Effects of different exercise training program on post-exercise V̇O2kinetics and V̇O2recovery delay in stable patients with coronary heart disease

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Skip to main content Home About Submit ALERTS / RSS Search for this keyword Advanced Search Effects of different exercise training program on post-exercise V̇O 2 kinetics and V̇O 2 recovery delay in stable patients with coronary heart disease View ORCID Profile Mathieu Gayda , Lukas-Daniel Trachsel , View ORCID Profile Pierre-Marie Leprêtre , View ORCID Profile Florent Besnier , View ORCID Profile Maxime Boidin , Julie Lalongé , View ORCID Profile Louis Bherer , Martin Juneau , Anil Nigam doi: https://doi.org/10.1101/2025.05.09.25325944 Mathieu Gayda 1 Preventive Medicine and Physical Activity (ÉPIC) Center, Montreal Heart Institute , Montreal, Canada 2 Department of Medicine, Faculty of Medicine, University of Montreal , Montreal, Canada 4 Research Center, Montreal Heart Institute , Montreal, Canada Ph.D Find this author on Google Scholar Find this author on PubMed Search for this author on this site ORCID record for Mathieu Gayda For correspondence: mathieu.gayda{at}icm-mhi.org Lukas-Daniel Trachsel 1 Preventive Medicine and Physical Activity (ÉPIC) Center, Montreal Heart Institute , Montreal, Canada 2 Department of Medicine, Faculty of Medicine, University of Montreal , Montreal, Canada 3 University Clinic for Cardiology, Inselspital, Bern University Hospital, University of Bern , Switzerland M.D Find this author on Google Scholar Find this author on PubMed Search for this author on this site Pierre-Marie Leprêtre 6 Centre d’Etudes des Transformations des Activités Physiques et Sportives (CETAPS) UR 3882, Université Rouen Normandie , Mont-Saint-Aignan, France 7 Unité de Réadaptation Cardiovasculaire, Centre Hospitalier de Corbie , Corbie, France Find this author on Google Scholar Find this author on PubMed Search for this author on this site ORCID record for Pierre-Marie Leprêtre Florent Besnier 1 Preventive Medicine and Physical Activity (ÉPIC) Center, Montreal Heart Institute , Montreal, Canada 2 Department of Medicine, Faculty of Medicine, University of Montreal , Montreal, Canada 4 Research Center, Montreal Heart Institute , Montreal, Canada PhD Find this author on Google Scholar Find this author on PubMed Search for this author on this site ORCID record for Florent Besnier Maxime Boidin 5 Research Institute for Sport and Exercise Sciences, Liverpool John Moores University , Liverpool, United Kingdom Ph.D Find this author on Google Scholar Find this author on PubMed Search for this author on this site ORCID record for Maxime Boidin Julie Lalongé 1 Preventive Medicine and Physical Activity (ÉPIC) Center, Montreal Heart Institute , Montreal, Canada 4 Research Center, Montreal Heart Institute , Montreal, Canada R.A Find this author on Google Scholar Find this author on PubMed Search for this author on this site Louis Bherer 1 Preventive Medicine and Physical Activity (ÉPIC) Center, Montreal Heart Institute , Montreal, Canada 2 Department of Medicine, Faculty of Medicine, University of Montreal , Montreal, Canada 4 Research Center, Montreal Heart Institute , Montreal, Canada Find this author on Google Scholar Find this author on PubMed Search for this author on this site ORCID record for Louis Bherer Martin Juneau 1 Preventive Medicine and Physical Activity (ÉPIC) Center, Montreal Heart Institute , Montreal, Canada 2 Department of Medicine, Faculty of Medicine, University of Montreal , Montreal, Canada 4 Research Center, Montreal Heart Institute , Montreal, Canada M.D Find this author on Google Scholar Find this author on PubMed Search for this author on this site Anil Nigam 1 Preventive Medicine and Physical Activity (ÉPIC) Center, Montreal Heart Institute , Montreal, Canada 2 Department of Medicine, Faculty of Medicine, University of Montreal , Montreal, Canada 4 Research Center, Montreal Heart Institute , Montreal, Canada M.D Find this author on Google Scholar Find this author on