Ventilatory Equivalent For CO2 Research Articles

The Abdominal Aortic Aneurysm Get Fit Trial: A Randomised Controlled Trial of Exercise to Improve Fitness in Patients with Abdominal Aortic Aneurysm

Ruptured abdominal aortic aneurysm (AAA) carries a mortality rate of up to 80%. Elective repair prevents rupture, but peri-operative mortality remains at 2% – 3%. This mortality rate and long term survival rate are associated with impaired peak oxygen uptake (peak VO2), oxygen uptake at anaerobic threshold (AT) and ventilatory equivalent for CO2 (VECO2) at AT on cardiopulmonary exercise testing (CPET). Improving fitness to optimise these variables could improve peri-operative and long term survival, but the required exercise training suitable for patients with AAA has yet to be established. This randomised controlled trial aimed to evaluate the effectiveness of 24 week, patient directed, community based exercise on CPET measured fitness in AAA surveillance patients. This was a prospective randomised controlled trial in a tertiary UK vascular centre conducted using CONSORT guidelines. Patients on AAA surveillance (n = 56) were randomly assigned to either (1) a 24 week community exercise programme (CEP) with choice of gym or home exercises, or (2) standard clinical care including advice on weight loss and exercise. The primary outcome was change in peak VO2 at 24 weeks, with secondary outcomes including AT, VECO2, cardiovascular biomarkers (lipid profile, pro-B-type natriuretic peptide, and high sensitivity C reactive protein, body mass index, and HRQoL. Follow up was at eight, 16, 24, and 36 weeks to evaluate duration of benefit. All analyses were performed on an intention to treat basis. CEP patients (n = 28) achieved mean (95% confidence interval [CI]) improvements from baseline in peak VO2 of 1.5 (95% CI 0.5 – 2.5), 2.1 (95% CI 1.1 – 3.2), 2.3 (95% CI 1.2 – 3.3), and 2.2 (95% CI 1.1, 3.3) mL/kg/min at 8, 16, 24, and 36 weeks, respectively. These changes in CEP patients were significantly greater than those seen in control patients at 16 (p = .002), 24 (p = .031), and 36 weeks (p < .001). There were also significant improvements in AT, triglyceride levels, and HRQoL in CEP patients. This CEP significantly improved those CPET parameters associated with impaired peri-operative and long term survival in patients following AAA repair. These improvements were maintained at 12 weeks following the end of the programme.

Analysis of Influencing Factors for Exercise Ventilation Efficiency of COPD Patients.

Dynamic pulmonary hyperinflation and abnormal air exchange are the primary causes of the exercise limitation of chronic obstructive pulmonary disease (COPD) patients. During exercise, COPD sufferers' lungs are dynamically hyperinflated. Increased inefficient ventilation reduces ventilation efficiency and causes a mismatch between ventilation volume and blood flow. The ventilatory equivalent for CO2 (VeqCO2) is a physiological parameter that can be measured using cardiopulmonary exercise testing. Therefore, the aim of this exploratory study was to perform cardiopulmonary exercise testing on people with COPD, investigate the impact of static pulmonary function on ventilation efficiency under the exercise state, and screen the predictive indicators of ventilation efficiency. Subject. The aim of this study was to look at the factors that influence the exercise ventilation efficiency of people with COPD. Method. A total of 76 people with COPD were recruited during the stable period. Age, gender, body height, body mass, and other basic information were recorded. The body mass index (BMI) was determined, and forced vital capacity (FVC), forced expiratory volume in one second (FEV1), residual volume/total lung capacity (RV/TLC), diffusing capacity of the lung for carbon monoxide (DLCO), and DLCO divided by the alveolar volume (DLCO/VA) were measured. The ventilatory equivalent for carbon dioxide (VE/VCO2) under the rest state (EqCO2rest), anaerobic threshold (EqCO2at), and maximum exercise state (EqCO2 max) were calculated to investigate the influencing factors for ventilation efficiency of people with COPD. Results. FEV1% was negatively correlated with EqCO2rest (r = −0.277, P value <0.05); FEV1/FVC % was negatively correlated with EqCO2rest and EqCO2at (r = −0.311, −0.287, P value <0.05); DLCO% was negatively correlated with EqCO2rest, EqCO2at, and EqCO2max (r = −0.408, −0.462, and −0.285, P value <0.05); DLCO/VA% was negatively correlated with EqCO2rest, EqCO2at, and EqCO2max (r = −0.390, −0.392, and −0.245, P value <0.05); RV/TLC was positively correlated with EqCO2rest and EqCO2at (r = 0.289, 0.258, P-value <0.05). The prediction equation from the multivariable regression analysis equation was Y = 40.04–0.075X (Y = EqCO2, X = DLCO/VA%). Conclusions. As the degree of ventilatory obstruction increased, the ventilation efficiency of the stable people with COPD under the exercise state showed a progressive decrease; the ventilation efficiency of the people with COPD decreased significantly under the maximum exercise state, and the ventilation capacity and diffusion capacity were the significant factors that affected the exercise ventilation efficiency. The diffusion function may predict the maximum ventilation efficiency and enable primary hospitals without exercise test equipment in developing countries to predict and screen patients at risk for current exercise based on limited information.

