scholarly journals Acute volume loading and exercise capacity in postural tachycardia syndrome

2014 ◽  
Vol 117 (6) ◽  
pp. 663-668 ◽  
Author(s):  
Rocío A. Figueroa ◽  
Amy C. Arnold ◽  
Victor C. Nwazue ◽  
Luis E. Okamoto ◽  
Sachin Y. Paranjape ◽  
...  
Keyword(s):  
Stroke Volume ◽  
Exercise Capacity ◽  
Cardiovascular Responses ◽  
Exercise Intolerance ◽  
Peak Exercise ◽  
Postural Tachycardia Syndrome ◽  
Volume Loading ◽  
Cardiac Atrophy ◽  
Postural Tachycardia ◽  
Maximal Effort

Postural tachycardia syndrome (POTS) is associated with exercise intolerance, hypovolemia, and cardiac atrophy, which may contribute to reduced stroke volume and compensatory exaggerated heart rate (HR) increases. Acute volume loading with intravenous (iv) saline reduces HR and improves orthostatic tolerance and symptoms in POTS, but its effect on exercise capacity is unknown. In this study, we determined the effect of iv saline infusion on peak exercise capacity (V̇o2peak) in POTS. Nineteen patients with POTS participated in a sequential study. V̇o2peak was measured on two separate study days, following administration of placebo or 1 liter of iv saline (NaCl 0.9%). Patients exercised on a semirecumbent bicycle with resistance increased by 25 W every 2 min until maximal effort was achieved. Patients exhibited blood volume deficits (−13.4 ± 1.4% ideal volume), consistent with mild to moderate hypovolemia. At baseline, saline significantly increased stroke volume (saline 80 ± 8 ml vs. placebo 64 ± 4 ml; P = 0.010), increased cardiac output (saline 6.9 ± 0.5 liter/min vs. placebo 5.7 ± 0.2 liter/min; P = 0.021), and reduced systemic vascular resistance (saline 992.6 ± 70.0 dyn-s/cm5 vs. placebo 1,184.0 ± 50.8 dyn-s/cm5; P = 0.011), with no effect on HR or blood pressure. During exercise, saline did not produce differences in V̇o2peak (saline 26.3 ± 1.2 mg·kg−1·min−1 vs. placebo 27.7 ± 1.8 mg·kg−1·min−1; P = 0.615), peak HR [saline 174 ± 4 beats per minute (bpm) vs. placebo 175 ± 3 bpm; P = 0.672] or other cardiovascular parameters. These findings suggest that acute volume loading with saline does not improve V̇o2peak or cardiovascular responses to exercise in POTS, despite improvements in resting hemodynamic function.

Reduced stroke volume during exercise in postural tachycardia syndrome

2007 ◽  
Vol 103 (4) ◽  
pp. 1128-1135 ◽  
Author(s):  
Shizue Masuki ◽  
John H. Eisenach ◽  
William G. Schrage ◽  
Christopher P. Johnson ◽  
Niki M. Dietz ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Peripheral Resistance ◽  
Cardiovascular Regulation ◽  
Open Circuit ◽  
Exercise Intolerance ◽  
Postural Tachycardia Syndrome ◽  
Cycle Exercise ◽  
Postural Tachycardia

Postural tachycardia syndrome (POTS) is characterized by excessive tachycardia without hypotension during orthostasis. Most POTS patients also report exercise intolerance. To assess cardiovascular regulation during exercise in POTS, patients ( n = 13) and healthy controls ( n = 10) performed graded cycle exercise at 25, 50, and 75 W in both supine and upright positions while arterial pressure (arterial catheter), heart rate (HR; measured by ECG), and cardiac output (open-circuit acetylene breathing) were measured. In both positions, mean arterial pressure, cardiac output, and total peripheral resistance at rest and during exercise were similar in patients and controls ( P > 0.05). However, supine stroke volume (SV) tended to be lower in the patients than controls at rest (99 ± 5 vs. 110 ± 9 ml) and during 75-W exercise (97 ± 5 vs. 111 ± 7 ml) ( P = 0.07), and HR was higher in the patients than controls at rest (76 ± 3 vs. 62 ± 4 beats/min) and during 75-W exercise (127 ± 3 vs. 114 ± 5 beats/min) (both P < 0.01). Upright SV was significantly lower in the patients than controls at rest (57 ± 3 vs. 81 ± 6 ml) and during 75-W exercise (70 ± 4 vs. 94 ± 6 ml) (both P < 0.01), and HR was much higher in the patients than controls at rest (103 ± 3 vs. 81 ± 4 beats/min) and during 75-W exercise (164 ± 3 vs. 131 ± 7 beats/min) (both P < 0.001). The change (upright − supine) in SV was inversely correlated with the change in HR for all participants at rest ( R2= 0.32), at 25 W ( R2= 0.49), 50 W ( R2= 0.60), and 75 W ( R2= 0.32) ( P < 0.01). These results suggest that greater elevation in HR in POTS patients during exercise, especially while upright, was secondary to reduced SV and associated with exercise intolerance.