PubMed Search for this author on this site Abstract Full Text Info/History Metrics Supplementary material Data/Code Preview PDF Abstract Post-exercise V̇O 2 kinetics and V̇O 2 recovery delay (RD) are clinical prognostic markers in cardiac patients, but have not been studied after exercise training in patients with coronary heart disease (CHD). We aimed to compare the effects of 12-weeks moderate-intensity continuous exercise training (MICET), low volume high-intensity interval training (LV-HIIT), or combined MICET/HIIT on O 2 deficit, post-exercise V̇O 2 kinetics, O 2 debt and V̇O 2 recovery delay (RD) in patients with CHD. Methods Patients with CHD were randomised in MICET, LV-HIIT or combined MICET/HIIT group for 12 weeks. Cardiopulmonary exercise test (CPET) parameters were assessed, and key exercise variables were calculated during and after exercise. CPET post-exercise kinetics time constant (r) (for V̇O 2 , V̇CO 2 , V̇ E and HR), O 2 deficit, O 2 debt and V̇O 2 recovery delay (RD) were calculated before and after training. Results A significant time effect (training) for r V̇O 2 (min) (p<0.05) was shown for all groups. Shorter r V̇O 2 values with small effect size (ES: 0.21 to 0.4) were noted for the combined MICET/HIIT and MICET groups. A significant time effect (p<0.01) was noted for O 2 debt that was increased after training (ES: 0.1 to 0.47). No significant statistical effect was shown for V̇O 2 RD and r V̇CO 2 , r V̇ E, r HR and O 2 deficit in all groups. Conclusions In patients with CHD, exercise training improved post-exercise V̇O 2 kinetic and the O 2 debt, with a higher impact of exercise dose (combined MICET/HIIT). Exercise training did not improved the V̇O 2 RD or other τ CPET recovery variables in CHD patients. Introduction Cardiopulmonary exercise testing (CPET) is the gold standard to assess cardiorespiratory fitness ( V̇ O 2 peak), a powerful indicator of disease severity and prognosis in patients with coronary heart disease (CHD) 1 , 2 . Exercise-based secondary prevention programs can improve V̇O 2 peak that is associated with a reduction of cardiovascular mortality and events in patients with CHD 3 – 5 . In addition to V̇ O 2 peak, other cardiopulmonary variables measured during CPET and its early post-exercise recovery phase can provide important complementary physiologic and metabolic information after exercise exposure of cardiac patients. Post-exercise V̇ O 2 kinetics is partly related to the recovery of phosphocreatine supply in the muscle, and is very sensitive to impairment of the O 2 delivery and diffusion in patients with chronic heart failure (CHF) 6 – 8 . V̇ O 2 kinetics during the early post-exercise recovery phase are considered independent of the exercise level but these values are affected by severe reduction in exercise capacity and abnormal cardiac response to exercise 9 , 10 . After exercise cessation, prolonged V̇ O 2 , ventilation ( V̇ E) and heart rate recovery kinetics has been associated with a worse clinical profile and outcomes in patients with CHF 6 , 8 , 11 . V̇ O 2 kinetics and O 2 debt, i.e. the difference between the resting rate of oxygen consumption and the elevated rate following an exercise, are also affected by the hemodynamic negative effect of not providing the body’s requested amount of O 2 generated during exercise (O 2 deficit) with values correlated with O 2 exercise delivery and exercise tolerance 10 . The value of the peak oxygen recovery delay (V̇O 2 RD), as defined as the time from the beginning of recovery until the V̇O 2 permanently falls below V̇O 2 peak, was also inversly related to cardiac output reserve, predicts time to heart transplantation and was associated with disease severity in patients with CHF 6 , 11 . In patients with CHD, abnormalities in post-exercise V̇ O 2 kinetics shape («Hump») and slowed V̇ O 2 kinetics have been related to myocardial ischemia 12 , 13 , while time constant (r) of V̇O 2 , V̇CO 2 and heart rate were not different between healthy subjects and patients with CHD 10 . With these