Changes In Total Peripheral Resistance Research Articles

The relative contribution of hemodynamic parameters to blood pressure decrease in classical orthostatic hypotension.

We studied the relative contributions of total peripheral resistance (TPR), stroke volume (SV) and heart rate (HR) to low blood pressure in classical orthostatic hypotension (cOH) on group and individual levels. We retrospectively analyzed tilt test records from cOH patients and age/sex-matched controls. We quantified relative effects of HR, SV and TPR on mean arterial pressure (MAP) with the log-ratio method. We studied relations of changes of HR, SV or TPR with the change of MAP across patients and variability of contributions of HR, SV and TPR to MAP. We also explored neurogenic vs. nonneurogenic causes. MAP responded to tilt with a decrease in patients (n = 80) and an increase in controls (n = 80). A too small TPR-increase contributed most to cOH, followed by a too large SV-decrease; both effects were partially corrected by a larger increase of HR. Only TPR changes consistently affected MAP change in patients and controls. TPR decreased almost exclusively in patients, most in those with severe cOH. Contributions of HR, SV and TPR to MAP did not differ between probable neurogenic and nonneurogenic causes. HR, SV and TPR all contributed to cOH, with a key role for TPR; a decrease of TPR was almost unique to patients and may be due to hyperventilation. The lack of differences between neurogenic and nonneurogenic causes needs further study.

Using an in-office passive leg raise to identify older adults with suboptimal blood pressure control.

Passive leg raise (PLR) is a simple, dynamic maneuver that has been used to increase preload to the heart. We hypothesize that PLR may offer a new and efficient office-based tool for assessing blood pressure (BP) control in older adults. One hundred and three veterans (≥60 years old) without known cardiovascular disease and varying degrees of blood pressure control were included in this cross-sectional cohort study. Twenty-four hour ambulatory BP monitoring identified Veterans with optimal and suboptimal BP control (≥125/75 mmHg). Bioimpedance electrodes (Baxter Medical, Deerfield, Illinois, USA) and brachial BP were used to calculate hemodynamic parameter changes across PLR states [pre-PLR, active PLR (3 min), and post-PLR]. Multiple linear regression was used to assess associations between BP control status with changes in hemodynamic parameters between PLR states. The 24-h ambulatory BP monitoring identified 43 (42%) older Veterans with optimal BP control (mean age of 70.5 ± 7.0 years) and 55 (54%) with suboptimal BP (mean age of 71.3 ± 8.7 years). Veterans with suboptimal BP control had significantly reduced change in total peripheral resistance (ΔTPR) (7.0 ± 156.0 vs. 127.3 ± 145.6 dynes s/cm5; P = 0.002) following PLR compared with Veterans with optimal BP control. Suboptimal BP control (β = -0.35, P = 0.004) had a significant association with reduced ΔTPR, even after adjusting for demographic variables. Measuring PLR-induced hemodynamic changes in the office setting may represent an alternative way to identify older adults with suboptimal BP control when 24-h ambulatory BP monitoring is not available.

Preconception Physical Exercise Is Associated with Phenotype-Specific Cardiovascular Alterations in Women at Risk for Gestational Hypertensive Disorders.

Background/Objectives: Gestational hypertensive disorders (GHD) pose significant maternal and fetal health risks during pregnancy. Preconception physical exercise has been associated with a lower incidence of GHD, but insights into the cardiovascular mechanisms remain limited. This study aimed to evaluate the effect of preconception physical exercise on the complete cardiovascular functions of women at risk for GHD in a subsequent pregnancy. Methods: A non-invasive hemodynamics assessment of arteries, veins, and the heart was performed on 40 non-pregnant women at risk for developing GHD in a subsequent pregnancy. Measurements of an electrocardiogram Doppler ultrasound, impedance cardiography and bio-impedance spectrum analysis were taken before and after they engaged in physical exercise (30-50 min, 3×/week, 4-6 months). Results: After a mean physical exercise period of 29.80 weeks, the total peripheral resistance (TPR), diastolic blood pressure and mean arterial pressure decreased in the total study population, without changing cardiac output (CO). However, in 42% (9/21) of women categorized with high or low baseline CO (>P75 or <P25 resp.), a shift in CO was observed towards the normal reference interquartile range (P25-P75). This was associated with improved hepatic venous and central arterial hemodynamic functions. Similar changes in TPR occurred in 38% (11/29) of women classified as having low or high baseline TPR. Conclusions: As in pregnancy, output- or resistance-dominant cardiovascular profiles already exist prior to conception. This study illustrates that preconception physical exercise shifts high or low CO and/or TPR towards the normal midrange, allowing women at risk for GHD to start a subsequent pregnancy with a more gestation-adaptable cardiovascular system.

