Maximal Lower Body Negative Pressure Research Articles

Paradoxical increase in E/e' during severe central hypovolemia in healthy humans

Abstract Introduction The ratio of mitral blood inflow to mitral annular tissue velocity in early diastole (E/e') is widely used as an index of left ventricular (LV) diastolic dysfunction. Theoretically, it is considered that e’ can correct the effect of LV relaxation on E, and thus E/e’ can be applied for the prediction of LV filling pressures in patients with cardiac diseases. However, recent guidelines indicate that E/e’ may not provide a reliable estimate of filling pressures in healthy subjects. Indeed, previous studies have reported that E/e' did not decrease during acute central hypovolemia because both E and e’ are similarly reduced by low preload condtions. However, it is possible that E/e' did not decrease since central hypovolemia are not critical in the previous studies. Purpose The purpose of the present study was to clarify the change of E/e’ during severe central ypovolemia induced by lower body negative pressure. Methods Twelve healthy men (25±5 years old) underwent 2D Doppler and 3D echocardiography during graded lower body negative pressure (LBNP) up to presyncope. We measured LV diastolic function indices by 2D echocardiography including septal and lateral mitral annular early diastolic velocities (e’), and early (E) and late (A) mitral inflow velocities. In addition, we measured LV function indices by 3D echocardiography including end-diastolic volume (EDV), end-systolic volume (ESV), stroke volume (SV), ejection fraction (EF), global longitudinal strain (GLS), global circumferential strain (GCS), twist and peak untwisting rate. We compared echocardiography indices before LBNP (Baseline) with those at maximal LBNP (LBNPmax) and at half of the maximal LBNP (LBNP1/2max). Results E/e’ (Baseline: 5.8±0.8, LBNP1/2max: 5.4±1.0, LBNPmax: 7.8±2.3, mean±SD, p<0.01, ANOVA) did not change at the LBNP1/2max but increased only at the LBNPmax. E (80±11, 59±10, 62±12 cm/sec, p<0.01) and E/A (2.2±0.8, 1.5±0.5, 1.0±0.3, p<0.01) decreased at the LBNP1/2max as compared to baseline but did not change from LBNP1/2max to LBNPmax. e’ (14.1±2.0, 11.1±1.5, 8.2±2.2 cm/sec, p<0.01) decreased in response to LBNP. LV EF (62±3, 55±5, 43±9 %, p<0.01), LV GLS (-20.5±2.8, -17.6±2.7, -13.6±4.7 %, p<0.01), and LV GCS (-31.2±3.7, -26.8±3.3, -19.4±5.3 %, p<0.01) decreased in response to LBNP. LV twist (15.2±5.1, 14.5±5.4, 20.9±7.7 °, p<0.01) and LV peak untwisting rate (-138±42, -164±50, -245±88 °/cm, p<0.01) increased only at the LBNPmax. Conclusion The present study for the first time showed that E/e’ paradoxically increased during acute severe hypovolemia in healthy humans. This paradox was likely caused by well-preserved E, while e’ decreased in response to acute severe central hypovolemia. The present finding also showed that peak untwisting rate was increased only at severe central hypovolemia, suggesting that the well-preserved E may be caused by high pressure gradient from left atrium to LV induced by enhanced LV untwisting suction function.Key results of this study①Key results of this study②

The Reciprocal Relationship Between Cardiac Baroreceptor Sensitivity and Cerebral Autoregulation During Simulated Hemorrhage in Humans

