Acute Plasma Volume Expansion Research Articles

Effects of Increased Preload on Cardiac Function in Younger vs Older Women

PURPOSE: Limitations in cardiac preload and/or compliance could underlie diminished stroke volume and ventricular remodeling adaptations to endurance exercise in older women. The present study tested the hypothesis that attenuated cardiac function in older women persists during acute increases in preload, both at rest and during exercise. METHODS: Nine younger (Y, 21-28 y) and ten older (O, 61-73 y) healthy, non-endurance trained women were studied 1) at rest in the supine and seated positions, and 2) during graded upright cycle ergometer exercise (20, 40, 60 and 80% of VO2peak), both before and after acute plasma volume (PV) expansion (via IV infusion of 5% albumin; 10ml/kg). Cardiac responses to postural change, exercise, and PV expansion were measured using echocardiography (rest and low intensity exercise) and open circuit C2H2 (exercise). RESULTS: Under resting normovolemic conditions, stroke volume (SV) was augmented in the supine (vs. upright) posture in both Y (61±9 vs. 52±8 ml/beat, P<0.05) and O (55±10 vs. 49±7 ml/beat, P<0.05) women. Hypervolemia augmented supine SV further in Y (68±4 ml/beat, P<0.05 vs. normovolemia), but not in O (55±10 ml/ beat, P>0.05 vs. normovolemia) women. These resting postural and hypervolemic effects were mediated by changes in end diastolic volume, and not secondary to age group differences in the extent of PV expansion (averaged +16% and +13% in Y and O, respectively) or estimated filling pressures (E/E’). E/A ratio during peak resting preload conditions (i.e., supine hypervolemia), moreover, was positively associated with VO2peak in Y, but not in O women. During upright exercise, hypervolemia increased SV an average of 15 ml/beat across all 4 work intensities in Y women (p<0.05 vs. normovolemia). This was in contrast to O women, who exhibited very small increases in SV during hypervolemic exercise (i.e., <5 ml/beat). CONCLUSIONS: Healthy older women appear to have a reduced ability (relative to younger women) to utilize acute increases in preload to raise left ventricular stroke volume, including during large muscle exercise. These findings likely reflect the combined effects of exceptional lusitropic function in younger women, and a less compliant ventricle in the aged female heart.

Effects of Acute Plasma Volume Expansion on Renal Perfusion, Filtration, and Oxygenation After Cardiac Surgery

Background In the present randomized study, we evaluated the differential effects of a colloid and a crystalloid fluid on renal oxygen delivery ( R D O 2 ), glomerular filtration (GFR), renal oxygen consumption ( R V ˙ O 2 ), and the renal oxygen supply–demand relationship (i.e. renal oxygenation) after cardiac surgery with cardiopulmonary bypass. Methods Thirty patients with normal preoperative renal function, undergoing uncomplicated cardiac surgery, were studied in the intensive care unit in the early postoperative period. Patients were randomized to receive a bolus dose of either a crystalloid (Ringers-acetate® 20 ml kg−1, n=15) or a colloid solution (Venofundin® 10 ml kg−1, n=15). Systemic haemodynamics were measured via a pulmonary artery catheter. Renal blood flow and GFR were measured by the renal vein retrograde thermodilution technique and by renal extraction of 51Cr-EDTA (=filtration fraction). Arterial and renal vein blood samples were obtained for measurements of renal oxygen delivery ( R D O 2 ) and R V ˙ O 2 . Renal oxygenation was estimated from the renal oxygen extraction. Results Despite an increase in cardiac index and renal blood flow with both fluids, neither of the fluids improved R D O 2 , because they both induced haemodilution. The GFR increased in the crystalloid (28%) but not in the colloid group. The crystalloid increased the filtration fraction (24%) and renal oxygen extraction (23%), indicating that the increase in GFR, the major determinant of R V ˙ O 2 , was not matched by a proportional increase in R D O 2 . Conclusions Neither the colloid nor the crystalloid improved R D O 2 when used for postoperative plasma volume expansion. The crystalloid-induced increase in GFR was associated with impaired renal oxygenation, which was not seen with the colloid. Clinical trial registration NCT01729364.