Editor's Choice – The Abdominal Aortic Aneurysm Get Fit Trial: A Randomised Controlled Trial of Exercise to Improve Fitness in Patients with Abdominal Aortic Aneurysm

Ruptured abdominal aortic aneurysm (AAA) carries a mortality rate of up to 80%. Elective repair prevents rupture, but peri-operative mortality remains at 2% - 3%. This mortality rate and long term survival rate are associated with impaired peak oxygen uptake (peak VO2), oxygen uptake at anaerobic threshold (AT) and ventilatory equivalent for CO2 (VECO2) at AT on cardiopulmonary exercise testing (CPET). Improving fitness to optimise these variables could improve peri-operative and long term survival, but the required exercise training suitable for patients with AAA has yet to be established. This randomised controlled trial aimed to evaluate the effectiveness of 24 week, patient directed, community based exercise on CPET measured fitness in AAA surveillance patients. This was a prospective randomised controlled trial in a tertiary UK vascular centre conducted using CONSORT guidelines. Patients on AAA surveillance (n= 56) were randomly assigned to either (1) a 24 week community exercise programme (CEP) with choice of gym or home exercises, or (2) standard clinical care including advice on weight loss and exercise. The primary outcome was change in peak VO2 at 24 weeks, with secondary outcomes including AT, VECO2, cardiovascular biomarkers (lipid profile, pro-B-type natriuretic peptide, and high sensitivity C reactive protein, body mass index, and HRQoL. Follow up was at eight, 16, 24, and 36 weeks to evaluate duration of benefit. All analyses were performed on an intention to treat basis. CEP patients (n= 28) achieved mean (95% confidence interval [CI]) improvements from baseline in peak VO2 of 1.5 (95% CI 0.5 - 2.5), 2.1 (95% CI 1.1 - 3.2), 2.3 (95% CI 1.2 - 3.3), and 2.2 (95% CI 1.1, 3.3) mL/kg/min at 8, 16, 24, and 36 weeks, respectively. These changes in CEP patients were significantly greater than those seen in control patients at 16 (p= .002), 24 (p= .031), and 36 weeks (p < .001). There were also significant improvements in AT, triglyceride levels, and HRQoL in CEP patients. This CEP significantly improved those CPET parameters associated with impaired peri-operative and long term survival in patients following AAA repair. These improvements were maintained at 12 weeks following the end of the programme.

Vitamin D Supplementation Partially Rescues Breathing Deficits in Mecp2 Hemizygous Null Mice, a Model of Rett Syndrome

Rett syndrome (RTT) is a severe X‐linked progressive neurodevelopmental disorder affecting ~1 in 10,000 females. It is the second most common genetic cause of cognitive disability in girls, after Down syndrome. Girls with this devastating disorder develop relatively normally for 6‐18 months, after which they undergo a period of rapid regression. They lose many motor skills, the growth of their brain slows, and they develop repetitive, autistic behaviors and seizures. Autonomic disruptions are a leading cause of early death in RTT, and rescue of breathing deficits is considered a primary goal in the development of therapeutic interventions. We initiated a proof‐of‐concept study by investigating male Mecp2 hemizygous null mice as they have the strongest phenotype which occurs at an early age; male Mecp2‐null (KO) mice have also been characterized thoroughly in the literature. We tested the hypothesis that Vitamin D supplementation (VitD) would ameliorate, or partially rescue breathing and cardiovascular deficits in Mecp2 KO mice. Mice were tested at 4 weeks of age (PRE), then placed on a control (1 IU Vitamin D/g) or VitD (50 IU Vitamin D/g) diet, and re‐tested at 8 weeks of age (POST). To examine our hypothesis, unrestrained barometric plethysmography was used to quantify breathing frequency (breaths/min), tidal volume (VT; mL/breath), VT/inspiratory time (VT/Ti; mL/sec), minute ventilation (VE; mL/min/g) and the ventilatory equivalent for CO2 (VE/VCO2) in both wildtype (WT; n=6) and Mecp2 KO (n=5) littermates. Data Sciences International Ponemah software was used to analyze flow tracings during exposure to air (20.93% O2, balanced N2). The MouseOx Plus by STARR Life Sciences was utilized to collect heart rate (HR) and oxygen saturation in freely moving conscious mice. Data are expressed as mean ± S.D., WT vs. KO. In the PRE group, Mecp2 KO mice had dysregulated breathing and HR as previously demonstrated in the literature (data not shown). In the POST VitD diet groups, VT (0.24±0.02 vs 0.15±0.06 mL/breath; p=0.01) and VT/Ti remained lower (2.085±0.313 vs. 1.291±0.583 mL/sec; p=0.017) in Mecp2 KO. However, breathing frequency (166±21 vs. 166±19 breaths/min), VE/g (1.07±0.12 vs. 0.99±0.57 mL/min/g), ratio of VE/VCO2 (112±47 vs. 103±46) and HR (582±84 vs. 532±59 beats/min) were similar between WT and KO. The number of oxygen desaturations were not significant between WT and KO, but the values were variable across groups and included a number of desaturations (12±7 vs. 5±7 desaturations/30 minutes), similar to findings we have previously described in young control mice. These data reveal a partial rescue of breathing and HR deficits in Mecp2 KO mice following 4 weeks of VitD. The reduced VT/Ti suggests an attenuated neural drive to breath in Mecp2 KO vs. WT that persists after VitD. Current studies are examining the responses to hypoxia and hypercapnia and will identify more information about oxygen and carbon dioxide sensing in these mice following control and VitD diets.