Tolerance to reduced central blood volume (e.g., via hemorrhage) depends upon cardiovascular and cerebrovascular mediated compensatory mechanisms to preserve cerebral perfusion. Prior studies have demonstrated a reciprocal relationship between the arterial baroreflex and cerebral autoregulation (CA) at rest and in response to acute hypotension. It is unknown if this reciprocal relationship persists during progressive and sustained hypotension simulating hemorrhage. We hypothesized that the reciprocal relationship between cardiac baroreceptor sensitivity (BRS) and CA would be maintained during a simulated hemorrhage induced by maximal lower body negative pressure (LBNP), and that the strength of this relationship would be greater in subjects with higher tolerance to this stress. Healthy young adults (n=51; 23F/28M, 26 ± 4 y) completed a step-wise LBNP protocol until the onset of presyncope. Subjects were classified as high tolerant (HT) if they completed at least the -60 mmHg stage of LBNP (≥ 20-min), and low tolerant (LT) if they became presyncopal prior to completing the -60 mmHg stage of LBNP (< 20-min), as previously defined by our group. Heart rate (HR), mean arterial pressure (MAP), stroke volume (SV), and middle cerebral artery velocity (MCAv) were measured continuously. The absolute change from baseline to presyncope (Δ) was calculated for each variable. Cardiac BRS was calculated as ΔHR divided by ΔMAP, and CA was calculated as ΔMCAv divided by ΔMAP. The relationship between BRS and CA was assessed with Pearson's correlation coefficients for the entire group of 51 subjects, and within the HT and LT sub-groups. Absolute change values for the hemodynamic responses were also compared between the two tolerance groups. By design, tolerance to LBNP was different between the groups (HT (n=30): 1775 ± 225 s vs. LT (n=21): 1184 ± 253 s; P<0.0001). Accordingly, HT subjects demonstrated a greater ΔSV (HT: -51 ± 17 ml vs. LT: -41 ± 13 ml; P=0.03) and a greater ΔHR (HT: +56 ± 17 bpm vs. LT: +34 ± 20 bpm; P<0.0001) in response to maximal LBNP. Interestingly, ΔMAP (HT: -18 ± 7 mmHg vs. LT: -19 ± 9 mmHg; P=0.51), ΔMCAv (HT: -17 ± 8 cm/s vs. LT: -19 ± 10 cm/s; P=0.52), BRS (HT: 4 ± 3 bpm/mmHg vs. LT: 3 ± 4 bpm/mmHg; P=0.24), and CA (HT: 1.2 ± 0.9 cm/s.mmHg-1 vs. LT: 1.5 ± 1.8 cm/s.mmHg-1; P=0.45) were similar between HT and LT subjects. In support of our hypothesis, there was a strong reciprocal relationship (R=0.77; P<0.0001) between BRS and CA in the group of 51 subjects. When independently assessing this relationship within each tolerance group, however, there was a stronger relationship in LT subjects (R=0.94; P<0.0001) compared to HT subjects (R=0.57; P<0.001). In support of our hypothesis, the reciprocal relationship between cardiac BRS and CA was maintained during sustained and progressive hypotension, but this relationship was stronger in subjects with lower tolerance to this stress. These findings suggest that despite a strong overall relationship in the interaction between BRS and CA, it may not be a primary compensatory mechanism that dictates tolerance to simulated hemorrhage in young healthy adults.

Ketamine: yay or neigh? Implications for cardiovascular regulation and considerations for field use.

Ketamine: yay or neigh? Implications for cardiovascular regulation and considerations for field use.

The Interaction Between Heart Systole and Cerebral Circulation During Lower Body Negative Pressure Test.

The time constant (τ[s]) estimates how fast the arterial part of the cerebrovascular bed fills with blood volume during the cardiac cycle, whereas a product of τ and heart rate (HR) (τ*HR[%]) assesses how this period of arterial filling is related to an entire heart cycle. In this study we aimed to investigate cerebral hemodynamics using τ and τ*HR during a progressive lower body negative pressure (LBNP) test.Transcranial Doppler cerebral blood flow velocity (CBFV), Finapres arterial blood pressure (ABP), and HR, along with end-tidal CO2, were simultaneously recorded in 38 healthy volunteers during an LBNP test. The τ was estimated using mathematical transformation of ABP and CBFV pulse waveforms. After a gradual shortening of τ from baseline (0.20 ± 0.06 s) to maximal LBNP before the onset of presyncope (0.15 ± 0.05 s), we observed a significant increase in τ at presyncope (0.24 ± 0.15 s; p = 0.0001). In the course of LBNP, the τ*HR did not significantly change from baseline (25.6 ± 5.7 % vs 26.6 ± 8.9 %, p = n.s.) except for presyncope, when it increased to 40.4 ± 21.1 % (p < 0.000001). Because the time needed to fill the arterial part of the cerebrovascular bed with blood is prolonged during presyncope, an increased part of the heart cycle seems to be spent on the cerebral blood supply.

