Systemic arterial compliance, systemic vascular resistance, and effective arterial elastance during exercise in endurance-trained men

Systemic arterial compliance (C) and vascular resistance (R) regulate effective arterial elastance (Ea), an index of artery load. Increases in Ea during exercise are due primarily to reductions of C and maintain optimal ventricular-arterial coupling. Because C at rest and left ventricular functional reserve are greater in endurance-trained (ET) compared with sedentary control (SC) humans, we hypothesized that reductions of C and increases in Ea are greater in ET than SC individuals. The aim of this study was to investigate C, R, and Ea during exercise in ET and SC humans. C, R, Ea, and cardiac cycle length (T) were measured at rest and during exercise of 40, 60, and 80% maximal oxygen uptake using Doppler ultrasonography in 12 SC and 13 ET men. C decreased in an exercise intensity-dependent manner in both groups, but its reductions were greater in the ET than SC subjects. Consequently, although C at rest was greater in the ET than SC group, the intergroup difference in C disappeared during exercise. Exercise-related changes in R/T were relatively slight and R/T was lower in the ET than the SC group, both at rest and during exercise. Although Ea at rest was lower in the ET than SC group, there were no intergroup differences in Ea at 40, 60, or 80% maximal oxygen uptake. We conclude that the reductions of C from rest to exercise are more marked in ET than SC humans. This may be related to the exercise-associated disappearance of the difference in Ea between ET and SC humans.     

Estimation of total systemic arterial compliance in humans

Systemic arterial compliance, a major component of aortic input impedance, was determined in 10 patients with congestive heart failure secondary to idiopathic dilated cardiomyopathy and 11 age-matched control subjects found free of detectable cardiovascular disease. Total arterial compliance was determined from high-fidelity ascending aortic pressure and velocity recordings using 1) the traditional monoexponential aortic diastolic pressure decay and 2) the direct solution of the equation, which describes the three-element windkessel model of the arterial system. Resting values for total arterial compliance (x10(-3) cm5/dyn) derived from method 1 were significantly correlated with compliance derived from method 2 (r = 0.89, P less than 0.01). However, method 1 values (control mean 1.15 +/- 0.27, heart failure mean 1.18 +/- 0.54) were consistently and significantly lower (P less than 0.001) than method 2 values (control mean 1.59 +/- 0.50, heart failure mean 1.38 +/- 0.60). Resting total arterial compliance in heart-failure patients was not significantly different from control subjects. Total arterial compliance did not significantly change with exercise in either group despite increases in arterial pressure. However, nitroprusside administration in the heart-failure group increased total arterial compliance both at rest and on exercise compared with the unmedicated state. These different methodological approaches to the estimation of total arterial compliance in humans resulted in significantly different absolute values for compliance, although both methods provided concordant results with respect to the response of arterial compliance to physiological and pharmacological interventions.(ABSTRACT TRUNCATED AT 250 WORDS)     

Relation of effective arterial elastance to arterial system properties

Effective arterial elastance (E(a)), defined as the ratio of left ventricular (LV) end-systolic pressure and stroke volume, lumps the steady and pulsatile components of the arterial load in a concise way. Combined with E(max), the slope of the LV end-systolic pressure-volume relation, E(a)/E(max) has been used to assess heart-arterial coupling. A mathematical heart-arterial interaction model was used to study the effects of changes in peripheral resistance (R; 0.6-1.8 mmHg x ml(-1) x s) and total arterial compliance (C; 0.5-2.0 ml/mmHg) covering the human pathophysiological range. E(a), E(a)/E(max,) LV stroke work, and hydraulic power were calculated for all conditions. Multiple-linear regression analysis revealed a linear relation between E(a), R/T (where T is cycle length), and 1/C: E(a) = -0.13 + 1.02R/T + 0.31/C, indicating that R/T contributes about three times more to E(a) than arterial stiffness (1/C). It is demonstrated that different pathophysiological combinations of R and C may lead to the same E(a) and E(a)/E(max) but can result in differences of 10% in stroke work and 50% in maximal power.     