scholarly journals Remote exposure to secondhand tobacco smoke is associated with lower exercise capacity through effects on oxygen pulse- a proxy of cardiac stroke volume

2021 ◽  
Author(s):  
Siyang Zeng ◽  
Michelle Dunn ◽  
Warren M Gold ◽  
Mehrdad Arjomandi
Keyword(s):  
Stroke Volume ◽  
Exercise Capacity ◽  
Tobacco Smoke ◽  
Cardiovascular Responses ◽  
Peak Exercise ◽  
Air Trapping ◽  
Exercise Limitation ◽  
Oxygen Pulse ◽  
Secondhand Tobacco Smoke ◽  
Cardiac Stroke Volume

Background: Prolonged past exposure to secondhand tobacco smoke (SHS) is associated with exercise limitation. Pulmonary factors including air trapping contribute to this limitation but the contribution of cardiovascular factors is unclear. Methods: To determine contribution of cardiovascular mechanisms to SHS-associated exercise limitation, we examined the cardiovascular responses to maximum effort exercise testing in 166 never-smokers with remote but prolonged occupational exposure to SHS and no known history of cardiovascular disease except nine with medically-controlled hypertension. We estimated the contribution of oxygen-pulse (proxy for cardiac stroke volume) and changes in systolic (SBP) and diastolic blood pressures (DBP) and heart rate (HR) over workload towards exercise capacity, and examined whether the association of SHS with exercise capacity was mediated through these variables. Results: Oxygen consumption (VO2Peak) and oxygen-pulse (O2-PulsePeak) at peak exercise were 1,516±431mL/min (100±23 %predicted) and 10.6±2.8mL/beat (117±25 %predicted), respectively, with 91 (55%) and 43 (26%) of subjects not being able to achieve their maximum predicted values. Sixty-two percent showed hypertensive response to exercise by at least one established criterion. In adjusted models, VO2Peak was associated directly with O2-Pulse and inversely with rise of SBP and DBP over workload (all P<0.05). Moreover, SHS exposure association with VO2Peak was mainly (84%) mediated through its effect on oxygen-pulse (P=0.034). Notably, although not statistically significant, a large proportion (60%) of air trapping effect on VO2Peak seemed to be mediated through oxygen-pulse (P=0.066). Discussion: In a never-smoker population with remote prolonged exposure to SHS, abnormal escalation of afterload and an SHS-associated reduction in cardiac output contributed to lower exercise capacity.

Abstract 2197: The Multi-System Effect of Exercise Training During Prolonged Bed Rest Deconditioning: An Integrated Approach to Countermeasure Development for the Heart, Lungs, Muscle and Bones

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Jeffrey Hastings ◽  
Eric Pacini ◽  
Felix Krainski ◽  
Shigeki Shibata ◽  
Manish Jain ◽  
...  
Keyword(s):  
Exercise Training ◽  
Exercise Capacity ◽  
Orthostatic Intolerance ◽  
Lower Body Negative Pressure ◽  
Bed Rest ◽  
Orthostatic Tolerance ◽  
Volume Loading ◽  
System Effect ◽  
Cardiac Atrophy ◽  
South Central

