Peak Exercise Heart Rate Research Articles

Exercise training enhances autonomic function after acute myocardial infarction: A randomized controlled study

IntroductionHeart rate recovery, defined as the fall in heart rate during the first minute after exercise, is an indicator of autonomic function, and has been found to be an independent predictor of mortality after acute myocardial infarction. Exercise training has several well-known benefits in terms of cardiorespiratory fitness, modifiable cardiovascular risk factors and prognosis after acute coronary events. However, there are no randomized controlled studies in the literature evaluating the effects of exercise training per se, controlling for changes in medication and diet, on heart rate recovery. Thus, this study aims to assess the effects of exercise training on autonomic function in coronary artery disease patients recovering from acute myocardial infarction. MethodsThirty-eight patients following a first acute myocardial infarction participated in this prospective randomized clinical trial. Patients were randomized into two groups: exercise training or control. The exercise group participated in an 8-week aerobic exercise program, while the control received standard medical care and follow-up. Changes in hemodynamics at rest and at peak exercise (heart rate, systolic and diastolic blood pressure, and rate pressure product), dietary intake, cardiorespiratory fitness, and heart rate recovery were assessed. ResultsMedication and diet remained unchanged in both groups during the study period. The exercise-training group improved resting hemodynamics, particularly resting heart rate (from 68.0±9.2 to 62.6±8.7bpm, p=0.030) and systolic blood pressure (from 135±7.1 to 125.6±11.3mmHg, p=0.012), cardiorespiratory fitness (from 30.8±7.8 to 33.9±8.3ml/min/kg, p=0.016), and heart rate recovery (from 20±6 to 24±5bpm, p=0.007). No significant changes were observed in the control group. ConclusionsExercise training improved autonomic function, assessed by heart rate recovery, resting heart rate and systolic blood pressure, in the absence of changes in diet or medication.

Exercise training enhances autonomic function after acute myocardial infarction: A randomized controlled study

IntroductionHeart rate recovery, defined as the fall in heart rate during the first minute after exercise, is an indicator of autonomic function, and has been found to be an independent predictor of mortality after acute myocardial infarction. Exercise training has several well-known benefits in terms of cardiorespiratory fitness, modifiable cardiovascular risk factors and prognosis after acute coronary events. However, there are no randomized controlled studies in the literature evaluating the effects of exercise training per se, controlling for changes in medication and diet, on heart rate recovery. Thus, this study aims to assess the effects of exercise training on autonomic function in coronary artery disease patients recovering from acute myocardial infarction. MethodsThirty-eight patients following a first acute myocardial infarction participated in this prospective randomized clinical trial. Patients were randomized into two groups: exercise training or control. The exercise group participated in an 8-week aerobic exercise program, while the control received standard medical care and follow-up. Changes in hemodynamics at rest and at peak exercise (heart rate, systolic and diastolic blood pressure, and rate pressure product), dietary intake, cardiorespiratory fitness, and heart rate recovery were assessed. ResultsMedication and diet remained unchanged in both groups during the study period. The exercise-training group improved resting hemodynamics, particularly resting heart rate (from 68.0±9.2 to 62.6±8.7bpm, p=0.030) and systolic blood pressure (from 135±7.1 to 125.6±11.3mmHg, p=0.012), cardiorespiratory fitness (from 30.8±7.8 to 33.9±8.3ml/min/kg, p=0.016), and heart rate recovery (from 20±6 to 24±5bpm, p=0.007). No significant changes were observed in the control group. ConclusionsExercise training improved autonomic function, assessed by heart rate recovery, resting heart rate and systolic blood pressure, in the absence of changes in diet or medication.

Exercise blood pressure response is related to asymmetric dimethylarginine and osteoprotegerin in hypertension