Effects of acute plasma volume expansion on renal perfusion, filtration, and oxygenation after cardiac surgery: a randomized study on crystalloid vs colloid

In the present randomized study, we evaluated the differential effects of a colloid and a crystalloid fluid on renal oxygen delivery (RD(O2)), glomerular filtration (GFR), renal oxygen consumption ((RV(O2))), and the renal oxygen supply-demand relationship (i.e., renal oxygenation) after cardiac surgery with cardiopulmonary bypass. Thirty patients with normal preoperative renal function, undergoing uncomplicated cardiac surgery, were studied in the intensive care unit in the early postoperative period. Patients were randomized to receive a bolus dose of either a crystalloid (Ringers-acetate 20 ml kg(-1), n=15) or a colloid solution (Venofundin) 10 ml kg(-1), n=15). Systemic haemodynamics were measured via a pulmonary artery catheter. Renal blood flow and GFR were measured by the renal vein retrograde thermodilution technique and by renal extraction of 51Cr-EDTA (=filtration fraction). Arterial and renal vein blood samples were obtained for measurements of renal oxygen delivery (RD(O2)) and RV(O2). Renal oxygenation was estimated from the renal oxygen extraction. Despite an increase in cardiac index and renal blood flow with both fluids, neither of the fluids improved RD(O2), because they both induced haemodilution. The GFR increased in the crystalloid (28%) but not in the colloid group. The crystalloid increased the filtration fraction (24%) and renal oxygen extraction (23%), indicating that the increase in GFR, the major determinant of RV(O2), was not matched by a proportional increase in RD(O2). Neither the colloid nor the crystalloid improved RD(O2) when used for postoperative plasma volume expansion. The crystalloid-induced increase in GFR was associated with impaired renal oxygenation, which was not seen with the colloid. NCT01729364.

Phosphodiesterase 4 inhibition attenuates plasma volume loss and transvascular exchange in volume‐expanded mice

We tested the hypothesis that inhibition of phosphodiesterase 4 (PDE4) with rolipram to increase vascular endothelial cAMP and stabilize the endothelial barrier would attenuate the action of endogenous atrial natriuretic peptide (ANP) to increase vascular permeability to the plasma protein albumin after an acute plasma volume expansion. After rolipram pretreatment (8 mg (kg body wt)(-1), intraperitoneal, 30 min) more than 95% of the peak increase in plasma volume after volume expansion (4.5% bovine serum albumin, 114 μl (g body wt)(-1) h(-1), 15 min) remained in the vascular space 75 min after the end of infusion, whereas only 67% of the fluid was retained in volume-expanded animals with no rolipram pretreatment. Rolipram significantly decreased 30 min fluorescently labelled albumin clearance (μl (g dry wt)(-1)) relative to untreated volume-expanded controls in skin (e.g. back, 10.4 ± 1.6 vs. 19.5 ± 3.6, P = 0.04), muscle (e.g. hamstring, 15.0 ± 1.9 vs. 20.8 ± 1.4, P = 0.04) and in colon, caecum, and rectum (average reduction close to 50%). The mass of muscle and skin tissue accounted for 70% of volume-expansion-dependent albumin shifts from plasma to interstitium. The results are consistent with observations that the PDE4 inhibitor rolipram attenuates ANP-induced increases in vascular permeability after infusion of exogenous ANP and observations of elevated central venous pressure after a similar volume expansion in mice with selective deletion of the endothelial ANP receptor. These observations may form the basis for new strategies to retain intravenous fluid containing macromolecules.

