Effects of lower body positive pressure on muscle sympathetic nerve activity response to head-up tilt

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 degrees 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 degrees 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.     

Hemodynamic consequences of rapid changes in posture in humans.

Tolerance to +G(z) gravitational stress is reduced when +G(z) stress is preceded by exposure to hypogravity (fraction, 0, or negative G(z)). For example, there is an exaggerated fall in eye-level arterial pressure (ELAP) early on during +G(z) stress (head-up tilt; HUT) when this stress is immediately preceded by -G(z) stress (head-down tilt; HDT). The aims of the present study were to characterize the hemodynamic consequences of brief HDT on subsequent HUT and to test the hypothesis that an elevation in leg vascular conductance induced by -G(z) stress contributes to the exaggerated fall in ELAP. Young healthy subjects (n = 3 men and 4 women) were subjected to 30 s of 30 degrees HUT from a horizontal position and to 30 s of 30 degrees HUT when HUT was immediately preceded by 20 s of -15 degrees HDT. Four bouts of HDT-HUT were alternated between five bouts of HUT in a counterbalanced designed to minimize possible time effects of repeated exposure to gravitational stress. One minute was allowed for recovery between tilts. Brief exposure to HDT elicited an exaggerated fall in ELAP during the first seconds of the subsequent HUT (-17.9 +/- 1.4 mmHg) compared with HUT alone (-12.4 +/- 1.2 mmHg, P <0.05) despite a greater rise in stroke volume (Doppler ultrasound) and cardiac output over this brief time period in the HDT-HUT trials compared with the HUT trials (thereafter stroke volume fell under both conditions). The greater fall in ELAP was associated with an exaggerated increase in leg blood flow (femoral artery Doppler ultrasound) and was therefore largely (70%) attributable to an exaggerated rise in estimated leg vascular conductance, confirming our hypotheses. Thus brief exposure to -G(z) stress leads to an exaggerated fall in ELAP during subsequent HUT, owing to an exaggerated increase in estimated leg vascular conductance.     

Influence of central venous pressure change on plasma vasopressin in humans

After overnight food and fluid restriction, nine healthy males were examined before, during, and after lower body positive pressure (LBPP) of 11 +/- 1 mmHg (mean +/- SE) for 30 min and before, during, and after graded lower body negative pressure (LBNP) of -10 +/- 1, -20 +/- 2, and -30 +/- 2 mmHg for 20 min each. LBPP and LBNP were performed with the subject in the supine position in a plastic box encasing the subject from the xiphoid process and down, thus including the splanchnic area. Central venous pressure (CVP) during supine rest was 7.5 +/- 0.5 mmHg, increasing to 13.4 +/- 0.8 mmHg (P less than 0.001) during LBPP and decreasing significantly at each step of LBNP to 2.0 +/- 0.5 mmHg (P less than 0.001) at 15 min of -30 +/- 2 mmHg LBNP. Plasma arginine vasopressin (AVP) did not change significantly in face of this large variation in CVP of 11.4 mmHg. Mean arterial pressure increased significantly during LBPP from 100 +/- 2 to 117 +/- 3 Torr (P less than 0.001) and only at one point during LBNP of -30 +/- 2 mmHg from 102 +/- 1 to 115 +/- 5 mmHg (P less than 0.05). Heart rate did not change during LBPP but increased slightly from 51 +/- 3 to 55 +/- 3 beats/min (P less than 0.05) only at 7 min of LBNP of -30 +/- 2 mmHg. Plasma osmolality, sodium, and potassium did not change during the experiment. Hemoglobin concentration increased during LBPP and LBNP, whereas hematocrit only increased during LBNP.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of cardiovascular response to passive tilt in young and elderly men