Mental stress augments central artery stiffness in young individuals of both sexes

Mental stress is a daily stimulus that can acutely activate the sympathetic nervous system. Whether sympathetic stimulation can augment central artery stiffness (CAS) has not yet been well documented. Moreover, sex differences in sympathetic neurovascular transduction have been reported. We assessed whether mental stress augments CAS in both sexes and whether any CAS increase is blunted in women compared with men. The hf-PWV (heart-femoral pulse wave velocity; index of CAS), MAP (mean arterial pressure), PP (pulse pressure), TPR (total peripheral resistance), and HR (heart rate) were measured in 26 young individuals (13 men, 13 women) at rest and throughout a 10-minute bout of stress induced by mental arithmetic. Data over the mental stress period were compared to the preceding baseline values and between sexes. Mental stress increased hf-PWV, MAP, PP, and HR from baseline throughout the entire stimulation period (p < .005). TPR diminished in the first minute of stimulation (p < .001) in both sexes and increased in the last minutes in women only (p < .005). Hf-PWV was lower in women than men (p < .001) at rest and during mental stress, but the changes from baseline were similar in both sexes. There were sex differences in the PP and TPR changes, which were evident at different times of stimulation. Mental stress increased CAS in both sexes throughout the stimulation period. Although values of CAS were lower in women both at rest and during mental stress, the CAS increase due to mental stress was similar in both sexes.

Abstract 13592: Gender Related Divergences in Cardiac and Vascular Function With Age

Introduction: Heart failure with preserved ejection fraction (HFpEF) is a disease of advanced aging that disproportionately affects women. Diastolic function changes with age and it is unknown if gender-related differences in progression exist. Understanding ages at which parameters of vascular and diastolic function diverge may provide insight into the differential risk of HFpEF between genders. Methods: Sedentary but healthy non-obese subjects aged 20-90 (n=178, 58% female; avg age 56 ± 13 yrs) underwent measures of pulmonary capillary wedge pressure (PCWP; right heart catheterization), blood pressure and cardiac output (acetylene rebreathe). Diastolic function was assessed by Doppler echocardiogram. A generalized linear model was used to estimate effects of age for each measured hemodynamic parameter as a function of gender. Results: Across age, women had higher systolic blood pressure (SBP) (age*gender p=0.025, age p&lt;0.001) and total peripheral resistance (TPR) (age*gender p=0.053, age p&lt;0.001). Changes in TPR were apparent at age 26 while SBP diverged at age 55. (Figure) Women had slower early diastolic recoil (e’) (age*gender p&lt;0.001) starting at age 55. While E wave velocity was lower in women, age-related decline was similar to men. E/e’ was higher in women (age*gender p=0.007) and diverged at a young age (28). PCWP declined with age similarly in both men and women. Systolic velocity (s’) declined in early middle age (42) in women (age*gender p=0.007, age p=0.002). Conclusions: Women experience greater changes in cardiac and vascular function with age than men. The age at which these parameters diverge differs, with evidence for decline in vascular function and cardiac contractility occurring at young ages in women while changes in SBP and diastolic recoil occur after age 55. Understanding lifestyle and hormonal factors that influence these differences may help elucidate HFpEF risk factors that are modifiable and serve as a target for therapy.

Control of blood pressure in the cold: differentiation of skin and skeletal muscle vascular resistance.