Emerging evidence suggests that emphasis should be shifted from the diagnostic to the prognostic perspective of treadmill exercise testing [1–5]. There is also a close association of a hypertensive response to exercise with endothelial dysfunction [6], accelerated carotid atherosclerosis [7], and left ventricular hypertrophy [8]. Focusing, on asymmetric dimethylarginine (ADMA) it has considerable cardiovascular effects mainly by modulating arterial resistance and structure in renal and systemic circulation [9–11] and its levels are increased in essential hypertension [12,13].Ontheotherhand,osteoprotegerin (OPG)represents a link between bone and vascular metabolism [14–16]. The aim of the present study was to explore the possible associations of a hypertensive response to exercise with ADMA and OPG levels in hypertension. The study population consisted of 420 non-diabetic consecutive males (all Caucasian) with untreated and uncomplicated stage I-II essential hypertension that were eligible for exercise treadmill testing [17]. Diagnosis of hypertension and ruling out of secondary forms of hypertensionwasdoneaccording to guidelines [18,19]. Exclusion criteria included atherosclerotic cardiovascular disease, valvular heart disease, fasting glucose N125 mg/dl, augmented serum creatinine concentration or overt proteinuria at the dipstick test and any other clinically significant systemic disease. We also excluded subjects with left bundle brunchblock, preexcitation syndromes, pacing rhythm, atrialfibrillation and signs of left ventricular hypertrophy or ischemic disease. Based on the exclusion criteria 304 essential hypertensives were selected. Office blood pressure measurement was performed according to guidelines [18,19] and ambulatory blood pressure was recorded as has been described in detail [20]. Study participants performed symptomlimited exercise testing according to the multistage Bruce protocol on a Quinton 5000 treadmill system (Quinton Instruments, Seattle, WA, USA) [21]. The highest systolic blood pressure value achieved during the exercise stress test was the peak exercise systolic blood pressure and accordingly a hypertensive response to exercise was defined as a peak exercise systolic blood pressure ≥210 mmHg, in line with the Framingham criteria [22] while reasons for exercise test termination have been previously described [23]. Significant differences were determined using the Student independent-samples t test or the chi-square test where appropriate. Correlation analyses were performed using the Pearson's correlation coefficient andmultiple regressionwas used to examine the independent predictors of peak systolic blood pressure. Statistical significance was set at pb0.05. From the initial population, 54 patients were excluded due to an ischemic response at the electrocardiogram or failure to achieve the age-predicted target heart rate, leaving a total of 250 subjects eligible for final analysis. Hypertensive patients with a hypertensive response to exercise were older, had higher body mass index, waist circumference, office and 24-h systolic blood pressure (Table 1), while exhibited greater ADMA and OPG levels (Table 2 and Fig. 1 upper and lower panel). Accounting for confounders, including age, body mass index, waist circumference, smoking status, office systolic/diastolic blood pressure, glucose and lipid levels did not abolish the significant difference in log ADMA and log OPG (pb0.05). The hypertensive response group exhibited lower peak exercise heart rate, attenuated total exercise time and more impaired exercise capacity (Table 3).

Exercise Heart Rate Acceleration Patterns during Atrial Fibrillation and Sinus Rhythm

Patients with atrial fibrillation sustain a significant lower exercise tolerance compared to those in sinus rhythm, even while seemingly in adequate rate-control. Exercise testing was performed during atrial fibrillation and after electric cardioversion for 30 patients who were initially treated with AV modifying agents and were considered in adequate rate control. Heart rate parameters were obtained during all exercise stages, and a graphic display of heart rate acceleration was obtained. For those patients who remained in sinus rhythm, an additional exercise test was performed after 1 month. During atrial fibrillation, heart rate at the completion of Bruce stage 1 and the peak exercise heart rate were significantly higher when compared to sinus rhythm (120 ± 10 bpm vs. 98 ± 11 bpm and 164 ± 16 bpm vs. 129 ± 11 bpm respectively, p < 0.001 for both). The time to peak exercise heart rate was significantly shorter during atrial fibrillation (3.5 ± 1 min vs. 6.5 ± 1.5 min, p < 0.001), and the total exercise duration was subsequently shorter as well (6 ± 2 min vs. 8.5 ± 2 min, p < 0.001). Treatment with beta-blockers prior to exercise did not affect the earlier peaking of the heart rate. After 1 month, similar time to peak heart rate and similar exercise performance were observed among patients, who remained in sinus rhythm, when compared to to the post-cardioversion exercise test. In patients with atrial fibrillation, exercise heart rate acceleration displays a specific pattern of early peaking. Earlier heart rate peaking occurs regardless of ample rate control while at rest or mild physical activity and contributes to overall lower exercise performance.