We propose to prevent the cardiac atrophy and orthostatic intolerance associated with prolonged bed rest using rowing ergometry/resistance training with aggressive volume loading on the day of testing. We hypothesize that prevention of cardiac atrophy will forestall cardiovascular deconditioning, leading to preserved exercise capacity and orthostatic tolerance. Twenty-four healthy subjects, ages 20 –55, were enrolled with 8 randomized to training (EX), 8 with training and volume loading (VOL), and 8 as sedentary (SED) controls. Testing included maximal upright exercise, orthostatic tolerance via graded lower body negative pressure (LBNP), cardiac MRI, as well as invasive cardiac pressure-volume measurements, performed at baseline and at the end of 5 weeks of 6° head down bedrest. Upright exercise capacity was preserved with training as measured by peak workrate and VO2max (EX/VOL: pre 195±46W, 34±7 ml/kg/min; post 202±42W, 33±4 ml/kg/min) but deteriorated in SED group (pre 171±55W, 34±8 ml/kg/min; post 145±51W, 27±7 ml/kg/min). MRI derived mass (% change: +6.3±9.9% EX/VOL vs. −5.5±3.7% SED) was increased by training. Exercise training appears to preserve LV chamber compliance (stiffness constants: EX/VOL: pre= 0.035±0.021, post = 0.036±0.029; SED: pre= 0.020±0.011, post = 0.028±0.007). Training also preserves hemodynamic variables measured at −40mmHg of LBNP, including stroke volume (EX: pre 44±12; post 38±9 ml, VOL: pre 49±30; post 45±29 ml, SED: pre 35±5; post 24±8 ml ). These preliminary data support our hypothesis that an optimized training program consisting of dynamic and resistance exercise can prevent part of the multisystem atrophy and orthostatic intolerance associated with prolonged bed rest. This defines a specific countermeasure that is practical, safe, and effective against the cardiovascular, muscle and bone deconditioning associated with prolonged bed rest. This information is relevant not only for astronauts exposed to long duration spaceflight, but also for patients with chronic reductions in physical activity, and those with disease processes that alter cardiac stiffness such as obesity, hypertension, heart failure or ischemic heart disease, plus normal aging and osteoporosis. This research has received full or partial funding support from the American Heart Association, AHA South Central Affiliate (Arkansas, New Mexico, Oklahoma & Texas).

scholarly journals Supine cycling plus volume loading prevent cardiovascular deconditioning during bed rest

2010 ◽  
Vol 108 (5) ◽  
pp. 1177-1186 ◽  
Author(s):  
Shigeki Shibata ◽  
Merja Perhonen ◽  
Benjamin D. Levine
Keyword(s):  
Exercise Training ◽  
Exercise Capacity ◽  
Orthostatic Intolerance ◽  
Lower Body Negative Pressure ◽  
Bed Rest ◽  
Left Ventricular ◽  
Orthostatic Tolerance ◽  
Volume Loading ◽  
Cardiac Atrophy ◽  
Cardiac Filling

There are two possible mechanisms contributing to the excessive fall of stroke volume (and its contribution to orthostatic intolerance) in the upright position after bed rest or spaceflight: reduced cardiac filling due to hypovolemia and/or a less distensible heart due to cardiac atrophy. We hypothesized that preservation of cardiac mechanical function by exercise training, plus normalization of cardiac filling with volume infusion, would prevent orthostatic intolerance after bed rest. Eighteen men and three women were assigned to 1) exercise countermeasure ( n = 14) and 2) no exercise countermeasure ( n = 7) groups during bed rest. Bed rest occurred in the 6° head-down tilt position for 18 days. The exercise regimen was prescribed to compensate for the estimated cardiac work reduction between bed rest and ambulatory periods. At the end of bed rest, the subjects were further divided into two additional groups for post-bed rest testing: 1) volume loading with intravenous dextran to normalize cardiac filling pressure and 2) no volume loading. Dextran infusion was given to half of the exercise group and all of the sedentary group after bed rest, leading ultimately to three groups: 1) exercise plus volume infusion; 2) exercise alone; and 3) volume infusion alone. Exercise training alone preserved left ventricular mass and distensibility as well as upright exercise capacity, but lower body negative pressure (LBNP) tolerance was still depressed. LBNP tolerance was maintained only when exercise training was accompanied by dextran infusion. Dextran infusion alone following bed rest without exercise maintained neither orthostatic tolerance nor upright exercise capacity. We conclude that daily supine cycle exercise sufficient to prevent cardiac atrophy can prevent orthostatic intolerance after bed rest only when combined with plasma volume restoration. This maintenance of orthostatic tolerance was achieved by neither exercise nor dextran infusion alone. Cardiac atrophy and hypovolemia are likely to contribute independently to orthostatic intolerance after bed rest.

scholarly journals Decreased Stroke Volume and Venous Return in School Children with Postural Tachycardia Syndrome

2021 ◽  
Vol 253 (3) ◽  
pp. 181-190
Author(s):  
Shino Jimbo ◽  
Yukihiko Fujita ◽  
Wakako Ishii ◽  
Hidemasa Namiki ◽  
Masataka Kato ◽  
...  
Keyword(s):  
Stroke Volume ◽  
School Children ◽  
Venous Return ◽  
Postural Tachycardia Syndrome ◽  
Postural Tachycardia

scholarly journals Reduced central blood volume and cardiac output and increased vascular resistance during static handgrip exercise in postural tachycardia syndrome