Reduced venous compliance: an important determinant for orthostatic intolerance in women with vasovagal syncope.

The influence of lower limb venous compliance on orthostatic vasovagal syncope (VVS) is uncertain. The most widespread technique to calculate venous compliance uses a nonphysiological quadratic regression equation. Our aim was therefore to construct a physiologically derived venous wall model (VWM) for calculation of calf venous compliance and to determine the effect of venous compliance on tolerance to maximal lower body negative pressure (LBNP). Venous occlusion plethysmography was used to study calf volume changes in 15 women with VVS (25.5 ± 1.3 yr of age) and 15 controls (22.8 ± 0.8 yr of age). The fit of the VWM and the regression equation to the experimentally induced pressure-volume curve was examined. Venous compliance was calculated as the derivative of the modeled pressure-volume relationship. Graded LBNP to presyncope was used to determine the LBNP tolerance index (LTI). The VWM displayed a better fit to the experimentally induced pressure-volume curve (P < 0.0001). Calf blood pooling was similar in the groups and was not correlated to the LTI (r = 0.204, P = 0.30). Venous compliance was significantly reduced at low venous pressures in women with VVS (P = 0.042) and correlated to the LTI (r = 0.459, P = 0.014) in the low pressure range. No correlation was found between venous compliance at high venous pressures and the LTI. In conclusion, the new VWM accurately adopted the curvilinear pressure-volume curve, providing a valid characterization of venous compliance. Reduced venous compliance at low venous pressures may adversely affect mobilization of peripheral venous blood to the central circulation during hypovolemic circulatory stress in women with VVS.

The heart cannot pump blood that it does not receive.

The heart cannot pump blood that it does not receive.

Time dynamics of cerebral blood flow during LBNP (1183.11)

Background: The time constant (τ) estimates how fast the arterial part of cerebral vascular bed is filled with blood volume during the cardiac systole. We have demonstrated previously that τ provides new insights into time dynamics in different cardiovascular diseases and during CO2 challenge in normal subjects. In this study we aimed to investigate time dynamics of cerebral blood flow using τ during progressive lower body negative pressure (LBNP) test.Material and Methods:Simultaneous recordings of TCD cerebral blood flow velocity (CBFV) in MCA, Finapres arterial blood pressure (ABP) and heart rate (HR) along with end‐tidal CO2 (EtCO2) were performed in 38 healthy volunteers (26 ± 4 years) during LBNP test. τ and τ*HR [beat] were estimated during lower body negative pressure ‐ using mathematical transformation of ABP and CBFV pulse waveforms. The analysis of variance (ANOVA) with Bonferroni post‐hoc test were used to compare the differences in hemodynamic variables between the stages of LBNP test. The level of significance was set as 0.05.Key Results / Statistics: From baseline to maximal LBNP before the onset of presyncope the gradual shortening of τ by 74±6% (mean ±95%CI) of baseline was observed with no further decrease in τ at presyncope (76±8%) ‐ see figure 1. The τ*HR did not change significantly in the course of LBNP up to the presyncope when it increased by 119±11% of baseline (p&lt;0.0013). At presyncope reduction in ABP was by 90±5% of baseline, in CBFV by 77±3% of baseline, and in EtCO2 by 81±5% of baseline whereas HR increased by 162±9% of baseline.Conclusion: The time constant Tau sheds light onto a new aspect of the pathophysiology of presyncope. Although the heart systole contributes an increasing part to the cerebral circulation the failure of cerebral circulation cannot be prevented. Tau*HR indicates a significant downslow of the cerebral circulation during LBNP just before the occurrence of presyncopal complaints.