Traditional Cardiovascular Disease Risk Factors Related to Heart Rate Responses at the Onset of Exercise

The standard exercise treadmill test (ETT) is known to be one of the most powerful, noninvasive tools for risk stratifying patients with or suspected of having cardiovascular disease (CVD). However, controversy exists regarding the heart rate (HR) profile in early exercise and its association with mortality in asymptomatic adults. Peak and post exercise HR responses are well known, but to determine clinical utility, HR responses at the onset of exercise in apparently healthy men and women must be better understood. PURPOSE: To identify the HR increase profile and determine the association of traditional CVD risk factors with an absolute change in HR at one minute and one-third (1/3) total exercise time in apparently healthy adults. METHODS: Retrospective examination of a symptom-limited maximal ETT was performed for asymptomatic, self-referred adult participants of a university-based fitness program between 1990-2006. Records were analyzed for HR responses from individuals (N=947) of both sexes representing a broad range of age and fitness levels (11-78 yrs; VO2peak: 16.5 to 49.4 ml·kg-1·min-1). The HR response of the BSU/Bruce ramp protocol was identified. The association of traditional CVD risk factors with absolute changes in HR at minute one and 1/3 of total exercise time from pre-test standing HR were identified. RESULTS: The mean HR increase at minute one was 18.4±9.1 and 22.9±10.9 beats (25th to 75th percentile range 13 to 26 beats) for men and women respectively (p<0.05). The mean HR increase at 1/3 total exercise time was 32.8±10.4 and 34.8±10.1 beats for men and women respectively (p<0.05). A significantly better CVD risk factor profile (lower systolic and diastolic BP, BMI, total cholesterol, triglycerides, higher VO2peak, and regular exercise) was associated with less of an increase in HR at minute one than a greater increase in HR, despite consisting of a greater percentage of current smokers. However, no significant difference in CVD risk factor profiles existed at 1/3 total exercise time. CONCLUSIONS: A lower HR increase at minute one of exercise was significantly associated with a better CVD risk factor profile but the same differences were not seen at 1/3 total exercise time. These data suggest a greater parasympathetic influence at the onset of exercise may be protective in an asymptomatic population.

Exercise Testing Identifies Patients at Increased Risk for Morbidity and Mortality Following Fontan Surgery

The objective of this study was to examine the relationship between exercise test data and mortality in patients who have had the Fontan procedure. The study was designed as a retrospective cohort study. The study was set in a tertiary care center. All study participants were Fontan patients ≥16 years old who had cardiopulmonary exercise tests at our institution between November 2002 and March 2010. The first exercise test with adequate effort during the study period was retained for analysis. We enrolled 146 patients at a median age of 21.5 years (16.0-51.6); 15.8 years (1.2-29.9) after Fontan surgery. The outcome measures were exercise test data (peak oxygen consumption, peak heart rate, etc.); mortality. Peak oxygen consumption averaged 21.2 ± 6.2 mL/kg/min, 57.1 ± 14.1% predicted. Follow-up data were collected 4.0 ± 2.0 years (range 0.3-7.7) after the exercise test. Sixteen patients (11%) died during follow-up; their peak oxygen consumption (16.3 ± 4.0 mL/kg/min) was significantly less than the survivors' (21.8 ± 6.2 mL/kg/min; P < .0001). Recursive partitioning and Cox proportional hazards modeling revealed that the hazard for death for patients with a peak oxygen consumption of <16.6 mL/kg/min was 7.5 (95% confidence interval: 2.6, 21.6; P < .0002) times that of patients with a higher peak oxygen consumption. Similarly, the hazard ratio for patients with peak-exercise heart rates of <122.5 bpm was 10.6 (3.0, 37.1; 0 < 0.0002). Data from exercise tests could also identify patients at increased risk for a combined morbidity/mortality end point. In adults with Fontan surgery, exercise test data can identify patients at increased risk of midterm morbidity and mortality.

Prognosis in patients achieving ≥10 METS on exercise stress testing: Was SPECT imaging useful?

