Reduction In Plasma Volume Research Articles

Changes in plasma volume associated with mental stress ischemia in patients with coronary artery disease

Psychological stress has been shown to trigger angina and myocardial ischemia in patients with coronary artery disease. However, the mechanisms by which stress may trigger cardiac events has yet to be fully elucidated. Twenty five patients underwent radionuclide ventriculography during a multiple stress challenge. Plasma volume was assessed during rest and at the end of the stress task. Flow-mediated dilatation was also measured. Controlling for endothelial function and medications, patients with ischemia had greater reductions in plasma volume than non-ischemic patients. Reduced plasma volume may be one mechanism by which mental stress may increase the risk for acute coronary events.

Impact of Acute Weight Loss and/or Thermal Stress on Rowing Ergometer Performance

The impact of acute weight loss on rowing performance was assessed when generous nutrient intake was provided in 2 h of recovery after making weight. Competitive rowers (N = 17) completed four ergometer trials, each separated by 48 h. Two trials were performed after a 4% body mass loss in the previous 24 h (WT) and two were performed after no weight restrictions, that is, unrestricted (UNR). In addition, two trials (1 x WT, 1 x UNR) were in a thermoneutral environment (NEUTRAL, mean 21.1 +/- SD 0.7 degrees C, 29.0 +/- 4.5% RH) and two were in the heat (HOT 32.4, +/- 0.4 degrees C, 60.4 +/- 2.7% RH). Trials were performed in a counterbalanced fashion according to a Latin square design. Aggressive nutritional recovery strategies (WT 2.3 g x kg(-1) carbohydrate, 34 mg x kg(-1) Na, 28.4 mL x kg(-1) fluid; UNR ad libitum) were employed in the 2 h after weigh-in. Both WT (mean 2.1, 95% CI 0.7-3.4 s; P = 0.003) and HOT (4.1, 2.7 - 5.4 s; P < 0.001) compromised 2000-m time-trial performance. Whereas WT resulted in hypohydration, the associated reduction in plasma volume explained only part of the performance compromise observed (0.2 s for every 1% decrement) Moreover, WT did not influence core temperature or indices of cardiovascular function. Acute weight loss compromised performance, despite generous nutrient intake in recovery, although the effect was small. Performance decrements were further exacerbated when exercise was performed in the heat.

Hyponatraemia for the clinical endocrinologist

Hyponatraemia for the clinical endocrinologist

Atrial natriuretic peptide: an essential physiological regulator of transvascular fluid, protein transport, and plasma volume

Atrial natriuretic peptide (ANP) acts acutely to reduce plasma volume by at least 3 mechanisms: increased renal excretion of salt and water, vasodilation, and increased vascular permeability. Authors of a study in this issue of the JCI performed a knockout of the receptor for ANP in vascular endothelia in order to distinguish the effects of ANP-dependent increases in vascular permeability from those of other endocrine actions of ANP in the regulation of plasma volume. The knockout mice exhibited reduced vascular permeability to plasma protein, resulting in chronically increased plasma volume, arterial hypertension, and cardiac hypertrophy. Renal excretion and vasodilation did not account for these changes. Thus ANP-induced increases in endothelial permeability may be critical to the ability of ANP to lower arterial blood pressure.

Renin-Aldosterone Paradox and Perturbed Blood Volume Regulation Underlying Postural Tachycardia Syndrome

