Remote exposure to secondhand tobacco smoke is associated with lower exercise capacity through effects on oxygen pulse- a proxy of 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.

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Acute volume loading and exercise capacity in postural tachycardia syndrome

Journal of Applied Physiology ◽

10.1152/japplphysiol.00367.2014 ◽

2014 ◽

Vol 117 (6) ◽

pp. 663-668 ◽

Cited By ~ 17

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.

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Non-invasive estimation of stroke volume during exercise from oxygen in heart failure patients

European Journal of Preventive Cardiology ◽

10.1177/2047487320920755 ◽

2020 ◽

pp. 204748732092075

Author(s):

Emanuele Accalai ◽

Carlo Vignati ◽

Elisabetta Salvioni ◽

Beatrice Pezzuto ◽

Mauro Contini ◽

...

Keyword(s):

Heart Failure ◽

Oxygen Uptake ◽

Stroke Volume ◽

Peak Exercise ◽

Heart Failure Patients ◽

Cardiopulmonary Exercise ◽

Oxygen Pulse ◽

Failure Severity ◽

Volume Estimates ◽

Heart Failure Severity

Aims In heart failure, oxygen uptake and cardiac output measurements at peak and during exercise are important in defining heart failure severity and prognosis. Several cardiopulmonary exercise test-derived parameters have been proposed to estimate stroke volume during exercise, including the oxygen pulse (oxygen uptake/heart rate). Data comparing measured stroke volume and the oxygen pulse or stroke volume estimates from the oxygen pulse at different stages of exercise in a sizeable population of healthy individuals and heart failure patients are lacking. Methods We analysed 1007 subjects, including 500 healthy and 507 heart failure patients, who underwent cardiopulmonary exercise testing with stroke volume determination by the inert gas rebreathing technique. Stroke volume measurements were made at rest, submaximal (∼50% of exercise) and peak exercise. At each stage of exercise, stroke volume estimates were obtained considering measured haemoglobin at rest, predicted exercise-induced haemoconcentration and peripheral oxygen extraction according to heart failure severity. Results A strong relationship between oxygen pulse and measured stroke volume was observed in healthy and heart failure subjects at submaximal (R2 = 0.6437 and R2 = 0.6723, respectively), and peak exercise (R2 = 0.6614 and R2 = 0.5662) but not at rest. In healthy and heart failure subjects, agreement between estimated and measured stroke volume was observed at submaximal (–3 ± 37 and –11 ± 72 ml, respectively) and peak exercise (1 ± 31 and 6 ± 29 ml, respectively) but not at rest. Conclusion In heart failure patients, stroke volume estimation and oxygen pulse during exercise represent stroke volume, albeit with a relevant individual data dispersion so that both can be used for population studies but cannot be reliably applied to a single subject. Accordingly, whenever needed stroke volume must be measured directly.

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Impact of COVID-19 on exercise pathophysiology. A combined cardiopulmonary and echocardiographic exercise study

Journal of Applied Physiology ◽

10.1152/japplphysiol.00710.2020 ◽

2021 ◽

Author(s):

Claudia Baratto ◽

Sergio Caravita ◽

Andrea Faini ◽

Giovanni Battista Perego ◽

Michele Senni ◽

...

Keyword(s):

Oxygen Consumption ◽

Exercise Capacity ◽

Vascular Function ◽

Exercise Physiology ◽

Cardiopulmonary Exercise Test ◽

Peak Oxygen Consumption ◽

Peak Exercise ◽

Exercise Limitation ◽

Arterial Blood ◽

Multisystem Involvement

Background. Survivors from COVID-19 pneumonia can present with persisting multisystem involvement (lung, pulmonary vessels, heart, muscle, red blood cells) that may negatively affect exercise capacity. Methods. We sought to determine the extent and the determinants of exercise limitation in COVID-19 patients at the time of hospital discharge. Results. Eighteen consecutive patients with COVID-19 and 1:1 age-, sex-, and body mass index- matched controls underwent: spirometry, echocardiography, cardiopulmonary exercise test and exercise echocardiography for the study of pulmonary circulation. Arterial blood was sampled at rest and during exercise in COVID-19 patients. COVID-19 patients lie roughly on the same oxygen consumption isophlets than controls both at rest and during submaximal exercise, thanks to supernormal cardiac output (p<0.05). Oxygen consumption at peak exercise was reduced by 30% in COVID-19 (p<0.001), due to a peripheral extraction limit. Additionally, within COVID-19 patients, hemoglobin content was associated with peak oxygen consumption (R2=0.46, p=0.002)Respiratory reserve was not exhausted (median [IRQ], 0.59 [0.15]) in spite of moderate reduction of forced vital capacity (79±40%)Pulmonary artery pressure increase during exercise was not different between patients and controls. Ventilatory equivalents for carbon dioxide were higher in COVID-19 patients than in controls (39.5 [8.5] vs 29.5 [8.8], p<0.001), and such an increase was mainly explained by increased chemosensitivity. Conclusions. When recovering from COVID-19, patients present with reduced exercise capacity and augmented exercise hyperventilation. Peripheral factors, including anemia and reduced oxygen extraction by peripheral muscles were the major determinants of deranged exercise physiology. Pulmonary vascular function seemed unaffected, despite restrictive lung changes.