BackgroundThe benefit of myocardial perfusion imaging (MPI) over exercise ECG stress testing alone is unclear in individuals attaining a workload of ≥10 METS. The purpose of this prospective study is to determine mortality and nonfatal cardiac events in patients at either intermediate pretest risk for CAD or patients with known CAD, achieving ≥10 METS regardless of peak exercise heart rate. The authors previously reported a low prevalence of significant ischemia in this patient cohort. MethodsBaseline characteristics, ECG stress test findings, and perfusion and function results from quantitative gated 99mTc-SPECT MPI were compared by achievement of a maximum age-predicted heart rate ≥85% in 509 consecutive patients who reached ≥10 METS. Events including all-cause and cardiac mortality, non-fatal myocardial infarction (MI), and late revascularization (>4 weeks after MPI) were prospectively collected. ResultsOf the 509 patients achieving ≥10 METS, follow-up for mortality was obtained in 463 (91%). Those lost to follow-up were older and had higher rates of tobacco use. The prevalences of CAD risk factors, prior known CAD, and MPI abnormalities were higher for the 68 patients failing to reach 85% of their target heart rate. The rate of ≥10% left-ventricular (LV) ischemia by MPI remained very low irrespective of attained heart rate (0.6% (3/463)). Six (1.2%) had an LVEF < 40%. Death occurred in 12 (2.6%) patients, one of which was classified as cardiac (0.1%/year). The other 11 deaths were related to cancer. Additionally, there were three nonfatal MIs (0.7 %) and one late revascularization (0.2%). Only one of these patients had any ischemia on MPI. No cardiac event patient had exercise ST depression or ≥5% LV ischemia. ConclusionsThus, patients at intermediate risk for CAD or known CAD achieving ≥10 METS have a very low prevalence of ≥10% LV ischemia and very low rates of cardiac mortality, nonfatal MI, and late revascularization, irrespective of heart rate achieved. Cardiac events did not correlate with abnormalities on the index MPI study. These results suggest that patients who attain ≥10 METS during exercise stress have an excellent prognosis over an intermediate term of follow-up, regardless of peak exercise heart rate achieved. The added value of MPI to standard exercise ECG testing in this population is questionable.

Exercise Testing and Training in Children With Congenital Heart Disease

The primary function of the cardiopulmonary system is to provide blood flow (and oxygen) in quantities sufficient to support the metabolic needs of the body. The capacity of the cardiopulmonary system to fulfill this function is maximally stressed when an individual's metabolic rate is increased, a condition that occurs most commonly during physical activity/exercise. A number of physiological changes accompany and facilitate the accommodation of the circulatory system to the hemodynamic demands of exercise (Figure 1). In normal individuals, these changes (which during upright exercise include a tripling of the resting heart rate, a >60% reduction in systemic and pulmonary vascular resistance, and a >50% increase in stroke volume) can ultimately produce a >5-fold increase in cardiac output. The increase in cardiac output is accompanied by enhanced ventricular preload (as the ventricles move up their Starling curves to accommodate the increased workload), a doubling of systolic and mean pulmonary artery pressures (most of the increase in pulmonary artery pressures is due to the concomitant rise in left-sided filling pressures; the increase in transpulmonary pressure gradient is relatively small), and a more modest increase in systemic arterial pressures.1,–,4 Figure 1. Some of the physiological changes that accompany and facilitate the accommodation of the circulatory system to the hemodynamic demands of exercise. RAp indicates right atrial pressure; LAp, left atrial pressure; PVR, pulmonary vascular resistance; SVR, systemic vascular resistance; PAp, pulmonary artery pressure; and AOp, aortic pressure. Congenital heart disease (CHD) may, in a variety of ways and to a variable extent, adversely affect these hemodynamic adaptations. For instance, patients with a Fontan procedure lack a pulmonary ventricle. They therefore cannot increase their pulmonary blood flow and pressures normally (and consequently cannot maintain their ventricular preload and systemic blood flow) during exercise.5 Patients with tetralogy of Fallot and …

Platelet reactivity in diabetic patients subjected to acute exercise stress test

Previous studies have reported ambiguous results regarding the effect of acute exercise on platelet reactivity in healthy and cardiac patients. We aimed to assess platelet reactivity among diabetic patients before and immediately after an acute exercise stress test. Patients (controls: mean age 53.1 ± 12.1 years; four males; body mass index 27.0 ± 5.7 kg/m(2); HbA(1c) 6.0 ± 1.1%, n = 8) and diabetic patients (52.9 ± 11.3; six males; body mass index 30.7 ± 2.2 kg/m(2); HbA(1c) 7.8 ± 1.7%, n = 8) referred for diagnostic nuclear exercise stress test were recruited. Blood samples obtained at rest and immediately post-exercise were stimulated with adenosine diphosphate (ADP), collagen and arachidonic acid. Expression of CD41 (pan-platelet marker) and CD62p (platelet stimulation marker) were measured by flow cytometry. Aspirin responsiveness was measured using VerifyNow. Although peak systolic blood pressure was significantly higher in the diabetics compared with nondiabetics (186.3 ± 25.4 vs. 157.1 ± 19.1, respectively, P = .028), peak exercise heart rate was similar (156.5 ± 8.3 vs. 155.5 ± 12.1 for diabetics and nondiabetics, respectively). No differences were observed between groups for aspirin resistance. Platelet stimulation with ADP exhibited significantly lower CD62p-positive cell population (%) in the diabetic patients both prior to and following the exercise stress test (P = .03). In addition, although not significant, platelet stimulation was higher post-exercise in the diabetic patients (6.3 ± 4.7% vs. 12.0 ± 5.6%, for pre- and post-exercise, respectively, P = .2) with no difference in controls (9.2 ± 5.5% vs. 8.9 ± 5.9%). Platelet stimulation in diabetic patients is blunted and might be explained by the prolonged exposure of platelets to multiple diabetic risk factors.