To test the hypothesis that altered hemodynamic responses to postural changes are associated with aging, cardiovascular responses to head-up tilt (HUT) and head-down tilt (HDT) were examined in 12 healthy young (average age, 24.6 +/- 1.7 years) and 12 healthy elderly (average age, 68.6 +/- 2.2 years) men. Subjects were passively tilted from supine to 30 degrees, 60 degrees, and 90 degrees HUT and HDT. Responses to these perturbations were determined 5 min after tilting with measures of heart rate (HR), blood pressure (SBP, DBP), and echocardiographically determined left ventricular diameter in systole and diastole (LVIDs, LVIDd). In HUT there were no significant age effects. In both young and elderly, SBP decreased significantly (p less than 0.05), and DBP and HR increased significantly. Ejection fraction (EF), mean arterial blood pressure (MABP), and rate-pressure product (RPP) were unchanged in both groups. In HDT, the hemodynamic responses of the young and elderly were in opposite directions and significant age effects were found for SBP, DBP, HR, LVIDs, EF, MABP, and RPP. In HDT, the young appear to increase cardiac output primarily due to an increase in EF and end-diastolic volume (LVIDd), while HR is unchanged and SBP is decreased. MABP is unchanged, suggesting a small decrease in total peripheral resistance. The elderly may increase cardiac output slightly, owing to an increase in LVIDd with no change in EF, and a large increase in HR. Afterload increased markedly, therefore attenuating any increase in cardiac output.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiovascular and hormonal response during a 4-week head-down tilt with and without exercise and LBNP countermeasures

To determine whether exercise and Lower Body Negative Pressure (LBNP) during 28 days of -6 degrees head-down tilt (HDT) would modify orthostatic tolerance and blood volume regulating hormones, twelve healthy men were assigned to either a no- countermeasure (No-CM, n=6), or a countermeasure (CM, n=6) group. LBNP sessions consisted of 15 minutes exposure to -30 mm Hg, on days 16, 18, 20 and 22-28 of HDT. Muscular exercise began on day 8 and consisted of combined graded dynamic and isometric resistance bilateral leg exercise on a specially designed supine ergometer, in two sessions of 15-20 min. each, every day, 6 days per week. A tilt test was performed before and at the end of HDT. Changes in resting plasma volume from control day (D-5) to HDT day 24 were -11.2% for No-CM and -2.2% for CM. After HDT three among the 6 subjects of the No-CM group presented presyncopal or syncopal symptoms, no tilt test was interrupted in CM group. Atrial Natriuretic Peptide (ANP) decreased at day 7 for the two groups and remained low during all the HDT period for No-CM group only. Plasma Renin Activity and Aldosterone increased at day 7 and remained elevated for the two groups. Norepinephrine and epinephrine were unchanged. Elevated diuresis and natriuresis were evident during the first day of HDT. However, renal excretory patterns were different between the two groups: indeed, a decrease of Na+, ANP and cGMP was observed only in No-CM at Day 13 during HDT. Our data showed that the subjects of the No-CM group experienced a greater increase in heart rate and a decrease in systolic blood pressure during tilt tests after HDT; nevertheless, after HDT, blood pressure was better maintained in CM group during the tilt test. The plasma volume decrease measured at the end of HDT was significantly lower in CM group, in contrast, these countermeasures were ineffective in preventing at least certain changes in blood volume regulating hormones.     