Minute ventilation/carbon dioxide production in patients with dysfunctional breathing.

Dysfunctional breathing refers to a multi-dimensional condition that is characterised by pathological changes in an individual's breathing. These changes lead to a feeling of breathlessness and include alterations in the biomechanical, psychological and physiological aspects of breathing. This makes dysfunctional breathing a hard condition to diagnose, given the diversity of aspects that contribute to the feeling of breathlessness. The disorder can debilitate individuals without any health problems, but may also be present in those with underlying cardiopulmonary co-morbidities. The ventilatory equivalent for CO2 (V eqCO2 ) is a physiological parameter that can be measured using cardiopulmonary exercise testing. This review will explore how this single measurement can be used to aid the diagnosis of dysfunctional breathing. A background discussion about dysfunctional breathing will allow readers to comprehend its multidimensional aspects. This will then allow readers to understand how V eqCO2 can be used in the wider diagnosis of dysfunctional breathing. Whilst V eqCO2 cannot be used as a singular parameter in the diagnosis of dysfunctional breathing, this review supports its use within a broader algorithm to detect physiological abnormalities in patients with dysfunctional breathing. This will allow for more individuals to be accurately diagnosed and appropriately managed.

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

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 &amp;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, &amp; dyspnea, respectively). The mean exercise duration was 9.85 min. The mean ventilatory reserve was within normal limits (&amp;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, &amp;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 (&amp;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.

Breathing and Respiratory Muscle Function in Senescent Wild‐type and Ts65Dn Male Mice

