Cardiovascular responses to upright and supine exercise in humans after 6 weeks of head-down tilt (−6°)

Seven healthy men performed steady-state dynamic leg exercise at 50 W in supine and upright postures, before (control) and repeatedly after 42 days of strict head-down tilt (HDT) (−6°) bedrest. Steady-state heart rate (f _c), mean arterial blood pressure, cardiac output (Q˙ _c), and stroke volume (SV) were recorded. The following data changed significantly from control values. The f _c was elevated in both postures at least until 12 days, but not at 32 days after bedrest. Immediately after HDT, SV and Q˙ _c were decreased by 25 (SEM 3)% and 19 (SEM 3)% in supine, and by 33 (SEM 5)% and 20 (SEM 3)% in upright postures, respectively. Within 2 days there was a partial recovery of SV in the upright but not in the supine posture. The SV and Q˙ _c during supine exercise remained significantly decreased for at least a month. Submaximal oxygen uptake did not change after HDT. We concluded that the cardiovascular response to exercise after prolonged bedrest was impaired for so long that it suggested that structural cardiac changes had developed during the HDT period. Accepted: 6 June 2000     

Cardiovascular responses to upright and supine exercise in humans after 6 weeks of head-down tilt (-6 degrees)

Seven healthy men performed steady-state dynamic leg exercise at 50 W in supine and upright postures, before (control) and repeatedly after 42 days of strict head-down tilt (HDT) (-6 degrees) bedrest. Steady-state heart rate (fc), mean arterial blood pressure, cardiac output (Qc), and stroke volume (SV) were recorded. The following data changed significantly from control values. The fc was elevated in both postures at least until 12 days, but not at 32 days after bedrest. Immediately after HDT, SV and Qc were decreased by 25 (SEM 3)% and 19 (SEM 3)% in supine, and by 33 (SEM 5)% and 20 (SEM 3)% in upright postures, respectively. Within 2 days there was a partial recovery of SV in the upright but not in the supine posture. The SV and Qc during supine exercise remained significantly decreased for at least a month. Submaximal oxygen uptake did not change after HDT. We concluded that the cardiovascular response to exercise after prolonged bedrest was impaired for so long that it suggested that structural cardiac changes had developed during the HDT period.     

Short-term cardiovascular responses to rapid whole-body tilting during exercise

Our objective was to characterize the responses of heart rate (HR) and arterial blood pressure (BP) to changes in posture during concomitant dynamic leg exercise. Ten men performed dynamic leg exercise at 50, 100, and 150 W and were rapidly and repeatedly tilted between supine (0°) and upright (80°) positions at 2-min intervals. Continuous recordings of BP and HR were made, and changes in central blood volume were estimated from transthoracic impedance. Short-lasting increases in BP were observed immediately upon tilting from the upright to the supine position (down-tilt), averaging +18 mmHg (50 W) to +31 mmHg (150 W), and there were equally short-lasting decreases in BP, ranging from −26 to −38 mmHg upon tilting from supine to upright (up-tilt). These components occurred for all pressure parameters (systolic, mean, diastolic, and pulse pressures). We propose that these transients reflect mainly tilt-induced changes in total peripheral resistance resulting from decreases and increases of the efficiency of the venous muscle pump. After 3–4 s (down-tilt) and 7–11 s (up-tilt) there were large HR transients in a direction opposite to the pressure transients. These HR transients were larger during the down-tilt (−15 to −26 beats · min⁻¹) than during the up-tilt (+13 to +17 beats · min⁻¹), and increased in amplitude with work intensity during the down-tilt. The tilt-induced HR fluctuations could be modelled as a basically linear function of an arterial baroreflex input from a site half-way between the heart and the carotid sinus, and with varying contributions of fast vagal and slow sympathetic HR responses resulting in attenuated tachycardic responses to hypotensive stimuli during exercise. Accepted: 24 August 1999     

Upright tilt resets dynamic transfer function of baroreflex neural arc to minify the pressure disturbance in total baroreflex control