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Improvement of alveolar-capillary membrane diffusing capacity with exercise training in chronic heart failure

Journal of Applied Physiology ◽

10.1152/japplphysiol.00365.2004 ◽

2004 ◽

Vol 97 (5) ◽

pp. 1866-1873 ◽

Cited By ~ 65

Author(s):

Marco Guazzi ◽

Giuseppe Reina ◽

Gabriele Tumminello ◽

Maurizio D. Guazzi

Keyword(s):

Heart Failure ◽

Cardiac Output ◽

Chronic Heart Failure ◽

Stroke Volume ◽

Gas Diffusion ◽

Peak Exercise ◽

Exercise Limitation ◽

Capillary Blood Volume ◽

Arteriolar Resistance ◽

Alveolar Capillary

Chronic heart failure (CHF) may impair lung gas diffusion, an effect that contributes to exercise limitation. We investigated whether diffusion improvement is a mechanism whereby physical training increases aerobic efficiency in CHF. Patients with CHF ( n = 16) were trained (40 min of stationary cycling, 4 times/wk) for 8 wk; similar sedentary patients ( n = 15) were used as controls. Training increased lung diffusion (DlCO, +25%), alveolar-capillary conductance (DM, +15%), pulmonary capillary blood volume (VC, +10%), peak exercise O2 uptake (peak V̇o2, +13%), and V̇o2 at anaerobic threshold (AT, +20%) and decreased the slope of exercise ventilation to CO2 output (V̇e/V̇co2, −14%). It also improved the flow-mediated brachial artery dilation (BAD, from 4.8 ± 0.4 to 8.2 ± 0.4%). These changes were significant compared with baseline and controls. Hemodynamics were obtained in the last 10 patients in each group. Training did not affect hemodynamics at rest and enhanced the increase of cardiac output (+226 vs. +187%) and stroke volume (+59 vs. +49%) and the decrease of pulmonary arteriolar resistance (−28 vs. −13%) at peak exercise. Hemodynamics were unchanged in controls after 8 wk. Increases in Dlco and DM correlated with increases in peak V̇o2 ( r = 0.58, P = 0.019 and r = 0.51, P = 0.04, respectively) and in BAD ( r = 0.57, P < 0.021 and r = 0.50, P = 0.04, respectively). After detraining (8 wk), Dlco, DM, VC, peak V̇o2, V̇o2 at AT, V̇e/V̇co2 slope, cardiac output, stroke volume, pulmonary arteriolar resistance at peak exercise, and BAD reverted to levels similar to baseline and to levels similar to controls. Results document, for the first time, that training improves DlCO in CHF, and this effect may contribute to enhancement of exercise performance.

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

Clinical Medicine Insights Circulatory Respiratory and Pulmonary Medicine ◽

10.1177/1179548418790564 ◽

2018 ◽

Vol 12 ◽

pp. 117954841879056 ◽

Cited By ~ 1

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.

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Use of Oxygen Pulse in Predicting Doppler-Derived Maximal Stroke Volume in Adolescents

Pediatric Exercise Science ◽

10.1123/pes.2014-0215 ◽

2015 ◽

Vol 27 (3) ◽

pp. 412-418 ◽

Cited By ~ 8

Author(s):

Vishwanath Unnithan ◽

Thomas W. Rowland

Keyword(s):