Physiological Demands of an Intermittent Futsal-Oriented High-Intensity Test

The aim of this study was to provide evidence for specific physiological demands of a futsal time-motion analysis devised progressive and intermittent shuttle-running test (futsal intermittent endurance test [FIET]). Eighteen full-time professional futsal players (age 20.6 +/- 3.1 years, body mass 71.6 +/- 8.5 kg, height 175 +/- 7.9 cm) volunteered to participate in this study. In a random order and on separate days, they performed the FIET and a treadmill test (TM) to assess aerobic fitness. Physiological demands were examined by monitoring exercise heart rates (HRs), O2, and blood-lactate concentration (BLac) during FIET and TM conditions. During the FIET, players covered 1,464 +/- 136 m attaining a mean speed at exhaustion of 16.5 +/- 0.6 km h. The mean FIET duration was of 13.24 +/- 1.13 minutes. Peak O2, HR, and BLac were 95 +/- 6.4, 99 +/- 2, and 108 +/- 25% of treadmill O2max, HRmax, and BLac, respectively. Large correlations were found between speed at ventilatory threshold and maximal speed at O2max with FIET performance (r = 0.60 and 0.61, p < 0.01, respectively). Peak O2 during the FIET was significantly lower than O2max. Although there was no mean difference between peak exercise HR in the TM and FIET conditions, significant intraindividual bias was evident. This study showed that FIET heavily stresses both the aerobic and anaerobic energy systems to a level that is similar to what was reported in futsal game play. Coaches may use the FIET to examine futsal players' ability to cope with intermittent high-intensity exercise. It is suggested that the highest HR found during the FIET should be regarded as peak HR and not as individual HRmax.

Characteristics of Exercise‐Induced Intrapulmonary Arteriovenous Fistula in Patients with Unexplained Exertional Dyspnea

Dynamic appearance of intrapulmonary arteriovenous fistula (AVF) during exercise may be associated with unexplained exertional dyspnea (UED) and can be diagnosed with an agitated saline contrast study during exercise echocardiography. However, the occurrence of AVF during exercise in patients with UED has not been well described. Thus, the frequency of exercise-induced intrapulmonary AVF in the outpatients with UED was retrospectively analyzed. Thirty-nine outpatients (age: 53 ± 12, 33 female) with UED underwent symptom-limited supine bicycle exercise echocardiography. Ten patients (26%) developed exercise-induced intrapulmonary AVF. Patients with and without AVF showed the similar peak exercise heart rate, systolic blood pressure, and rate-pressure product. The patients with AVF demonstrated a small but significant decrease in arterial oxygen saturation with exercise as compare to baseline (95.6 ± 2.8% at peak, vs. 97.5 ± 2.5% at baseline, P < 0.05 with a paired Student t-test). Our study suggests that exercise-induced intrapulmonary AVF is relatively common in the outpatients with UED and associated with mild exercise desaturation; however, the mechanism of desaturation could not be determined by this study. Further investigation to characterize and determine the clinical significance of AVF is warranted.

