None listed
Conditions
Brief summary
Considering that obese patients with obstructive sleep apnea syndrome (OSA) and increases epicardial adipose tissue (EAT) thickness display sympathetic over activation at baseline conditions, we sought to investigate the effect of this autonomic dysfunction on HRR. Whereas several studies have demonstrated attenuated heart rate recovery (HRR) in obese patients with either OSA or EAT accumulation, whether overlap of both conditions may further impair HRR has not been previously reported. The main objective of our study was to test whether post-exercise HRR in obese patients would be independently associated with OSA condition and EAT increase.
Interventions
Obese patients BMI >30 will be enrolled to perform polysomnography test, cardio-pulmonary exercise testing and echocardiography. Relationship between heart rate recovery, epicardial fat thickness and obstructive sleep apnea will be studied. Cardiopulmonary exercise testing was performed according to standardized procedures using an electromagnetic braked cycle ergometer. by cardiologists experienced in exercise physiology. Exercise protocol involved an initial 3 minutes of rest, followed by unloaded cycling for 2 minutes of unload cycling with a progressively increment every minute (10 watt/minute) until exhaustion at a pedaling frequency of 60-65 rpm. Subjects were continuously monitored using 12-lead ECG (Case, GE Healthcare, France). Blood pressure assessed were recorded every 2-minutes. Subjects respired through an oro-nasal mask (Hans Rudolf 7450 SeriesV2™ Mask, CareFusion, France). Breath-by-breath cardiopulmonary data (PowerCube-Ergo, Ganshorn Medizin Electronic GmbH, Niederlauer, Germany) were measured at rest, warm up and incremental exercise testing. Before each test, oxygen (O2) and carbon dioxide (CO2) analyzers and flow mass sensor were calibrated using available precision gas mixture and a 3-L syringe, respectively. Minute ventilation (VE), oxygen uptake (VO2), carbon dioxide output (VCO2) were recorded as concurrent 10-s moving averages, as was determined ventilation anaerobic threshold by the V-slope method. Ventilatory reserve was calculated as (MVV – peak VE) / MVV * 100, where MVV is maximal voluntary ventilation estimated as FEV1 multiplied by 35. Peak values were averaged over the last 30 s of exercise. Patient effort was considered to be maximal if two of the following occurred: predicted maximal work is achieved, predicted maximal heart rate (HR) is achieved, VE/VO2 > 45 and RER > 1.10, as recommended by the ATS/ACCP. At peak exercise, subjects assessed Borg-perceived exertion ratings for both respiratory and leg discomfort. During the study period, mean values between qualified replicate tests performed weekly on control subjects were 3.1 ± 4.2 %, 3.4 ± 3.2 %, 2.1 ± 2.2 %, for peak VO2, VCO2 and VE, respectively. Peak oxygen pulse (O2 pulse) was calculated and was expressed in mL per beat and as percentage of predicted value by dividing the predicted peak VO2 by predicted peak HR. VE/VCO2 slope was calculated off-line as a linear regression function using 10-s averaged values and excluding the non-linear part of the relationship after the respiratory compensation point (where non-linear rise in V’E occurred relative to VCO2 in the presence of decrease of end-tidal pressure of CO2). The percentage of HR reserve used at peak exercise referred to [(HRstage-HRrest) / (220-age in years-HRrest)] * 100, where HR is heart rate. Heart rate recovery was defined as the change in heart rate from peak exercise to 1 minute (HRR-1) and 3 minutes (HRR-3) later.
Sponsors
Eligibility
Inclusion criteria
obese BMI > 30
Exclusion criteria
macrovascular sequellea of metabolic syndrome, such as hypertension, heart failure, coronary artery disease, renal failure