Effective arterial elastance as an index of pulmonary vascular load

The aim of this study was to test whether the simple ratio of right ventricular (RV) end-systolic pressure (Pes) to stroke volume (SV), known as the effective arterial elastance (Ea), provides a valid assessment of pulmonary arterial load in case of pulmonary embolism- or endotoxin-induced pulmonary hypertension. Ventricular pressure-volume (PV) data (obtained with conductance catheters) and invasive pulmonary arterial pressure and flow waveforms were simultaneously recorded in two groups of six pure Pietran pigs, submitted either to pulmonary embolism (group A) or endotoxic shock (group B). Measurements were obtained at baseline and each 30 min after injection of autologous blood clots (0.3 g/kg) in the superior vena cava in group A and after endotoxin infusion in group B. Two methods of calculation of pulmonary arterial load were compared. On one hand, Ea provided by using three-element windkessel model (WK) of the pulmonary arterial system [Ea(WK)] was referred to as standard computation. On the other hand, similar to the systemic circulation, Ea was assessed as the ratio of RV Pes to SV [Ea(PV) = Pes/SV]. In both groups, although the correlation between Ea(PV) and Ea(WK) was excellent over a broad range of altered conditions, Ea(PV) systematically overestimated Ea(WK). This offset disappeared when left atrial pressure (Pla) was incorporated into Ea [Ea * (PV) = (Pes - Pla)/SV]. Thus Ea * (PV), defined as the ratio of RV Pes minus Pla to SV, provides a convenient, useful, and simple method to assess the pulmonary arterial load and its impact on the RV function.     

Hemodynamic correlates of effective arterial elastance in mitral stenosis before and after balloon valvotomy

Colin, Patrice, Michel Slama, Alec Vahanian, YvesLecarpentier, Gilbert Motté, and Denis Chemla. Hemodynamiccorrelates of effective arterial elastance in mitral stenosis beforeand after balloon valvotomy. J. Appl.Physiol. 83(4): 1083-1089, 1997.This study hadthe purpose of documenting the hemodynamic correlates of effectivearterial elastance (Ea; i.e., an accurate estimate of hydraulic load)in mitral stenosis (MS) patients. The main hypothesis tested was thatEa relates to the total vascular resistance (R)-to-pulse intervalduration (T) ratio(R/T) in MS patients both before andafter successful balloon mitral valvotomy (BMV). High-fidelity aorticpressure recordings were obtained in 10 patients (40 ± 12 yr)before and 15 min after BMV. Ea value was calculated as the ratio ofthe steady-state end-systolic aortic pressure (ESAP) to stroke volume(thermodilution). Ea increased after BMV (from 1.55 ± 0.63 to 1.83 ± 0.71 mmHg/ml; P < 0.05). Throughout the procedure, there was a strong linearrelationship between Ea and R/T: Ea = 1.09R/T  0.01 mmHg/ml,r = 0.99, P = 0.0001. This ultimately dependedon the powerful link between ESAP and mean aortic pressure [MAP;r = 0.99, 95% confidence interval for the difference (MAP  ESAP) from 18.5 to +4.5 mmHg].Ea was also related to total arterial compliance (area method) and towave reflections (augmentation index), although to a lesser extent. After BMV, enhanced and anticipated wave reflections were observed, andthis was likely to be explained by decreased arterial compliance. Thepresent study indicated that Ea depended mainly on the steady componentof hydraulic load (i.e., R) and on heart period (i.e., T) in MS patients.

     

Theory of the measurement of arterial compliance in humans

Experimental determinations of the arterial complianceC are discussed, based on a simplified formula involving the systolic and diastolic pressures, the period of diastole and the peripheral resistance. The resistance is expressed in terms of the cardiac output and the mean arterial pressure during diastole. which is derived from an assumed exponential pressure-time curve and leads to a still simpler expression forC. The cardiac output is obtained by a rebreathing method that yields arterial and venous P_{CO 2}, the latter from extrapolation based on a linear difference equation. The experimental standard error of the compliance in terms of those of the various physiological parameters is considered. Numerical examples are given for a healthy man.     

Contribution of plasma proteins to splanchnic and total anabolic utilization of dietary nitrogen in humans