Maintenance of arterial pressure (AP) under orthostatic stress against gravitational fluid shift and pressure disturbance is of great importance. One of the mechanisms is that upright tilt resets steady-state baroreflex control to a higher sympathetic nerve activity (SNA). However, the dynamic feedback characteristics of the baroreflex system, a hallmark of fast-acting neural control, remain to be elucidated. In the present study, we tested the hypothesis that upright tilt resets the dynamic transfer function of the baroreflex neural arc to minify the pressure disturbance in total baroreflex control. Renal SNA and AP were recorded in ten anesthetized, vagotomized and aortic-denervated rabbits. Under baroreflex open-loop condition, isolated intracarotid sinus pressure (CSP) was changed according to a binary white noise sequence at operating pressure +/- 20 mmHg, while the animal was placed supine and at 60 degrees upright tilt. Regardless of the postures, the baroreflex neural (CSP to SNA) and peripheral (SNA to AP) arcs showed dynamic high-pass and low-pass characteristics, respectively. Upright tilt increased the transfer gain of the neural arc (resetting), decreased that of the peripheral arc, and consequently maintained the transfer characteristics of total baroreflex feedback system. A simulation study suggests that postural resetting of the neural arc would significantly increase the transfer gain of the total arc in upright position, and that in closed-loop baroreflex the resetting increases the stability of AP against pressure disturbance under orthostatic stress. In conclusion, upright tilt resets the dynamic transfer function of the baroreflex neural arc to minify the pressure disturbance in total baroreflex control.     

Resetting of the arterial baroreflex increases orthostatic sympathetic activation and prevents postural hypotension in rabbits

Since humans are under ceaseless orthostatic stress, the mechanism to maintain arterial pressure (AP) under orthostatic stress against gravitational fluid shift is of great importance. We hypothesized that (1) orthostatic stress resets the arterial baroreflex control of sympathetic nerve activity (SNA) to a higher SNA, and (2) resetting of the arterial baroreflex contributes to preventing postural hypotension. Renal SNA and AP were recorded in eight anaesthetized, vagotomized and aortic-denervated rabbits. Isolated intracarotid sinus pressure (CSP) was increased stepwise from 40 to 160 mmHg with increments of 20 mmHg (60 s for each CSP level) while the animal was placed supine and at 60 deg upright tilt. Upright tilt shifted the CSP–SNA relationship (the baroreflex neural arc) to a higher SNA, shifted the SNA–AP relationship (the baroreflex peripheral arc) to a lower AP, and consequently moved the operating point to marked high SNA while maintaining AP. A simulation study suggests that resetting in the neural arc would double the orthostatic activation of SNA and increase the operating AP in upright tilt by 10 mmHg, compared with the absence of resetting. In addition, upright tilt did not change the CSP–AP relationship (the baroreflex total arc). A simulation study suggests that although a downward shift of the peripheral arc could shift the total arc downward, resetting in the neural arc would compensate this fall and prevent the total arc from shifting downward to a lower AP. In conclusion, upright tilt increases SNA by resetting the baroreflex neural arc. This resetting may compensate for the reduced pressor responses to SNA in the peripheral cardiovascular system and contribute to preventing postural hypotension.     

Difference in human cardiovascular response between upright and supine recovery from upright cycle exercise

Cardiovascular responses were examined in seven healthy male subjects during 10 min of recovery in the upright or supine position following 5 min of upright cycle exercise at 80% peak oxygen uptake. An initial rapid decrease in heart rate (f _c) during the early phase of recovery followed by much slower decrease was observed for both the upright and supine positions. The average f _c at the 10th min of recovery was significantly lower (P < 0.05) in the supine position than in the upright position, while they were both significantly greater than the corresponding pre-exercise levels (each P < 0.05). Accordingly, the amplitude of the high frequency (HF) component of R-R interval variability (by spectrum analysis) in both positions was reduced with a decrease in mean R-R interval, the relationship being expressed by a regression line – mean R-R interval = 0.006 × HF amplitude + 0.570 (r = 0.905, n = 28, P < 0.001). These results would suggest that the slower reduction in f _c following the initial rapid reduction in both positions is partly attributable to a retardation in the restoration of the activity of the cardiac parasympathetic nervous system. Post-exercise upright stroke volume (SV, by impedance cardiography) decreased gradually to just below the pre-exercise level, whereas post-exercise supine SV increased markedly to a level similar to that at rest before exercise. The resultant cardiac output (Q˙ _c) and the total peripheral vascular resistance (TPR) in the upright and supine positions returned gradually to their respective pre-exercise levels in the corresponding positions. At the 10th min of recovery, both average SV and Q˙ _c were significantly greater (each P < 0.005) in the supine than in the upright position, while average TPR was significantly lower (P < 0.05) in the supine than in the upright position. In contrast, immediately after exercise, mean blood pressure dropped markedly in both the supine and upright positions, and their levels at the 10th min of recovery were similar. Therefore we concluded that arterial blood pressure is maintained relatively constant through various compensatory mechanisms associated with f _c, SV, Q˙ _c, and TPR during rest and recovery in different body positions. Accepted: 4 September 1999     

