Clinical impact of a structured exercise-training program in a sample of North African male patients with stable angina: A pilot study

High resting heart rate (RHR) is associated with multiple morbidity in chronic obstructive pulmonary disease (COPD) patients. Factors regarding the effectiveness of exercise training (ET) on RHR in COPD patients are unclear. The main objective of the current study is to determine the predictors of the eventual change in RHR after ET. One hundred and ten COPD patients (mean age: 63.1 ± 8.1years, FEV1%: 43.6 ± 16.6) who participated in the ET program that consisted of supervised breathing, aerobic, strengthening, and stretching exercises for 8weeks, 2days a week, were included in the study. RHR, pulmonary functions, 6-min walk distance (6-MWD), Modified Medical Research Council Dyspnea Scale, St. George Respiratory Questionnaire, and Hospital Anxiety and Depression scores were compared before and after ET. Multivariate regression analysis was performed to correlate factors related to changes in RHR before and after exercise. There was a significant improvement in RHR after the ET program (p < 0.001). Improvement in RHR was correlated with baseline RHR, 6-MWD, partial arterial oxygen pressure, dyspnea sensation, forced expiratory volume in the first second (r = 0.516, -0.388, -0.489, 0.369, -0.360, p < 0.05, respectively), and change in 6-MWD, partial arterial oxygen pressure, and symptom score (r = 0.523, 0.451, -0.325, p < 0.05, respectively) after ET. Baseline RHR, 6-MWD, and the change in 6-MWD were the independent factors that predicted the change in RHR after ET. Patients with a high RHR and low functional capacity and whose functional capacity improves more have a greater decrease in RHR after the ET program. By considering these related factors, clinicians can focus on improving the cardiovascular system in COPD patients. NCT04890080 (retrospectively registered-date of registration: 05.17.2021).

Introduction: In a normal healthy adult, sympathetic and parasympathetic system should be in synergy. Measuring resting heart rate is a one of the methods to assess health condition. It can be affected by different factors such as exercise, mental health, any disease, etc. Normal subjects with reduced heart rate are associated with better cardiovascular health. Physical inactivity is associated with high level of inflammatory markers. Increased inflammatory markers are related to inflammation and chronic diseases. The C-Reactive Protein (CRP) is a biomarker of inflammatory diseases. High CRP level is a potent risk factor for obesity, diabetes, atherosclerosis, etc. Aim: To study the effect of short term resistance and endurance exercise training on resting heart rate in healthy young adults, CRP, Body Mass Index (BMI) and also to compare the changes between two exercise groups. Materials and Methods: A cross-sectional study was conducted from May 2019 to May 2020 in the Department of Physiology at King George’s Medical University, Lucknow, Uttar Pradesh, India. The study included 60 healthy young adults with normal BMI (18.5-24.9 kg/m2) and age between 18-25 years. Subjects were equally divided into Group I- Resistance exercise and Group II endurance groups. Subjects did moderate intensity exercise (based on maximum heart rate) for five days in a week for eight weeks. Endurance group did jogging. Resistance group did push-up, pull-up and squats. Target heart rate during moderate intensity of activities was 64-76% of maximum heart rate. Heart rate measurement was done before the start of exercise and after five to seven minutes of exercise when it reached 64-76% of maximum heart rate. It was measured by pulse oximeter. Follow-up was done after eight weeks of exercise training in both the groups. Evaluation was done by comparing resting heart rate and CRP level before the start of training and after the completion of training programme. Statistical analysis was done using student t-test and paired t-test. Results: Mean age of subjects of group I was found to be higher (19.98±1.26 years) as compared to group II (19.97±0.98 years). Mean pre intervention BMI of both the groups was found to be similar (21.97±1.78 kg/m2). No statistically significant change in resting heart rate was found in both resistance group (p=0.096) and endurance group (p=0.326) after exercise training. Statistically significant increase in CRP was found in resistance group (p&lt;0.001) and endurance group (p&lt;0.001). The increment in CRP was more in endurance group (55.04%) than resistance group (35.34%). Conclusion: Short duration of exercises increase inflammation but no significant effect on resting heart rate was seen.