What is the central question of this study? Why does blood pressure increases during cold air exposure? Specifically, what is the contribution of skin and skeletal muscle vascular resistance during whole body versus isolated face cooling? What is the main finding and its importance? Whole-body cooling caused an increase in blood pressure through an increase in skeletal muscle and cutaneous vascular resistance. However, isolated mild face cooling caused an increase in blood pressure predominately via an increase in cutaneous vasoconstriction. The primary aim of this investigation was to determine the individual contribution of the cutaneous and skeletal muscle circulations to the cold-induced pressor response. To address this, we examined local vascular resistances in the cutaneous and skeletal muscle of the arm and leg. Thirty-four healthy individuals underwent three different protocols, whereby cold air to clamp skin temperature (27°C) was passed over (1) the whole-body, (2) the whole-body, but with the forearm pre-cooled to clamp cutaneous vascular resistance, and (3) the face. Cold exposure applied to the whole body or isolated to the face increased mean arterial pressure (all, P<0.001) and total peripheral resistance (all, P<0.047) compared to thermal neutral baseline. Whole-body cooling increased femoral (P<0.005) and brachial artery resistance (P<0.003) compared to thermoneutral baseline. Moreover, when the forearm was pre-cooled to remove the contribution of cutaneous resistance (P=0.991), there was a further increase in lower arm vasoconstriction (P=0.036) when whole-body cooling was superimposed. Face cooling also caused a reflex increase in lower arm cutaneous (P=0.009) and brachial resistance (P=0.050), yet there was no change in femoral resistance (P=0.815) despite a reflex increase in leg cutaneous resistance (P=0.010). Cold stress causes an increase in blood pressure through a change in total peripheral resistance that is largely due to cutaneous vasoconstriction with face cooling, but there is additional vasoconstriction in the skeletal muscle vasculature with whole-body cooling.

Mechanism-based pharmacodynamic model for propofol haemodynamic effects in healthy volunteers☆

BackgroundThe adverse haemodynamic effects of the intravenous anaesthetic propofol are well known, yet few empirical models have explored the dose–response relationship. Evidence suggests that hypotension during general anaesthesia is associated with postoperative mortality. We developed a mechanism-based model that quantitatively characterises the magnitude of propofol-induced haemodynamic effects during general anaesthesia. MethodsMean arterial pressure (MAP), heart rate (HR) and pulse pressure (PP) measurements were available from 36 healthy volunteers who received propofol in a step-up and step-down fashion by target-controlled infusion using the Schnider pharmacokinetic model. A mechanistic pharmacodynamic model was explored based on the Snelder model. To benchmark the performance of this model, we developed empirical models for MAP, HR, and PP. ResultsThe mechanistic model consisted of three turnover equations representing total peripheral resistance (TPR), stroke volume (SV), and HR. Propofol-induced changes were implemented by Emax models on the zero-order production rates of the turnover equations for TPR and SV. The estimated 50% effective concentrations for propofol-induced changes in TPR and SV were 2.96 and 0.34 μg ml−1, respectively. The goodness-of-fit for the mechanism-based model was indistinguishable from the empirical models. Simulations showed that predictions from the mechanism-based model were similar to previously published MAP and HR observations. ConclusionsWe developed a mechanism-based pharmacodynamic model for propofol-induced changes in MAP, TPR, SV, and HR as a potential approach for predicting haemodynamic alterations. Clinical trial registrationNCT02043938

α-Adrenergic receptor blockade attenuates pressor response during mental stress in young black adults.

Black individuals exhibit increased blood pressure (BP) responses to sympathetic stimulation that are associated with an increased risk of hypertension (HTN). We tested the hypothesis that α1‐adrenergic blockade inhibits the increased BP response during and after 45‐min stress in young normotensive Black adults, which may be mediated, in part, by dampened vasoconstriction and decreased renal sodium retention. Utilizing a double‐masked randomized, crossover study design, 51 normotensive Black adults (31 ± 8 yr) were treated with either a placebo or 1 mg/day of prazosin for 1 week. On the final day of each treatment, hemodynamic measures and urinary sodium excretion (UNaV) were collected before (Rest), during (Stress) and after (Recovery) 45 min of mental stress induced via a competitive video game task. During the Stress period, diastolic BP and total peripheral resistance (TPR) were significantly lower with prazosin compared to placebo (p < .05 for both). Similarly, we observed lower systolic BP, diastolic BP, and TPR during the Recovery period with prazosin versus placebo (p < .05 for both). There was no effect of prazosin on stress‐associated UNaV. The change in systolic BP from Rest to Recovery was positively associated with the change in TPR with both treatments (p < .05 for both). In summary, prazosin treatment dampened BP reactivity to 45‐min mental stress and lowered post‐stress BP over the recovery period, which was linked to reduce TPR in young normotensive Black adults. These results suggest that α1‐adrenergic receptor activity may contribute to BP responses and delayed BP recovery to prolonged mental stress through increased vasoconstriction in Black adults.

Factors mediating the pressor response to isometric muscle contraction: An experimental study in healthy volunteers during lower body negative pressure.