Patients with postural tachycardia syndrome (POTS) experience considerable disability, but in most, the pathophysiology remains obscure. Plasma volume disturbances have been implicated in some patients. We prospectively tested the hypothesis that patients with POTS are hypovolemic compared with healthy controls and explored the role of plasma renin activity and aldosterone in the regulation of plasma volume. Patients with POTS (n=15) and healthy controls (n=14) underwent investigation. Heart rate (HR), blood pressure (BP), plasma renin activity, and aldosterone were measured with patients both supine and upright. Blood volumes were measured with 131I-labeled albumin and hematocrit. Patients with POTS had a higher orthostatic increase in HR than controls (51+/-18 versus 16+/-10 bpm, P<0.001). Patients with POTS had a greater deficit in plasma volume (334+/-187 versus 10+/-250 mL, P<0.001), red blood cell volume (356+/-128 versus 218+/-140 mL, P=0.010), and total blood volume (689+/-270 versus 228+/-353 mL, P<0.001) than controls. Despite the lower plasma volume in patients with POTS, there was not a compensatory increase in plasma renin activity (0.79+/-0.58 versus 0.79+/-0.74 ng x mL(-1) x h(-1), P=0.996). There was a paradoxically low level of aldosterone in the patients with POTS (190+/-140 pmol/L versus 380+/-230 pmol/L; P=0.017). Patients with POTS have paradoxically unchanged plasma renin activity and low aldosterone given their marked reduction in plasma volume. These patients also have a significant red blood cell volume deficit, which is regulated by the renal hormone erythropoietin. These abnormalities suggest that the kidney may play a key role in the pathophysiology of POTS.

Effects of gender and hypovolemia on sympathetic neural responses to orthostatic stress

We tested the hypothesis that women have blunted sympathetic neural responses to orthostatic stress compared with men, which may be elicited under hypovolemic conditions. Muscle sympathetic nerve activity (MSNA) and hemodynamics were measured in eight healthy young women and seven men in supine position and during 6 min of 60 degrees head-up tilt (HUT) under normovolemic and hypovolemic conditions (randomly), with approximately 4-wk interval. Acute hypovolemia was produced by diuretic (furosemide) administration approximately 2 h before testing. Orthostatic tolerance was determined by progressive lower body negative pressure to presyncope. We found that furosemide produced an approximately 13% reduction in plasma volume, causing a similar increase in supine MSNA in men and women (mean +/- SD of 5 +/- 7 vs. 6 +/- 5 bursts/min; P = 0.895). MSNA increased during HUT and was greater in the hypovolemic than in the normovolemic condition (32 +/- 6 bursts/min in normovolemia vs. 44 +/- 15 bursts/min in hypovolemia in men, P = 0.055; 35 +/- 9 vs. 45 +/- 8 bursts/min in women, P < 0.001); these responses were not different between the genders (gender effect: P = 0.832 and 0.814 in normovolemia and hypovolemia, respectively). Total peripheral resistance increased proportionately with increases in MSNA during HUT; these responses were similar between the genders. However, systolic blood pressure was lower, whereas diastolic blood pressure was similar in women compared with men during HUT, which was associated with a smaller stroke volume or stroke index. Orthostatic tolerance was lower in women, especially under hypovolemic conditions. These results indicate that men and women have comparable sympathetic neural responses during orthostatic stress under normovolemic and hypovolemic conditions. The lower orthostatic tolerance in women is predominantly because of a smaller stroke volume, presumably due to less cardiac filling during orthostasis, especially under hypovolemic conditions, which may overwhelm the vasomotor reserve available for vasoconstriction or precipitate neurally mediated sympathetic withdrawal and syncope.

Antitumor Effects of a Monoclonal Antibody that Binds Anionic Phospholipids on the Surface of Tumor Blood Vessels in Mice

We recently reported that anionic phospholipids, principally phosphatidylserine, become exposed on the external surface of viable vascular endothelial cells in tumors, possibly in response to oxidative stresses present in the tumor microenvironment. In the present study, we tested the hypothesis that a monoclonal antibody directed against anionic phospholipids might exert antitumor effects by causing vascular damage in tumors. A new mouse immunoglobulin G3 monoclonal antibody, 3G4, was raised that binds anionic phospholipids in the presence of serum or beta2-glycoprotein I. The antibody was tested for its ability to localize to tumor vessels and exert antitumor effects in mice. 3G4 recognized anionic phospholipids on the external membrane of H(2)O(2)-treated endothelial cells and in vitro. It localized specifically to tumor vascular endothelium and to necrotic tumor cells after injection into severe combined immunodeficient mice bearing orthotopic MDA-MB-435 tumors. Treatment with 3G4 retarded the growth of four different tumors in mice. It reduced the growth of established orthotopic MDA-MB-231 and MDA-MB-435 human breast tumors in mice by 75% and 65% respectively, large L540 human Hodgkin's tumors by 50%, and small syngeneic Meth A fibrosarcomas by 90%. Histologic examination revealed vascular damage, a reduction in vascular density, and a reduction in tumor plasma volume. Treatment with 3G4 induced the binding of monocytes to tumor endothelium and infiltration of macrophages into MDA-MB-435 and MDA-MB-231 tumors. No toxicity to the mice was observed. 3G4 localizes specifically to complexes of anionic phospholipids and serum proteins on the surface of vascular endothelial cells in tumors in mice. This results in damage to tumor vasculature and suppression of tumor growth.