20-Hz whole body vibration training fails to counteract the decrease in leg muscle volume caused by 14 days of 6° head down tilt bed rest

A 6° head down tilt bed rest (HDT) was used to simulate the effects of muscle unloading in space. We tested whether vibration training (VT) reduces the decrease in leg muscle volume induced by 14 days HDT. In two study phases eight healthy male subjects received both (1) HDT and VT or (2) HDT and a control intervention. Twice daily five intervals of 1 min VT were performed (20 Hz, 2–4 mm) in upright standing position followed by 1 min breaks in seated position. The control intervention included identical procedures except the vibration plate was off. Before and the day after HDT volumes of upper and lower leg muscles were measured using magnetic resonance imaging. HDT combined with control intervention caused a significant (P < 0.05) decrease in the volumes of muscles by −4 to −6.5%. VT failed to counteract the decrease in leg muscle volume induced by HDT.     

Carotid-cardiac baroreflex function does not influence blood pressure regulation during head-up tilt in humans

The influence of the carotid-cardiac baroreflex on blood pressure regulation was evaluated during supine rest and 40 degrees head-up tilt (HUT) in 9 healthy young subjects with and without full cardiac vagal blockade. The carotid baroreflex responsiveness, or maximal gain (G(MAX)), was assessed from the beat-to-beat changes in heart rate (HR) and mean arterial pressure (MAP) by the variable neck pressure and suction technique ranging in pressure from +40 to -80 Torr, with and without glycopyrrolate (12.0 +/- 1.0 microg/kg body weight; mean +/- SE). In the supine position, glycopyrrolate increased the HR to 91 +/- 3 bpm, from 54 +/- 3; MAP to 89 +/- 2 mmHg, from 76 +/- 2; and cardiac output to 6.8 +/- 0.3 l.min(-1), from 4.9 +/- 0.3 (P < 0.05). The G(MAX) of the carotid baroreflex control of HR was reduced to -0.06 +/- 0.01 bpm.mmHg(-1), from -0.30 +/- 0.02 (P < 0.05) with no significant effect on the G(MAX) of the carotid baroreflex control of MAP. During HUT the carotid baroreflex control of MAP was unchanged, though the G(MAX) of the carotid baroreflex control of HR was increased (P < 0.05). During HUT, central blood volume, assessed by electrical thoracic admittance, and total vascular conductance were decreased with and without glycopyrrolate. Furthermore, glycopyrrolate reduced G(MAX) of the carotid baroreflex control of HR during HUT (P < 0.05) with no significant effect on G(MAX) of the carotid baroreflex control of MAP. These data suggest that during supine rest and HUT-induced decreases in central blood volume, the carotid baroreflex control of HR is mediated primarily via parasympathetic activity. Furthermore, the maintenance of arterial blood pressure during postural stress is primarily mediated by arterial and cardiopulmonary reflex regulation of sympathetic activity and its effects on the systemic vasculature.     

Baroreflex impairment during rapid posture changes at rest and exercise after 120 days of bed rest

Orthostatic intolerance is common after space flight and head-down tilt (HDT) bed rest. We hypothesized that HDT-induced impairments of arterial blood pressure (AP) control would be more marked during exercise and that recovery of baroreflex function after very long-term HDT would be delayed. Six subjects were studied before (BDC) during (day 60, D60; D113) and after (recovery day 0, R0; R3; R15) 120 days of HDT. Supine resting subjects were exposed to repeated 1 min passive tilts to upright at 3-min interval. During 50 W steady-state exercise corresponding tilt had a 2-min duration at 4-min interval. The amplitudes of the tilt-induced transient beat-by-beat deviations in AP and rate (HR) were determined during the gravity transients. At rest these deviations did not change over time, but during exercise the total peak-to-nadir range of deviations in systolic AP (SAP) at up-tilt and down-tilt increased to 168±16% (mean±SEM) of BDC at D113 with no clear recovery upto and including R15. Counter-regulatory HR responses were not increased proportionally and especially not tachycardic responses to up-tilt, resulting in a reduction of baroreflex sensitivity (ΔRR-interval/ΔSAP) by 55±9% of BDC at D113 with no recovery upto and including R15. We conclude that prolonged bed rest cause long-lasting impairments in AP control and baroreflex function in exercising humans.     