Phosphodiesterase 4 inhibition attenuates plasma volume loss and transvascular exchange in volume expanded mice

Phosphodiesterase 4 inhibition attenuates plasma volume loss and transvascular exchange in volume expanded mice

Angiotensin II Type 1 Receptors and Systemic Hemodynamic and Renal Responses to Stress and Altered Blood Volume in Conscious Rabbits

We examined how systemic blockade of type 1 angiotensin (AT1-) receptors affects reflex control of the circulation and the kidney. In conscious rabbits, the effects of candesartan on responses of systemic and renal hemodynamics and renal excretory function to acute hypoxia, mild hemorrhage, and plasma volume expansion were tested. Candesartan reduced resting mean arterial pressure (MAP, −8 ± 2%) without significantly altering cardiac output (CO), increased renal blood flow (RBF, +38 ± 9%) and reduced renal vascular resistance (RVR, −32 ± 6%). Glomerular filtration rate (GFR) was not significantly altered but sodium excretion (UNa+V) increased fourfold. After vehicle treatment, hypoxia (10% inspired O2 for 30 min) did not significantly alter MAP or CO, but reduced heart rate (HR, −17 ± 6%), increased RVR (+33 ± 16%) and reduced GFR (−46 ± 16%) and UNa+V (−41 ± 17%). Candesartan did not significantly alter these responses. After vehicle treatment, plasma volume expansion increased CO (+35 ± 7%), reduced total peripheral resistance (TPR, −26 ± 5%), increased RBF (+62 ± 23%) and reduced RVR (−32 ± 9%), but did not significantly alter MAP or HR. It also increased UNa+V (803 ± 184%) yet reduced GFR (−47 ± 9%). Candesartan did not significantly alter these responses. After vehicle treatment, mild hemorrhage did not significantly alter MAP but increased HR (+16 ± 3%), reduced CO (−16 ± 4%) and RBF (−18 ± 6%), increased TPR (+18 ± 4%) and tended to increase RVR (+18 ± 9%, P = 0.1), but had little effect on GFR or UNa+V. But after candesartan treatment MAP fell during hemorrhage (−19 ± 1%), while neither TPR nor RVR increased, and GFR (−64 ± 18%) and UNa+V (−83 ± 10%) fell. AT1-receptor activation supports MAP and GFR during hypovolemia. But AT1-receptors appear to play little role in the renal vasoconstriction, hypofiltration, and antinatriuresis accompanying hypoxia, or the systemic and renal vasodilatation and natriuresis accompanying plasma volume expansion.

Plasma Volume Expansion Resulting from Intravenous Glucose Tolerance Test

Objective. To quantify the degree of plasma volume expansion that occurs during an intravenous glucose tolerance test (IVGTT). Methods. Twenty healthy volunteers (mean age, 28 years) underwent IVGTTs in which 0.3 g/kg of glucose 30% was injected as a bolus over 1 min. Twelve blood samples were collected over 75 min. The plasma glucose and blood hemoglobin concentrations were used to calculate the volume distribution (V d) and the clearance (CL) of both the exogenous glucose and the injected fluid volume. Results. The IVGTT caused a virtually instant plasma volume expansion of 10%. The half-life of the glucose averaged 15 min and the plasma volume expansion 16 min. Correction of the fluid kinetic model for osmotic effects after injection reduced CL for the infused volume by 85%, which illustrates the strength of osmosis in allocating fluid back to the intracellular fluid space. Simulations indicated that plasma volume expansion can be reduced to 60% by increasing the injection time from 1 to 5 min and reducing the glucose load from 0.3 to 0.2 g/kg. Conclusion. A regular IVGTT induced an acute plasma volume expansion that peaked at 10% despite the fact that only 50–80 mL of fluid were administered.