Effect of posture on arterial baroreflex control of heart rate in humans

Altered baroreflex function may contribute to the cardiovascular changes associated with weightlessness. Since central blood volume (CBV) increases during simulated weightlessness we have examined the possibility that acute changes in CBV may modify baroreceptor function. We used graded head-up tilt (HUT) and head-down tilt (HDT) to induce changes in CBV, and neck suction to stimulate carotid baroreceptors, in 6 subjects. The increase in pulse interval induced by a negative pressure of 8.2 kPa (62 mm Hg) imposed for 10 s while supine was compared with the increase while tilted for 8 min at +/- 15 degrees, +/- 30 degrees and +/- 45 degrees. During HDT at 15 degrees the pulse interval over the first 5 cardiac cycles following suction onset was 51 +/- (SEM) 18 ms longer (p less than 0.05), at 30 degrees it was 61 +/- 20 ms longer (p less than 0.05), and at 45 degrees it was 74 +/- 35 ms longer (p less than 0.01), compared with supine. During HUT at 15 degrees the pulse interval was 25 +/- 9 ms shorter (p less than 0.05) than when supine, but was not significantly different at 30 degrees and 45 degrees. These responses occurred independently of changes in brachial blood pressure. Attenuation was also observed after 5 min (56 +/- 17 ms; less than 0.05), and after 40 min (25 +/- 9 ms; p less than 0.05) of 60 degrees HUT compared with supine. We conclude that posture does modify arterial baroreflex control of heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)     

Plasma prolactin responses to acute changes in central blood volume in man

The present study examined the relationship between plasma prolactin (PRL) and central blood volume (CBV) in man. 6 adult males lay in a lower body pressure box at a thermoneutral ambient temperature (27 degrees C) on three occasions. On each occasion a 70-min control period was followed by a 20-min exposure to a lower body pressure of either 0 mm Hg, -20 (lower body negative pressure; LBNP), or +10 mm Hg (lower body positive pressure; LBPP), followed by a 60-min recovery period. Blood was drawn and urine collected at 30-min intervals. Blood pressure and heart rate were monitored at 30-min intervals during control and recovery periods and at 10-min intervals during lower body pressure exposure. Neither 0 mm Hg, LBNP, nor LBPP altered plasma osmolality, sodium, or potassium levels. Increasing CBV by LBPP increased systemic blood pressure (p less than 0.01) but had no effect on heart rate, plasma PRL, or urine osmolality. LBNP, in contrast, increased heart rate (p less than 0.05). Half of the subjects undergoing LBNP developed presyncopal symptoms, characteristic of a vasovagal reaction which includes precipitous hypotension. Subjects developing these symptoms tended to exhibit an increase in plasma PRL and an increase in urine osmolality. Asymptomatic subjects demonstrated no change in plasma PRL or urine osmolality. In addition, subjects exhibiting a PRL response to LBNP had a higher control period plasma PRL baseline (231%) than did asymptomatic subjects. These data suggest that while plasma PRL levels are not sensitive to nonhypotensive changes in CBV, they do respond to hypotensive decreases in CBV and/or its associated nausea.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hemodynamic and neuroendocrine predictors of lower body negative pressure (LBNP) intolerance in healthy young men.

Exposure to LBNP results in body fluid shift to lower extremities similarly as under influence of orthostatic stress. In susceptible persons it leads to syncope. For better understanding why certain individuals are more susceptible to orthostatic challenges it seemed necessary to collect more data on hemodynamic and neuroendocrine adjustments occurring before onset of presyncopal symptoms Accordingly, in this study heart rate (HR), blood pressure (BP), stroke volume (SV), cardiac output (CO), hematocrit, plasma catecholamines, adrenomedullin, ACTH and plasma renin activity (PRA) were measured in 24 healthy men during graded LBNP (-15, -30 and -50 mmHg). Thirteen subjects completed the test (HT group) whereas 11 had presyncope signs or symptoms at -30 mmHg or at the beginning of -50 mmHg (LT group). Comparison of these groups showed that LT subjects had lower baseline total peripheral resistance and higher plasma adrenomedullin. During LBNP plasma catecholamine and PRA increases were even greater in LT than in HT group while plasma adrenomedullin elevations were similar in both groups. Plasma ACTH increased only in LT group following presyncope symptoms. Low tolerant group showed more rapid decline of SV and CO than HT subjects from the beginning of LBNP. It is suggested that measurements of SV at the level of LBNP which did not evoke any adverse symptoms may be of predictive value for lower orthostatic tolerance.     