Whilst both cardiac output (CO) and total peripheral resistance (TPR) determine mean arterial blood pressure (MAP), their relative importance in the pressor response to isometric exercise remains unclear. This study aimed to elucidate the relative importance of these two different factors by examining pressor responses during cardiopulmonary unloading leading to step-wise reductions in CO. Hemodynamics were investigated in 11 healthy individuals before, during and after two-minute isometric exercise during lower body negative pressure (LBNP; -20mmHg and -40mmHg). The blood pressure response to isometric exercise was similar during normal and reduced preload, despite a step-wise reduction in CO during LBNP (-20mmHg and -40mmHg). During -20mmHg LBNP, the decreased stroke volume, and consequently CO, was counteracted by an increased TPR, while heart rate (HR) was unaffected. HR was increased during -40 mmHg LBNP, although insufficient to maintain CO; the drop in CO was perfectly compensated by an increased TPR to maintain MAP. Likewise, transient application of LBNP (-20mmHg and -40mmHg) resulted in a short transient drop in MAP, caused by a decrease in CO, which was compensated by an increase in TPR. This study suggests that, in case of reductions of CO, changes in TPR are primarily responsible for maintaining the pressor response during isometric exercise. This highlights the relative importance of TPR compared to CO in mediating the pressor response during isometric exercise.

The influence of aircraft noise exposure on the systemic and renal haemodynamics.

Epidemiological studies found a link between aircraft noise exposure and increased incidence of arterial hypertension and cardiovascular disease, but the underlying pathophysiological mechanisms are not fully understood. Clinical studies have shown that mental stress affects the systemic and renal haemodynamic, but no such study was performed with noise exposure as stress factor. We analysed systemic and renal effects of 25 min standardized aircraft noise in a sham controlled clinical study including 80 healthy men and 34 male patients with hypertension. Systemic haemodynamic parameters were measured using electrocardiography and impedance cardiography. The renal haemodynamic was assessed using steady state input clearance with infusion of para-aminohippuric acid and inulin for glomerular filtration rate and renal plasma flow, respectively. In the systemic circulation of hypertensive patients, there was an increase in total peripheral resistance (TPR) (1420 ± 387 vs. 1640 ± 516 dyn·s·cm-5, P = 0.001) and a decrease in cardiac index (CI) (2.9 ± 0.8 vs. 2.6 ± 0.8 L/(min·m2, P < 0.001) 25 min after the start of noise exposure, which was not present during sham procedure (P = 0.10, P = 0.86). In healthy individuals a procedure induced increase in TPR and decrease in CI was present after noise (TPR: 995 ± 239 vs. 1106 ± 308 dyn·s·cm-5, P = 0.001, CI: 3.6 ± 0.7 vs. 3.3 ± 0.9 L/(min·m2, P < 0.001) and sham application (TPR: P = 0.002, CI: P < 0.001). However, in healthy individuals changes in TPR (P = 0.450) and CI (P = 0.605) from baseline until 25 min after the start of the intervention did not differ between noise and sham exposure. In the renal circulation of hypertensive patients and healthy individuals the response did not differ between noise and sham procedure. In hypertensive but not healthy men we observed a systemic vasoconstrictive response after aircraft noise exposure accompanied by a decrease in CI. No significant changes were observed in the renal circulation. Our results suggest that male hypertensive patients are more susceptible for noise-induced changes of vascular resistance in the systemic circulation.

Aerobic fitness and sympathetic responses to spontaneous muscle sympathetic nerve activity in young males