Down Syndrome (DS) results from trisomy 21 and is the most common cause of mental retardation in the US. People with DS display reduced muscle tone and cardiorespiratory complications that may contribute to breathing disturbances. Ts65Dn (Ts) mice, a model of DS, exhibit increased apnea frequency at 3 months of age (7±9 vs. 36±28; wild‐type (WT) vs. Ts) that persists at 6 (19± 7 vs. 77±58) and 12 months (5±6 vs. 64±77; p&lt;0.001 for age, strain, and age by strain). People with DS have increased life expectancy and it is unknown how breathing changes across the lifespan in this population. We tested the hypothesis that ~20‐month‐old Ts mice would have altered ventilation compared to age‐matched WT mice. To test this hypothesis, unrestrained barometric plethysmography was used to quantify breathing frequency (breaths/min), tidal volume (VT; mL), VT/inspiratory time (VT/Ti; mL/sec), minute ventilation (VE; mL/min) and ventilatory equivalent for CO2 (VE/VCO2) in 18 to 22‐month‐old male WT (n=12) and Ts (n=13) mice. Data Sciences International Ponemah software was used to analyze flow tracings during exposure to air (20.93% O2, balanced N2). Data are expressed as mean±S.D., WT vs. Ts. A main effect of strain was uncovered using MANOVA (p=0.033). Breathing frequency (171±33 vs. 136±41 breaths/min; p=0.025) and VE (74.6±25.7 vs. 50.3±15.5 mL/min; p=0.010) approached the a priori cutoff (Bonferroni correction, p&lt;0.01). VT (0.439±0.112 vs. 0.377±0.075 mL/breath; p=0.123) and the ratio of VE/VCO2 (45.5 ±22.0 vs. 42.4±19.8; p=0.715) were not different. VT/Ti (3.65±1.03 vs. 2.49±0.759 mL/sec; p=0.004) was reduced in Ts vs. WT, which suggests Ts mice have a reduced ventilatory drive. Since people with DS demonstrate evidence of muscle weakness, we examined diaphragm (DIA) and sternohyoid (SH; representative pharyngeal dilator) muscle function in WT (DIA n=10, SH n=9) and Ts (DIA n=7, SH n=7) mice. Twitch (2.2±1.1 vs 2.3±1.0 N/cm2; p=0.835) and tetanic (11.2±7.3 vs. 11.6±4.8 N/cm2; p=0.900) force, and the force frequency‐relationship (p=.766) for SH muscle were equivalent between groups. Similarly, no differences were observed for DIA twitch (6.0±2.7 vs. 5.2±2.1 N/cm2; p=0.438) and tetanic (20.7±6.0 vs. 19.9±2.8 N/cm2; p=0.758) force, or the force‐frequency relationship (p=0.339). Diaphragm function was preserved in aged Ts mice which is in line with similar VT between groups. These data reveal the increased propensity for apnea in Ts mice is independent of upper airway muscle weakness and may alternatively be of neural origin. Current studies are examining motor control of the upper airway in Ts mice.Support or Funding InformationThis work was funded by 1R15HD076379 (LRD), 3R15HD076379 (LRD). Additional support was granted by the Le Moyne College McDevitt Center Undergraduate Research Fellowship in Natural Science (MS‐N, MR), and the Le Moyne College Biological Sciences Department.

Exercise oscillatory ventilation in heart failure and in pulmonary arterial hypertension

BackgroundPatients with pulmonary arterial hypertension (PAH) and with heart failure (HF) have increased ventilatory responses to exercise in proportion to disease severity. Exercise-associated oscillatory ventilation (EOV) predicts poor outcome in HF. Whether EOV occurs in PAH is unknown. MethodsWe analyzed the initial cardiopulmonary exercise tests (CPETs) and right heart catheterization data of 109 patients with PAH and in 107 patients with HF consecutively referred to our center. ResultsThe PAH patients were aged 54±16years and their NYHA functional class was 2.8±0.5. The HF patients were aged 53±13years and NYHA 2.4±0.6. Hemodynamic data were obtained in only 36 of them. The patients with PAH compared to those with HF had a lower peak VO2 (13±5 vs 17±5mL/kg/min, p<0.001) and a higher ventilatory equivalent for CO2 (VE/VCO2) slope (55±21 vs 34±7, p<0.001). Mean pulmonary artery pressure was higher (50±10 vs 29±11mmHg) and wedge pressure lower (10±3 vs 19±5mmHg) in PAH patients, but cardiac output was not different (4.0±1.3 vs 4.2±1.2L/min). EOV was present in 22 patients (21%) with HF and in no patient with PAH. ConclusionsPatients with PAH compared to HF with slightly better functional class have a lower aerobic exercise capacity and higher ventilatory responses, but no EOV. An increase in pulmonary artery wedge pressure rather than a low cardiac output may be necessary condition of EOV in HF.

Abnormalities of the Ventilatory Equivalent for Carbon Dioxide in Patients with Chronic Heart Failure

Introduction. The relation between minute ventilation (VE) and carbon dioxide production (VCO2) can be characterised by the instantaneous ratio of ventilation to carbon dioxide production, the ventilatory equivalent for CO2 (VEqCO2). We hypothesised that the time taken to achieve the lowest VEqCO2 (time to VEqCO2 nadir) may be a prognostic marker in patients with chronic heart failure (CHF). Methods. Patients and healthy controls underwent a symptom-limited, cardiopulmonary exercise test (CPET) on a treadmill to volitional exhaustion. Results. 423 patients with CHF (mean age 63 ± 12 years; 80% males) and 78 healthy controls (62% males; age 61 ± 11 years) were recruited. Time to VEqCO2 nadir was shorter in patients than controls (327 ± 204 s versus 514 ± 187 s; P = 0.0001). Univariable predictors of all-cause mortality included peak oxygen uptake (X 2 = 53.0), VEqCO2 nadir (X 2 = 47.9), and time to VEqCO2 nadir (X 2 = 24.0). In an adjusted Cox multivariable proportional hazards model, peak oxygen uptake (X 2 = 16.7) and VEqCO2 nadir (X 2 = 17.9) were the most significant independent predictors of all-cause mortality. Conclusion. The time to VEqCO2 nadir was shorter in patients with CHF than in normal subjects and was a predictor of subsequent mortality.