Platelet Reactivity in Diabetic Patients Subjected to Acute Exercise Stress Test

Background: Previous studies reported ambiguous results about the effect of acute exercise on platelet reactivity (PR) in healthy and cardiac patients. Aim: To assess PR among diabetic patients before and immediately after an acute exercise stress test (EST). METHODS: Patients (controls: mean age 53.1±12.1yr; 4M; BMI 27.0±5.7kg/m2; HbA1c 6.0±1.1%, n=8) and diabetic patients (52.9±11.3; 6M; BMI 30.7±2.2kg/m2; HbA1c 7.8±1.7%, n=8) referred for diagnostic nuclear EST were recruited. Blood samples obtained at rest and immediately post exercise were stimulated with ADP, collagen, and arachidonic acid. Expression of CD41 (pan platelet marker) and CD62p (platelet activation marker) were measured by flow cytometry. Aspirin responsiveness was measured using VerifyNow. RESULTS: Though peak systolic blood pressure was significantly higher in the diabetics compared with controls (186.3±25.4 vs. 157.1±19.1, p=0.028), peak exercise heart rate was similar (155.5±12.1 vs. 156.5±8.3 for controls and diabetics). No differences were observed among groups for aspirin resistance. Platelet stimulation with ADP exhibited significantly lower CD62p positive cell population (%) in the diabetic patients both prior to and following EST, p=0.03 (figure). In addition, though not significant, platelet stimulation was higher post exercise in the diabetic patients (6.3±4.7% vs. 12.0±5.6%, for pre and post exercise, respectively, p=0.2) with no difference in controls (9.2±5.5% vs. 8.9±5.9%). CONCLUSION: PR in diabetic patients is blunted and not affected by acute exercise, probably due to prolonged exposure of platelets to multiple diabetic risk factors.Figure: No caption provided.

Three-month exercise and weight loss program improves heart rate recovery in obese persons along with cardiopulmonary function

Heart rate recovery (HRR) after exercise is an independent risk factor for cardiovascular disease and mortality, and it is well known to be modifiable by weight loss. We investigated whether HRR was mainly improved by better cardiopulmonary function or by alteration of the metabolic profile. The weight loss program included 2h of group exercise per week and individual dietary instruction by a qualified dietician every week. Clinical assessment (including HRR) was done before and after the 3-month program. The subjects were 125 obese persons without a past history of stroke, cardiovascular events, or use of medications who participated in and completed our exercise plus weight loss program. HRR (35.61+/-12.83 to 45.34+/-13.6 beats/min, p<0.0001) was significantly faster after the program. The change in HRR was significantly correlated (p<0.05) with the changes in body weight, body mass index, percent body fat, waist circumference, hip circumference, resting heart rate, peak exercise heart rate, exercise time, maximal work load, physical working capacity divided by body weight (PWC75%HRmax/weight), subcutaneous fat area, visceral fat area, low-density lipoprotein cholesterol, and leptin. Multivariate analysis showed that the change in HRR was significantly correlated (p<0.05) with the changes in resting heart rate, peak exercise heart rate, and PWC75%HRmax/weight. Our data demonstrated that HRR can be improved in obese subjects by a 3-month exercise and weight loss program. Improvement in cardiopulmonary function by exercise seems to be the main contributor to the increment of HRR.

A Preliminary Study of Subsymptom Threshold Exercise Training for Refractory Post-Concussion Syndrome

To evaluate the safety and effectiveness of subsymptom threshold exercise training for the treatment of post-concussion syndrome (PCS). Prospective case series. University Sports Medicine Concussion Clinic. Twelve refractory patients with PCS (6 athletes and 6 nonathletes). Treadmill test to symptom exacerbation threshold (ST) before and after 2 to 3 weeks of baseline. Subjects then exercised 5 to 6 days per week at 80% ST heart rate (HR) until voluntary peak exertion without symptom exacerbation. Treadmill testing was repeated every 3 weeks. Adverse reactions to exercise, PCS symptoms, HR, systolic blood pressure (SBP), achievement of maximal exertion, and return to work/sport. Pretreatment, ST occurred at low exercise HR (147 + or - 27 bpm) and SBP (142 + or - 6 mm Hg). After treatment, subjects exercised longer (9.75 + or - 6.38 minutes to 18.67 + or - 2.53 minutes, P = .001) and achieved peak HR (179 + or - 17 bpm) and SBP (156 + or - 13 mm Hg), both P < .001 versus pretreatment, without symptom exacerbation. Time series analysis showed significant change in rate of symptom reduction for all subjects and reduced mean symptom number in 8/11. Rate of PCS symptom improvement was related to peak exercise HR (r = -0.55, P = .04). Athletes recovered faster than nonathletes (25 + or - 8.7 vs 74.8 + or - 27.2 days, P = .01). No adverse events were reported. Athletes returned to sport and nonathletes to work. Treatment with controlled exercise is a safe program that appears to improve PCS symptoms when compared with a no-treatment baseline. A randomized controlled study is warranted.