conflicting results, the prevalence of the V̇O 2 RD and its hemodynamic relationship has not been studied in patients with CHD. Previous study in healthy subjects suggested that initial aerobic fitness and exercise training improved post exercise V̇ O 2 kinetics 14 – 16 . In patients with CHF, previous studies demonstrated that various exercise training program (aerobic, resistance plus respiratory or interval training) improved post-exercise V̇ O 2 kinetics after submaximal 17 , 18 or maximal exercise 19 , via mainly improvement of muscular O 2 delivery. There are actually no studies investigating the effects of different exercise training programs on O 2 deficit, post-exercise V̇ O 2 kinetics, O 2 debt, and the V̇O 2 RD in patients with CHD. The main aims of our study were to assess the effects of moderate-intensity continuous exercise training (MICET), low volume high-intensity interval training (LV-HIIT), or combined MICET/HIIT on O 2 deficit, post-exercise V̇O 2 kinetics, O 2 debt, and V̇O 2 RD in patients with CHD. We hypothesised that exercise training will improve post-exercise V̇ O 2 kinetics and the V̇O 2 RD in patients with CHD, with stronger effects for higher exercise dose. Material and methods Study design and participants This retrospective study is based on data from three prospective randomized exercise intervention trials conducted in patients with CHD 20 – 24 . All studies protocols were approved by the Research Ethics and New Technology Development Committee of the Montreal Heart Institute, and were registered on ClinicalTrials.gov ( ClinicalTrials.gov identifier numbers: NCT03414996 , NCT02048696 , NCT03443193 ) and written informed consent was obtained by each patient. All patients were referred for a structured aerobic exercise training program at the ÉPIC Center of the Montreal Heart Institute and were involved in a training intervention study. All patients with CHD were under optimal medical therapy after coronary revascularisation. Measurement Baseline clinical assessment (i.e. medical history, physical examination and anthropometric measurements, including body composition analysis (bioimpedance, Tanita, model BC418, Japan), transthoracic echocardiography (GE, Vivid 9, USA) and CPET were performed at baseline and after completion of each of the program. Maximal cardiopulmonary exercise testing (CPET) Maximal CPET was performed on a cycle ergometer (Ergoline 800S, Bitz, Germany) according to the latest join recommendations and as previously published 21 , 22 , 24 , 25 . Following a 3-minute warm up phase at an initial work load of 20 W, an incremental exercise test with 15 Watt increments per min until exhaustion at a pedalling speed > 60 rpm was performed. The recovery phase consisted of 2 minutes of active recovery at 20 W at pedalling speed between 50 and 60 rpm, followed by 3 minutes of passive recovery. Gas exchange parameters were continuously measured at rest, during exercise, and during recovery using a metabolic system (Oxycon Pro, CareFusion, Jaeger, Germany), breath by breath basis and then averaged every 15 sec. as recently published 21 – 24 . There was a continuous ECG monitoring (Marquette, case 12, St. Louis, Missouri). Blood pressure and rate of perceived exertion (RPE) were measured each 3 min throughout the test. The highest V̇O 2 value reached during the exercise phase was considered as the V̇O 2 peak, and this value was used for the calculation of the O 2 pulse (V̇O 2 /HR) according to the recent recommendations 21 , 22 , 24 , 25 . Oxygen deficit calculation O 2 deficit was calculated by subtracting the measured V̇O 2 during exercise phase (warm-up and incremental exercise phase) from the theoretical V̇O 2 value computed based on the energy cost to develop 1 watt on an electromagnetic brake ergometer 26 . Post exercise CPET variables Recovery (or post-exercise) was defined by the period after exercise cessation at peak effort and was activated manually by the operator during CPET testing. Recovery CPET variable were measured during 5 minutes (2 min of active recovery and then 3 min of passive recovery). The post exercise CPET kinetics (V̇O 2 , V̇CO 2 , V̇ E) were assessed with Oxycon Pro software utilities Tau ( τ) mathematical function (Oxycon Pro CareFusion, Jaeger, Germany), indicated by mono exponential function 8 , 27 , 28 : where a1 is the CPET (V̇O 2 , V̇CO 2 , V̇ E, HR) value at the beginning of recovery, a is the asymptote value (value at end of 5 min-recovery), r is tau (or time constant : time need to reach 63% of the gain) 8 , 27 , 28 . The V̇O 2 recovery delay (V̇O 2 RD) was calculated according to recent previous methodology 6 and defined as the time from the beginning of recovery until the V̇O 2 permanently falls below V̇O 2 peak. As well, heart rate recovery (HRR) at 1 minute was calculated by subtracting heart rate at 1 min recovery from the maximal heart rate at peak exercise 20 . O 2 debt was calculated by taking the exercise-final V̇O 2 as the peak of the curve and integrating V̇O 2 from there until it decayed to the rest value 26 . Exercise training intervention (aerobic and resistance training) The aerobic exercise training intervention consisted of three different training modalities: moderate-intensity continuous exercise training (MICET), low volume high-intensity interval training (LV-HIIT), and a combined HIIT/MICET, as previously reported 20 – 24 . All patients performed 2 to 3 exercise training sessions a week on a bicycle ergometer. Resistance training (RT) was then performed following each endurance session 21 , 22 , 24 . The training load was calculated for the aerobic training component according to the adapted model of Calvert et al. 29 . More details regarding aerobic and resistance training protocols are available in Supplementary materials File S1. Statistical analyses Data are presented as means ± standard deviation for continuous variables and presented as frequencies and percentages for categorical variables. Statistical analyses were performed using GraphPad Prism 9.0 (GraphPad Software, Inc., La Jolla, California, USA). Normal distribution was verified with a Shapiro-Wilk test and baseline characteristics were compared between groups using either a t -test or a Mann-Whitney test, a chi-square test was used for categorical variables. Mixed model analysis (groups x time) was used to study the CPET parameters across time and between groups. Models with group, time and group x time interaction as independent variables were used. The group x time interaction was the main focus of the analysis as it tested the difference in the change (post-pre) between the three groups. Multiple comparison test was done using Šídák test to localize differences, with adjusted p-value. The magnitude of the effect size was compared using Cohen’s d scale and was considered either trivial (d <0.2), small (0.2 < d < 0.5), moderate (0.5 < d 0.8). A p -value < 0.05 was considered statistically significant. Results Clinical characteristics The clinical characteristics are presented in table 1 . In the final analysis, we included a total of 82 patients with CHD (Combined MICET/HIIT=38, HIIT n=26, MICET=18). Patients in the combined MICET/HIIT had a lower prevalence of post ACS, lower use of dual antiplatelet therapy, higher weekly training sessions (p<0.05) vs. the other groups (HIIT, MICET). Resting DBP was higher for combined HIIT/HIIT vs. HIIT (p<0.05). Resting LVEF was lower in the MICET group vs. the 2 others (p<0.05). Training load was higher for Combined MICET/HIIT and MICET vs. HIIT (p<0.0001). Otherwise, there were no differences with regards to baseline clinical characteristics ( Table 1 ) . View this table: View inline View popup Table 1: Clinical characteristics of patients with CHD randomized to combined MICET/HIIT, HIIT, or MICET. Exercise and recovery CPET parameters The exercise and recovery CPET parameters for the three groups (combined MICET-HIIT, HIIT, MICET) are presented in table 2 . There was significant time effect (training) regarding τ V̇O 2 (min) (p<0.01) with no interaction. The τ V̇O 