Resting heart rate is directly associated and maximal exercise-induced heart rate inversely associated with cardiovascular mortality, and therefore their difference might contain prognostic information from both variables. The comparative long-term prognostic values of maximal exercise-induced heart rate and of the difference between it and resting heart rate were studied in apparently healthy middle-aged men. Resting heart rate and maximal exercise-induced heart rate were measured, and their difference calculated, in 1960 apparently healthy men aged 40-59 years, and mortality was recorded over a period of 16 years. Conventional coronary risk factors were assessed at baseline. Both the difference between the two heart rates and the maximal exercise-induced heart rate were strongly, independently and inversely associated with cardiovascular mortality after adjustment for age, smoking, systolic blood pressure, lung function, glucose tolerance, serum cholesterol level, serum triglycerides level, physical fitness and exercise ECG findings. The adjusted relative risk of cardiovascular death in heart-rate difference quartiles 3 and 4 compared with that in quartile 1 (the lowest heart-rate difference quartile) was 0.54 (95% confidence interval 0.33-0.86; P = 0.009). The corresponding value for maximal exercise-induced heart rate was 0.56 (95% confidence interval 0.34-0.89; P = 0.018). Within the lowest heart-rate difference quartile, but not within the lowest maximal exercise-induced heart rate quartile, a further, strong, negative gradient in cardiovascular mortality was observed. In the high working capacity range, low heart-rate difference but not low maximal exercise-induced heart rate predicted very high cardiovascular disease mortality. Heart-rate difference and maximal exercise-induced heart rate were also inversely associated with non-cardiovascular disease mortality. Both heart-rate difference and maximal exercise-induced heart rate were strong, graded, long-term predictors of cardiovascular mortality among apparently healthy middle-aged men, independent of age, physical fitness and conventional coronary risk factors. However, low heart-rate difference was a better predictor than low maximal exercise-induced heart rate for recognizing individuals who were at particularly high risk of dying prematurely from cardiovascular diseases.

Coronary artery disease is the leading cause of morbidity and mortality around the world. Autonomic nervous system abnormalities are associated with coronary artery disease and its complications. Exercise stress tests are routinely used for the detection of the presence of coronary artery disease. In this study, we observed the association between heart rate profile during exercise and the severity of coronary artery disease. One hundred and sixty patients with abnormal exercise treadmill test (> or =1 mm horizontal or downsloping ST-segment depression; 119 men, 41 women; mean age = 57 +/- 9 years) were included in the study. Use of any drug affecting heart rate was not permitted. Resting heart rate before exercise, maximum heart rate during exercise, and resting heart rate after exercise (5 min later) were measured and two parameters were calculated: heart rate increment (maximum heart rate - resting heart rate before exercise) and heart rate decrement (maximum heart rate - resting heart rate after exercise). All patients underwent selective coronary angiography and subclassified into two groups according to stenotic lesion severity. Group 1 had at least 50% of stenotic lesion and group 2 had less than 50%. Patients in the first group had increased resting heart rate, decreased maximum heart rate, decreased heart rate increment, and decreased heart rate decrement compared with second group. All patients were classified into tertiles of resting heart rate, heart rate increment, and heart rate decrement level to evaluate whether these parameters were associated with severity of coronary artery stenosis in the study. The multiple-adjusted odds ratio of the risk of severe coronary atherosclerosis was 21.888 (95% confidence interval 6.983-68.606) for the highest tertile of resting heart rate level compared with the lowest tertile. In addition, the multiple-adjusted odds ratio of the risk of severe coronary atherosclerosis was 20.987 (95% confidence interval 6.635-66.387) for the lowest tertile of heart rate increment level compared with the highest tertile and 2.360 (95% confidence interval 1.004-5.544) for the lowest tertile of heart rate decrement level compared with the highest tertile. Altered autonomic nervous system regulation affects heart rate profile, increased resting heart rate, decreased heart rate increment, and decreased heart rate decrement, during exercise and this effect is strongly and independently associated with the severity of coronary artery disease.

Nordic walking versus walking without poles for rehabilitation with cardiovascular disease: Randomized controlled trial

In African-American (AA) adults, β-blockers (BB) have been reported to be less efficacious treating cardiac disease compared with whites (CAUC). This has been attributed to genetic polymorphisms of β-receptors. It is unknown if racial differences affect response to BB in pediatric patients with arrhythmias. AA and CAUC ≤ 18 years of age were included if they underwent treadmill stress testing while receiving metoprolol, atenolol, nadolol, or carvedilol. Patient demographics, resting heart rate (HR), maximum HR, and BB variables were collected. CAUC patients were matched on a 2:1 basis by age and sex to AA patients. Patients were blunted if HR was <90 % of maximum predicted HR for same-age patients on a modified Bruce protocol treadmill stress test. Long-term follow-up for breakthrough arrhythmias was documented. 78 patients were included (26 AA, 52 CAUC). No differences were noted in demographics, medication dose, BB or arrhythmia type, or baseline, maximal, or % HR change (p = not significant [NS]). On univariate analysis, fewer AA achieved a blunted HR during treadmill testing compared with CAUC (65 vs. 86%, p = 0.03). On multivariate analysis, AA were less likely to have an HR blunted by BB (OR 0.18, 95% confidence interval [CI] 0.04-0.75, p = 0.02) compared with CAUC. During the 1-year follow-up period, AA trended toward having one (58 vs. 40%, p = 0.14) or multiple instances (38 vs. 26%, p = 0.26) of breakthrough arrhythmia on cardiac Holter monitor testing. Race appears to affect the efficacy of BB therapy in pediatric patients with arrhythmias. Future studies to identify genetic polymorphisms in this patient subset are necessary.