Modulation of body fluids and angiotensin II receptors in a rat model of intra‐uterine growth restriction

We previously reported that sodium restriction during pregnancy reduces plasma volume expansion and promotes intra-uterine growth restriction (IUGR) in rats while it activates the renin-angiotensin-aldosterone system (RAAS). In the present study, we proceeded to determine whether expression of the two angiotensin II (ANGII) receptor subtypes (AT(1) and AT(2)) change in relation to maternal water-electrolyte homeostasis and fetal growth. To this end, pregnant (gestation day 15) and non-pregnant Sprague-Dawley rats were randomly assigned to two groups fed either normal, or Na(+)-restricted diets for 7 days. At the end of the treatment period, plasma aldosterone and renin activity as well as plasma and urine electrolytes were measured. Determinations for AT(1) and AT(2) mRNA and protein were made by RNase protection assay and photoaffinity labelling, respectively, using a number of tissues implicated in volume regulation and fetal growth. In non-pregnant rats, Na(+) restriction decreases Na(+) excretion without altering plasma volume, plasma Na(+) concentration or the expression of AT(1) and AT(2) mRNA or protein in the tissues examined. In normally fed pregnant rats when compared to non-pregnant controls, AT(1) mRNA increases in the hypothalamus as well as pituitary and declines in uterine arteries, while AT(1) protein decreases in the kidney and AT(2) mRNA declines in the adrenal cortex. In pregnant rats, Na(+) restriction induces a decrease in plasma Na(+), an increase in plasma urea, as well as a decline in renal urea and creatinine clearance rates. Protein levels for both AT(1) and AT(2) in the pituitary and AT(2) mRNA in the adrenal cortex are lower in the Na(+)-restricted pregnant group when compared to normally fed pregnant animals. Na(+) restriction also induces a decrease in AT(1) protein in the placenta. In conclusion, these results suggest that pregnancy may increase sensitivity to Na(+) depletion by the tissue-specific modulation of ANGII receptors. Finally, these receptors may be implicated in the IUGR response to low Na(+).

Orthostatic blood pressure control before and after spaceflight, determined by time-domain baroreflex method

Reduction in plasma volume is a major contributor to orthostatic tachycardia and hypotension after spaceflight. We set out to determine time- and frequency-domain baroreflex (BRS) function during preflight baseline and venous occlusion and postflight orthostatic stress, testing the hypothesis that a reduction in central blood volume could mimic the postflight orthostatic response. In five cosmonauts, we measured finger arterial pressure noninvasively in supine and upright positions. Preflight measurements were repeated using venous occlusion thigh cuffs to impede venous return and "trap" an increased blood volume in the lower extremities; postflight sessions were between 1 and 3 days after return from 10- to 11-day spaceflight. BRS was determined by spectral analysis and by PRVXBRS, a time-domain BRS computation method. Although all completed the stand tests, two of five cosmonauts had drastically reduced pulse pressures and an increase in heart rate of approximately 30 beats/min or more during standing after spaceflight. Averaged for all five subjects in standing position, high-frequency interbeat interval spectral power or transfer gain did not decrease postflight. Low-frequency gain decreased from 8.1 (SD 4.0) preflight baseline to 6.8 (SD 3.4) postflight (P = 0.033); preflight with thigh cuffs inflated, low-frequency gain was 9.4 (SD 4.3) ms/mmHg. There was a shift in time-domain-determined pulse interval-to-pressure lag, Tau, toward higher values (P < 0.001). None of the postflight results were mimicked during preflight venous occlusion. In conclusion, two of five cosmonauts showed abnormal orthostatic response 1 and 2 days after spaceflight. Overall, there were indications of increased sympathetic response to standing, even though we can expect (partial) restoration of plasma volume to have taken place. Preflight venous occlusion did not mimic the postflight orthostatic response.