Lower aerobic fitness increases the risk of developing hypertension. Muscle sympathetic nerve activity (MSNA) is important for the beat-by-beat regulation of blood pressure. Whether the cardiovascular consequences of lower aerobic fitness are due to augmented transduction of MSNA into vascular responses is unclear. We tested the hypothesis that aerobic fitness is inversely related to peak increases in total peripheral resistance (TPR) and mean arterial pressure (MAP) in response to spontaneous MSNA bursts in young males. Relative peak oxygen consumption (VO2peak, indirect calorimetry) was assessed in 18 young males (23 ± 3years; 41 ± 8ml/kg/min). MSNA (microneurography), cardiac intervals (electrocardiogram) and arterial pressure (finger photoplethysmography) were recorded continuously during supine rest. Stroke volume and cardiac output (CO) were estimated via the ModelFlow method. TPR was calculated as MAP/CO. Changes in TPR and MAP were tracked for 12 cardiac cycles following heartbeats associated with or without spontaneous bursts of MSNA. Overall, aerobic fitness was inversely correlated to the peak ΔTPR (0.8 ± 0.7mmHg/l/min; R = -0.61, P = 0.007) and ΔMAP (2.3 ± 0.8mmHg; R = -0.69, P < 0.001), but not with the peak ΔCO (0.2 ± 0.1l/min; P = 0.50), MSNA burst frequency (14 ± 5 bursts/min; P = 0.43) or MSNA relative burst amplitude (65 ± 12%; P = 0.13). Heartbeats without an associated burst of MSNA did not increase TPR, MAP or CO. Although unrelated to traditional MSNA characteristics, aerobic fitness was inversely associated with spontaneous sympathetic neurovascular transduction in young males. This may be a potential mechanism by which aerobic fitness modulates the regulation of arterial blood pressure through the sympathetic nervous system.

Difference in cardiovascular response during orthostatic stress in Parkinson's disease and multiple system atrophy.

Although orthostatic hypotension is more prominent in multiple system atrophy (MSA) than in Parkinson's disease (PD), there is no study comparing the degree of decrease in total peripheral resistance and cardiac response during orthostatic stress between both diseases. In this study, we examined whether there is a difference in cardiovascular response between MSA and PD. We examined the results of the head-up tilt test in 68 patients with MSA, 28 patients with cardiac non-denervated PD, and 70 patients with cardiac denervated PD whose total peripheral resistance after 60° tilting was lower than the value at 0°. Differences in cardiac output and blood pressure changes were compared against the decrease in total peripheral resistance. There was no difference in the degree of decrease in total peripheral resistance among the three groups. However, the slope of the regression line revealed that the increase in cardiac output against the change in total peripheral resistance was significantly lower in the MSA group than in the cardiac non-denervated and denervated PD groups, and that the decrease in systolic blood pressure against the change in total peripheral resistance was significantly greater in the MSA group than in the cardiac non-denervated and denervated PD groups. In MSA, the cardiac response during orthostatic stress is lower than that in PD, possibly underlying the fact that orthostatic hypotension is more prominent in MSA than in PD.

Sympathetic nervous system activity and reactivity in women with gestational diabetes mellitus.

IntroductionGestational diabetes mellitus (GDM) is associated with vascular dysfunction. Sympathetic nervous system activity (SNA) is an important regulator of vascular function, and is influenced by glucose and insulin. The association between GDM and SNA (re)activity is unknown. We hypothesize that women with GDM would have increased SNA during baseline and during stress.MethodsEighteen women with GDM and 18 normoglycemic pregnant women (controls) were recruited. Muscle SNA (MSNA; peroneal microneurography) was assessed at rest, during a cold pressor test (CPT) and during peripheral chemoreflex deactivation (hyperoxia). Spontaneous sympathetic baroreflex gain was quantified versus diastolic pressure at rest and during hyperoxia.ResultsAge, gestational age (third trimester) and pre‐pregnancy body mass index and baseline MSNA was not different among the groups. Women with GDM had a similar increase in MSNA, but a greater pressor response to CPT compared to controls (% change in MAP 17 ± 7% vs. 9 ± 9%; p = .004). These data are consistent with a greater neurovascular transduction in GDM (% change in total peripheral resistance/% change in burst frequency [BF]: 15.9 ± 30.2 vs. −5.2 ± 16.4, p = .03). Interestingly, women with GDM had a greater reduction in MSNA during hyperoxia (% change in BF −30 ± 19% vs. −6 ± 17%; p = .01).ConclusionWomen diagnosed with GDM have similar basal SNA versus normoglycemic pregnant women, but greater neurovascular transduction, meaning a greater influence of the sympathetic nerve activity in these women. We also document evidence of chemoreceptor hyperactivity, which may influence SNA in women with GDM but not in controls.

The cross-sectional association between diabetes and orthostatic hypotension in community-dwelling older people.