Phosphodiesterase IV inhibitor Rolipram attenuates ANP‐dependent intravascular fluid loss

Mice with deletion of the endothelial ANP receptor (guanylyl cyclase A receptor) (EC GC‐A KO mice) have expanded intravascular volumes and retain infused fluid in the vascular space (Schreier et al. Endocrinol 149: 4193, 2008). We have previously demonstrated in isoflurane anesthetized wild type C57BL/6 mice that pretreatment with Rolipram (8 mg/kg IP, 30 min), a phosphodiesterase IV inhibitor that raises intracellular cAMP and stabilizes the endothelial barrier, attenuates the ANP‐dependent increase in vascular permeability (FASEB J 23:950.12, 2009). To test the extent that ANP‐dependent changes in vascular permeability regulate vascular volume, we infused ANP (500 ng/kg·min) and measured a hematocrit increase from 41% to 47%, an 11% reduction in plasma volume. This infusion rate raises plasma ANP to physiological levels near those measured after an acute plasma volume expansion. Rolipram pretreatment completely blocks this ANP‐dependent fluid loss. EC GC‐A KO mice also show no increase in hematocrit with ANP infusion relative to their control littermates. Thus Rolipram appears to be as effective to attenuate ANP‐mediated fluid loss as EC GC‐A KO. We predict that mice similarly pretreated to stabilize the endothelial barrier will retain fluid in the vascular space when given plasma volume expansion. (Supported by pilot funds from Clinical and Translational Science Center, UC Davis UL1 RR024146; NCRR).

Reply to Zavorsky

reply: Dr. Zavorsky's letter ([5][1]) demonstrates a poor understanding of gas exchange physiology in that his claim to have measured pulmonary O2 uptake (Vo2) kinetics following acute plasma volume expansion (APVE) in a previous study ([6][2]) is utterly without foundation. In the study of

Plasma volume expansion does not influence oxygen uptake kinetics in trained cyclists

LETTERS TO THE EDITORPlasma volume expansion does not influence oxygen uptake kinetics in trained cyclistsGerald S. ZavorskyGerald S. ZavorskyPublished Online:01 Feb 2007https://doi.org/10.1152/japplphysiol.01029.2006MoreSectionsPDF (29 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations to the editor: I have read the recent article by Berger and colleagues (1) on the effects of plasma volume expansion on oxygen uptake kinetics, peak oxygen uptake, and performance during high-intensity cycling exercise. These researchers have shown that after 7 ml/kg infusion of a plasma volume expander (∼580 ml), and a reduction in hemoglobin concentration by 8%, there was no difference in oxygen uptake kinetics. Nonetheless, maximal oxygen uptake and time to exhaustion increased by 6 and 16%, respectively (1).The lack of a change in oxygen uptake kinetics is not new. The authors have failed to discuss the results of two similar companion papers published recently in which minute ventilation and oxygen uptake kinetics were unchanged from plasma volume expansion compared with control (2, 3). Specifically, a reduction in oxygen delivery during intense exercise by 377 ml/min from plasma volume expansion (3) did not influence oxygen uptake kinetics (2). The similarities between the work of Berger et al. (1) and ours are numerous. First, we both used colloids to expand plasma volume by approximately the same amount. Second, the decrease in hemoglobin concentration caused by plasma volume expansion was approximately the same. Third, we both used high-intensity cycling exercise protocols. Although the aims of our papers were different, our data are worth mentioning because they are highly related to the work of Berger et al. What is different in our results was that contrary to Berger et al., we did not see any change in the peak oxygen uptake after 6.5 min of very strenuous cycling exercise after plasma volume expansion (500 ml Pentaspan), but we did see a significant change in arterial blood acidity (2). However, unlike Berger et al., our subjects were highly trained, and perhaps the level of fitness precluded any increase in oxygen uptake from plasma volume expansion despite lowering arterial pH (2). As well, unlike the study of Berger et al., we also measured cardiac output and stroke volume in our subjects and found no changes in these parameters from expansion. This implies that right ventricular filling was not limited in our very fit subjects. In the case of Berger et al., right ventricular filling may have been limited in these “lower fit” subjects as evidenced by the increase in peak oxygen pulse (1). Therefore, the issue of whether performance and/or maximal oxygen uptake and/or cardiac output is improved with plasma volume expansion still needs to be studied further in various populations (i.e., highly fit vs. recreationally active vs. sedentary subjects), but the issue of whether it affects oxygen uptake kinetics, in my opinion, is answered.REFERENCES1 Berger NJ, Campbell IT, Wilkerson DP, Jones AM. Influence of acute plasma volume expansion on V̇o2 kinetics, V̇o2 peak, and performance during high-intensity cycle exercise. J Appl Physiol 101: 707–714, 2006.Link | ISI | Google Scholar2 Zavorsky GS, Walley KR, Hunte GS, McKenzie DC, Sexsmith GP, Russell JA. Acute hypervolaemia improves arterial oxygen pressure in athletes with exercise-induced hypoxaemia. Exp Physiol 88: 555–564, 2003.Crossref | ISI | Google Scholar3 Zavorsky GS, Walley KR, Hunte GS, McKenzie DC, Sexsmith GP, Russell JA. Acute hypervolemia lengthens red cell pulmonary transit time during exercise in endurance athletes. Respir Physiol Neurobiol 131: 255–268, 2002.Crossref | ISI | Google ScholarAUTHOR NOTESAddress for reprint requests and other correspondence: G. S. Zavorsky, Dept. of Anesthesia, McGill Univ. Health Center, Montreal, Quebec, Canada H3G 1A4 (e-mail: [email protected]) Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation Cited ByReply to ZavorskyAndrew M. Jones, Nicolas J. Berger, Daryl P. Wilkerson, and Iain T. Campbell1 February 2007 | Journal of Applied Physiology, Vol. 102, No. 2 More from this issue > Volume 102Issue 2February 2007Pages 828-828 Copyright & PermissionsCopyright © 2007 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.01029.2006PubMed17284661History Published online 1 February 2007 Published in print 1 February 2007 Metrics