JOURNAL/jscr/04.03/00124278-201103000-00034/OV0312/v/2021-02-09T093750Z/r/image-png o2max and ventilatory threshold of trained cyclists are not affected by 28-day l-arginine supplementation

The ergogenic effect of L-arginine on an endurance-trained population is not well studied. The few studies that have investigated L-arginine on this population have not been conducted in a laboratory setting or measured aerobic variables. The purpose of the current study is to determine if 28 days of L-arginine supplementation in trained male cyclists affects VO2max and ventilatory threshold (VT). Eighteen (18) endurance-trained male cyclists (mean ± SD, age: 36.3 ± 7.9 years; height: 182.4 ± 4.6 cm; and body mass: 79.5 ± 4.7 kg) performed a graded exercise test (GXT; 50 W + 25 W·min) before and after 28 days of supplementation with L-arginine (ARG; 2 × 6 g·d) or placebo (PLA; cornstarch). The GXT was conducted on the subject's own bicycle using the RacerMate CompuTrainer (Seattle, WA, USA). VO2 was continuously recorded using the ParvoMedics TrueOne 2400 metabolic cart (Salt Lake City, UT, USA) and VT was established by plotting the ventilatory equivalent for O2 (VE/VO2) and the ventilatory equivalent for CO2 (VE/VCO2) and identifying the point at which VE/VO2 increases with no substantial changes in VE/VCO2. L-arginine supplementation had no effect from initial VO2max (PL, 58.7 ± 7.1 ml·kg·min; ARG, 63.5 ± 7.3 ml·kg·min) to postsupplement VO2max (PL, 58.9 ± 6.0 ml·kg·min; ARG, 63.2 ± 7.2 ml·kg·min). Also, no effect was seen from initial VT (PL, 75.7 ± 4.6% VO2max; ARG, 76.0 ± 5.3% VO2max) to postsupplement VT (PL, 74.3 ± 8.1% VO2max; ARG, 74.2 ± 6.4% VO2max). These results indicate that L-arginine does not impact VO2max or VT in trained male cyclists.

Developing pulmonary vasculopathy in systemic sclerosis, detected with non-invasive cardiopulmonary exercise testing.

BackgroundPatients with systemic sclerosis (SSc) may develop exercise intolerance due to musculoskeletal involvement, restrictive lung disease, left ventricular dysfunction, or pulmonary vasculopathy (PV). The latter is particularly important since it may lead to lethal pulmonary arterial hypertension (PAH). We hypothesized that abnormalities during cardiopulmonary exercise testing (CPET) in patients with SSc can identify PV leading to overt PAH.MethodsThirty SSc patients from the Harbor-UCLA Rheumatology clinic, not clinically suspected of having significant pulmonary vascular disease, were referred for this prospective study. Resting pulmonary function and exercise gas exchange were assessed, including peakVO2, anaerobic threshold (AT), heart rate- VO2 relationship (O2-pulse), exercise breathing reserve and parameters of ventilation-perfusion mismatching, as evidenced by elevated ventilatory equivalent for CO2 (VE/VCO2) and reduced end-tidal pCO2 (PETCO2) at the AT.ResultsGas exchange patterns were abnormal in 16 pts with specific cardiopulmonary disease physiology: Eleven patients had findings consistent with PV, while five had findings consistent with left-ventricular dysfunction (LVD). Although both groups had low peak VO2 and AT, a higher VE/VCO2 at AT and decreasing PETCO2 during early exercise distinguished PV from LVD.ConclusionsPreviously undiagnosed exercise impairments due to LVD or PV were common in our SSc patients. Cardiopulmonary exercise testing may help to differentiate and detect these disorders early in patients with SSc.

Ventilatory Changes After Active Heat Acclimation for Multiday Ultramarathon Races in the Sahara Desert

To determine the effect of active heat acclimation (HA) on ventilatory responses, 4 endurance‐trained athletes (42.0 ± 5.7 y, mean ± SD) underwent 10 day of activity in 35–40°C and ~15% RH conditions to prepare for multiday ultramarathon races in the Sahara desert. Exercise during HA included 1 h/day of running at ≥50% maximal oxygen consumption (VO2max). Physiological assessments included pre‐ and post‐HA VO2max, heart rate (HR), esophageal (Tes), rectal (Tre), and skin temperatures (4 sites). Pre‐ and post‐HA VO2max values were not significantly different (52.8 ± 4.0 vs 52.0 ± 4.6 mL·kg−1·min−1, p = 0.35). Attainment of HA was confirmed by a significant reduction in exercise HR (p &lt; 0.01) and trends (p=0.12) for reductions in both Thermal Comfort ratings and Borg Ratings of Perceived Exertion over the 10‐d HA period. During incremental exercise, from pre‐ to post‐HA, the ventilatory equivalent for O2 (VE/VO2) increased from 28.6 ± 1.0 to 30.2 ± 1.0 (p = 0.06), whereas the ventilatory equivalent for CO2 (VE/VCO2) showed no change (29.6 ± 0.8 vs 29.8 ± 2.0, p = 0.37). These preliminary data suggest that active HA increases ventilatory responses independently of an exercise training effect.Supported by NSERC, Canadian Foundation for Innovation.