Severe Acute Hemolytic Transfusion Reaction Following ABO-Mismatched Platelet Transfusion: Should ABO-Mismatched Platelet Transfusion Policy Be Evaluated.

Transfusion of ABO-mismatched platelets is common practice. Although a unit of single donor apheresis platelet (SDP) contains as much plasma and passive anti-A or/and anti-B antibodies (allo-agglutinins) as a unit of fresh frozen plasma, ABO- mismatched platelet transfusions are considered safe and hemolytic transfusion reactions have only rarely been reported. We report a case of a 67-year old male, blood group A, with mantle cell lymphoma who received 1 SDP for chemotherapy induced thrombocytopenia. Several prior platelet transfusions had been uneventful. After 150 ml of irradiated, leukoreduced, SDP from blood group O donor had been infused, he developed nausea, light-headiness, chills, and back pain. He became bradycardic and hypotensive. Platelet transfusion was discontinued and intravenous dexamethasone and rapid saline infusion was administered. Later, his hemoglobin dropped from 10.6 to 7.4 g/dl and total serum bilirubin increased by 9 fold. A direct antiglobulin test (DAT) on post-transfusion sample demonstrated 1+ reactivity at room temperature. An elution test performed on the patient's circulating red blood cells contained anti-A antibodies. These results are consistent with a severe acute hemolytic transfusion reaction. The donor anti-A and anti-B antibodies titers at room temperature and at 37°C were 512 and 2048 with A1 cells and 128 and 256 with B cells, respectively.This case illustrates the rare possibility of hemolytic transfusion reaction occurring as a result of ABO-mismatched platelets from group O donor with high-titer anti-A antibodies. SDP (in contrast to pooled platelets) offers the advantages of reduced risk of infection transmission and alloimmunization by limiting exposure to one donor only. However, it increases the opportunity for hemolytic transfusion reaction to occur if the donor has high-titer antibodies which would have been diluted if pooled platelets were used. As SDP use becomes more widespread, the risk of clinically significant hemolytic reactions is likely to increase, especially in seriously ill patients who tolerate these reactions particularly poorly. Moreover, increasingly, apheresis platelets are being donated by a small group of highly motivated donors, raising the chances of repeated transfusions from the same donors. We propose that the safety of ABO-mismatched platelet transfusions be re-evaluated. Effectiveness (and costs) of potential preventive strategies such as screening all SDP units for high-titer antibodies and/or plasma volume reduction of all mismatched SDP units should be studied.

Long-term bed rest-induced reductions in stroke volume during rest and exercise: cardiac dysfunction vs. volume depletion

Long-term head-down-tilt bed rest (HDT) causes cardiovascular deconditioning, attributed to reflex dysfunctions, plasma volume reduction, or cardiac impairments. Our objective with the present study was to evaluate the functional importance and relative contribution of these during rest and exercise in supine and upright postures. We studied six subjects before (baseline), during [days 60 (D60) and 113 (D113)], and after [recovery days 0 (R0), 3 (R3), and 15 (R15)] 120 days of -6 degrees HDT. We determined cardiac output, stroke volume (SV), mean arterial pressure, and heart rate during rest and exercise in supine and upright postures. Cardiac output and SV decreased significantly in all four conditions, but the time courses differed for rest and exercise. Upright resting SV was decreased by 24 +/- 9% at D60 compared with baseline but had recovered already at R3. Supine exercise SV decreased more slowly (by 5 +/- 8% at D60 and by 18 +/- 4% at D113) and recovered more slowly after HDT termination. Steady-state mean arterial pressure showed no changes. Heart rate had increased by 18 +/- 4% at D60 and had recovered partially at R3. Our data indicate that long-term HDT causes both a rapid, preload-dependent reduction in SV, most evident during rest in the upright position, and a more slowly developing cardiac dysfunction, most evident during supine exercise. However, the ability to maintain blood pressure and to perform sustained low levels of dynamic exercise is not influenced by HDT.