The present study was conducted to determine the effects of 8-week aerobic and resistance training on body composition values of sedentary male individuals. A total of 30 healthy sedentary male subjects volunteered to participate in the study and were divided into two groups randomly: aerobic training group (n = 15, age = 34.0 ± 5.22 years), and resistance training group (n = 15, age = 34.2 ± 6.12). Body heights of the participants were measured and their body compositions body weight (BW), body mass index (BMI), basal metabolic rate (BMR), body fat percentage (BFP), body fat mass (BFM), lean body mass (LBM) were measured with bioelectric impedance analysis (BIA) device, and then evaluated. Their resting heart rates were determined, and maximum heart rates were calculated with the Karvonen formula. The Brzycki Equation was used to predict one-repetition maximum strength. There were statistically significant decreases in BW, BMI, BFP and BFM values of the aerobic training group (p&lt;0.05). There was no significant difference between pre- and post-test values of BMR and LBM (p&gt;0.05). BW and BMI values of the resistance training group did not show a significant difference in pre-test and post-test (p&gt;0.05). Significant decreases were found in BFP and BFM values (p&lt;0.05). The increase in BMR and LBM values were found to be statistically significant (p&lt;0.05). There were significant differences between BW, BMI, BMR, BFM and LBM values in the comparison of pre- and post-test values of the aerobic and resistance training groups (p&lt;0.05). However, there was no statistically significant difference in BFP (p&gt;0.05). In conclusion, it was found out that regular aerobic and resistance training caused positive effects on body composition of sedentary male individuals.

Heart rate recovery (HRR) during exercise testing is an independent predictor of prognosis. The relative predictive power of computational analysis of HRR as a function of resting and maximum heart rate (HR) compared with direct measurement of the drop in HR has not been determined. We aimed to improve on the prognostic value of HRR by the use of mathematical representations of HRR kinetics. In all, 2,193 patients who underwent exercise testing, coronary angiography, and clinical evaluation were followed up for 10.2 +/- 3.6 years. Mathematical functions were used to model HRR as a function of resting (HR(Rest)), maximum HR (HR(Peak)) and time (t): (a) HRR= HR(Rest) + (HR(peak) - HR(Rest)) X e(-kt) and (b) HRR= HR(Rest) + (HR(peak) - HR(Rest)) e(-kt2) Equation (b) provided the best fit of the recovery HR curve. An abnormal HRR at 2 min was a better predictor of mortality than HRR at 1, 3, or 5 min. At 2 min, HRR also predicted mortality better than computational models of HRR, relating HRR as a function of maximum and resting HRs. After adjusting for univariately significant predictors of mortality, HRR, age, exercise capacity, and maximum HR were chosen in order as the best predictors of mortality. Even though the computational models of HRR and the determination of HRR at different time intervals were significant predictors of mortality, the simple discrete measure of HRR at 2 min was the best predictor of mortality. At 2 min, HRR outperformed age, METs, and maximum exercise HR in predicting all-cause mortality.