Orthostatic hypotension is a recognized complication of diabetes, but studies examining prevalence in diabetes are limited. The aim of this study was to ascertain the prevalence of orthostatic hypotension and the pattern of orthostatic BP response in a cohort of people with diabetes aged ≥50 years, embedded within the Irish Longitudinal Study of Ageing. Orthostatic hypotension was defined as a drop in systolic blood pressure (SBP) ≥20mmHg or drop in diastolic blood pressure (DBP) ≥10mmHg at 30s after standing. Diabetes was defined by self-report but cross-checked against HbA1c and medication records. Multilevel mixed effects linear regression models were used to compare orthostatic BP in people with and without diabetes. Some 3222 people were included, 7% (213 of 3222) of whom had diabetes. Prevalence of orthostatic hypotension in the group with diabetes was 22% (46 of 213) vs. 13% in those without diabetes; χ2 = 12.43; P < 0.001. Multilevel models demonstrated prolonged recovery of DBP in people with diabetes, with only 41% (87 of 213) returning to baseline by 60s. Logistic regression models demonstrated that diabetes was associated with a significantly increased likelihood of orthostatic hypotension (odds ratio 1.84, 95% confidence interval 1.30-2.59; P=0.001) and this remained robust after controlling for covariates. Over one-fifth of older people with diabetes had orthostatic hypotension. Recovery of DBP is related to dynamic changes in total peripheral resistance and impairment of this baroreflex-mediated response may explain the higher prevalence in diabetes. Given the prognostic implications when co-existing with diabetes, orthostatic hypotension may represent a potentially modifiable risk factor for adverse outcomes in late-life diabetes.

P139 Does Early Life Programming Influence Arterial Stiffness and Central Hemodynamics in Adulthood? Could Birth Cohort Effects be of Importance?

ObjectiveOur aim was to investigate possible associations between birth weight (BW) and adult carotid-femoral Pulse Wave Velocity (cfPWV) and augmentation pressure index (AIx).DesignThis study including 1598 participants, 340 elderly subjects and 1258 young-middle aged subjects from the Malmö Offspring Study with data on birth weight and gestational age (GA). Participants underwent cfPWV and AIx measurements with Sphygmocor® (AtCor, Australia). Analysis of data was performed with multiple linear regression models with adjustments for age, sex, GA, and risk factors. Furthermore, comparisons were made between participants born prematurely or at term, or born small-for-gestational-age (SGA) or appropriate-for-gestational-age (AGA).ResultsBirth weight was positively associated with cfPWV after full adjustment (b = 0.057; p < 0.001), Figure 1, a finding that remained significant in the younger age group 18–27 years (b = 0.138, p = 0.008). Furthermore, birth weight was inversely associated with AIx (b = −0.058, p = 0.001). Subjects born SGA had significantly higher AIx (p = 0.007) and MAP (p = 0.037) compared to AGA born. Preterm-born subjects showed significantly higher systolic blood pressure compared to term-born (p = 0.034). Also, BW was inversely associated with MAP (b = −0.058, p = 0.017) and SBP (b = −0.047, p = 0.031), respectively.ConclusionOur findings suggest that changes in total peripheral resistance, rather than decreased arterial stiffness, may explain the observed inverse association between birth weight and SBP. Furthermore, the association between birth weight and cfPWV, shown strongest in the youngest age group (birth cohort), could possibly be explained by increasing maternal overweight/obesity. This calls for screening of risk factors in subjects with adverse conditions at birth.Figure 1Simple regression of birth weight and pulse wave velocity.