Effect of lower body negative pressure on orthostatic tolerance and cardiac function during 21 days head-down tilt bed rest

The purpose of the present study was to investigate the changes of orthostatic tolerance and cardiac function during 21 d head-down tilt (HDT) bed rest and effect of lower body negative pressure in the first and the last week in humans. Twelve healthy male volunteers were exposed to -6 degrees HDT bed rest for 21 d. Six subjects received -30 mmHg LBNP sessions for 1 h per day from the 1st to the 7th day and from the 15th to the 21st day of the HDT, and six others served as control. Orthostatic tolerance was assessed by means of standard tilt test. Stroke volume (SV), cardiac output (CO), preejection period (PEP) and left ventricular ejection time (LVET) were measured before and during HDT. Before HDT, all the subjects in the two groups completed the tilt tests. After 10 d and 21 d of HDT, all the subjects of the control group and one subject of the LBNP group could not complete the tilt test due to presyncopal or syncopal symptoms. The mean upright time in the control group (15.0 +/- 3.2 min) was significantly shorter than those in the LBNP group (19.7 +/- 0.9 min). SV and CO decreased significantly in the control group on days 3 and 10 of HDT, but remained unchanged throughout HDT in the LBNP group. A significant increase in PEP/LVET was observed on days 3 and 14 of HDT in both groups. The PEP/LVET in the LBNP group was significantly lower on day 3 of HDT, while LVET in the LBNP group was significantly higher on days 3, 7 and 14 of HDT than those in the control group. The results of this study suggest that brief daily LBNP sessions used in the first and the last weeks of 21 d HDT bed rest were effective in diminished the effect of head-down tilt on orthostatic tolerance, and LBNP might partially improve cardiac pumping function and cardiac systole function.     

Reduced orthostatic tolerance following 4 h head-down tilt

The cardiovascular responses to a 10-min 1.22 rad (70 degrees) head-up tilt orthostatic tolerance test (OST) was observed in eight healthy men following each of a 5-min supine baseline (control), 4 h of 0.1 rad (6 degrees) head-down tilt (HDT), or 4 h 0.52 rad (30 degrees) head-up tilt (HUT). An important clinical observation was presyncopal symptoms in six of eight subjects following 4 h HDT, but in no subjects following 4 h HUT. Immediately prior to the OST, there were no differences in heart rate, stroke volume, cardiac output, mean arterial pressure and total peripheral resistance for HDT and HUT. However, stroke volume and cardiac output were greater for the control group. Mean arterial pressure for the control group was less than HDT but not HUT. Over the full 10-min period of OST, the mean arterial pressure was not different between groups. Heart rate increased to the same level for all three treatments. Stroke volume decreased across the full time period for control and HDT, but only at 3 and 9 min for HUT. There was a higher total peripheral resistance in the HDT group than control or HUT. The pre-ejection period to left ventricular ejection time ratio was less in HDT than for control or HUT groups. These data indicate a rapid adaptation of the cardiovascular system to 4 h HDT that appears to be inappropriate on reapplication of a head to foot gravity vector. We speculate that the cause of the impaired orthostatic tolerance is decreased tone in venous capacitance vessels so that venous return is inadequate.     

Differential effects of lower body negative pressure and upright tilt on splanchnic blood volume

Upright posture and lower body negative pressure (LBNP) both induce reductions in central blood volume. However, regional circulatory responses to postural changes and LBNP may differ. Therefore, we studied regional blood flow and blood volume changes in 10 healthy subjects undergoing graded lower-body negative pressure (-10 to -50 mmHg) and 8 subjects undergoing incremental head-up tilt (HUT; 20 degrees , 40 degrees , and 70 degrees ) on separate days. We continuously measured blood pressure (BP), heart rate, and regional blood volumes and blood flows in the thoracic, splanchnic, pelvic, and leg segments by impedance plethysmography and calculated regional arterial resistances. Neither LBNP nor HUT altered systolic BP, whereas pulse pressure decreased significantly. Blood flow decreased in all segments, whereas peripheral resistances uniformly and significantly increased with both HUT and LBNP. Thoracic volume decreased while pelvic and leg volumes increased with HUT and LBNP. However, splanchnic volume changes were directionally opposite with stepwise decreases in splanchnic volume with LBNP and stepwise increases in splanchnic volume during HUT. Splanchnic emptying in LBNP models regional vascular changes during hemorrhage. Splanchnic filling may limit the ability of the splanchnic bed to respond to thoracic hypovolemia during upright posture.     