Splanchnic tissues are largely involved in the postprandial utilization of dietary amino acids, but little is yet known, particularly in humans, about the relative contributions of different splanchnic protein pools to splanchnic and total postprandial anabolism. Our aim was to develop a compartmental model that could distinguish dietary nitrogen (N) incorporation among splanchnic constitutive, plasma (splanchnic exported), and peripheral proteins after a mixed-protein meal in humans. Eight healthy subjects were fed a single mixed meal containing 15N-labeled soy protein, and dietary N postprandial kinetics were measured in plasma free amino acids, proteins, and urea and urinary urea and ammonia. These experimental data and others previously obtained for dietary N kinetics in ileal effluents under similar experimental conditions were used to develop the compartmental model. Six hours after the mixed-meal ingestion, 31.5, 7.5, and 21% of ingested N were predicted to be incorporated into splanchnic constitutive, splanchnic exported, and peripheral proteins, respectively. The contribution of splanchnic exported proteins to total splanchnic anabolism from dietary N was predicted to be approximately 19% and to remain steady throughout the simulation period. Model behavior and its predictions were strongly in line with current knowledge of the system and the scarce, specific data available in the literature. This model provides the first data concerning the anabolism of splanchnic constitutive proteins in the nonsteady postprandial state in humans. By use of only slightly invasive techniques, this model could help to assess how the splanchnic anabolism is modulated under different nutritional or pathophysiological conditions in humans.     

The association of oxidative stress with arterial compliance and vascular resistance in a bi-ethnic population: the SABPA study

A loss of arterial elasticity increases the risk for cardiovascular events. Oxidative injury to the vessel wall may be one of the underlying mechanisms influencing arterial elasticity. We compared markers of oxidative stress, antioxidant capacity, inflammation, windkessel compliance (Cwk), and total peripheral resistance (TPR) in black and white South Africans. Associations of arterial compliance and vascular resistance (as indicated by TPR) with oxidative stress, antioxidant capacity and inflammatory markers were also investigated. We included 146 black and 181 white men and women. Measurements from the Finometer device were used to calculate Cwk and TPR while thiobarbituric acids reactive substances (TBARS), glutathione peroxidase (GPx), C-reactive protein (CRP), and interleukin-6 (IL-6) were analyzed in serum or urine samples. Black participants had higher TPR, TBARS, GPx, CRP, and IL-6 levels (all p?≤?0.018) and lower Cwk (both p?≤?0.013) compared to white participants. Multiple regression analyses revealed independent associations of Cwk (β?=??0.27, p?=?0.015) and TPR (β?=?0.18, p?=?0.018) with TBARS in black participants, while Cwk (β?=??0.10; p?=?0.019) and TPR (β?=?0.13, p?=?0.047) were independently associated with GPx in white participants. Decreased arterial compliance and increased vascular resistance associated with increased oxidative damage independent of hypertensive status in black participants. These results suggest that oxidative stress plays a role in early vascular changes in a black population prone to the development of cardiovascular disease.     

Acute effects of resistance exercise on arterial compliance.

Decreased central arterial compliance is an emerging risk factor for cardiovascular disease. Resistance training is associated with reductions in the elastic properties of central arteries. Currently, it is not known whether this reduction is from one bout of resistance exercise or from an adaptation to multiple bouts of resistance training. Sixteen healthy sedentary or recreationally active adults (11 men and 5 women, age 27 +/- 1 yr) were studied under parallel experimental conditions on 2 separate days. The order of experiments was randomized between resistance exercise (9 resistance exercises at 75% of 1 repetition maximum) and sham control (seated rest in the exercise room). Baseline hemodynamic values were not different between the two experimental conditions. Carotid arterial compliance (via simultaneous B-mode ultrasound and applanation tonometry) decreased and beta-stiffness index increased (P < 0.01) immediately and 30 min after resistance exercise. Immediately after resistance exercise, carotid systolic blood pressure increased (P < 0.01), although no changes were observed in brachial systolic blood pressure at any time points. These measures returned to baseline values within 60 min after the completion of resistance exercise. No significant changes in these variables were observed during the sham control condition. These results indicate that one bout of resistance exercise acutely decreases central arterial compliance, but this effect is sustained for <60 min after the completion of resistance exercise.     

Systemic venous circulation. Waves propagating on a windkessel: relation of arterial and venous windkessels to systemic vascular resistance