Peak Oxygen Uptake During the Six-minute Walk Test in Diffuse Interstitial Lung Disease and Pulmonary Hypertension

IntroductionThe six-minute walk test (6MWT) is widely used in evaluating diffuse interstitial lung disease (ILD) and pulmonary hypertension (PH). However, their physiological determining factors have not been well defined. ObjectiveTo evaluate the physiological changes that occur in ILD and PH during the 6MWT, and compare them with the cardiopulmonary exercise test (CPET). Material and MethodsThirteen patients with ILD and 14 with PH were studied using the 6MWT and CPET on an ergometer cycle. The respiratory variables were recorded by means of telemetry during the 6MWT. ResultsOxygen consumption (VO2), respiratory and heart rate reached a plateau from minute 3 of the 6MWT in both diseases. The VO2 did not differ from the peak value in the CPET (14±2 and 15±2ml/kg/min, respectively, in ILD; 16±6 and 16±6ml/kg/min, in PH). The arterial oxygen saturation decreased in both diseases, although it was more marked in ILD (−12±5%, P<.01). The ventilatory equivalent for CO2 (VE/VCO2) in PH during the 6MWT was strongly associated with functional class (FC) (85±14 in FC III-IV, 44±6 in FC I-II; P<.001). ConclusionsThe 6MWT in ILD and PH behaves like a maximal effort test, with similar VO2 to the CPET, demonstrating a limit in oxygen transport capacity. Monitoring using telemetry during the 6MWT may be useful for the clinical evaluation of patients with ILD or PH.

Periodic Breathing Promotes Circulatory Oscillations at Rest and during Exercise in Patients with Heart Failure

Instability of breathing control in HF patients is manifest as periodic breathing (PB) and characterized by regular and marked oscillations of minute ventilation (VE) and tidal volume (VT) in a crescendo-decrescendo pattern. PB has been associated with decreased exercise capacity and adverse prognosis. Previous studies suggest circulatory oscillations may accompany oscillation of VE though this has not been well characterized. Augmented intrathoracic pressure changes during periods of increased VE may promote phasic increases of venous return and pulmonary blood flow. Hypothesis: In HF patients with PB, the predicted (by modified alveolar gas equation) decline of end-tidal carbon dioxide (PetCO2) associated with increased VE is offset by increased circulatory CO2 delivery to the lungs. Methods: 50 consecutive patients with HF and PB were identified by cardiopulmonary exercise. Exercise PB was defined as >25% variation of amplitude (peak VE-nadir VE/mean VE) persisting >60% exercise duration. Breath by breath gas exchange measurements obtained at rest and during exercise included oxygen uptake (VO2), CO2 production (VCO2), ventilatory equivalent for CO2 (VE/VCO2), PetCO2, VE, and VT. Predicted PetCO2 was estimated by the modified alveolar gas equation: VE = (.863∗VCO2)/PaCO2∗(1-VD/VT), where PetCO2 was substituted for arterial CO2 tension (PaCO2). Ventilatory dead space (VD) was presumed to be constant. Results: (Table) During peak periods of VE at rest, 50% max and max work the measured decline of PetCO2 was less than predicted (Pred PetCO2) from measured VE and due to proportionately greater increase of VCO2.Tabled 1Rest (n=50)50% max (n=50)Max (n=50)NadirPeakNadirPeakNadirPeakMean (60 secs)VT(L)0.51.00.61.41.41.81.6VE(L/min)7.4019.615.534.243.167.056VCO2(ml/min)141481375881110216481425VEVCO257424540404240PetCO2(mmHg)32313331312930Pred PetCO232203318312430 Open table in a new tab Conclusion: In HF patients with PB, the decline of PetCO2 observed during periods of increased VE is less than predicted by the modified alveolar gas equation and likely attributable to phasic augmentation of circulatory CO2 delivery to the lungs. Cardiopulmonary interaction in HF patients with PB includes phasic increases of pulmonary blood flow which promotes modulation and stabilization of PaCO2.