Renal and hormonal responses to isotonic saline infusion after 3 days' head‐down tilt vs. supine and seated positions

Aim: The study aimed to determine whether prolonged exposure to simulated microgravity produces a level of thoracic volume receptor loading similar to that seen in the upright position or immediately after lying down. Methods: We used a cross‐over design to compare responses to a saline infusion in eight healthy subjects during a 4‐day, ?6° head‐down tilt (HDT) and in the acute seated and acute supine positions. Results: The first 24 h of HDT were associated with greater urinary excretion of water and sodium (UV, UNaV) than seated and acute supine [cumulative UV, 3035 ± 219, 2311 ± 156 (P < 0.05), and 2448 ± 182 mL (P < 0.05), respectively; cumulative UNaV, 256 ± 19, 180 ± 11 (P < 0.05), and 189 ± 15 mmol (P < 0.05), respectively]. Haemoglobin and haematocrit were increased after 24 h and plasma volume decreased after 48 h of HDT (P < 0.05). With prolongation of HDT, UV and UNaV returned near the baseline values, and plasma atrial natriuretic factor (ANF) and renin values returned to acute seated levels; in acute supine, ANF values were higher and renin lower than in the two other positions. After a 30‐min infusion of 20 mL kg^?1 isotonic saline on the fourth HDT day or during acute seated or acute supine, sodium excretion within 4 h was similar during HDT and acute seated (83 ± 6 and 84 ± 9 mmol, respectively) and greater during supine (104 ± 8 mmol, P < 0.05). The renin decrease was greater in HDT and seated than in supine. The plasma ANF increase was greater during HDT than during supine; during seated, plasma ANF was unchanged. Conclusion: These data suggest that, after 4 days of HDT, thoracic volume receptor loading returns to the same level as in the seated position, leading to blunted responses to volume expansion as compared with the acute supine position.     

Renal and hormonal responses to isotonic saline infusion after 3 days' head-down tilt vs. supine and seated positions

AIM: The study aimed to determine whether prolonged exposure to simulated microgravity produces a level of thoracic volume receptor loading similar to that seen in the upright position or immediately after lying down. METHODS: We used a cross-over design to compare responses to a saline infusion in eight healthy subjects during a 4-day, -6 degree head-down tilt (HDT) and in the acute seated and acute supine positions. RESULTS: The first 24 h of HDT were associated with greater urinary excretion of water and sodium (UV, UNaV) than seated and acute supine [cumulative UV, 3035 +/- 219, 2311 +/- 156 (P < 0.05), and 2448 +/- 182 mL (P < 0.05), respectively; cumulative UNaV, 256 +/- 19, 180 +/- 11 (P < 0.05), and 189 +/- 15 mmol (P < 0.05), respectively]. Haemoglobin and haematocrit were increased after 24 h and plasma volume decreased after 48 h of HDT (P < 0.05). With prolongation of HDT, UV and UNaV returned near the baseline values, and plasma atrial natriuretic factor (ANF) and renin values returned to acute seated levels; in acute supine, ANF values were higher and renin lower than in the two other positions. After a 30-min infusion of 20 mL kg(-1) isotonic saline on the fourth HDT day or during acute seated or acute supine, sodium excretion within 4 h was similar during HDT and acute seated (83 +/- 6 and 84 +/- 9 mmol, respectively) and greater during supine (104 +/- 8 mmol, P < 0.05). The renin decrease was greater in HDT and seated than in supine. The plasma ANF increase was greater during HDT than during supine; during seated, plasma ANF was unchanged. CONCLUSION: These data suggest that, after 4 days of HDT, thoracic volume receptor loading returns to the same level as in the seated position, leading to blunted responses to volume expansion as compared with the acute supine position.     