Effect of Sex on Cardiovascular Responses to Acute Sympathoexcitatory Stressors

Over the past twenty years, an increasing number of studies have compared baseline cardiovascular regulation between men and women. These studies have provided strong support for an effect of sex on cardiovascular outcomes, and implicate the sympathetic nervous system as a mediator of many of these differences. However, many of these studies have been conducted under baseline conditions, despite the fact that humans are seldom in a true “baseline” state (i.e., quiet, supine rest). Therefore, the purpose of this study was to investigate the effect of sex on cardiovascular responses to sympatho‐excitatory stimuli in young healthy individuals. We examined cardiovascular responses to the cold pressor test (CPT) and a voluntary end‐expiratory apnea (APN) in 5 women and 4 men. We hypothesized that women would demonstrate a reduced change in total peripheral resistance (TPR) and therefore blood pressure (BP) responses to these stimuli compared with men. Men and women were of similar age (men: 24 ± 2 y, women: 24 ± 1; p=0.8) and BMI (men: 26 ± 6 kg/m2, women: 22 ± 1; p=0.2). Baseline mean arterial pressure (MAP) was higher in men than women (87 ± 7 vs77 ± 4 mmHg, respectively; p=0.03), while baseline TPR (men: 25.7 ± 2.7 vs women: 23.2 ± 6.6 mmHg/L/min; p=0.5) and cardiac output (3.4 ± 0.4 vs 3.5 ± 0.9 L/min; p=0.9) were similar between the sexes. CPT was associated with a significant increase in MAP from baseline which was not different between the sexes (men: 90 ± 3 vs women: 92 ± 13mmHg; main effect of condition: p=0.03, effect of sex: p=0.7). Likewise, TPR increased in response to CPT, but again this response did not differ between the sexes (men: 27.0 ± 7.1, vs women: 25.8 ± 5.4 mmHg/L/min; main effect of condition: p=0.04, effect of sex: p=0.3). APN‐EX was associated with a similar increase in DBP (men: 83 ± 6 vs women: 69 ± 25 mmHg; main effect of condition: p=0.03, effect of sex: p=0.3) as well as TPR (men: 33.0 ± 4.8 vs women: 29.0 ± 13.9 mmHg/L/min; main effect of condition: p=0.01, effect of sex: p=0.6). In conclusion, cardiovascular responses to the CPT, a generalized sympathetic stressor, as well as to APN, which activates the chemoreflex, were similar between the young healthy men and women. These data refute our hypothesis, and suggest that cardiovascular responsiveness during these sympatho‐excitatory stimuli does not differ between the sexes.Support or Funding InformationThis project was supported by a Natural Sciences and Engineering Research Council Discovery Grant (CWU). TEA and YC were supported by the McGill Department of Kinesiology and Physical Education Graduate Excellence Fellowship.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

The Differences Between Winners and Losers in Competition: the Relation of Cognitive and Emotional Aspects During a Competition to Hemodynamic Responses

Sympathetic nervous activity plays an important role in behavior related to competition. However, the hemodynamic response patterns of winners and losers during competition remain largely unknown. This study examined the differences between winners’ and losers’ hemodynamic and psychological responses (their evaluation of perceived demands and resources and their positive and negative emotions) to competition. The participants included 30 university students, who completed a competitive mirror-drawing task (three times) in pairs as their cardiac output (CO) and total peripheral resistance (TPR) were measured. Additionally, they were required to answer a question regarding their subjective psychological state before and during the competition. The participants were assigned to a Winner or a Loser group based on outcomes. The Winner group presented greater CO changes than the Loser group, while the Loser group displayed greater TPR changes than the Winner group. Moreover, the Winner group scored significantly higher on resource/demand evaluation than the Loser group. Although we observed no significant differences in terms of negative emotion, only the Winner group showed increased positive emotions from precompetition to competition. This evidence suggests that winners and losers display different patterns of enhanced sympathetic-cardiovascular responses to competition; winners are characterized by a myocardial response pattern, while losers are characterized by a vascular response pattern. The psychological responses that depend on one’s position during a competition provide information on the quality of hemodynamic responses to competition.

Blunted cardiovascular responses to exercise in Parkinson's disease patients: role of the muscle metaboreflex.

Patients with Parkinson's disease (PD) exhibit attenuated cardiovascular responses to exercise. The underlying mechanisms that are potentially contributing to these impairments are not fully understood. Therefore, we sought to test the hypothesis that patients with PD exhibit blunted cardiovascular responses to isolated muscle metaboreflex activation following exercise. For this, mean blood pressure, cardiac output, and total peripheral resistance were measured using finger photoplethysmography and the Modelflow method in 11 patients with PD [66 ± 2 yr; Hoehn and Yahr score: 2 ± 1 a.u.; time since diagnosis: 7 ± 1 yr; means ± SD) and 9 age-matched controls (66 ± 3 yr). Measurements were obtained at rest, during isometric handgrip exercise performed at 40% maximal voluntary contraction, and during postexercise ischemia. Also, a cold pressor test was assessed to confirm that blunted cardiovascular responses were specific to exercise and not representative of generalized sympathetic responsiveness. Changes in mean blood pressure were attenuated in patients with PD during handgrip (PD: ∆25 ± 2 mmHg vs. controls: ∆31 ± 3 mmHg; P < 0.05), and these group differences remained during postexercise ischemia (∆17 ± 1 mmHg vs. ∆26 ± 1 mmHg, respectively; P < 0.01). Additionally, changes in total peripheral resistance were attenuated during exercise and postexercise ischemia, indicating blunted reflex vasoconstriction in patients with PD. Responses to cold pressor test did not differ between groups, suggesting no group differences in generalized sympathetic responsiveness. Our results support the concept that attenuated cardiovascular responses to exercise observed in patients with PD are, at least in part, explained by an altered skeletal muscle metaboreflex. NEW & NOTEWORTHY Patients with Parkinson's disease (PD) presented blunted cardiovascular responses to exercise. We showed that cardiovascular response evoked by the metabolic component of the exercise pressor reflex is blunted in patients with PD. Furthermore, patients with PD presented similar pressor response during the cold pressor test compared with age-matched controls. Altogether, our results support the hypothesis that attenuated cardiovascular responses to exercise observed in patients with PD are mediate by an altered skeletal muscle metaboreflex.