Mechanisms contributing to low orthostatic tolerance in women: the influence of oestradiol

The impact of 17β-oestradiol (E2) exposure on autonomic control of orthostasis in young women is unclear. We tested the hypothesis that autonomic cardiovascular regulation is more sensitive to E2 exposure in women with low orthostatic tolerance. Women underwent an initial maximal lower body negative pressure (LBNP) test to place them into a low (LT, n = 7, 22 ± 1 years old, body mass index 22 ± 1 kg m(-2)) or a high orthostatic tolerance group (HT, n = 7, 22 ± 1 years old, body mass index 24 ± 1 kg m(-2)). We then suppressed endogenous reproductive hormone production using a gonadotrophin-releasing hormone antagonist (GnRHant) for 10 days, with E2 administration during the last 7 days of GnRHant. We measured R-R interval and beat-by-beat blood pressure during the modified Oxford protocol, and changes in heart rate, blood pressure and forearm vascular resistance (FVR) during submaximal LBNP. During submaximal LBNP, FVR increased in HT (ANOVA P < 0.05) but not in LT (ANOVA P > 0.05), and stroke volume was lower in LT relative to HT at all levels of LBNP (P < 0.05). Compared with GnRHant, E2 administration shifted FVR lower in LT (ANOVA P < 0.05), with no effect in HT. Administration of E2 increased baroreflex control of heart rate (derived from the modified Oxford protocol) in LT (GnRHant 10.7 ± 2.5 ms mmHg(-1) vs. E2 16.1 ± 2.4 ms mmHg(-1), P < 0.05) but not in HT (GnRHant 13.4 ± 1.9 ms mmHg(-1) vs. E2 15.3 ± 2.4 ms mmHg(-1), n.s.). In conclusion, blunted peripheral vasoconstriction and lower stroke volume contribute to compromised orthostatic tolerance in women; this inability to vasoconstrict is further exacerbated by exposure to E2. Furthermore, E2 administration increases baroreflex-mediated heart rate responses to orthostasis in low orthostatic tolerant women, which is likely to be a compensatory mechanism for the blunted peripheral vascular resistance and lower central volume.

Progesterone enhances adrenergic control of skin blood flow in women with high but not low orthostatic tolerance

Women are more susceptible to orthostatic intolerance. Peripheral α-adrenergic responsiveness is important in orthostasis and is lower in women compared to men, and is modulated by female sex hormones. We tested the hypothesis that oestradiol attenuates peripheral cutaneous adrenergic responses in women with low orthostatic tolerance (LT), whereas progesterone enhances adrenergic responses in women with high orthostatic tolerance (HT). After completing a maximal lower body negative pressure test to determine level of orthostatic tolerance (cumulative stress index, CSI), women self administered a gonadotropin releasing hormone (GnRH) antagonist for 16 days to suppress endogenous sex hormone production. Oestradiol (E2, 0.2 mg day−1, patch; days 4–16), and progesterone (P4, 200 mg day−1, oral; days 12–16) were administered. Skin blood flow responses to graded intradermal microdialysis infusions of noradrenaline (NA) were measured during GnRH antagonist, E2, and E2+P4, in eight HT (s.e.m. = 22 ± 1 years, CSI −871 ± 86 mmHg min) and eight LT (21 ± 1 years, CSI −397 ± 65 mmHg min) women. In separate probes, NA was infused alone, and co-infused with the nitric oxide synthase inhibitor NG-monomethyl-l-arginine (l-NMMA, 10 mm), the non-selective cyclooxygenase inhibitor ketorolac tromethamine (Keto, 10 mm), and combined l-NMMA + Keto (10 mm each). Progesterone administration enhanced adrenergic responses in HT women (logEC50 GnRH −4.02 ± 0.39, E2+P4 −5.18 ± 0.31, P < 0.05); this response was reversed with Keto (E2+P4 logEC50 NA+Keto −3.82 ± 0.35, P < 0.05). In contrast, no change in adrenergic responsiveness occurred in LT women during any hormone condition. These data indicate differential regulation of cutaneous adrenergic responses by progesterone via the cyclooxygenase pathway in women with high and low orthostatic tolerance.