Is there "cardiovascular drift" during and after simulated orthostasis in humans?

This study investigates the time course of hemodynamic variables during and after simulated orthostasis (lower body suction at 55mmHg for 30 mins: LBNP-55). Individual strategies of blood pressure defense could be observed; LBNP-55 increased heart rate and reduced stroke volume, but was non-hypotensive. During 20 minutes post-LBNP, heart rate was decreased as well as stroke volume index below pre-LBNP values. The reduced cardiac index together with unchanged mean arterial pressure gave a highly significant increase of peripheral resistance after LBNP. The validity of stroke volume results under the experimental conditions given needs to be clarified.     

Effect of lower-body positive pressure on postural fluid shifts in men

To quantify the effect of 60 mm Hg lower-body positive pressure (LBPP) on orthostatic blood-volume shifts, the mass densities (+/- 0.1 g.1-1) of antecubital venous blood and plasma were measured in five men (27-42 years) during combined tilt table/antigravity suit inflation and deflation experiments. The densities of erythrocytes, whole-body blood, and of the shifted fluid were computed and the magnitude of fluid and protein shifts were calculated during head-up tilt (60 degrees) with and without application of LBPP. During 30-min head-up tilt with LBPP, blood density (BD) and plasma density (PD) increased by 1.6 +/- 0.3 g.1-1, and by 0.8 +/- 0.2 g.1-1 (+/- SD) (N = 9), respectively. In the subsequent period of tilt without LBPP, BD and PD increased further to + 3.6 +/- 0.9 g.1-1, and to + 2.0 +/- 0.7 g.1-1 (N = 7), compared to supine control. The density increases in both periods were significant (p less than 0.05). Erythrocyte density remained unaltered with changes in body position and pressure suit inflation/deflation. Calculated shifted-fluid densities (FD) during tilt with LBPP (1006.0 +/- 1.1 g.1-1, N = 9), and for subsequent tilt after deflation (1002.8 +/- 4.1 g.1-1, N = 7) were different from each other (p less than 0.03). The plasma volume decreased by 6.0 +/- 1.2% in the tilt-LBPP period, and by an additional 6.4 +/- 2.7% of the supine control level in the subsequent postdeflation tilt period. The corresponding blood volume changes were 3.7 +/- 0.7% (p less than 0.01), and 3.5 +/- 2.1% (p less than 0.05), respectively. Thus, about half of the postural hemo-concentration occurring during passive head-up tilt was prevented by application of 60 mm Hg LBPP.     