Abstract 721: The Exercise Pressor Response to Lower Extremity Dynamic Exercise is Accompanied by an Abnormal Change in Total Peripheral Resistance in Peripheral Arterial Disease Subjects

Patients with peripheral arterial disease (PAD) have an exaggerated pressor response to dynamic exercise of the affected limb. We tested the hypothesis that this response is mediated by an increase in total peripheral resistance (TPR). We measured heart rate, blood pressure, stroke volume, cardiac output (CO), and total peripheral resistance (TPR) during exercise in 9 subjects with PAD and 9 age matched controls using continuous finger arterial pressure monitoring (Finometer). Finometer derived values were adjusted to values obtained by echocardiography, and brachial pressure at baseline. The average age and ABI was 65 ± 7 and 1.06 ± 0.07 in controls, and 66 ± 7 and 0.64 ± 0.08 in PAD. Participants performed dynamic plantar flexion at progressive workloads of 2 to 12kg (increased by 1kg/min until onset of fatigue/pain) using their symptomatic leg or leg with lower ABI. Those who reached 12kg continued exercise at a constant load until onset of fatigue/pain or a maximum of 4 minutes. Participants were then asked to perform an isometric handgrip exercise at 30% of maximum voluntary contraction (MVC) until fatigue. Results are shown in Table 1. There were no differences in hemodynamic parameters at baseline. The average weight at end of plantar flexion was 12.0 ± 0.2 and 9.2 ± 2.5 kg (p&lt;0.0001) for control and PAD. Perceived exertion (Borg scale) and pain (NPRS scale) at end of exercise was 15 ± 2 and 0, and 15 ± 2 and 6 ± 3 in control and PAD. Plantar flexion elicited a significantly higher rise in blood pressure in PAD compared to control. TPR decreased in controls, but slightly increased in PAD. In contrast, isometric handgrip elicited a similar pressor response, as well as changes in CO and TPR in both groups. We conclude that the exaggerated pressor response in PAD is mediated by an abnormal response in TPR, which counteracts the normal vasodilatory response to dynamic leg exercise seen in controls. This response appears to be specific to dynamic plantar flexion exercise in PAD.

Cardiovascular responses to isometric handgrip exercise in young patients with recurrent vasovagal syncope.

Arterial blood pressure (BP) increased in healthy humans in response to isometric handgrip (IHG), but the pattern of the relative contribution of cardiac output (CO) and total peripheral resistance (TPR) changes to the pressor response is different among individuals. We investigated weather patients with recurrent vasovagal syncope (VVS) have a similar pattern of individual CO, TPR and pressor responses to IHG, as healthy subjects. 32 patients (27.5 ± 2.6 years), and 30 age-matched controls. Autonomic function was evaluated using finger-photoplethysmography to measure BP and heart rate (HR) response to gravitational stress (ΔBP, ΔHR), Valsalva maneuver (VM) and baroreflex sensitivity (BRS), and BP HR and CO changes during IHG. ΔBP, ΔHR, VM and IHG tests did not show significant difference between VVS patients and controls, although BRS was lower in VVS group (p < 0.05). Pattern of individual pressor, CO and TPR responses to IHG was significantly different between VVS patients and healthy subjects (Chi square, p = 0.0246). In 100% of the healthy subjects BP increased during IHG, but in a 19% of the patients BP (CO and TPR) did not increased during IHG. In VVS patients, the autonomic tests (ΔBP, ΔHR, VM and BRS) showed no significant differences between the group with BP increase and the group without pressor response. In VVS patients, the pattern of individual CO and TPR changes to IGH is different from healthy subjects. VVS patients may present an abnormal regulation of cardiovascular responses to IHG, with preserved cardiovagal and cardiac sympathetic function.