Effect of blood volume on plasma volume shift during exercise

To assess the relationship between blood volume (BV) and the reduction in plasma volume (PV) during exercise in individual variations, we measured BV and changes in PV in thirteen male volunteers during treadmill exercise until exhaustion. The lactate threshold (LT), as a predictor of aerobic exercise capacity, was calculated from the exercise intensity at the point of plasma lactate concentration buildup to 4 mmol. The relationship of peak VO 2 with BV indicated a significant positive correlation. The strong positive relation between the shifts in PV and total PV, and resulted in a maintenance of the circulating BV.

Reduced plasma volume and mesenteric vascular reactivity in obese Zucker rats.

Obese Zucker rats (OZR) are mildly hypertensive with an apparently elevated sympathetic vasomotor tone compared with lean Zucker rats (LZR). Studies have also suggested enhanced adrenergic pressor reactivity in OZR but assumed comparable baroreflexes, or blood volume-to-body weight ratio, to LZR. In 15-wk-old OZR and LZR, we measured plasma volume and vascular reactivity to norepinephrine (NE) and phenylephrine (PE) with doses evaluated by body weight and plasma volume. Plasma volume measured by dye dilution (Evans blue; 200 microl of 0.5%) showed that OZR had comparable blood volumes to LZR but lower blood volume-to-body weight ratio (3.4 +/- 0.2 ml/100 g) than LZR (5.7 +/- 0.2 ml/100 g, P < 0.05). Ganglionic blockade (mecamylamine, 4 mg/kg) in isoflurane-anesthetized rats produced larger decreases in arterial pressure in OZR compared with LZR (52 +/- 2 vs. 46 +/- 2 mmHg). Pressor responses to NE (0.01-10 microg/kg) were exaggerated with doses analyzed by body weight but not analyzed by drug quantity. Pressor responses to PE (1-24 microg/kg) showed no difference with doses analyzed by body weight, but, analyzed by drug quantity, OZR showed a slight decrease in pressor reactivity. PE-induced increases in vascular resistance were exaggerated in the hindlimb circulation of OZR, normal in the renal circulation, and attenuated in the mesenteric circulation. The timing of the peak pressor response to PE corresponded with the increase in mesenteric vascular resistance, followed by rises in hindlimb and renal resistance. These data suggest that systemic adrenergic pressor reactivity is not enhanced in OZR, despite exaggerated vascular reactivity in the hindlimb of the OZR.

Angiotensin II Sensitivity in Nonpregnant Formerly Preeclamptic Women and Halthy Parous Contorls

In women prone to develop hypertensive complications, vascular reactivity fails to decrease in early pregnancy. Since hypertensive syndromes of pregnancy seem to be superimposed on a preexisting disorder, we tested the hypothesis that in formerly preeclamptic women, as compared to healthy parous controls, circulatory reactivity to angiotensin II is enhanced in the follicular phase of the menstrual cycle. Sixty formerly preeclamptic women were subdivided into a hypertensive (HYPERT, n = 14), a normotensive thrombophilic (THROMB, n = 26), and a normotensive nonthrombophilic (ASYMPT, n = 20) subgroup. In these women and in 11 healthy parous controls we assessed at least 5 months postpartum at day 5 (+/-2) of the menstrual cycle the following variables: body weight, height, plasma volume, reactivity to infused angiotensin II of arterial blood pressure, heart rate, glomerular filtration rate (GFR), effective renal blood flow, and the hormones of the renin-angiotensin-aldosterone (RAAS) axis. At baseline, THROMB did not differ from controls. In contrast, ASYMPT exhibited slight overweight, reduced plasma volume, and reduced renal blood flow. HYPERT much resembled ASYMPT except for the overweight, renal perfusion, and GFR. Infusion of angiotensin II led to comparable decreases in renal perfusion and filtration, and to increases in blood pressure. However, sensitivity to this substance correlated inversely with relative and absolute sizes of the plasma volume compartment. Circulatory sensitivity to infused angiotensin II is comparable between nonpregnant formerly preeclamptic women and healthy parous controls. However, responsiveness to this agent is enhanced among women with a contracted plasma volume compartment, a condition commonly observed among formerly preeclamptic women.