There is a lack of randomized clinical trials (RCTs) exploring the outcomes of cardiopulmonary rehabilitation programmes (CPRPs) on submaximal aerobic capacity of long COVID-19 patients (LC19Ps). This RCT aimed to evaluate the effect of an ambulatory CPRP on the 6-min walk test (6MWT) data (main outcome: 6-min walk distance (6MWD)) of LC19Ps. Conducted as a single-blinded RCT, the study included Tunisian LC19Ps with persistent dyspnoea (i.e. modified medical research council (mMRC) level ≥2) at least three months postdiagnosis. LC19Ps were randomly assigned to the intervention (IG, n = 20) or control (CG, n = 10) groups. Pre- and post-CPRP evaluations included dyspnoea assessments (Borg and mMRC scales), anthropometric data, spirometry, and 6MWT. The CPRP (i.e. 18 sessions over six weeks) encompassed warm-up, aerobic training, resistance training, respiratory exercises, and therapeutic education. The CPRP significantly improved i) dyspnoea, i.e. IG exhibited larger reductions compared to the CG in Borg (-3.5 ± 2.0 vs. -1.3 ± 1.5) and mMRC (-1.5 ± 0.8 vs. -0.1 ± 0.3) scales, and ii) 6MWD, i.e. IG demonstrated larger improvements compared to the CG in 6MWD (m, %) (168 ± 99 vs. 5 ± 45 m, 28 ± 8 vs. 1 ± 8%, respectively), and resting heart rate (bpm, % maximal predicted heart rate) (-9 ± 9 vs. 1 ± 7 bpm; -5 ± 6 vs. 0 ± 4%, respectively), with small effect sizes. In the IG, the 1.5-point decrease in mMRC and the 168 m increase in 6MWD exceeded the recommended minimal clinical important differences of 1 point and 30 m, respectively. CPRP appears to be effective in enhancing the submaximal exercise capacity of LC19Ps, particularly in improving 6MWD, dyspnoea, and resting heart rate. RCT registration: www.pactr.org; PACTR202303849880222.

it is well known that athletes have a low resting heart rate, i.e., a resting bradycardia and heart rates below 30 beats/min have been reported ([7][1]). For example, Wikipedia states that the Tour de France cyclist, Miguel Indurain, had a resting heart rate of 28 beats/min when race fit. The

To assess the clinical significance of silent myocardial ischemia (SMI) in the elderly, 113 patients with stable angina who showed ischemic ST depression during treadmill stress testing were studied by dipyrimadole thallium imaging and coronary arteriography. They were divided into two groups: 44 patients with silent ST depressions and 69 patients with painful ST depressions. The groups were compared for scintigraphic and coronary arteriographic features as well as prognosis. There was a significantly greater proportion of older patients (> or = 65 years) in the group with SMI (64%) than in the group with painful ischemia (38%) (p < 0.01), although there was no difference in the mean ages of the two groups. The prevalence of multivessel coronary stenosis was not significantly different between the two groups (45% in the SMI group and 61% in the group with painful ischemia). Treadmill stress testing showed no differences in exercise duration, maximal heart rate, maximal systolic blood pressure, or maximal ST depression between the two groups. Dipyrimadamole thallium imaging revealed similar results in the site of reversible defects (RD), i.e. 76% in the anterior area and 24% in the inferior area in patients with SMI, and 83% in the anterior area and 17% in the inferior area in patients with painful ischemia. However, the size of RD was significantly smaller in patients with SMI, i.e. 14.6 +/- 6.1 segments in patients with SMI and 18.7 +/- 8.3 segments in patients with painful ischemia (p < 0.05). Although a significantly higher proportion of patients with painful ischemia (48%) underwent PTCA or CABG as their initial therapy as compared to those with SMI (16%), there was no significant difference in the cardiac event rate between the two groups initially treated medically. Among patients with stable angina, those with SMI may have a smaller amount of ischemic myocardium and may be older in a greater proportion than those with painful ischemia. Dipyrimadole thallium imaging is useful in the assessment of SMI in the elderly.

382 Effects of a 4-Months High-Intensity Interval Training Associated With Resistance Training Program on Cognitive Performance, Cerebral Oxygenation, Exercise Capacity and Cardiac Output in Middle-Aged Overweight Subjects: A Pilot Study

Aims/IntroductionHeart rate recovery (HRR) after exercise is considered to be a new index of autonomic dysfunction associated with cardiovascular disease and mortality. The present study aimed to investigate the risk factors of HRR and the effects of exercise on the abnormal HRR in type 2 diabetes.Materials and MethodsA total of 123 type 2 diabetes patients were recruited, and the oral glucose tolerance test and exercise test were carried out to analyze the risk factors associated with abnormal HRR. Among these patients, 42 patients with abnormal HRR were further randomized to either the conventional therapy group (CT group; n = 20) or the intensive therapy group (IT group; n = 22). The CT group patients underwent metformin and diet control, whereas the IT group additionally underwent a combined moderate intensity aerobic and resistance training three times per week for 12 weeks. The results of blood sample analysis and HRR were recorded before and after the training.ResultsAbnormal HRR was related to fasting blood glucose, glycosylated hemoglobin, low‐density lipoprotein cholesterol, and resting and maximum heart rates (P < 0.05 for both). After training, the IT group had significantly lower levels of fasting blood glucose, glycosylated hemoglobin and resting heart rate than the CT group (all P < 0.01 or P < 0.005). Significant improvement in HRR and metabolic equivalents was observed in the IT group compared with the CT group (P < 0.05).ConclusionsThese data suggested that combined aerobic and resistance training improved cardiac autonomic dysfunction as measured by HRR in type 2 diabetes patients. This might be due to better improvement of glycemic control, resting heart rate and physical fitness.