2 was shorter with trivial to small effect size for the combined MICET-HIIT and MICET groups (ES: 0.21 and 0.40). No significant time, group or interaction effect was noted for τ V̇CO 2 , τ V̇ E, τ HR, V̇O 2 RD and O 2 deficit for all groups (p>0.05). The prevalence of V̇O 2 RD was of 43% (pre: n=35) at baseline and of 47% after training (n=38), and remained unchanged (p=0.63). A significant time effect (p0.05). A significant interaction and time effect (p<0.05) was found for O 2 pulse and values were improved after training in the combined HIIT/MICET, HIIT groups and particularly in the MICET group (ES: 0.27 to 0.59). The training load was lower in the LV-HIIT group vs the 2 others groups (P<0.0001) and higher in the MICET group vs. combined HIIT/MICET (P<0.05) (see Table 1 ) . View this table: View inline View popup Table 2: Exercise and recovery cardiopulmonary exercise test parameters in CHD patients randomized to combined MICET/HIIT, LV-HIIT, or MICET. Discussion In this study, we have assessed the effects of different aerobic exercise training program (Combined HIIT/MICET, LV-HIIT, and MICET) on post-exercise V̇O 2 kinetics, O 2 deficit, O 2 debt, and V̇O 2 RD in patients with CHD. Our main findings were that: 1) aerobic exercise training improves τ V̇O 2 in particular for higher exercise dose program (Combined HIIT/MICET, MICET); 2) Exercise training did no improves V̇O 2 RD or other τ CPET recovery variables; 3) Exercise training improved O 2 pulse in particular for higher exercise dose program (Combined HIIT/MICET, MICET). To our knowledge, there is few data on the effect of different exercise training program on post-exercise V̇O 2 kinetics, V̇O 2 RD, O 2 deficit and debt in patients with CHD. Regarding τ V̇O 2 , this was the only CPET τ that was improved after exercise training in our CHD patients. We should note that the higher effects size were noted in the combined group (HIIT/MICET) and to a lesser degree in the MICET group (ES:-0.21/-0.40). These two groups had the higher exercise dose. Our results are in agreement with 2 previous exercise training studies in CHF patients. Kemp et al. showed an acceleration of submaximal τ V̇O 2 after 12 weeks of exercise training (HIIT, resistance and respiratory training) in CHF patients 17 . Similarly, Spee et al showed an improvement of τ V̇O 2 after 12 weeks of HIIT in CHF patients 18 . In these 2 studies, comparison were done to an inactive control group of CHF patients. This CPET recovery parameter is of great clinical importance, it was shown to be related to lower exercise tolerance, cardiac abnormalities/ischemia and muscle oxidative metabolism in cardiac patients 8 , 12 , 13 . These improvements may be explained by several mechanisms that include an increased O 2 utilization by the peripherals muscles via enhanced mitochondrial function 30 , 31 and/or and increased O 2 delivery by the muscle vasculature via an improved vasodilatory capacity 17 , 18 . Another potential mechanism may be due to improved cardiac output during exercise, as suggested by previous studies in CHD patients 12 , 13 , and from our improved O 2 pulse after training. Regarding other τ CPET variables (V̇CO 2 and V̇E), their kinetics were not improved after training in our patients. Studies on τ V̇CO 2 and τ V̇E were mostly realized with CHF patients 8 , 10 , 32– 34 , and none have explored the impact of exercise training on these variables in cardiac patients. τ V̇CO 2 and τ V̇E were shown to be prolonged in the more severe CHF patients vs. less severe ones or healthy subjects 8 , 10 , 32– 34 . Therefore, τ V̇CO 2 might originate from the CO 2 production from the aerobic metabolism, the plasmatic buffering of metabolic acidosis by the bicarbonates pool, that should be expired by ventilation. As well, τ V̇E value was suggested to reflect the breathing pattern recovery from peak exercise, and stimuli from mecano and chemoreceptors controlling ventilation 32 . Regarding V̇O 2 RD, we showed no impact of exercise training on this variable in our CHD patients. As