Peripheral microvascular responses to norepinephrine in women with orthostatic intolerance

We determined the effects of estradiol (E2) and progesterone (P4) on the cutaneous microvasculature during adrenergic (norepinephrine, NE) stimulation in eight orthostatic tolerant (OT) and eight intolerant (OI) women. We hypothesized that 1) OI have a blunted vasoconstrictor response to NE compared to OT; and 2) that female sex hormones modulate vasoconstriction. A cumulative stress index (CSI) during maximal lower body negative pressure determined orthostatic tolerance. Endogenous E2 and P4 was suppressed with daily administration of a GnRH antagonist (GnRH) for 16 days; we gave E2 (0.2 mg/day, patch) on days 4–16, and P4 (200 mg/day, pills) on days 13–16. We measured skin blood flow (laser Doppler flowmetry) during graded NE infusions (skin microdialysis) during GnRH, E2, and E2+P4. CSI was 871±86 and 397±65 for OT and OI respectively (P &lt; 0.05). The vasoconstrictor response to NE during GnRH was similar between groups (log EC50: OT −3.9, CI −4.9 to −3.1; OI −4.4, CI −5.4 to −3.4). Combined E2+P4 enhanced the vasoconstrictor response in OT (EC50 −4.8, CI −5.6 to −4.1) but was reversed with Ketorolac (−3.8, −4.6 to −3.0). Hormones did not alter vasoconstriction in OI (EC50 −4.3, CI −5.0 to −3.7; −4.9, CI −5.5 to −4.4). Adrenergic response in skin microvasculature was similar between OT and OI. Although OI were insensitive to hormone treatments, P4 augments cutaneous adrenergic responses in OT. HL071159.

Cardiovascular Responses to Maximal Graded and Acute Lower Body Negative Pressure

This investigation attempted to determine whether heart-rate and blood pressure responses to maximal acute lower body negative pressure (LBNP) are exacerbated compared with maximal graded LBNP in active older (n = 9, 70 +/- 7 yr) and endurance-trained younger (n = 10, 23 +/- 3 yr) individuals. Heart rate increased earlier during graded LBNP in the younger group (-40 mm Hg vs. tolerance) and was significantly higher than that of the older adults at the point of tolerance. Mean arterial pressure (MAP) decreased more in the older than the younger individuals during graded LBNP. LBNP-tolerance index was significantly greater in the younger group (309 +/- 52 vs. 255.6 +/- 48 mm Hg/min). Acute doses of LBNP elicited slower heart-rate responses in the older group. Despite these age-related differences, MAP responses were not different between groups with acute LBNP, so age per se does not appear to predispose individuals to orthostatic intolerance.

Limitations of End-Tidal CO2 as an Early Indicator of Central Hypovolemia in Humans

Objective. This study tested the hypothesis that pulmonary end-tidal CO2 (PETCO2) tracks reductions in central blood volume in human volunteers exposed to progressive central hypovolemia. Methods. Measurements of PETCO2, systolic (SBP), diastolic (DBP), andmean arterial (MAP) blood pressures, heart rate (HR), stroke volume (SV), andrespiratory rate (RR) were obtained in 50 healthy human subjects during baseline supine rest andexposure to progressive reductions of central blood volume produced by application of lower body negative pressure (LBNP). Results. As increasing amounts of LBNP were applied, SBP, DBP, MAP, HR, SV, andPETCO2 decreased (p < 0.001). RR was not altered (p = 1.0). The decrease in PETCO2 did not begin to occur until 40% of maximal LBNP was applied. While PETCO2 decreased progressively thereafter, the range of baseline values (28.8–49.2 mmHg) varied more than the reduction in PETCO2 elicited by maximal LBNP (baseline = 40.1 ± 0.6 mmHg; maximal LBNP = 29.8 ± 1.0 mmHg). The earliest significant alteration was observed in SV, which occurred at 20% of maximal LBNP. MAP did not decline significantly until 80% of maximal LBNP was reached. PETCO2 was correlated positively with SV (r2 = 0.87). Conclusions. Although PETCO2tracked decreases in SV in this human model of progressive central hypovolemia, reductions in PETCO2were small relative to the range of baseline values. Thus, monitoring such small reductions in PETCO2 as an early warning of imminent cardiovascular collapse during hemorrhage may not be clinically useful without monitors capable of providing continuous trending.