Renal and hormonal effects of water deprivation in late-term pregnant rats.

Water-retaining hormones are stimulated during pregnancy allowing normal volume expansion. Because pregnant rats actively retain water, we postulate that water deprivation (WD) would cause a greater reduction in plasma volume in pregnant than in nonpregnant rats. To test this hypothesis, Sprague-Dawley pregnant and nonpregnant rats were water-deprived for 48 hours. At day 19 of pregnancy, or in the corresponding day in nonpregnant rats, they were randomly assigned to either a WD or a control (C) pair-fed group (n=10 to 12 per group). WD significantly reduced body weight, food intake, and creatinine clearance, and increased urinary osmolality in nonpregnant and pregnant rats. WD reduced plasma volume in a similar proportion in nonpregnant and pregnant rats (nonpregnant rats C=13.1+/-0.4, WD=11.0+/-0.2; pregnant rats C=19.4+/-0.7, WD=16.8+/-0.5 mL, P<0.001). Both groups of pregnant rats had a similar reduction in blood pressure. Plasma renin activity (nonpregnant rats C=6.1+/-1.1, WD=20.5+/-2.0; pregnant rats C=49+/-9.7, WD=94+/-12 ng angiotensin I/mL per hour, P<0.001) and plasma aldosterone levels were increased by pregnancy and further increased by WD. WD significantly reduced urinary kallikrein. WD caused a significant reduction in fetal but not placental weights. Present data indicate that 48-hour WD reduced renal kallikrein and further stimulated water-retaining hormones. We speculate that these are compensatory changes contributing to the maintenance of pregnancy in response to WD.

Platelet activation, sympathetic tone, and plasma volume in nulligravid women of reproductive age.

Preeclampsia is associated with increased platelet activation, increased sympathetic activity, and decreased plasma volume. We sought to estimate the relationship of plasma volume, sympathetic activity, or both to platelet activation in nonpregnant nulligravid women. We studied 37 healthy nulligravid subjects during the follicular phase of the menstrual cycle. After intravenous access was obtained, subjects rested in the supine position for 15 minutes. Blood was drawn without venous constriction for measurement of plasma catecholamines (epinephrine and norepinephrine) and complete blood count. Antigenic markers of platelet activation, CD63 and CD61-CD14 (platelet-monocyte aggregates), were measured with flow cytometry. Plasma volume was estimated in the supine position by using Evans blue dye and is expressed in milliliters and corrected for body mass index (BMI). We compared data from the lowest plasma volume/BMI quartile with the 2 middle quartiles combined and with the upper quartile. Data are expressed as mean +/- standard deviation. P <.05 was considered significant. Subjects were aged 26.5 +/- 5.0 years, BMI was 24.0 +/- 3.0 kg/m(2), and plasma volume was 2,685 +/- 429 mL. We identified no significant relationship of platelet concentration to plasma volume/BMI between quartile groups (P =.944). However, there was a significant difference between quartiles for %CD63 expression (P =.013) and for CD61/CD14 expression (P =.018), with the lowest quartile demonstrating elevated platelet activation. We found evidence that enhanced platelet activation is associated with reduced plasma volume, but not with plasma catecholamine concentrations. There was no association of platelet concentration with reduced plasma volume. We speculate that elements of the clinical syndrome of preeclampsia coexist as a subclinical phenotype before pregnancy.