Impaired Heart Rate Recovery and Chronotropic Incompetence in Patients With Heart Failure With Preserved Ejection Fraction

This study assessed the chronotropic response to exercise and heart rate (HR) recovery after exercise in a carefully phenotyped group of patients with heart failure with preserved left ventricular ejection fraction (HfpEF) and a control group of similar age and gender distribution. We studied 41 patients with HfpEF, 41 healthy controls, and 16 hypertensive controls. None were taking HR-limiting medications. All study participants had clinical examination, 12-lead ECG, pulmonary function test, echocardiogram, and metabolic exercise test with HR monitoring throughout exercise. Chronotropic response was measured by the percentage of the HR reserve used during maximal exercise and the peak exercise HR as a percentage of predicted maximal HR. Patients with HfpEF were generally women (70%), overweight, aged 69+/-8 years. Controls were of similar gender (63%) and age (67+/-6 years). Patients with HfpEF had significantly reduced peak VO(2) compared with controls (20+/-4 mL kg(-1) min(-1) versus 31+/-6 mL kg(-1) min(-1), P<0.001) and greater minute ventilation-carbon dioxide production relationship (V(E)/V(CO2)) slope) (33+/-6 versus 29+/-4, P<0.001). Chronotropic incompetence was significantly more common in patients with HfpEF compared with matched healthy controls as measured by the percentage of the HR reserve used during maximal exercise (63% versus 2%, <0.001) and percentage of predicted maximal HR (34% versus 2%, <0.001). In addition, abnormal HR recovery 1-minute after exercise (defined as the reduction in the HR from peak exercise 1-minute after exercise) was also significantly more common in patients with HfpEF compared with controls (23% versus 2%, P=0.01). Hypertensive controls showed similar chronotropic response to peak exercise and HR recovery after exercise as healthy controls. Patients with HfpEF have impaired chronotropic incompetence during maximal exercise and abnormal HR recovery after exercise.

Exercise Echocardiography in Cryopreserved Aortic Homografts: Comparison of a Prototype Stentless, a Stented Bioprosthesis, and Native Aortic Valves

Aortic valve replacement with a cryopreserved aortic homograft (CH) is an attractive alternative to bioprosthesis implantation. The aim of the study was to compare the hemodynamic performance of CH implanted with aortic root inclusion compared to prototype stentless (SS) bioprosthesis, standard stented (SD) bioprosthesis, and a native aortic valve. Hemodynamics and Doppler echocardiographic measurements such as left ventricular ejection fraction, aortic valve orifice area index (AVOAI), mean and maximal transvalvular gradients, were obtained at rest and immediately after exercise in 28 patients after aortic valve replacement with CH (n = 10), SS (n = 9), or SD (n = 9), and in a control group (CG) of 15 normal volunteers. Rest and peak exercise heart rate and workload achieved were not different among the groups. Baseline AVOAI was larger for CH and CG compared to SS and SD groups (P < 0.05). Maximal and mean transvalvular pressure gradients at rest were lower for CH compared to SS and SD groups (P < 0.05), but higher than CG (P < 0,05). Implanted aortic CH had better hemodynamic performance than SS and SD bioprosthesis and similar to native normal aortic valves, both at rest and immediately after exercise.

Adjuvant Trastuzumab Induces Ventricular Remodeling Despite Aerobic Exercise Training

To examine the effect of aerobic training in mitigating trastuzumab-mediated left ventricular (LV) remodeling in women with human epidermal growth factor receptor 2 (HER2)-positive breast cancer. Seventeen women (53 +/- 7 years) with HER2-positive breast cancer did aerobic training during the first 4 months of adjuvant trastuzumab. Peak oxygen consumption and magnetic resonance imaging assessment of LV volumes, mass, and rest and peak (dobutamine stress) ejection fraction were assessed before and after 4 months of trastuzumab. Participants attended 59% +/- 32% of prescribed exercise sessions at 78% +/- 6% of peak heart rate. Peak exercise heart rate, systolic and diastolic blood pressure, power output, and oxygen consumption were not different after training (all P-values > 0.05). Exercise adherence predicted change in peak oxygen consumption (r = 0.77; P = 0.000). Resting end-diastolic (pre: 120 +/- 23 mL versus post: 133 +/- 16 mL) and end-systolic volumes (pre: 44 +/- 12 mL versus post: 55 +/- 11 mL) and mass (pre: 108 +/- 21 g versus post: 114 +/- 18 g) increased, whereas ejection fraction (pre: 64% +/- 4% versus post: 59% +/- 4%) decreased from baseline to post-intervention (all P-values < 0.05). Peak ejection fraction was lower after 4 months (pre: 79 +/- 4 versus post: 76 +/- 6%; P = 0.087). Initiation of adjuvant trastuzumab therapy is associated with LV cavity dilation and reduced ejection fraction despite aerobic exercise training. The long-term consequences of trastuzumab-induced LV remodeling and the means to prevent LV dysfunction require further study.