Virtual conductance, real hypotension: what happens when we stand up too fast?

cardiovascular physiologists have long been curious about the mechanisms of fainting, and the goal of understanding why people faint under a variety of conditions has taken researchers to the ends of the Earth, and beyond. Some of these investigations have focused on adaptation to extreme

Cardiovascular Responses To Maximal Graded And Acute Lbnp In Older And Endurance Trained Younger Individuals

Aging and endurance exercise training appear to affect responses to maximal orthostatic stress. However, the direction of the effect is equivocal with some studies showing that the above conditions increase orthostatic tolerance with others finding that these states are associated with decreased orthostatic tolerance or no difference in tolerance. PURPOSE: To determine if heart rate and blood pressure responses to maximal acute lower body negative pressure (LBNP) are exacerbated compared to maximal graded LBNP in endurance trained younger and healthy older individuals. METHODS: Nineteen participants (young: n = 10, 23 + 3 yr, 60.3 + 16 ml/kg/min; older: n = 9, 70 + 7yr, 75% on 6-min walk test) underwent graded LBNP to presyncope or 4 minutes at −100 mmHg. Subsequently, participants were exposed to acute LBNP for 4 minutes at −50 mmHg and 4 minutes at the point of tolerance determined by the graded protocol. Heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP) and mean arterial pressure (MAP) were measured continuously with a Dinamap. RESULTS: LBNP tolerance index was significantly greater in the younger group (311+ 53 vs. 248+18). SBP, DBP and MAP were significantly higher in the older group at −50 mmHg in the graded protocol compared to the younger group. No difference in variables was seen at tolerance in the graded protocol, or during −50 mmHg and the tolerance point during the acute protocol in either group. HR was greater and SBP was lower at the point of tolerance in the graded protocol compared to the acute protocol for both groups. CONCLUSIONS: Young endurance trained individuals appear to be more tolerant to graded simulated orthostatic stress than older physically active humans. Graded LBNP may apply more cardiovascular stress than acute LBNP due to the prolonged exposure, therefore for practical purposes, determining tolerance using acute exposures to LBNP may be more indicative of cardiovascular responses to orthostasis.

The Effects of Aging and Physical Activity on Doppler Measures of Diastolic Function

Healthy aging results in changes in Doppler measures of diastolic function. It is unclear whether these alterations are a specific manifestation of the aging process or reflect a cardiac adaptation to a more sedentary lifestyle. It was hypothesized that healthy, but sedentary, aging would result in slowing of diastolic filling and myocardial relaxation, whereas lifelong endurance training would prevent such changes. Doppler data were measured in young subjects and sedentary and fit seniors across a broad range of loading conditions. Thirteen sedentary healthy (70+/-4 years) and 12 fit Masters athlete (68+/-3 years) seniors were recruited. Twelve young healthy (32+/-9 years) subjects were used for comparison. Pulmonary capillary wedge pressure and Doppler variables were measured at the 6 loading conditions of baseline (twice), -15 and -30 mm Hg lower body negative pressure, and 2 levels of saline solution infusion. Doppler variables consisted of early and late mitral inflow velocity (E/A) ratio, isovolumetric relaxation time (IVRT), tissue Doppler velocities (TDI Emean), and propagation velocity of mitral inflow. Aging resulted in a decrease in E/A ratio (p<0.001), TDI Emean (p<0.001), and propagation velocity of mitral inflow (p<0.001) and an increase in IVRT (p=0.001). Lifelong endurance training did not completely prevent the changes in E/A ratio (p=0.212), IVRT (p=0.546), or propagation velocity of mitral inflow (p=1.00). Fit seniors were able to achieve E/A ratios of 1.0 during baseline and saline solution infusion. TDI Emean was higher in fit versus sedentary seniors at baseline (p=0.012) and during maximal lower body negative pressure (p=0.036), but not during saline solution infusion (p=0.493). In conclusion, age-associated abnormalities in Doppler measures of myocardial filling and relaxation are only partially minimized by lifelong endurance training and therefore may be more specific to the aging process than secondary to years of deconditioning.

