and was defined as the arterial baroreflex function. There was a close relationship between MSNA and diastolic arterial pressure in each subject at rest and during static exercise and PE-CA. The slope of the relationship significantly increased by >300% during static exercise ( P < 0.001), and the x-axis intercept (diastolic arterial pressure level) increased by 13 mmHg during exercise ( P< 0.001). These alterations in the baroreflex relationship were completely maintained during PE-CA. It is concluded that static handgrip exercise is associated with a resetting of the operating range and an increase in the reflex gain of the arterial barorelex control of MSNA.

The present study was performed to test the hypothesis that application of lower body positive pressure (LBPP) during orthostasis would reduce the baroreflex-mediated enhancement in sympathetic activity in humans. Eight healthy young men were exposed to a 70° head-up tilt (HUT) on application of 30 mmHg LBPP. Muscle sympathetic nerve activity (MSNA) was microneurographically recorded from the tibial nerve, along with hemodynamic variables. We found that in the supine position with LBPP, MSNA remained unchanged (13.4 ± 3.3 vs. 11.8 ± 2.3 bursts/min, without vs. with LBPP; P > 0.05), mean arterial pressure was elevated, but arterial pulse pressure and heart rate did not alter. At 70° HUT with LBPP, the enhanced MSNA response was reduced (33.8 ± 5.0 vs. 22.5 ± 2.2 bursts/min, without vs. with LBPP; P < 0.05), mean arterial pressure was higher, the decreased pulse pressure was restored, and the increased heart rate was attenuated. We conclude that the baroreflex-mediated enhancement in sympathetic activity during HUT was reduced by LBPP. Application of LBPP in HUT induced an obvious cephalad fluid shift as well as a restoration of arterial pulse pressure, which reduced the inhibition of the baroreceptors. However, the activation of the intramuscular mechanoreflexes produced by 30 mmHg LBPP might counteract the effects of baroreflexes.

To elucidate the effects of linear acceleration on muscle sympathetic nerve activity (MSNA) in humans, 16 healthy men were tested in a linear accelerator. Measurements of MSNA, electrocardiogram, blood pressure, and thoracic impedance were undertaken during linear acceleration. Sinusoidal linear acceleration with peak values at ±0.10, ±0.15, and ±0.20 G was applied in anteroposterior (±Gx, n = 10) or lateral (±Gy, n = 6) directions. The total activity and burst rate of MSNA decreased significantly during forward, backward, left, or right linear accelerations. The total activity of MSNA decreased to 50.5 ± 6.9, 52.5 ± 4.4, 71.2 ± 9.6, and 67.6 ± 8.2% from the baselines (100%) during linear accelerations with peak values at ±0.20 G in the four directions, respectively. These results suggest that dynamic stimulation of otolith organs in horizontal directions in humans might inhibit MSNA directly in order to quickly redistribute blood to muscles during postural reflexes induced by passive movement, which supports the concept that the vestibular system contributes to sympathetic regulation in humans.

Background. Fluid shift induced by postural change causes autonomic neural responses of the cardiovascular system that buffer blood pressure fluctuation. The aim of the study was to clarify the effects of aging on cardiovascular autonomic functions in response to gravity-related fluid shift that unloads or loads the baroreceptors in human subjects. Methods. A chest electrocardiogram, blood pressure by Finapres, and stroke volume by impedance method were measured in healthy young men (23‐31 years old) and healthy elderly men (74‐80 years old) during supine rest, at 90 8 head-up tilt and thermoneutral head-out water immersion. Spectral analysis was applied to the time series data of the R-R intervals (heart rate variability [HRV]) and systolic blood pressure (blood pressure variability [BPV]). The arterial baroreflex gain for heart rate was estimated using frequency transfer function analysis. Results. The young subjects had stable blood pressure, despite the larger amount of fluid shift induced by both tilt and immersion, and had marked changes in HRV and BPV. The elderly subjects failed to maintain stable blood pressure during these perturbations, despite less fluid shift and no significant changes in HRV and BPV. The arterial baroreflex gain for heart rate was not changed in the elderly subjects, whereas the gain decreased with upright in the young subjects and showed an increasing tendency during immersion compared with upright posture. Conclusions. These findings suggest that the adaptivity of the autonomic nervous system to gravity-related fluid shift is reduced in elderly people, and this may cause blood pressure instability. RAVITY is a natural physical stimulus that humans live with. It affects cardiovascular function because we change posture in our active daily life (upright, sitting, squatting, and lying), which influences hydrostatic pressure gradient from the foot to the head. Changing one’s posture resets the hydrostatic pressure gradient, and a gravity-related fluid shift is produced along the Gz axis. This shift induces neural responses of the autonomic nervous system that regulate cardiovascular functions to buffer blood pressure fluctuations induced by postural changes.

To examine how long-lasting microgravity simulated by 6 degrees 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 degrees 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 degrees HUT was not different between before and after HDBR, but mean blood pressure decreased in 60 degrees 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.

To clarify how neural and humoral mechanisms operate to control cardiovascular unctions in man under weightlessness, the response of sympathetic nerve activity was observed in healthy human subjects by means of microneurographic technique with the changes of several hemodynamic parameters and hormonal responses during thermoneutral head-out water immersion. Muscle sympathetic nerve activity was markedly suppressed by head-out immersion, concomitantly with a reduction of the leg volume, an increase of the stroke volume and a reduction of total peripheral resistance. At the same time, plasma level of norepinephrine, vasopressive and antidiuretic hormones (ADH, aldosterone, renin activity, angiotensin I·II) were reduced, while vasodepressive and diuretic hormone (ANP) was markedly increased. The systemic blood pressure was maintained almost unchanged during head-out water immersion. The suppressive response of sympathetic nerve activity seemed to be age-dependent. This response was less prominent in the elderly than in young subjects. It is concluded that the suppressive response of muscle sympathetic activity plays an important role to maintain hemodynamic homeostasis under weightlessness to compensate for the cephalad fluid shift and the resultant increase of the stroke volume in cooperation with the hormonal responses.

The sympathetic nervous system plays an important role to maintain the homeostasis of vital functions in humans against environmental stimuli. Sympathetic nerve responses to environmental stimuli in humans have been assessed conventionally using rather indirect methods by analyzing the responses of effector organs or by measuring the changes in plasma norepinephrine level. Meanwhile, the microneurography technique has enabled us to approach the sympathetic nervous system in humans more directly. By applying this technique, it has become possible to investigate how the human sympathetic nervous system responds to different kinds of environmental stimuli. In this paper, the usefulness of microneurography as a research tool in environmental physiology is shown together with a review of microneurographic findings on sympathetic nerve responses to environmental stimuli in humans.

We hypothesized that muscle sympathetic nerve activity (MSNA) and cardiovascular responses to the conventional head-up tilt (HUT) are different from those to head-up suspension (HUS) because of antigravity muscle activity. The MSNA from the tibial nerve, heart rate, blood pressure, stroke volume, cardiac output, and calf blood flow were measured in 13 healthy young subjects. Left atrial diameter was measured by two-dimensional echocardiography in another nine subjects. The resting MSNA and cardiovascular responses at a low level (20°) of orthostasis were similar during both modes. At higher levels (40 and 60°), the responses of MSNA, heart rate, stroke volume, and cardiac output were significantly stronger and there was a smaller reduction in calf blood flow during HUT than during HUS ( P < 0.05). Left atrial diameter was decreased significantly from the resting values during HUT and HUS without any significant difference between the modes of orthostasis. The results provide evidence that the engagement of antigravity muscles during HUT may have additive effects on sympathetic vasoconstrictor and cardiovascular responses to orthostatic stress.