Cardiovascular and hormonal changes with different angles of head-up tilt in men

The purpose of this study was to assess the endocrine status, thoracic impedance, blood concentration, and hemodynamic dose-responses using different angles of passive head-up tilt (HUT) ranging from 12 degrees to 70 degrees in the same subjects. Measurements were performed during 20 min supine position (pre-HUT), 30 min upright (HUT12, HUT30, HUT53, or HUT70), and 20 min supine (post-HUT); subjects 70 min in the supine position only (HUT0) served as resting controls. Norepinephrine increased above resting control values by 19, 44, 80, and 102%; epinephrine by 30, 41, 64, and 68%; aldosterone by 29, 62, 139, and 165%; plasma renin activity n. s., 41, 91, and 89%; vasopressin n.s., 27, 47, and 59%; thoracic bioimpedance n. s., 8, 13, and 16%; heart rate n. s., 5, 26, and 45%, and mean arterial pressure n. s., 5, 7, and 10%; at min 27 of HUT12, HUT30, HUT53, and HUT70, respectively. Pulse pressure decreased with HUT53 and HUT70 by 4 and 10%. Hematocrit increased by 0.2, 1.7, 6.3, and 7.2%, respectively. Blood density increased by 2.3 and 3.0 g/l, plasma density by 1.7 and 1.8 g/l with HUT53 and HUT70. After finishing HUT, heart rate fell to values which stayed below pre-HUT, and also below resting control levels for > or = 5 min ("post-orthostatic bradycardia") even after the lowest orthostatic load (HUT12). Thoracic impedance and arterial pressure remained increased after terminating HUT30, HUT53, and HUT70. In conclusion, passive orthostatic loading of different extent produces specific dose-responses of different magnitude in the endocrine system, blood composition, thoracic impedance, and hemodynamic variables. The heart rate is depressed even after HUT12, while arterial blood pressure and thoracic impedance exceed pre-stimulus levels after greater head-up tilt, indicating altered cardiovascular response after passive orthostasis.     

Cardiac hemodynamics at rest and during LBNP after 4 days and 6 weeks in HDT

The first objective was to assess the left ventricle function at rest, at the end of a short term (4 days) HDT, and at the end of a long term (6 weeks) HDT. The second objective was to check if these short and long HDT induced any abnormal cardiac hemodynamic response to LBNP (lower body negative pressure) test that could be related to orthostatic intolerance.     

Effects of lower body positive pressure on muscle sympathetic nerve activity response [correction of respopnse] to head-up tilt

The benefits of lower body positive pressure (LBPP) are generally accepted for clinical treatment in medical emergencies caused by massive bleeding to maintain the systemic blood pressure. They are also used by NASA post spaceflight for preventing orthostatic hypotension in the astronauts. However, controversy still exists concerning the mechanisms underlying LBPP benefits. The purpose of this study was to test the hypothesis that the baroreflex-mediated enhancement in sympathetic activity would be attenuated by LBPP during an orthostatic challenge in humans. Specifically, we studied 1) the sympathetic activity responses by the microneurographic technique, using direct intraneural measurement of muscle sympathetic nerve activity (MSNA); and 2) the contributions of preload and afterload to the chances in MSNA response during orthostasis on application of LBPP. To accomplish these issues, MSNA was recorded microneurographically along with noninvasive measurement of the cardiovascular variables in all the subjects during exposure to a 70 degrees HUT with 30-mm Hg LBPP.     

Effect of lymphatic outflow pressure on lymphatic albumin transport in humans.

The effects of posture on the lymphatic outflow pressure and lymphatic return of albumin were examined in 10 volunteers. Lymph flow was stimulated with a bolus infusion of isotonic saline (0.9%, 12.6 ml/kg body wt) under four separate conditions: upright rest (Up), upright rest with lower body positive pressure (LBPP), supine rest (Sup), and supine rest with lower body negative pressure (LBNP). The increase in plasma albumin content (Delta Alb) during the 2 h after bolus saline infusion was greater in Up than in LBPP: 82.9 +/- 18.5 vs. -28.4 mg/kg body wt. Delta Alb was greater in LBNP than in Sup: 92.6 vs. -22.5 +/- 18.9 mg/kg body wt (P < 0.05). The greater Delta Alb in Up and Sup with LBNP were associated with a lower estimated lymphatic outflow pressure on the basis of the difference in central venous pressure (Delta CVP). During LBPP, CVP was increased compared with Up: 3.8 +/- 1.4 vs. -1.2 +/- 1.2 mmHg. During LBNP, CVP was reduced compared with Sup: -3.0 +/- 2.2 vs. 1.7 +/- 1.0 mmHg. The translocation of protein into the vascular space after bolus saline infusion reflects lymph return of protein and is higher in Up than in Sup. Modulation of CVP with LBPP or LBNP in Up and Sup, respectively, reversed the impact of posture on lymphatic outflow pressure. Thus posture-dependent changes in lymphatic protein transport are modulated by changes in CVP through its mechanical impact on lymphatic outflow pressure.     