Influence of acute plasma volume expansion on O2 kinetics, O2peak, and performance during high-intensity cycle exercise

Influence of acute plasma volume expansion on O2 kinetics, O2peak, and performance during high-intensity cycle exercise

Influence of acute plasma volume expansion on V̇o2 kinetics, V̇o2peak, and performance during high-intensity cycle exercise

The purpose of this study was to examine the influence of acute plasma volume expansion (APVE) on oxygen uptake (V(O2)) kinetics, V(O2peak), and time to exhaustion during severe-intensity exercise. Eight recreationally active men performed "step" cycle ergometer exercise tests at a work rate requiring 70% of the difference between the gas-exchange threshold and V(O2max) on three occasions: twice as a "control" (Con) and once after intravenous infusion of a plasma volume expander (Gelofusine; 7 ml/kg body mass). Pulmonary gas exchange was measured breath by breath. APVE resulted in a significant reduction in hemoglobin concentration (preinfusion: 16.0 +/- 1.0 vs. postinfusion: 14.7 +/- 0.8 g/dl; P < 0.001) and hematocrit (preinfusion: 44 +/- 2 vs. postinfusion: 41 +/- 3%; P < 0.01). Despite this reduction in arterial O(2) content, APVE had no effect on V(O2) kinetics (phase II time constant, Con: 33 +/- 15 vs. APVE: 34 +/- 12 s; P = 0.74), and actually resulted in an increased V(O2peak) (Con: 3.90 +/- 0.56 vs. APVE: 4.12 +/- 0.55 l/min; P = 0.006) and time to exhaustion (Con: 365 +/- 58 vs. APVE: 424 +/- 64 s; P = 0.04). The maximum O(2) pulse was also enhanced by the treatment (Con: 21.3 +/- 3.4 vs. APVE: 22.7 +/- 3.4 ml/beat; P = 0.04). In conclusion, APVE does not alter V(O2) kinetics but enhances V(O2peak) and exercise tolerance during high-intensity cycle exercise in young recreationally active subjects.