Einfluss der CPAP-Therapie auf die ventilatorische Effizienz am Tage bei Patienten mit obstruktivem Schlafapnoe-Syndrom

Obstructive sleep apnea syndrome (OSAS) is a nocturnal breathing disorder with possibly negative consequences on daytime control of ventilatory drive. We therefore investigated ventilatory efficiency, defined as the ventilatory equivalent for CO2 (VaE/VaCO2), in patients with OSAS during exercise before and under treatment with continuous positive airway pressure (CPAP). In 21 patients with untreated OSAS, ventilatory efficiency, described as the slope (DeltaVaE vs. VaCO2) and the lowest ratio (VaE/VaCO2 min) of the ventilatory equivalent for CO2, was determined below the anaerobic threshold using spiroergometry. A follow-up after at least 6 months of CPAP therapy was performed in 16 of these patients and in 5 CPAP-neglecting patients with OSAS, who served as controls. In 21 patients with untreated OSAS, DeltaVaE vs. VaCO2 was significantly and VaE/VaCO2 min non-significantly lower, revealing better ventilatory efficiency, compared to normal values. In 16 patients, ventilatory efficiency did not change after on average 305.7 +/- 104.8 nights of CPAP-therapy, compared to 5 controls. OSAS is not associated with a disturbed ventilatory efficiency during exercise. Long-term CPAP-therapy does not change ventilatory efficiency during exercise in patients with OSAS. The improved ventilatory efficiency during exercise compared to normal controls may be due to differences concerning anthropometric data (e. g., obesity, hypertension) and cardiopulmonary exercise-test (45 degrees lying position).

Effects of acute hypoxia on the estimation of the lactate threshold from ventilatory gas exchange indices during an incremental exercise test.

The purpose of this study was to investigate the validity of non-invasive lactate threshold estimation using ventilatory and pulmonary gas exchange indices under condition of acute hypoxia. Seven untrained males (21.4+/-1.2 years) performed two incremental exercise tests using an electromagnetically braked cycle ergometer: one breathing room air and other breathing 12 % O2. The lactate threshold was estimated using the following parameters: increase of ventilatory equivalent for O2 (VE/VO2) without increase of ventilatory equivalent for CO2 (VE/VCO2). It was also determined from the increase in blood lactate and decrease in standard bicarbonate. The VE/VO2 and lactate increase methods yielded the respective values for lactate threshold: 1.91+/-0.10 l/min (for the VE/VO2) vs. 1.89+/-0.1 l/min (for the lactate). However, in hypoxic condition, VE/VO2 started to increase prior to the actual threshold as determined from blood lactate response: 1.67+/-0.1 l/min (for the lactate) vs. 1.37+/-0.09 l/min (for the VE/VO2) (P=0.0001), i.e. resulted in pseudo-threshold behavior. In conclusion, the ventilatory and gas exchange indices provide an accurate lactate threshold. Although the potential for pseudo-threshold behavior of the standard ventilatory and gas exchange indices of the lactate threshold must be concerned if an incremental test is performed under hypoxic conditions in which carotid body chemosensitivity is increased.

VE and VCO2 remain tightly coupled during incremental cycling performed after a bout of high-intensity exercise.

The purpose of the present study was to determine whether the linear relationship between CO2 output (VCO2) and pulmonary ventilation (VE) is altered during incremental cycling performed after exercise-induced metabolic acidosis. Ten untrained, female subjects performed two incremental cycling tests (15 W x min(-1) up to 165 W) on separate days. One incremental exercise test was conducted without prior exercise, whereas the other test was preceded by a 1-min bout of maximal cycling. The ventilatory equivalent for O2 (VE/VO2) was only elevated above control values at 15-60 W during incremental cycling performed after high-intensity exercise. In contrast, the ventilatory equivalent for CO2 (VE/VCO2) was significantly increased above control levels at nearly every work stage of incremental work (all except 165 W). Hyperventilation relative to VCO2 was confirmed by the significantly lower end-tidal CO2 tension (P(ET)CO2) obtained throughout the incremental cycling that was performed after high-intensity exercise (except at 165 W). VE and VCO2 were significantly correlated under both treatment conditions (r > 0.99; P < 0.001). Moreover, both the slope and y-intercept of the linear regression were found to be significantly elevated during the incremental cycling performed after high-intensity cycling compared to control conditions (P < 0.01). The increase in the slope of the VE-VCO2 relationship during incremental exercise performed under these conditions does not represent an uncoupling of VE from VCO2, but could be accounted for by the significantly lower P(ET)CO2 observed during exercise.