Cardiovascular responses to apneic facial immersion during altered cardiac filling.

The hypothesis that reduced cardiac filling, as a result of lower body negative pressure (LBNP) and postexercise hypotension (PEH), would attenuate the reflex changes to heart rate (HR), skin blood flow (SkBF), and mean arterial pressure (MAP) normally induced by facial immersion was tested. The purpose of this study was to investigate the cardiovascular control mechanisms associated with apneic facial immersion during different cardiovascular challenges. Six subjects randomly performed 30-s apneic facial immersions in 6.0 +/- 1.2 degrees C water under the following conditions: 1) -20 mmHg LBNP, 2) +40 mmHg lower body positive pressure (LBPP), 3) during a period of PEH, and 4) normal resting (control). Measurements included SkBF at one acral (distal phalanx of the thumb) and one nonacral region of skin (ventral forearm), HR, and MAP. Facial immersion reduced HR and SkBF at both sites and increased MAP under all conditions (P < 0.05). Reduced cardiac filling during LBNP and PEH significantly attenuated the absolute HR nadir observed during the control immersion (P < 0.05). The LBPP condition did not result in a lower HR nadir than control but did result in a nadir significantly lower than that of the LBNP and PEH conditions (P < 0.05). No differences were observed in either SkBF or MAP between conditions; however, the magnitude of SkBF reduction was greater at the acral site than at the nonacral site for all conditions (P < 0.05). These results suggest that the cardiac parasympathetic response during facial immersion can be attenuated when cardiac filling is compromised.     

15 degrees head-down tilt attenuates the postexercise reduction in cutaneous vascular conductance and sweating and decreases esophageal temperature recovery time.

The following study examined the effect of 15 degrees head-down tilt (HDT) on postexercise heat loss and hemodynamic responses. We tested the hypothesis that recovery from dynamic exercise in the HDT position would attenuate the reduction in the heat loss responses of cutaneous vascular conductance (CVC) and sweating relative to upright seated (URS) recovery in association with an augmented hemodynamic response and an increased rate of core temperature decay. Seven male subjects performed the following three experimental protocols: 1) 60 min in the URS posture followed by 60 min in the 15 degrees HDT position; 2) 15 min of cycle ergometry at 75% of their predetermined V(O2 peak) followed by 60 min of recovery in the URS posture; or 3) 15 min of cycle ergometry at 75% of their predetermined V(O2 peak) followed by 60 min of recovery in the 15 degrees HDT position. Mean skin temperature, esophageal temperature (T(es)), skin blood flow, sweat rate, cardiac output (CO), stroke volume (SV), heart rate (HR), total peripheral resistance, and mean arterial pressure (MAP) were recorded at baseline, end exercise, 2, 5, 8, 12, 15, and 20 min, and every 5 min until end of recovery (60 min). Without preceding exercise, HDT decreased HR and increased SV (P < or = 0.05). During recovery after exercise, a significantly greater MAP, SV, CVC, and sweat rate and a significantly lower HR were found with HDT compared with URS posture (P < or = 0.05). Subsequently, a significantly lower T(es) was observed with HDT after 15 min of recovery onward (P < or = 0.05). At the end of 60 min of recovery, T(es) remained significantly elevated above baseline with URS (P < or = 0.05); however, T(es) returned to baseline with HDT. In conclusion, extended recovery from dynamic exercise in the 15 degrees HDT position attenuates the reduction in CVC and sweating, thereby significantly increasing the rate of T(es) decay compared with recovery in the URS posture.