Effect of body tilt angle on fatigue and EMG activities in lower limbs during cycling

This study compared the rate of fatigue and lower limb EMG activities during high-intensity constant-load cycling in upright and supine postures. Eleven active males performed seven cycling exercise tests: one upright graded test, four fatigue tests (two upright, two supine) and two EMG tests (one upright, one supine). During the fatigue tests participants initially performed a 10 s all-out effort followed by a constant-load test with 10 s all-out bouts interspersed every minute. The load for the initial two fatigue tests was 80% of the peak power (PP) achieved during the graded test and these continued until failure. The remaining two fatigue tests were performed at 20% PP and were limited to the times achieved during the 80% PP tests. During the EMG tests subjects performed a 10 s all-out effort followed by a constant-load test to failure at 80% PP. Normalised EMG activities (% maximum, NEMG) were assessed in five lower limb muscles. Maximum power and maximum EMG activity prior to each fatigue and EMG test were unaffected by posture. The rate of fatigue at 80% PP was significantly higher during supine compared with upright posture (−68 ± 14 vs. −26 ± 6 W min⁻¹, respectively, P < 0.05) and the divergence of the fatigue responses occurred by the second minute of exercise. NEMG responses were significantly higher in the supine posture by 1–4 min of exercise. Results show that fatigue is significantly greater during supine compared with upright high-intensity cycling and this effect is accompanied by a reduced activation of musculature that is active during cycling.     

Spontaneous arterial baroreflex control of the heart rate during head-down tilt in heat-stressed humans

The purpose of this study was to elucidate the effect of raised body temperature per se during acute heat stress on the spontaneous arterial baroreflex control of heart rate (f _c) in humans. To investigate whether unloading of cardiopulmonary baroreceptors during whole-body heating would alter the arterial baroreflex control of f _c, we controlled loading of the cardiopulmonary baroreceptors by head-down tilt (HDT) at angles of 5°, 10°, 15°, and 30° during heat stress produced by hot-water-perfused suits. The sensitivity of the arterial baroreceptor-cardiac reflex was calculated from the spontaneous changes in beat-to-beat arterial pressure and f _c. As an index of cardiopulmonary baroreceptor loading, the left atrial diameter (LAD) was measured by echocardiography. During whole-body heating, the LAD decreased with the rising body core temperature and increased with the HDT. The decreased LAD during heating almost recovered to the normothermic control level by 10° HDT. In the supine position, cardiac baroreflex sensitivity remained unchanged during heating. Arterial pressure, f _c and cardiac baroreflex sensitivity were not changed by HDT ranging from 5° to 30° during heating. These results suggest that cardiac baroreflex sensitivity remain unchanged during graded loading of the cardiopulmonary baroreceptors in heat-stressed humans. Also, we conclude that the sensitivity of the spontaneous arterial baroreflex controlling the f _c is not influenced by raised body temperature per se during acute heat stress. Electronic Publication     

Human vagal baroreflex sensitivity fluctuates widely and rhythmically at very low frequencies

Arterial pressure fluctuates rhythmically in healthy supine resting humans, who, from all outward appearances, are in a 'steady-state'. Others have asked, If baroreflex mechanisms are functioning normally, how can arterial pressure be so variable? We reanalysed data from nine healthy young adult men and women and tested the hypotheses that during brief periods of observation, human baroreflex sensitivity fluctuates widely and rhythmically. We estimated vagal baroreflex sensitivity with systolic pressure and R–R interval cross-spectra measured over 15 s segments, moved by 2 s steps through 20-min periods of frequency- and tidal volume-controlled breathing. We studied each subject at the same time on three separate days, with fixed protocols that included two physiological states, supine and passive 40 deg upright tilt, before and after β-adrenergic, cholinergic, and angiotensin converting enzyme blockade. Minimum, mean and maximum (± s.d. ) supine control baroreflex sensitivities averaged 5 ± 3, 18 ± 6, and 55 ± 22 ms mmHg⁻¹. In most subjects, moderate ongoing fluctuations of baroreflex sensitivity were punctuated by brief major peaks, yielding frequency distributions that were skewed positively. Fast Fourier transforms indicated that baroreflex sensitivity fluctuations (expressed as percentages of total power) concentrated more in very low, 0.003–0.04 Hz, than ultra low, 0.0–0.003 Hz, frequencies (77 ± 7 versus 11 ± 8%, P ≤ 0.001, rank sum test). Autoregressive centre frequencies averaged 0.012 ± 0.003 Hz. The periodicity of very low frequency baroreflex sensitivity fluctuations was not influenced significantly by upright tilt, or by variations of autonomic drive or angiotensin activity. Our analysis indicates that during ostensibly 'steady-state' conditions, human vagal baroreflex sensitivity fluctuates in a major way, at very low frequencies.     