Influence of Acute Plasma Volume Expansion on Oxygen Uptake Kinetics in Severe-Intensity Exercise

Influence of Acute Plasma Volume Expansion on Oxygen Uptake Kinetics in Severe-Intensity Exercise

Saline volume expansion and cardiovascular physiology: novel observations, old explanations, and new questions

In a clinical investigation, Kumar and coworkers reported the hemodynamic events that accompany plasma volume expansion over 3 hours in healthy adult volunteers, and found that increases in stroke volume (SV) may be related to increases in left ventricular (LV)/right ventricular (RV) end-diastolic volume, as they expected, but also to decreases in LV/RV end-systolic volume. The latter finding suggests increased contractility and/or decreased afterload, which do not fit with their perception that clinicians ascribe increases in SV to increases in end-diastolic volume based on Starling's work. Increased ejection fraction and decreased vascular resistances were also observed. The same authors recently reported novel data suggesting that reduced blood viscosity may account for the observed reduction in vascular resistances with saline volume expansion. However, the variances in preload and afterload, along with uncertainty in estimates of contractility, substantially limit their ability to define a primary mechanism to explain decreases in LV end-systolic volume. A focus on using ejection fraction to evaluate the integrated performance of the cardiovascular system is provided to broaden this analytic perspective. Sagawa and colleagues described an approach to estimate the relationship, under clinical conditions, between ventricular and arterial bed elastances (i.e. maximal ventricular systolic elastance [Emax] and maximal arterial systolic elastance [Ea]), reflecting ventricular–arterial coupling. I used the mean data provided in one of the reports from Kumar and coworkers to calculate that LV Emax decreased from 1.09 to 0.96 mmHg/ml with saline volume expansion, while Ea decreased from 1.1 to 0.97 mmHg/ml and the SV increased (i.e. the increase in mean SV was associated with a decrease in mean afterload while the mean contractility decreased). The results reported by Kumar and coworkers invite further studies in normal and critically ill patients during acute saline-induced plasma volume expansion and hemodilution. If reduced viscosity decreases afterload, then this raises the questions by what mechanism, and what is the balance of benefit and harm associated with reduced blood viscosity affecting oxygen delivery? Why the mean Emax might decrease must be evaluated with respect to benefit in reducing ventricular work or a negative inotropic effect of saline.

Acute hypervolemia does not improve arterial oxygenation in maximally exercising thoroughbred horses.

Recently, it was reported that acute hypervolemia improves arterial oxygen tension in human athletes known to experience exercise-induced arterial hypoxemia. Since exercise-induced arterial hypoxemia is routinely observed in racehorses and is known to limit performance, we examined whether pre-exercise induction of acute hypervolemia would similarly benefit arterial oxygenation in maximally exercising thoroughbred horses. Two sets of experiments, namely, placebo [intravenous (IV) physiological saline] and acute hypervolemia (IV 7.2% NaCl, causing an 18.2% expansion of plasma volume) studies were carried out in random order on 13 healthy, exercise-trained thoroughbred horses, 7 days apart. An incremental exercise protocol leading to 120 s of galloping at 14 m s(-1) on a 3.5% uphill incline was used. Galloping at this workload elicited maximal heart rate and induced pulmonary hemorrhage in all horses in both treatments. In the placebo study, arterial oxygen tension decreased to 76.1 (2) mmHg (P<0.0001) at 30 s of maximal exertion, but further significant changes did not occur as exercise duration increased to 120 s [arterial oxygen tension 72.4 (2) mmHg]. A significant arterial hypoxemia also developed in galloping horses in the acute hypervolemia study [arterial oxygen tension at 30 and 120 s was 76.7 (1.7) and 71.9 (1.6) mmHg, respectively], but significant differences between treatments could not be demonstrated. In both treatments, a similar desaturation of arterial hemoglobin was also observed at 30 s of maximal exercise, which intensified with increasing exercise duration as hyperthermia, acidosis and hypercapnia intensified. Thus, acute expansion of plasma volume did not benefit arterial oxygenation in maximally exercising thoroughbred horses.