Norepinephrine and cardiovascular responses to maximal exercise in Parkinson's disease on and off medication

The aim of this experiment is to understand how Parkinson's disease (PD) medication affects the autonomic responses of individuals during an acute exercise stress test. Fourteen people with PD and fifteen healthy individuals age-matched between 50 and 80 years performed a modified Bruce protocol. Subjects with PD performed the test once off medication (PD-off) and then 1 week later on medication (PD-on). Heart rate (HR), blood pressure (BP), VO(2), and norepinephrine (NE) levels were taken at rest and at peak exercise. At peak exercise HR, BP, and NE values for the PD-on and PD-off group were all significantly lower than healthy controls, regardless of whether subjects were on their medication. Autonomic abnormalities during exercise in this population appear to be disease manifested and not impacted by medications used to treat PD. We can assume, both on and off medication, this population will show markedly lower BP, HR, and NE responses.

The Role of Mood Disorders in Exercise-Induced Cardiovascular Reactivity

Increased cardiovascular (CV) reactivity has been associated with worse CV prognosis. Though mood disorders (MDs) have been associated with increased CV reactivity during behavioral stressors, the extent to which MDs and their interaction with coronary heart disease (CHD) influences exercise-induced CV reactivity has not been evaluated. Five hundred twenty-six patients underwent nuclear exercise stress testing. Cardiovascular parameters were assessed at rest, every 2 minutes during exercise, and at peak exercise. MDs were measured using a structured psychiatric interview, the Primary Care Evaluation of Mental Disorders, and CHD was defined as having a history of myocardial infarction, revascularization, heart failure, and/or cerebrovascular event. CHD patients exhibited lower peak exercise heart rate (F = 9.40, p = .002) compared with patients without CHD. Submaximal data showed that patients with CHD had a slower rate of increase of heart rate (F = 4.29, p = .04) and diastolic blood pressure (F = 3.27, p = .04). There was an interaction of CHD and MDs, indicating that in patients with CHD, the rate of submaximal increase in systolic blood pressure (F = 3.08, p = .047) and rate-pressure product (F = 5.13, p = .006) was greater in patients with a MD compared with those without a MD. These differences were not observed in patients with no CHD. No other main or interaction effects of MDs and CHD were observed. Though MDs alone do not seem to be associated with higher levels of stress CV reactivity, their combination with CHD leads to increased submaximal exercise-induced CV reactivity. Prospective studies are needed to explore the causal relationship between these variables.

Heart rate recovery and prognosis in heart failure patients

The aim of this study is to evaluate the usefulness of heart rate recovery (HRRec) for assessing risk of death in heart failure (HF) patients. Echocardiographic and clinical exercise data were analyzed retrospectively on 712 HF patients (EF < or = 45%). HRRec was calculated as peak exercise heart rate - heart rate at 1 min of active recovery. Patients were followed for all-cause mortality (5.9 +/- 3.3 years follow-up). Groups were identified according to HRRec: group-1 (HRR < or = 4 bpm), group-2 (5 < or = HRR < or = 9 bpm), and group-3 (HRR > or = 10). Kaplan-Meier analysis estimated survival of 91, 64, and 43% (group-1); 94, 76, and 63% (group-2); and 92, 82, and 70% (group-3) at 1, 5, and 10 years, respectively. Ranked HRRec independently predicted mortality after adjusting for age, gender, NYHA class, LVEF and BMI, but was not independent of exercise time, peak V(O)(2) and V(E)/V(CO)(2) at nadir. HRRec is a useful prognostic marker in patients with HF, particularly when gas exchange measures are not available.