Ventilation and Gas Exchange during Exercise in Sickle Cell Anemia

Adults with sickle cell anemia (SCA) have restrictive lung impairment, increased alveolar dead space, and hypoxemia. These factors, together with increased anaerobic metabolism, are thought to cause exercise hyperventilation. To assess the role of each of these in children, 34 patients with SCA and 16 control subjects performed pulmonary function and exercise tests. Twenty-eight patients with SCA had spirometric values and lung volumes, and all but two patients with SCA had arterial saturation greater than 91% during exercise. Despite a low VO2max (30.07 +/- 6.55 ml/min/kg), the ventilatory anaerobic threshold (VAT) in the patients occurred at a similar %VO2max as in the control subjects (69 +/- 9% versus 63 +/- 12%). The slope of the delta VE/delta VCO2 relationship for sub-VAT work was steeper in the patients (29.4 +/- 6.5 versus 24.7 +/- 5.2, p = 0.01), and the ventilatory equivalent for CO2 (VE/VCO2) in steady-state exercise was greater in the patients than in the control subjects (33.2 +/- 3.5 versus 30.8 +/- 3.5, p = 0.03). End-tidal PCO2 did not differ (38.3 +/- 3.0 versus 39.2 +/- 3.1), indicating equivalent alveolar ventilation. The patients had a higher dead space:tidal volume ratio (VD/VT) than did the control subjects (0.204 +/- 0.033 versus 0.173 +/- 0.024, p = 0.0005). The PaCO2 was significantly lower in those with lower Hb, but there was no difference in pH. In conclusion, children with SCA have an increased exercise ventilatory response caused in part by increased physiologic dead space, and in part by their low Hb. The greater dead space may be the result of sickle cells impairing capillary perfusion to ventilated alveoli.

Lactate and ventilatory thresholds: disparity in time course of adaptations to training.

We tested the hypothesis that the lactate threshold (Tlac) during incremental exercise could be increased significantly during the first 3 wk of endurance training without any concomitant change in the ventilatory threshold (Tvent). Tvent is defined as O2 uptake (VO2) at which ventilatory equivalent for O2 [expired ventilation per VO2 (VE/VO2)] increased without a simultaneous increase in the ventilatory equivalent for CO2 (VE/VCO2). Weekly measurements of ventilatory gas exchange and blood lactate responses during incremental and steady-rate exercise were performed on six subjects (4 male; 2 female) who exercised 6 days/wk, 30 min/session at 70-80% of pretraining VO2max for 3 wk. Pretraining Tlac and Tvent were not significantly different. After 3 wk of training, significant increases (P less than 0.05) occurred for mean (+/- SE) VO2max (392 +/- 103 ml/min) and Tlac (482 +/- 135 ml/min). Tvent did not change during the 3 wk of training, despite significant (P less than 0.05) reductions in VE responses to both incremental and steady-rate exercise. Thus ventilatory adaptations to exercise during the first 3 wk of exercise training were not accompanied by a detectable alteration in the ventilatory "threshold" during a 1-min incremental exercise protocol. The mean absolute difference between pairs of Tlac and Tvent posttraining was 499 ml/min. Despite the significant training-induced dissociation between Tlac and Tvent a high correlation between the two parameters was obtained posttraining (r = 0.86, P less than 0.05). These results indicate a coincidental rather than causal relationship.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of endurance exercise training on ventilatory function in older individuals.

To evaluate the effect of endurance training on ventilatory function in older individuals, 1) 14 master athletes (MA) [age 63 +/- 2 yr (mean +/- SD); maximum O2 uptake (VO2max) 52.1 +/- 7.9 ml . kg-1 . min-1] were compared with 14 healthy male sedentary controls (CON) (age 63 +/- 3 yr; VO2max of 27.6 +/- 3.4 ml . kg-1 . min-1), and 2) 11 sedentary healthy men and women, age 63 +/- 2 yr, were reevaluated after 12 mo of endurance training that increased their VO2max 25%. MA had a significantly lower ventilatory response to submaximal exercise at the same O2 uptake (VE/VO2) and greater maximal voluntary ventilation (MVV), maximal exercise ventilation (VEmax), and ratio of VEmax to MVV than CON. Except for MVV, all of these parameters improved significantly in the previously sedentary subjects in response to training. Hypercapnic ventilatory response (HCVR) at rest and the ventilatory equivalent for CO2 (VE/VCO2) during submaximal exercise were similar for MA and CON and unaffected by training. We conclude that the increase in VE/VO2 during submaximal exercise observed with aging can be reversed by endurance training, and that after training, previously sedentary older individuals breathe at the same percentage of MVV during maximal exercise as highly trained athletes of similar age.