Compared with arterial hemodynamics, there has been relatively little study of venous hemodynamics. We propose that the venous system behaves just like the arterial system: waves propagate on a time-varying reservoir, the windkessel, which functions as the reverse of the arterial windkessel. During later diastole, pressure increases exponentially to approach an asymptotic value as inflow continues in the absence of outflow. Our study in eight open-chest dogs showed that windkessel-related arterial resistance was approximately 62% of total systemic vascular resistance, whereas windkessel-related venous resistance was only approximately 7%. Total venous compliance was found to be 21 times larger than arterial compliance (n = 3). Inferior vena caval compliance (0.32 +/- 0.015 ml x mmHg(-1) x kg(-1); mean +/- SE) was approximately 14 times the aortic compliance (0.023 +/- 0.002 ml x mmHg(-1) x kg(-1); n = 8). Despite greater venous compliance, the variation in venous windkessel volume (i.e., compliance x windkessel pulse pressure; 7.8 +/- 1.1 ml) was only approximately 32% of the variation in aortic windkessel volume (24.3 +/- 2.9 ml) because of the larger arterial pressure variation. In addition, and contrary to previous understanding, waves generated by the right heart propagated upstream as far as the femoral vein, but excellent proportionality between the excess pressure and venous outflow suggests that no reflected waves returned to the right atrium. Thus the venous windkessel model not only successfully accounts for variations in the venous pressure and flow waveforms but also, in combination with the arterial windkessel, provides a coherent view of the systemic circulation.     

Exercise and arterial adaptation in humans: uncoupling localized and systemic effects

Previous studies have established effects of exercise training on arterial wall thickness, remodeling, and function in humans, but the extent to which these changes are locally or systemically mediated is unclear. We examined the brachial arteries of the dominant (D) and nondominant (ND) upper limbs of elite racquet sportsmen and compared them to those of matched healthy inactive controls. Carotid and superficial femoral artery responses were also assessed in both groups. High-resolution duplex ultrasound was used to examine resting diameter, wall thickness, peak diameter, and blood flow. We found larger resting arterial diameter in the preferred arm of the athletes (4.9 ± 0.5 mm) relative to their nonpreferred arm (4.3 ± 0.4 mm, P < 0.05) and both arms of control subjects (D: 4.1 ± 0.4 mm; ND: 4.0 ± 0.4, P < 0.05). Similar limb-specific differences were also evident in brachial artery dilator capacity (5.5 ± 0.5 vs. 4.8 ± 0.4, 4.8 ± 0.6, and 4.8 ± 0.6 mm, respectively; P < 0.05) following glyceryl trinitrate administration and peak blood flow (1,118 ± 326 vs. 732 ± 320, 737 ± 219, and 698 ± 174 ml/min, respectively; P < 0.05) following ischemic handgrip exercise. In contrast, athletes demonstrated consistently lower wall thickness in carotid (509 ± 55 μm), brachial (D: 239 ± 100 μm; ND: 234 ± 133 μm), and femoral (D: 479 ± 38 μm; ND: 479 ± 42 μm) arteries compared with control subjects (carotid: 618 ± 74 μm; brachial D: 516 ± 100 μm; ND: 539 ± 129 μm; femoral D: 634 ± 155 μm; ND: 589 ± 112 μm; all P < 0.05 vs. athletes), with no differences between the limbs of either group. These data suggest that localized effects of exercise are evident in the remodeling of arterial size, whereas arterial wall thickness appears to be affected by systemic factors.     

Acetylcholine's effect on vascular resistance and compliance in the pulmonary circulation

Acetylcholine's effect on the distribution of vascular resistance and compliance in the canine pulmonary circulation was determined under control and elevated vascular tone by the arterial, venous, and double occlusion techniques in isolated blood-perfused dog lungs at both constant flow and constant pressure. Large and small blood vessel resistances and compliances were studied in lungs given concentrations of acetylcholine ranging from 2.0 ng/ml to 200 micrograms/ml. The results of this study indicate that acetylcholine dilates large arteries at low concentrations (less than or equal to 20 ng/ml) and constricts small and large veins at concentrations of at least 2 micrograms/ml. Characterization of acetylcholine's effects at constant pulmonary blood flow indicates that 1) large artery vasodilation may be endothelial-derived relaxing factor-mediated because the dilation is blocked with methylene blue; 2) a vasodilator of the arachidonic acid cascade (blocked by ibuprofen), probably prostacyclin, lessens acetylcholine's pressor effects; 3) when vascular tone was increased, acetylcholine's hemodynamic effects were attenuated; and 4) acetylcholine decreased middle compartment and large vessle compliance under control but not elevated vascular tone. Under constant pressure at control vascular tone acetylcholine increases resistance in all segments except the large artery, and at elevated vascular tone the pressor effects were enhanced, and large artery resistance was increased.     