Increases in central blood volume modulate carotid baroreflex resetting during dynamic exercise in humans

We sought to determine if resetting of the carotid-vasomotor baroreflex function curve during exercise is modulated by changes in central blood volume (CBV). CBV was increased during exercise by altering: (1) subject posture (supine versus upright) and (2) pedal frequency (80 versus 60 revolutions min⁻¹ (r.p.m.)); while oxygen uptake (     ) was kept constant. Eight male subjects performed three exercise trials: upright cycling at 60 r.p.m. (control); supine cycling at 60 r.p.m. (SupEX) and upright cycling at 80 r.p.m. to enhance the muscle pump (80EX). During each condition, carotid baroreflex (CBR) function was determined using the rapid neck pressure (NP) and neck suction (NS) protocol. Although mean arterial pressure (MAP) was significantly elevated from rest (88 ± 2 mmHg) during all exercise conditions ( P < 0.001), the increase in MAP was lower during SupEX (94 ± 2 mmHg) and 80EX (95 ± 2 mmHg) compared with control (105 ± 2 mmHg, P < 0.05). Importantly, the blood pressure responses to NP and NS were maintained around these changed operating points of MAP. However, in comparison to control, the carotid-vasomotor baroreflex function curve was relocated downward and leftward when CBV was increased during SupEX and 80EX. These alterations in CBR resetting occurred without any differences in     or heart rate between the exercise conditions. Thus, increasing CBV and loading the cardiopulmonary baroreflex reduces the magnitude of exercise-induced increases in MAP and CBR resetting. These findings suggest that changes in cardiopulmonary baroreceptor load influence carotid baroreflex resetting during dynamic exercise.     

Lung-deflating ability of rib cage and abdominal muscles in rabbits

Anesthetized, apneic, mechanically ventilated rabbits were placed into a tilting plethysmograph that a rubber diaphragm, tightly fitting the animal's body just below the xiphoid process, separated into a rib cage and abdominal chamber. Expired volumes (DeltaV) and abdominal pressure changes (DeltaPab) were assessed in supine and upright posture during maximal rib cage (RCC) and/or abdominal compression (ABC) by pressurizing either or both chambers, and during maximal stimulations of abdominal muscles (ABS). With RCC, DeltaV supine and upright amounted to 16+/-4.9 (mean+/-S.D.) and 20.9+/-7% of the vital capacity in supine posture (VCs) and to 75.8+/-14.5 and 44.8+/-13.9% of the expiratory reserve volume (ERV) in corresponding posture, DeltaPab being negligible. With ABC, DeltaV was 13.7+/-2 and 38.9+/-7.3% VCs and 68.4+/-14.8 and 84.4+/-10.5% ERV, respectively. Both DeltaV and DeltaPab were similar with ABC and ABS, independent of posture. If this applies also to RCC and expiratory rib cage muscle contraction, maximal expiratory effects of the latter (a) are larger in upright than supine posture; (b) contribute to ERV more in supine than upright posture; and (c) are similar to those caused by ABS in supine, but substantially smaller in upright posture.     

Role of Baroreflex Sensitivity in Predicting Tilt Training Response in Patients with Neurally Mediated Syncope

PurposeAn association between baroreflex sensitivity (BRS) and the response to tilt training has not been reported in patients with neurally mediated syncope (NMS). This study sought to investigate the role of BRS in predicting the response to tilt training in patients with NMS.ResultsAfter tilt training, 52 patients (91.2%) achieved three consecutive negative responses to the HUT. In the supine position before upright posture during the first session of tilt training for responders and non-responders, the mean BRS was 18.17±10.09 ms/mm Hg and 7.99±5.84 ms/mm Hg (p=0.008), respectively, and the frequency of BRS ≥8.945 ms/mm Hg was 45 (86.5%) and 1 (20.0%; p=0.004), respectively. Age, male gender, frequency of syncopal events before HUT, type of NMS, phase of positive HUT, total number of tilt training sessions, and mean time of tilt training did not differ between the study groups. In the multivariate analysis, BRS <8.945 ms/mm Hg in the supine position (odds ratio 23.10; 95% CI 1.20-443.59; p=0.037) was significantly and independently associated with non-response to tilt training.ConclusionThe BRS value in the supine position could be a predictor for determining the response to tilt training in patients with NMS who are being considered for inpatient tilt training.     