Effects of Gender and Hypovolemia on Sympathetic Neural Response to Orthostatic Stress

1463 PURPOSE: To test the hypothesis that women have blunted vasomotor sympathetic responses to orthostatic stress compared to men, which may be elicited under hypovolemic condition. METHODS: Muscle sympathetic nerve activity (MSNA), plasma catecholamines and hemodynamics were measured in 6 healthy women (29.7 ± 2.7 yrs, mean ± SEM) and 7 control men supine, and during 6-min of 60° head-up tilt (HUT) under both normovolemic and hypovolemic conditions (in random order), with ∼4 wk interval. Acute hypovolemia was produced by administration of a diuretic (furosemide 20 mg, iv) ∼2 h before testing. RESULTS: Furosemide produced an ∼8% reduction in plasma volume, resulting in an ∼40% increase in resting MSNA in both genders. MSNA was increased during HUT, while the change from supine to upright (ΔMSNA) was greater in the hypovolemic than normovolemic condition (18.0 ± 2.7 in normovolemia vs. 24.4 ± 4.5 bursts/min in hypovolemia in males, and 22.5 ± 3.2 vs. 30.5 ± 4.1 bursts/min in females; both P<0.05); these responses were not different between genders. Normalized total activity increased identically during HUT in males and females under both conditions. Plasma norepinephrine increased during HUT, the increment was greater in the hypovolemic than normovolemic condition (P<0.05), and the response was also similar between genders. Total peripheral resistance increased similarly in males and females during HUT, however, the increment was not different between normovolemic and hypovolemic conditions. Blood pressure was lower and stroke volume was smaller (both P < 0.05), while heart rate was similar in females compared to males during HUT under normovolemic and hypovolemic conditions. CONCLUSION: These results reject the hypothesis. It is concluded that men and women have comparable vasomotor sympathetic responses to orthostatic stress under both normovolemic and hypovolemic conditions. Supported partially by AHA Texas Affiliate Post Doctoral Fellowship Grant 0225017Y, and The Wallace, Barbara, and Kelly King Foundation Trust.

The Effect of Acute Exercise upon Postprandial Lipemia Following Correction for Plasma Volume Shifts

1489 PURPOSE: To examine the influence of plasma volume (PV) adjustments on our previously reported finding that isocaloric bouts of acute strength (ST) and aerobic training (AT) had no effect on fasting and postprandial plasma lipoprotein concentrations in 13 healthy normolipidemic males (age, 20.9 ± 0.6 years). METHODS: Subjects participated in three postprandial lipemia tests, one control (CON) and the other two 14-hours following isocaloric bouts of ST and AT. During all 3 tests, venous samples were obtained in a 12-hr fasted state and after the consumption of a high fat breakfast (55 g fat, 149 g carbohydrate, 22 g protein). Blood samples were analyzed for plasma triglyceride (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C) and glucose. Changes in PV were determined using the fasting CON trial hematocrit (Hct) and hemoglobin (Hb) values as the reference point from which all blood samples from the CON trial and exercise trials were compared. TG was monitored hourly for 6 hours from which the incremental (INCAUC) and total (TOTAUC) areas under the 6-hour TG curve were calculated. Differences between CON, ST and AT trials, with and without PV corrections. RESULTS: Hb was significantly higher in the fasting AT blood sample compared to the fasting CON sample (CON, 11.48 ± 0.78; AT, 14.13 ± 0.65; ST, 13.46 ± 0.53 mg/dl). The AT and ST fasting blood samples displayed 18 and 14 % reductions in PV, respectively. After PV correction there was no effect on fasting plasma TG or HDL-C concentrations. However, fasting plasma TC (CON, 172.5 ± 7.3; AT 138.1 ± 7.5; ST 149.2 ± 8.2 mg/dl) and glucose (CON, 85.9 ± 1.7 AT 70.8 ± 1.5; ST 69.6 ± 1.6 mg/dl) were significantly lower (P<0.05) following both exercise bouts. The 6-hour plasma TG INCAUC (CON, 355.0 ± 60.4; ST 183.5 ± 36.6; AT, 130.3 ± 30.1 mg/dl × 6h) and glucose TOTAUC (CON, 531.6 ± 19.8; ST 432.4 ± 20.1; AT, 419.8 ± 23.2 mg/dl × 6h) were significantly reduced during both exercise trials. CONCLUSION: These data suggest that PV corrections over multiple tests may provide a clearer picture of the effect of exercise treatments upon PPL. Given uncertainty over the exact cause of post exercise PV shifts and the large PV variation between trials in this study it is suggested that fluid and salt intakes be controlled during the 24-hours preceding fat tolerance tests.