Sympathetic neural discharge and vascular resistance during exercise in humans

The purpose of this study was to determine the relationship between changes in efferent muscle sympathetic nerve activity (MSNA) to the lower leg and calf vascular resistance (CVR) during isometric exercise in humans. We made intraneural (microneurographic) determinations of MSNA in the right leg (peroneal nerve) while simultaneously measuring calf blood flow to the left leg, arterial pressure, and heart rate in 10 subjects before (control), during, and after (recovery) isometric handgrip exercise performed for 2.5 min at 15, 25, and 35% of maximal voluntary contraction (MVC). Heart rate and arterial pressure increased above control within the initial 30 s of handgrip at all levels, and the magnitudes of the increases at end contraction were proportional to the intensity of the exercise. In general, neither MSNA nor CVR increased significantly above control levels during handgrip at 15% MVC. Similarly, neither variable increased above control during the initial 30 s of handgrip at 25 and 35% MVC; however, during the remainder of the contraction period, progressive, parallel increases were observed in MSNA and CVR (P less than 0.05). The correlation coefficients relating changes in MSNA to changes in CVR for the individual subjects averaged 0.63 +/- 0.07 (SE) (range 0.30-0.91) and 0.94 +/- 0.06 (range 0.80-0.99) for the 25 and 35% MVC levels, respectively. During recovery, both MSNA and CVR returned rapidly toward control levels. These findings demonstrate that muscle sympathetic nerve discharge and vascular resistance in the lower leg are tightly coupled during and after isometric arm exercise in humans. Furthermore, the exercise-induced adjustments in the two variables are both contraction intensity and time dependent.     

Sex differences in carotid baroreflex control of arterial blood pressure in humans: relative contribution of cardiac output and total vascular conductance

It is presently unknown whether there are sex differences in the magnitude of blood pressure (BP) responses to baroreceptor perturbation or if the relative contribution of cardiac output (CO) and total vascular conductance (TVC) to baroreflex-mediated changes in BP differs in young women and men. Since sympathetic vasoconstrictor tone is attenuated in women, we hypothesized that carotid baroreflex-mediated BP responses would be attenuated in women by virtue of a blunted vascular response (i.e., an attenuated TVC response). BP, heart rate (HR), and stroke volume were continuously recorded during the application of 5-s pulses of neck pressure (NP; carotid hypotension) and neck suction (NS; carotid hypertension) ranging from +40 to -80 Torr in women (n = 20, 21 ± 0.5 yr) and men (n = 20, 21 ± 0.4 yr). CO and TVC were calculated on a beat-to-beat basis. Women demonstrated greater depressor responses to NS (e.g., -60 Torr, -17 ± 1%baseline in women vs. -11 ± 1%baseline in men, P < 0.05), which were driven by augmented decreases in HR that, in turn, contributed to larger reductions in CO (-60 Torr, -15 ± 2%baseline in women vs. -6 ± 2%baseline in men, P < 0.05). In contrast, pressor responses to NP were similar in women and men (e.g., +40 Torr, +14 ± 2%baseline in women vs. +10 ± 1%baseline in men, P > 0.05), with TVC being the primary mediating factor in both groups. Our findings indicate that sex differences in the baroreflex control of BP are evident during carotid hypertension but not carotid hypotension. Furthermore, in contrast to our hypothesis, young women exhibited greater BP responses to carotid hypertension by virtue of a greater cardiac responsiveness.     

Alterations of calf venous and arterial compliance following acclimation to heat administered at a fixed daily time in humans

We investigated the effects of heat acclimation on venous and arterial compliance in humans. Four male and four female volunteers were exposed to an ambient temperature of 40°C and relative humidity of 40% for 4 h (1330–1730 hours) per day for 9–10 consecutive days. The calf venous compliance (CV) was estimated using venous occlusion plethysmography with a mercury-in-silastic strain gauge placed around the right calf at its maximum girth. The compliance of the small (CSA) and large (CLA) arteries were assessed by reflective and capacitance compliance by analyzing the radial artery blood pressure waveforms, basing on the use of a modified Windkessel model. The calf CV, CSA, CLA, systolic and diastolic blood pressures, heart rate and core temperature were determined twice a day, 0930–1100 hours (AM test) and 1500–1630 hours (PM test), in both heat-acclimated and non-heat-acclimated (control) conditions. Heat acclimation appeared to decrease blood pressures, heart rate and significantly lowered core temperature only in the PM test. In the control condition, the calf CV was not affected by the time of day and the CSA was significantly depressed in the PM test. After acclimation to heat, the calf CV significantly increased and the CSA did not decrease in the PM test. The results presented suggest that repeated heat exposure in humans, for 4 h at a fixed time daily, increases the calf CV and the CSA particularly during the period when the subjects were previously exposed to heat.