Acute hypervolaemia improves arterial oxygen pressure in athletes with exercise-induced hypoxaemia.

The aim of this study was to determine the effect of acute plasma volume expansion on arterial blood-gas status during 6.5 min strenuous cycling exercise comparing six athletes with and six athletes without exercise-induced arterial hypoxaemia (EIAH). We hypothesized that plasma volume expansion could improve arterial oxygen pressure in a homogeneous sample of athletes - those with EIAH. In this paper we have extended the analysis and results of our recently published surprising findings that lengthening cardiopulmonary transit time did not improve arterial blood-gas status in a heterogeneous sample of endurance cyclists. One 500 ml bag of 10 % Pentastarch (infusion condition) or 60 ml 0.9 % saline (placebo) was infused prior to exercise in a randomized, double-blind fashion on two different days. Power output, cardiac output, oxygen consumption and arterial blood gases were measured during strenuous exercise. Cardiac output and oxygen consumption were not affected by acute hypervolaemia. There were group x condition interaction effects for arterial oxygen pressure and alveolar-arterial oxygen pressure difference, suggesting that those with hypoxaemia experienced improved arterial oxygen pressure (+4 mmHg) and lower alveolar-arterial oxygen pressure difference (-2 mmHg) with infusion. In conclusion, acute hypervolaemia improves blood-gas status in athletes with EIAH. The impairment of gas exchange occurs within the first minute of exercise, and is not impaired further throughout the remaining duration of exercise. This suggests that arterial oxygen pressure is only minimally mediated by cardiac output.

Acute plasma volume expansion in the untrained alters the hormonal response to prolonged moderate-intensity exercise.

To investigate the role of an increase in plasma volume (PV), characteristically observed with short-term endurance training, on the endocrine response to prolonged moderate intensity exercise, eight untrained males (VO2 peak = 3.52 +/- 0.12 l x min(-1)) performed 90 min of cycle ergometry at approximately 60% VO2peak both before (CON) and following (PVX) PV expansion. Acute PV expansion, which was accomplished using a solution of Dextran (6%) or Pentispan (10%) (6.7 ml kg(-1)), resulted in a calculated 15.8+/-2.2% increase (p<0.05) in PV. The prolonged exercise resulted in increases (p<0.05) in plasma vasopressin (AVP), plasma rennin activity (PRA), aldosterone (ALD), atrial naturetic peptide (alpha-ANP), and the catecholamines norepinephrine (NE) and epinephrine (EPI). PVX blunted the increases (p<0.05) in AVP, PRA, ALD, NE and EPI, during the exercise itself. The concentration of alpha-ANP was also lower (p<0.05) during exercise following PVX, an effect that could be attributed to the lower resting levels. No differences in osmolality was observed between conditions. These results demonstrate that PVX alters the fluid regulatory hormonal response in untrained subjects to moderate intensity dynamic exercise in a manner similar to that observed following short-term training induced alterations in PV. The specific mechanisms responsible for these alterations remain unclear, but appear to be related directly to the increase in PV.

Effect of acute plasma volume expansion on thermoregulation and exercise performance in the heat.

We investigated the effects of acute plasma volume expansion on exercise performance in the heat. Six moderately trained men cycled for 40 min at 64 +/- 2% peak pulmonary oxygen uptake (VO2peak) followed by an individual performance time trial, where subjects completed a set amount of work (267 +/- 15 kJ) in as little time as possible. Exercise trials were performed at 35 degrees C with a relative humidity of 40%. Subjects performed two exercise trials: one after 13.1 +/- 1% acute plasma volume expansion (PVE), which was achieved by the intravenous infusion of 8 mL x kg(-1) body weight of Hemaccel (35 g x L(-1) polygeline, 145 mmol x L(-1) Na+, and 145 mmol x L(-1) Cl-) and the other without prior treatment (CON). Core temperature, skin blood flow, and heart rate progressively increased (P < 0.05) during exercise, but no differences were observed between trials. Plasma glucose and lactate were similar at rest and during exercise, as was VO2 during exercise. Exercise performance was not influenced by plasma volume expansion (CON 17.5 +/- 0.4 min and PVE 17.1 +/- 0.2 min). These data suggest that, in moderately trained men, plasma volume expansion alone does not enhance thermoregulatory function and exercise performance during moderate intensity exercise in the heat.