The Effect of Acute Exercise upon Postprandial Lipemia Following Correction for Plasma Volume Shifts

1489 PURPOSE: To examine the influence of plasma volume (PV) adjustments on our previously reported finding that isocaloric bouts of acute strength (ST) and aerobic training (AT) had no effect on fasting and postprandial plasma lipoprotein concentrations in 13 healthy normolipidemic males (age, 20.9 ± 0.6 years). METHODS: Subjects participated in three postprandial lipemia tests, one control (CON) and the other two 14-hours following isocaloric bouts of ST and AT. During all 3 tests, venous samples were obtained in a 12-hr fasted state and after the consumption of a high fat breakfast (55 g fat, 149 g carbohydrate, 22 g protein). Blood samples were analyzed for plasma triglyceride (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C) and glucose. Changes in PV were determined using the fasting CON trial hematocrit (Hct) and hemoglobin (Hb) values as the reference point from which all blood samples from the CON trial and exercise trials were compared. TG was monitored hourly for 6 hours from which the incremental (INCAUC) and total (TOTAUC) areas under the 6-hour TG curve were calculated. Differences between CON, ST and AT trials, with and without PV corrections. RESULTS: Hb was significantly higher in the fasting AT blood sample compared to the fasting CON sample (CON, 11.48 ± 0.78; AT, 14.13 ± 0.65; ST, 13.46 ± 0.53 mg/dl). The AT and ST fasting blood samples displayed 18 and 14 % reductions in PV, respectively. After PV correction there was no effect on fasting plasma TG or HDL-C concentrations. However, fasting plasma TC (CON, 172.5 ± 7.3; AT 138.1 ± 7.5; ST 149.2 ± 8.2 mg/dl) and glucose (CON, 85.9 ± 1.7 AT 70.8 ± 1.5; ST 69.6 ± 1.6 mg/dl) were significantly lower (P<0.05) following both exercise bouts. The 6-hour plasma TG INCAUC (CON, 355.0 ± 60.4; ST 183.5 ± 36.6; AT, 130.3 ± 30.1 mg/dl × 6h) and glucose TOTAUC (CON, 531.6 ± 19.8; ST 432.4 ± 20.1; AT, 419.8 ± 23.2 mg/dl × 6h) were significantly reduced during both exercise trials. CONCLUSION: These data suggest that PV corrections over multiple tests may provide a clearer picture of the effect of exercise treatments upon PPL. Given uncertainty over the exact cause of post exercise PV shifts and the large PV variation between trials in this study it is suggested that fluid and salt intakes be controlled during the 24-hours preceding fat tolerance tests.

Acute Effects of an Oral Calcium Load on Markers of Bone Metabolism During Endurance Cycling Exercise in Male Athletes

Although sport and physical activity are generally considered as positive factors for bone metabolism some endurance trainings such as running and bicycling have few or no beneficial or even deleterious effects on bone mineral density. The present study was designed to investigate the acute effect of an intensive endurance cycling exercise on biochemical bone markers. Furthermore, the effect of the oral intake of 1 g calcium load, by drinking high-calcium mineral water, just prior to and during the exercise was checked. Twelve well-trained elite male triathletes aged 23-37 years were explored. The serum concentrations of calcium, phosphate, PTH, bone alkaline phosphatase (BALP) and C-terminal cross-linking telopeptide of type 1 collagen (CTX) were measured before, during and after a 60 min 80% VO2max cycle ergometer exercise. Since cycling exercise was accompanied by a reduction in plasma volume the total amount of biochemical bone markers was calculated. When the exercise was performed without calcium load both serum concentrations and total amount of CTX began to increase progressively 30 min after the start of the exercise and were still significantly elevated, by 45-50%, 2h after the end of the exercise. Ingestion of high-calcium mineral water completely suppressed the CTX response. By contrast serum concentrations and total amount of BALP fluctuated and showed no significant difference with or without calcium load. The present study demonstrates that the burst of osteoclastic activity acutely induced by an endurance cycling exercise can be suppressed by the previous intake of a calcium load afforded by drinking high-calcium mineral water.