2007 ◽  
Vol 293 (3) ◽  
pp. H1908-H1917 ◽  
Author(s):  
Julian M. Stewart ◽  
Indu Taneja ◽  
Marvin S. Medow
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Blood Volume ◽  
Peripheral Resistance ◽  
Exercise Intolerance ◽  
Low Flow ◽  
Postural Tachycardia Syndrome ◽  
Central Blood Volume ◽  
Normal Flow ◽  
Postural Tachycardia

Postural tachycardia syndrome (POTS) is characterized by exercise intolerance and sympathoactivation. To examine whether abnormal cardiac output and central blood volume changes occur during exercise in POTS, we studied 29 patients with POTS (17–29 yr) and 12 healthy subjects (18–27 yr) using impedance and venous occlusion plethysmography to assess regional blood volumes and flows during supine static handgrip to evoke the exercise pressor reflex. POTS was subgrouped into normal and low-flow groups based on calf blood flow. We examined autonomic effects with variability techniques. During handgrip, systolic blood pressure increased from 112 ± 4 to 139 ± 9 mmHg in control, from 119 ± 6 to 143 ± 9 in normal-flow POTS, but only from 117 ± 4 to 128 ± 6 in low-flow POTS. Heart rate increased from 63 ± 6 to 82 ± 4 beats/min in control, 76 ± 3 to 92 ± 6 beats/min in normal-flow POTS, and 88 ± 4 to 100 ± 6 beats/min in low-flow POTS. Heart rate variability and coherence markedly decreased in low-flow POTS, indicating uncoupling of baroreflex heart rate regulation. The increase in central blood volume with handgrip was absent in low-flow POTS and blunted in normal-flow POTS associated with abnormal splanchnic emptying. Cardiac output increased in control, was unchanged in low-flow POTS, and was attenuated in normal-flow POTS. Total peripheral resistance was increased compared with control in all POTS. The exercise pressor reflex was attenuated in low-flow POTS. While increased cardiac output and central blood volume characterizes controls, increased peripheral resistance with blunted or eliminated in central blood volume increments characterizes POTS and may contribute to exercise intolerance.

scholarly journals Hemodynamic and Ventilatory Responses during Exercise in Pediatric Patients with Pulmonary Embolism

Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 9-10
Author(s):  
Mackenzie Parker ◽  
Ayesha Zia ◽  
Tony Babb ◽  
Michael D. Nelson
Keyword(s):  
Pulmonary Embolism ◽  
Exercise Capacity ◽  
Pediatric Patients ◽  
Left Ventricular ◽  
Work Rate ◽  
Exercise Intolerance ◽  
Peak Exercise ◽  
Ventricular Ejection Fraction ◽  
Peak Vo2 ◽  
The Mean

Background Pediatric patients with pulmonary embolism (PE) suffer from exercise intolerance and dyspnea on exertion, often without right heart dysfunction or pulmonary hypertension - at least at rest. The pathophysiology of the exercise limitation following pediatric PE therefore remains incompletely understood. Objectives To extend our understanding of exercise intolerance in pediatric patients with PE by examining ventilatory and hemodynamic responses to exercise. Methods To accomplish our goal, we instituted a standardized institutional protocol to systematically assess exercise capacity in pediatric PE patients in the first 3 months following diagnosis. Between February 2019- June 2020, 15 patients underwent resting pulmonary function tests and an incremental symptom-limited cardiopulmonary exercise testing (CPET) to obtain peak exercise in 8-12 minutes. All patients had received anticoagulation for at least 3 months. In all patients, right and left ventricular systolic and/or diastolic dysfunction at rest was ruled out by transthoracic echocardiography. Continuous measurements were made of minute ventilation (VE), oxygen uptake (VO2), carbon dioxide production (VCO2), heart rate (HR), and blood pressure. Predicted values for peak VO2 and work rate were generated from predictive equations. Patients with impaired exercise capacity, defined as &lt;80% of age-, sex- and ideal lean body mass predicted, and dyspnea on exertion underwent further exercise cardiac magnetic resonance (exCMR) imaging using an MR compatible ergometer. Biventricular volumes and contractility, RV longitudinal strain, and RV to pulmonary artery coupling were assessed at rest and with exercise. Results Baseline, clinical characteristics, and CPET data are shown in Tables 1 and 2. Forced Vital Capacity was normal without signs of airway obstruction. Three patients failed to reach their predicted physiologic limits during exercise, and CPET was terminated by the patient prematurely (e.g., muscular exertion, fatigue, & dyspnea, respectively). The mean exercise duration was 9.85 min. The mean ventilatory reserve was within normal limits (&gt;15%) in all but 1 patient. VO2/work rate was normal with normal VO2 at the anaerobic threshold (mean 1541ml/kg/min, SD:731). Exercise capacity, as measured by peak VO2 was reduced, that is, &lt;80% of predicted, in 5 out of the 15 patients (30%). Of these, three patients had echocardiography evidence of RV dysfunction at PE diagnosis, which had resolved at the time of CPET. There were no differences in the mean exercise time and maximal work rate achieved in those with low exercise capacity relative to normal capacity. The ventilatory equivalent for CO2 (VE/VCO2) at peak exercise was elevated (&gt;35) in three of the five patients with decreased exercise capacity. The O2 pulse was attenuated in patients with decreased exercise capacity when compared to those with normal exercise capacity (7.5 mL.beat -1 vs. 12.9-1; p=0.037). Of the two patients who underwent exCMR; one showed reduced right ventricular ejection fraction (38%), abnormal RV strain (-11.3%), elevated right sided pressures signified by interventricular flattening upon inspiration during free breathing scan and an uncoupled RV to the pulmonary circulation. Conclusions Reduced exercise capacity is common after PE and not evident by resting evaluations. Pediatric PE patients with low exercise capacity and dyspnea seem to be characterized by either an abnormal pulmonary vascular response to exercise or decreased ventilatory efficiency. Larger studies are needed to better understand exercise pathophysiology after pediatric PE. Disclosures No relevant conflicts of interest to declare.