Stroke Volume ◽

Work Load ◽

Open Circuit ◽

Peak Exercise ◽

Stress Tests ◽

Healthy Adolescent ◽

Oxygen Pulse ◽

Surrogate Measure ◽

Circuit Techniques ◽

High Level

Clinical exercise physiologists and physicians administering stress tests in the young have used oxygen pulse as a surrogate measure of stroke volume. It is important to recognize 1) the accuracy of O2 pulse in predicting maximal stroke volume during exercise, and 2) the normal pattern of O2 pulse during a progressive exercise test. This study examined both of these issues in a cohort of 44 healthy adolescent males and females (ages 14–16 years) who performed routine progressive cycle exercise to exhaustion. Gas exchange variables were measured by standard open circuit techniques. Stroke volume at rest and during exercise was assessed by the Doppler ultrasound method. At peak exercise O2 pulse correlated closely with stroke volume (r = .73) with a SEE of 12.6 ml·beat-1. Values of maximal O2 pulse in nonathletic boys and girls were 13.3 ± 2.5 and 11.0 ± 1.7 ml·beat-1, respectively. After the initial workload, a steady rise was observed in O2 pulse, entirely reflecting an increasing arterial venous oxygen difference, with a slope of approximately 4 ml/beat per 100 watts work load. The findings support the use of O2 pulse as a valid predictor of stroke volume during exercise in youth with a moderately high level of accuracy.

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3415 Percent Predicted Peak Exercise Oxygen Pulse Is a Marker of Cardiac Reserve Following Thoracic Radiotherapy

Journal of Clinical and Translational Science ◽

10.1017/cts.2019.302 ◽

2019 ◽

Vol 3 (s1) ◽

pp. 133-133

Author(s):

Justin McNair Canada ◽

Elisabeth Weiss ◽

John Grizzard ◽

Ronald Evans ◽

Ryan Garten ◽

...

Keyword(s):

Radiation Dose ◽

Stroke Volume ◽

Diffuse Fibrosis ◽

Peak Exercise ◽

Central Hemodynamics ◽

Thoracic Radiotherapy ◽

Oxygen Pulse ◽

Volume Response ◽

History Of ◽

Response To Exercise

OBJECTIVES/SPECIFIC AIMS: Cardiac radiation exposure following anti-cancer (CA) thoracic radiotherapy (RT) treatment increases risk of heart failure in a dose-dependent manner with a predominantly restrictive cardiomyopathy phenotype and is characterized by a diffuse fibrosis within the myocardium. The peak oxygen pulse (O2Pulse) determined at cardiopulmonary exercise testing (CPET) is the quotient of oxygen consumption (VO2) divided by the heart rate (HR) at peak exercise. Through deduction of the Fick equation (VO2 = cardiac output (CO) x arteriovenous oxygen difference) it provides a noninvasive estimate of the stroke volume response to exercise. Knowledge of the relationship between cardiac radiation dose and O2Pulse may provide mechanistic insight into the cardiac reserve of the CA survivor following thoracic RT. METHODS/STUDY POPULATION: Patients without a history of cardiovascular disease with a history of thoracic RT for CA treatment with significant incidental heart exposure (≥5 Gray (Gy) to ≥10% of the heart volume) underwent treadmill CPET to determine cardiorespiratory fitness and cardiac magnetic resonance (CMR) imaging to quantify central hemodynamics and for myocardial tissue characterization. The mean cardiac radiation dose (MCRD) and %volume of heart dose was determined from dose-volume histograms reflective of the dose contributions from all RT treatments for each patient. The oxygen pulse (milliliters (mL) of O2 per heart beat) was determined by dividing the absolute VO2 by the HR (beats per minute, bpm) at peak exercise and reported as %-predicted values to account for age and gender differences. Data are reported as number (%) or median (interquartile range). A stepwise multivariate linear regression model was created from significant univariate RT and CMR variables to determine independent predictors of %O2Pulse. RESULTS/ANTICIPATED RESULTS: Thirty patients (age = 63 [57-67] years, 18 [60%] female, 2.0 [0.1-28.7] years since completion of RT) underwent study procedures. The peak VO2=1376 mL·min-1 (62% of predicted) and peak HR = 150 (122-164) bpm resulted in a peak O2Pulse of 9.2 mL/beat (82% of predicted). The MCRD = 5.6 [3.7-17.8] Gy was inversely associated with %O2Pulse at univariate analysis (R = −0.514, p < .01), but was not retained at multivariate analysis. The CMR-derived CO ([4.9 (4.09-5.90) Liters/minute], β = +.374, p < .01), CMR-extracellular volume ([ECV, 26.9 (24.8-29.2)%], β = −.536, p < .01), and volume of the heart exposed to ≥30 Gy ([2.5 (0-15.0)Gy], (β = −.345, p = .01) were retained in the model (R2 = .709, F(3,19) = 15.438, p < .001) and were independent predictors of the %O2Pulse. DISCUSSION/SIGNIFICANCE OF IMPACT: In patients with significant heart exposure following RT, %O2Pulse (a surrogate of stroke volume response to exercise) is inversely associated with cardiac radiation dose and is related to central hemodynamics (CO) and markers of diffuse fibrosis (ECV).

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