Effects of Age and Fitness on Tolerance to Lower Body Negative Pressure

The purpose of this investigation was to determine the effects of age and fitness on tolerance to maximal lower body negative pressure (LBNP). Ten older fit (OF) [73.9 +/- 2 years; 39.0 +/- 2 ml.kg(-1).min(-1) (age and estimated VO(2)peak, respectively)], 10 older unfit (OU) (70.9 +/- 1 years; 27.1 +/- 2 ml.kg(-1).min(-1)), 10 young fit (YF) (22.6 +/- 0.5 years; 57.1 +/- 2 ml.kg(-1).min(-1)), and 10 young unfit (YU) (23.1 +/- 1 years; 41.1 +/- 2 ml.kg(-1).min(-1)) participants underwent graded LBNP of -10 mmHg every 4 minutes to either presyncope or -100 mmHg. Compared to the other groups, YF had an earlier increase in heart rate (-40 mmHg vs the last stage; YF vs OF, OU, and YU, respectively) and decline in stroke volume (-20 mmHg vs -40 mmHg; YF vs OF, OU, and YU, respectively). OU had a higher resting mean arterial pressure; this difference was maintained until the last stage. OF had an earlier decline in total peripheral conductance than the other groups (-20 mmHg vs -40 mmHg). Tolerance to maximal LBNP did not differ among the groups. Despite differences in the responses to submaximal LBNP, neither age nor cardiovascular fitness affect tolerance to maximal LBNP.

Effects Of A 6-month Endurance-training Program On Venous Compliance And Maximal LBNP In Older Adults

Aging and chronic exercise training influence leg venous compliance. Venous compliance affects responses to an orthostatic stress. The extent to which exercise training in a previously sedentary older population will affect venous compliance and tolerance to the simulated orthostatic stress of maximal lower body negative pressure (LBNP) is unknown. PURPOSE To determine the influence of a 6-month endurance-training program on calf venous compliance and responses and tolerance to maximal LBNP in older men and women. METHODS Twenty participants (Exercise group: n =10, 5 males, 5 females; Control group: n =10, 6 males, 4 females; all>60 y.) underwent graded LBNP to presyncope or 4 minutes at −100 mmHg before and after a 6-month endurance-training program. Utilizing venous occlusion plethysmography, calf venous compliance was determined in both groups using the first derivative of the pressure-volume relation during cuff pressure reduction before training, at 3 months, and at the end of the training program. RESULTS The exercise group improved their fitness with the 6-month endurance training program while the control group did not change (14 vs <1%, respectively; p<0.05). LBNP tolerance did not differ between groups or across trials (p=0.47). Venous compliance was not different between groups or trials either initially or after 3 months of endurance training, but tended to be greater in the exercise group after 6 months of training (p=0.08). CONCLUSION These data suggest that a 6 month endurance training program can improve venous compliance without affecting tolerance to maximal LBNP in older participants.

Effects of a 6-mo endurance-training program on venous compliance and maximal lower body negative pressure in older men and women