Reduced stroke volume during exercise in postural tachycardia syndrome

2009 ◽  
Vol 145 (1-2) ◽  
pp. 1-2
Author(s):  
S Masuki ◽  
JH Eisenach ◽  
WG Schrage ◽  
CP Johnson ◽  
NM Dietz ◽  
...  
Keyword(s):  
Stroke Volume ◽  
Postural Tachycardia Syndrome ◽  
Postural Tachycardia

scholarly journals Exercise Stroke Volume in Adult Cystic Fibrosis: A Comparison of Acetylene Pulmonary Uptake and Oxygen Pulse

2018 ◽  
Vol 12 ◽  
pp. 117954841879056 ◽  
Author(s):  
Erik H Van Iterson ◽  
Sarah E Baker ◽  
Courtney M Wheatley ◽  
Wayne J Morgan ◽  
Thomas P Olson ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Stroke Volume ◽  
Cardiopulmonary Exercise Testing ◽  
Exercise Intolerance ◽  
Peak Exercise ◽  
Oxygen Pulse ◽  
Pulmonary Uptake ◽  
Hemodynamic Assessment ◽  
Valid Estimate ◽  
The Impact

Cardiac hemodynamic assessment during cardiopulmonary exercise testing (CPET) is proposed to play an important role in the clinical evaluation of individuals with cystic fibrosis (CF). Cardiac catheterization is not practical for routine clinical CPET. Use of oxygen pulse (O2pulse) as a noninvasive estimate of stroke volume (SV) has not been validated in CF. This study tested the hypothesis that peak exercise O2pulse is a valid estimate of SV in CF. Measurements of SV via the acetylene rebreathe technique were acquired at baseline and peak exercise in 17 mild-to-moderate severity adult CF and 25 age-matched healthy adults. We calculated [Formula: see text]. Baseline relationships between SV and O2pulse were significant in CF ( r = .80) and controls ( r = .40), persisting to peak exercise in CF ( r = .63) and controls ( r = .73). The standard error of estimate for O2pulse-predicted SV with respect to measured SV was similar at baseline (14.1 vs 20.1 mL) and peak exercise (18.2 vs 13.9 mL) for CF and controls, respectively. These data suggest that peak exercise O2pulse is a valid estimate of SV in CF. The ability to noninvasively estimate SV via O2pulse during routine clinical CPET can be used to improve test interpretation and advance our understanding of the impact cardiac dysfunction has on exercise intolerance in CF.

scholarly journals Low-dose propranolol and exercise capacity in postural tachycardia syndrome: A randomized study

Neurology ◽  
2013 ◽  
Vol 80 (21) ◽  
pp. 1927-1933 ◽  
Author(s):  
A. C. Arnold ◽  
L. E. Okamoto ◽  
A. Diedrich ◽  
S. Y. Paranjape ◽  
S. R. Raj ◽  
...  
Keyword(s):  
Exercise Capacity ◽  
Low Dose ◽  
Randomized Study ◽  
Postural Tachycardia Syndrome ◽  
Postural Tachycardia
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