Acute plasma volume expansion alters cardiovascular but not thermal function during moderate intensity prolonged exercise

To investigate the hypothesis that the increase in plasma volume (PV) that typically occurs with training results in improved cardiovascular and thermal regulation during prolonged exercise, eight untrained males (V(O2)peak = 3.52 +/- 0.12 L x min(-1)) performed 90 min of cycle ergometry at 62% V(O2)peak before and after acute PV expansion. Subjects were infused with a PV-expanding solution (dextran (6%) or Pentaspan (10%)) equivalent to 6.7 mL x kg(-1) body mass (PVX) or acted as their own control (CON) in a randomized order. PVX resulted in a calculated 15.8% increase in resting PV, which relative to CON, was maintained throughout the exercise (P < 0.05). During PVX, heart rate was lower (P < 0.05) and stroke volume and cardiac output were higher (P < 0.05) during the exercise. Mean arterial pressure and total peripheral resistance, although altered by exercise (P < 0.05), were not different between the two conditions. Core temperature, which was progressively increased by the exercise (P < 0.01), was not affected by PVX. A similar decrease in body weight was observed between the conditions as a result of the exercise (P < 0.01). These results indicate that acute PVX alters cardiovascular performance without affecting the thermoregulatory response to prolonged cycle exercise.

Blood volume, aerobic power, and endurance performance: potential ergogenic effect of volume loading.

Blood volume (BV) and hemoglobin concentration ([Hb]) play important roles in oxygen transport. Manipulation of both BV and [Hb] can markedly affect systemic oxygen transport and maximal aerobic capacity (VO2max). However, the role of BV in oxygen transport and aerobic performance is not well understood. It has recently been postulated that an acute expansion of BV using plasma volume (PV), independent of changes in [Hb], may represent a potential ergogenic property. Therefore, the primary objective of this review was to determine the potential ergogenic properties of volume loading. An extensive research of Medline and Sport-Discus along with cross-referencing was conducted. Articles were included on the basis of their relevancy to the purpose of this review. Only articles published in English were included in the analysis. All study designs using human participants were reviewed. A systematic analysis of data regarding the effect of BV on the determination of oxygen transport, aerobic capacity, and endurance performance was conducted. Particular emphasis was given to articles that examined BV as the key independent variable. Articles relevant to the evaluation of the impact of BV on aerobic capacity and endurance performance were reviewed according to the strengths of the individual study designs. Seven investigations evaluated the impact of acute changes in BV, independent of changes in [Hb], on VO2max. Of these investigations, three revealed that acute manipulations of BV result in no change or a slight reduction in VO2max. Three investigations revealed a significant improvement in VO2max after acute PV expansion. One investigation revealed a nonsignificant increase in VO2max after acute PV expansion. Seven investigations evaluated the impact of acute changes in BV, independent of changes in [Hb], on endurance performance: two revealed a significant improvement in endurance performance after acute PV expansion, and five revealed an unchanged or reduced endurance performance after acute PV expansion. The majority of investigations showing an improvement in VO2max and/or endurance performance after acute PV expansion were conducted using untrained individuals. Volume loading does not result in an improvement in VO2max and/or endurance performance in endurance athletes. Volume loading in untrained individuals may improve VO2max, but does not bring these individuals to the aerobic capacity of endurance-trained athletes. Also, volume loading generally does not lead to improvement in endurance performance, irrespective of its effects on VO2max.