Aging and chronic exercise training influence leg venous compliance. Venous compliance affects responses to an orthostatic stress. The extent to which exercise training in a previously sedentary older population will affect venous compliance and tolerance to the simulated orthostatic stress of maximal lower body negative pressure (LBNP) is unknown. The purpose of this investigation is to determine the influence of a 6-mo endurance-training program on calf venous compliance and responses and tolerance to maximal LBNP in older men and women. Twenty participants (exercise group: n = 10, 5 men, 5 women; control group: n = 10, 6 men, 4 women; all >60 yr) underwent graded LBNP to presyncope or 4 min at -100 mmHg before and after a 6-mo endurance-training program. Utilizing venous occlusion plethysmography, calf venous compliance was determined in both groups using the first derivative of the pressure-volume relation during cuff pressure reduction before training, at 3 mo, and at the end of the training program. The exercise group improved their fitness with the 6-mo endurance-training program, whereas the control group did not change (14 +/- 3 vs. <1 +/- 2%; P < 0.05). LBNP tolerance did not differ between groups or across trials (P = 0.47). Venous compliance was not different between groups or trials, either initially or after 3 mo of endurance training, but tended to be greater in the exercise group after 6 mo of training (P = 0.08). These data suggest that a 6-mo endurance-training program may improve venous compliance without affecting tolerance to maximal LBNP in older participants.

Effects of Age and Fitness on Tolerance to Lower Body Negative Pressure

0177 Orthostatic hypotension has and has not been reported among the elderly and endurance athletes may or may not have reduced tolerance to orthostatic stress. One of the limitations of many of the aging studies is in the use of submaximal rather than maximal orthostatic stress and a focus on either aging or fitness, not both. Purpose: The purpose of this investigation was to determine the effects of age and fitness on tolerance to maximal lower body negative pressure. Methods: Ten older fit (OF; 73.9 + 2 yo; 39.0 + 2 ml·kg-1·min-1), ten older unfit (OU; 70.9 + 1 yo; 27.1 + 2 ml·kg-1·min-1), ten young fit (YF; 22.6 + 0.5 yo; 57.1 + 2 ml·kg-1·min-1) and ten young unfit (YU; 23.1 + 1 yo; 41.1 + 2 ml·kg-1·min-1) participants underwent graded LBNP to either presyncope or −100 mmHg. Results: Compared to the other groups, YF had an earlier increase in HR (−40 mmHg vs the last stage, p<0.05) and decline in stroke volume (−20 mmHg vs −40 mmHg, p<0.05). OU had a higher resting mean arterial pressure; this difference was maintained until the last stage (p<0.05). OF had an earlier decline in total peripheral conductance than the other groups (−20 mmHg vs −40 mmHg, p<0.05). Tolerance to maximal LBNP did not differ between the groups. Conclusion: Despite differences in the responses to submaximal LBNP, which suggest that mechanisms to maintain blood pressure are different, neither age nor cardiovascular fitness affect tolerance to LBNP.

Effects of Age and Fitness on Tolerance to Lower Body Negative Pressure

0177 Orthostatic hypotension has and has not been reported among the elderly and endurance athletes may or may not have reduced tolerance to orthostatic stress. One of the limitations of many of the aging studies is in the use of submaximal rather than maximal orthostatic stress and a focus on either aging or fitness, not both. Purpose: The purpose of this investigation was to determine the effects of age and fitness on tolerance to maximal lower body negative pressure. Methods: Ten older fit (OF; 73.9 + 2 yo; 39.0 + 2 ml·kg-1·min-1), ten older unfit (OU; 70.9 + 1 yo; 27.1 + 2 ml·kg-1·min-1), ten young fit (YF; 22.6 + 0.5 yo; 57.1 + 2 ml·kg-1·min-1) and ten young unfit (YU; 23.1 + 1 yo; 41.1 + 2 ml·kg-1·min-1) participants underwent graded LBNP to either presyncope or −100 mmHg. Results: Compared to the other groups, YF had an earlier increase in HR (−40 mmHg vs the last stage, p<0.05) and decline in stroke volume (−20 mmHg vs −40 mmHg, p<0.05). OU had a higher resting mean arterial pressure; this difference was maintained until the last stage (p<0.05). OF had an earlier decline in total peripheral conductance than the other groups (−20 mmHg vs −40 mmHg, p<0.05). Tolerance to maximal LBNP did not differ between the groups. Conclusion: Despite differences in the responses to submaximal LBNP, which suggest that mechanisms to maintain blood pressure are different, neither age nor cardiovascular fitness affect tolerance to LBNP.