well, the prevalence of V̇O 2 RD was not reduced after training for all patients. V̇O 2 RD is a prognosis marker in CHF patients and is linked to a reduced cardiac output, stroke volume, V̇O 2 /work slope during exercise and cardiac filling pressure in CHF patients 6 , 11 . This is the first study reporting V̇O 2 RD value in CHD patients and the impact of different exercise training program on this index. As expected, our V̇O 2 RD values (from 10.8 s to 14.7 s) are much shorter than previously published in patients with CHF 6 , 11 . As well, this remain unclear how exercise training may impact (shorten or reduce prevalence) this new CPET index. We showed that O 2 pulse (a surrogate marker of stroke volume) was improved in combined and MICET group, but that does not seemed to transfer to reduction of V̇O 2 RD values or prevalence. Regarding O 2 deficit, this element was not improved after training in our CHD patients. High inter-individual variability in O 2 deficit values were observed that may explain a lack of significant training effect. As well, we calculated this O 2 deficit during the warm-up period that may differ from previous studies. Our result disagree form a previous study in CHF patients 35 showing that continuous aerobic exercise training reduced the O 2 deficit and the anaerobic contribution during a constant submaximal exercise test. This O 2 deficit represents the anaerobic metabolism (ATP/phosphocreatine system and anaerobic glycolysis) plus the O 2 stored in the blood and muscle (hemo/myoglobin) that is used to produce additional ATP (in addition to ATP produced by aerobic metabolism) during incremental exercise and is dependent of the exercise intensity 26 . This is particular true at the start of exercise and for intensities above first ventilatory threshold, where O 2 deficit will increase during a ramp type test 26 . For the O 2 debt, the values were increased after training (time effect) in our CHD patients, in particular for the combined group with a higher ES noted. We should mention that the O 2 debt after an incremental test has been linked to exercise intensity, this debt being higher for more intense level of exercise 26 . This might be particularly the case, for the combined (HIIT/MICET) and MICET groups, that improved their V̇O 2 peak (data not shown) and therefore reached a higher exercise intensity post-training. Limitations In our study, data of three prospective randomised control trials were pooled for analysis from one single institution and with the participants composed mainly of men. However, a carefully selected and very homogenous population of patients with CHD was part of this study. We used low volume HIIT protocol (passive recovery) in the HIIT group 22 – 24 that is not the most commonly used in clinical research in patients with CHD 36 , 37 . In addition, short to long HIIT protocols were used in the combined HIIT/MICET group 21 . Therefore, the exercise volume (or dose) differed between the groups, with a higher dose in the combined one. Regarding CPET kinetics calculation, we used an incremental ramp protocol, and we did not performed a constant work rate test that could have produced more comparable results with previous studies. Conclusions We showed that aerobic exercise training with difference training modalities (HIIT, MICET, combined HIIT/MICET) improved τ V̇O 2 in patients with CHD, with greater effects for higher exercise dose program. Exercise training (whatever the modality) did not improved V̇O 2 RD time of prevalence, as well as τ CPET recovery variables in our patients with CHD sample. Our work confirms the benefits of exercise training in τ V̇O 2 in patients with CHD, suggesting a potential better functional status, cardiac function and muscle oxidative metabolism. Further RCT exercise training studies including more women with CHD or patients with others CHD etiology (post-acute MI or post-acute coronary syndrome) are necessary. Data Availability All data produced in the present work are contained in the manuscript