Patients with catecholaminergic polymorphic ventricular tachycardia (CPVT) are at risk for malignant ventricular arrhythmias during exercise and emotions which may lead to sudden cardiac death. Beta-blockers (BB) are the mainstay of therapy in patients with CPVT, but studies comparing the efficacy of different types of BB are scarce. Our objective was to determine the efficacy of different types of BB in reducing the ventricular arrhythmia (VA) severity on exercise stress test (EST) in patients with CPVT. Data was derived from the International CPVT Registry, a large retrospective cohort study. We included patients who had an EST before (pre-EST) and after start of BB (post-EST). We divided the cohort into five groups based on the first prescribed BB and compared pre-EST and post-EST. We included 428 patients (median age 18.5 [11.7–39.6] years, 240 (56.%) female), 155 (36.2%) probands) of whom 38 (8.9%) used atenolol, 131 (30.6%) bisoprolol, 82 (19.2%) metoprolol, 124 (29.0%) nadolol and 53 (12.4%) propranolol. Sex and history of aborted cardiac arrest were similar in all groups. The age at start of BB differed (p&amp;lt;0,001): patients using bisoprolol were oldest (35.0 [15.7–35.3]) while patients using propranolol were youngest (12.3 [8.8–24.9]). Median daily BB dose in mg/kg was: 1.0 [0.8–2.3] for atenolol, 0.06 [0.05–0.10] for bisoprolol, 0.9 [0.6–1.5] for metoprolol, 1.1 [0.9–1.6] for nadolol and 1.5 [1.1–2.8] for propranolol. Resting heart rate on pre-EST and post-EST was similar in all groups. Patients using metoprolol had a significantly higher maximum heart rate post-EST compared to nadolol and propranolol (161±18 vs 136±19 and 130±22 bpm, p=0,002 and p=0,001, respectively). The VA severity decreased significantly after BB (147 (37.9%) (non-sustained) ventricular tachycardia ((NS)VT) and 120 (30.9%) no or isolated ventricular premature beat (iVPB) pre-EST vs 46 (11.4%) (NS)VT and 184 (45.7%) iVPB post-EST, p&amp;lt;0,001). Examining the different groups, the VA severity decreased significantly after BB in all but atenolol (13 (40.6%) (NS)VT and 8 (25.0%) iVPB pre-EST vs 9 (25.0%) (NS)VT and 15 (41.7%) iVPB post-EST, p=0,103). Based on these results we conclude that all beta-blockers except atenolol are effective in reducing the VA severity on EST in patients with CPVT. Funding Acknowledgement Type of funding source: Public grant(s) – EU funding. Main funding source(s): E-Rare Joint Transnational Call for Proposals 2015 “Improving Diagnosis and Treatment of Catecholaminergic Polymorphic Ventricular Tachycardia: Integrating Clinical and Basic Science”

In patients with coronary artery disease, the target intensity-level of exercise training is usually based on a training heart rate that aims to be close to the upper level of metabolic aerobic exercise. We intended to evaluate whether a training heart rate calculated with the Karvonen formula after a conventional exercise test is comparable with the heart rate at the anaerobic threshold in patients after myocardial infarction treated with beta-blockers and if not to propose a new formula. In this multicenter prospective study, 115 consecutive beta-blocked patients recovering from myocardial infarction performed a cardiopulmonary exercise test to determine the anaerobic threshold. The training heart rate determined by the Karvonen formula was compared with the heart rate at the anaerobic threshold in a derivation sample (n=58) and a validation sample (n=57) of patients. The Karvonen training heart rate was significantly lower than the heart rate at the anaerobic threshold (91+/-5 versus 102+/-17 bpm, P<0.0001) in the first sample of patients and this difference was clinically relevant in 40% of patients. Thus, a 'modified Karvonen training heart rate', equal to 0.8xx(maximum heart rate-resting heart rate)+resting heart rate, was calculated by linear regression in the derivation sample and prospectively assessed in the validation sample. The modified Karvonen training heart rate was closer to the heart rate at the anaerobic threshold than the Karvonen training heart rate, and the difference between the modified Karvonen training heart rate and the heart rate at the anaerobic threshold was clinically relevant in only 5% of patients. The Karvonen formula underestimates the heart rate at the anaerobic threshold in beta-blocked patients, which may lead to undertraining of patients with coronary artery disease; we propose another formula more adapted to these patients.