Arterial blood pressure and carotid baroreflex function during arm and combined arm and leg exercise in humans

AIM: During arm cranking (A) blood pressure is higher than during combined arm and leg exercise (A + L), while the carotid baroreflex (CBR) is suggested to reset to control a higher blood pressure in direct relation to work intensity and the engaged muscle mass. METHOD: This study evaluated the function of the CBR by using neck pressure and neck suction during upright A, L and A + L in 12 subjects and, in order to evaluate a potential influence of the central blood volume on the CBR, also during supine A in five subjects. Exercise intensities for A and L were planned to elicit a heart rate response of c. 100 and 120 beats min(-1), respectively, in the upright position and both workloads were maintained during A + L and supine A. RESULTS: The CBR operating point, corresponding to the pre-stimulus blood pressure, was 88 +/- 6 mmHg (mean +/- SE) at rest. During upright A, L and A + L and supine A it increased to 109 +/- 9, 95 +/- 7, 103 +/- 7 and 104 +/- 4 mmHg, respectively, and it was thus higher during upright A than during A + L and supine A (P < 0.05). In addition, the CBR threshold and saturation pressures, corresponding to the minimum and maximum carotid sinus pressure, respectively, were higher during upright A than during supine A, A + L, L and at rest (P < 0.05) with no significant change in the maximal reflex gain. CONCLUSION: These findings demonstrate that during combined arm and leg and exercise in the upright position the CBR resets to a lower blood pressure than during arm cranking likely because the central blood volume is enhanced by the muscle pump of the legs.     

Development of a miniature motor-driven pulsatile LVAD driven by a fuzzy controller

We have been developing a small, lightweight motor-driven pulsatile left ventricular assist device (LVAD) with a ball screw. The motor-driven LVAD consists of a brushless DC motor and a ball screw. The attractive magnetic force between Nd–Fe–B magnets (with a diameter of 5 mm and a thickness of 1.5 mm) mounted in holes in a silicone rubber sheet (thickness 2 mm) and an iron plate adhered onto the a diaphragm of the blood pump can provide optimum active blood filling during the pump filling phase. The LVAD has a stroke volume of 55 ml and an overall volume of 285 ml; it weighs 360 g. The controller mainly consists of a fuzzy logic position and velocity controller to apply doctors' and engineers' knowledge to control the LVAD. Each unit of the controller consists of a functionally independent program module for easy improvement of the controller's performance. The LVAD was evaluated in in vitro experiments using a mock circulation. A maximum pump outflow of 5.1 l/min was obtained at a drive rate of 95 bpm against an afterload of 95 mmHg, and active filling using the attractive magnetic force provided a pump output of 3.6 l/min at a drive rate of 75 bpm under a preload of 0 mmHg. The operating efficiency of the LVAD was measured at between 8% and 10.5%. While the LVAD can provide adequate pump outflow for cardiac assistance, further upgrading of the software and improvement of the blood pump are required to improve pump performance and efficiency.     

Differential effect of head-up tilt on cardiovagal and sympathetic baroreflex sensitivity in humans

The purpose of this study was to determine the effect of baroreceptor unloading on the sensitivity of the cardiovagal and sympathetic arms of the baroreflex during upright posture. Beat-by-beat R-R interval, arterial blood pressure and cardiac output (Doppler ultrasound), as well as muscle sympathetic nerve activity (MSNA) were recorded during periods in supine (Supine) and 60 deg head-up tilt (HUT) positions (n = 8 volunteers). Cardiovagal baroreflex sensitivity (BRS) was measured by the spontaneous sequence analysis method using systolic blood pressure and R-R interval, while sympathetic BRS was determined using the slope of the linear relationship between decreasing segments of diastolic blood pressure (DBP) and corresponding increases in MSNA. On changing to HUT, mean R-R interval and cardiac output decreased, while mean measures of MSNA, DBP and total peripheral resistance increased (P < 0.05). Cardiovagal BRS decreased from Supine to 60 deg HUT (19 +/- 2 ms mmHg(-1) versus 7.6 +/- 1.2 ms mmHg(-1); P < 0.01). In contrast, sympathetic BRS increased from -6.1 +/- 1.4 a.u. mmHg(-1) in Supine to -14 +/- 2 a.u. mmHg(-1) in HUT (P < 0.01). Thus, HUT produced differential effects on cardiac versus sympathetic BRS. The data suggest that dynamic baroreflex-mediated cardiovascular control is dominated by sympathetic control during baroreceptor unloading.