Footnotes Funding: The study was funded by the Mirella and Lino Saputo Research Chair in Cardiovascular Diseases and the Prevention of Cognitive Decline from Université de Montréal at the Montreal Heart Institute, the Montreal Heart Institute Foundation and the EPIC Center Foundation. Competing Interests: None Clinical protocols: ( ClinicalTrials.gov identifier numbers: NCT03414996 , NCT02048696 , NCT03443193 ) Data Availability Statement : none References 1. ↵ Kodama S , Saito K , Tanaka S , et al. Cardiorespiratory fitness as a quantitative predictor of all-cause mortality and cardiovascular events in healthy men and women: a meta-analysis . Jama . 2009 ; 301 : 2024 – 2035 . 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Share Effects of different exercise training program on post-exercise V̇O 2 kinetics and V̇O 2 recovery delay in stable patients with coronary heart disease Mathieu Gayda , Lukas-Daniel Trachsel , Pierre-Marie Leprêtre , Florent Besnier , Maxime Boidin , Julie Lalongé , Louis Bherer , Martin Juneau , Anil Nigam medRxiv 2025.05.09.25325944; doi: https://doi.org/10.1101/2025.05.09.25325944 Share This Article: Copy Citation Tools Effects of different exercise training program on post-exercise V̇O 2 kinetics and V̇O 2 recovery delay in stable patients with coronary heart disease Mathieu Gayda , Lukas-Daniel Trachsel , Pierre-Marie Leprêtre , Florent Besnier , Maxime Boidin , Julie Lalongé , Louis Bherer , Martin Juneau , Anil Nigam medRxiv 2025.05.09.25325944; doi: https://doi.org/10.1101/2025.05.09.25325944 Citation Manager Formats BibTeX Bookends EasyBib EndNote (tagged) EndNote 8 (xml) Medlars Mendeley Papers RefWorks Tagged Ref Manager RIS Zotero Tweet Widget Facebook Like Google Plus One Subject Area Sports Medicine Subject Areas All Articles Addiction Medicine (568) Allergy and Immunology (863) Anesthesia (300) Cardiovascular Medicine (4435) Dentistry and Oral Medicine (444) Dermatology (382) Emergency Medicine (608) Endocrinology (including Diabetes Mellitus and Metabolic Disease) (1509) Epidemiology (15227) Forensic Medicine (30) Gastroenterology (1124) Genetic and Genomic Medicine (6597) Geriatric Medicine (668) Health Economics (997) Health Informatics (4534) Health Policy (1368) Health Systems and Quality Improvement (1613) Hematology (540) HIV/AIDS (1264) Infectious Diseases (except HIV/AIDS) (15916) Intensive Care and Critical Care Medicine (1103) Medical Education (623) Medical Ethics (146) Nephrology (667) Neurology (6599) Nursing (346) Nutrition (998) Obstetrics and Gynecology (1144) Occupational and Environmental Health (957) Oncology (3332) Ophthalmology (974) Orthopedics (369) Otolaryngology (420) Pain Medicine (436) Palliative Medicine (130) Pathology (663) Pediatrics (1693) Pharmacology and Therapeutics (691) Primary Care Research (711) Psychiatry and Clinical Psychology (5447) Public and Global Health (9230) Radiology and Imaging (2198) Rehabilitation Medicine and Physical Therapy (1370) Respiratory Medicine (1196) Rheumatology (593) Sexual and Reproductive Health (712) Sports Medicine (530) Surgery (712) Toxicology (99) Transplantation (289) Urology (265) (function(){function c(){var b=a.contentDocument||a.contentWindow.document;if(b){var d=b.createElement('script');d.innerHTML="window.__CF$cv$params={r:'a002a6bd586c06f7',t:'MTc3OTUyNDUzMA=='};var a=document.createElement('script');a.src='/cdn-cgi/challenge-platform/scripts/jsd/main.js';document.getElementsByTagName('head')[0].appendChild(a);";b.getElementsByTagName('head')[0].appendChild(d)}}if(document.body){var a=document.createElement('iframe');a.height=1;a.width=1;a.style.position='absolute';a.style.top=0;a.style.left=0;a.style.border='none';a.style.visibility='hidden';document.body.appendChild(a);if('loading'!==document.readyState)c();else if(window.addEventListener)document.addEventListener('DOMContentLoaded',c);else{var e=document.onreadystatechange||function(){};document.onreadystatechange=function(b){e(b);'loading'!==document.readyState&&(document.onreadystatechange=e,c())}}}})();