Effect of physical training on quality of life and oxygen consumption in patients with congestive heart failure. The effects of exercise training on fatigue and dyspnea in heart failure. Heart failure and a controlled trial investigating outcomes of exercise training (HF-ACTION): design and rationale. Exercise capacity, physical activity patterns and outcomes six years after cardiac rehabilitation in patients with heart failure. Effects on quality of life, symptoms and daily activity 6 months after termination of an exercise training programme in heart failure patients. Effects of exercise training in patients with heart failure: the Exercise Rehabilitation Trial (EXERT). Exercise training in patients with heart failure. A randomized, controlled trial. Effects of exercise training on peak performance and quality of life in congestive heart failure patients. Antiremodeling effect of long-term exercise training in patients with stable chronic heart failure: results of the Exercise in Left Ventricular Dysfunction and Chronic Heart Failure (ELVD-CHF) Trial. Effects of a home-based exercise program on clinical outcomes in heart failure. Anti-inflammatory effects of exercise training in the skeletal muscle of patients with chronic heart failure. Randomised controlled trial of cardiac rehabilitation in elderly patients with heart failure. Regular physical exercise corrects endothelial dysfunction and improves exercise capacity in patients with chronic heart failure. Quality of life, psychological and physiological changes following exercise training in patients with chronic heart failure. Physical training in patients with chronic heart failure of ischemic origin: effect on exercise capacity and left ventricular remodeling. Physical training in patients with stable chronic heart failure: effects on cardiorespiratory fitness and ultrastructural abnormalities of leg muscles. Effects of exercise training on left ventricular function and peripheral resistance in patients with chronic heart failure: A randomized trial. Aerobic training decreases B-type natriuretic peptide expression and adrenergic activation in patients with heart failure. Randomized, controlled trial of long-term moderate exercise training in chronic heart failure: effects on functional capacity, quality of life, and clinical outcome.
To assess changes in quality of life (QoL) and oxygen consumption produced by two different patterns of physical training in patients with congestive heart failure (CHF).
                42 men (mean age 55.9+/-8.1 years) with ischaemic CHF lasting 3.1+/-1.0 years. Patients were randomised into three groups each consisting of 14 men: group A--with constant workload, group B-with progressive/increasing workload, each trained up to 6 months and group C--not trained. QoL was assessed at baseline and at 6 months by means of the Psychological General Well-being Index (PGWB) and the Subjective Symptoms Assessment Profile (SSA-P). Cardiopulmonary exercise test and echocardiography were performed twice.
                At 6 months improvement in PGWB total index was observed, both in groups A and B (p<0.01). Men from groups A and B reported less cardiac symptoms (p<0.01), emotional distress (p<0.01), peripheral circulatory symptoms (p<0.01) and dizziness (p<0.01) in SSA-P. Improvement in sexual life was observed only in group B (p<0.01). Overall improvement of QoL was greater in group B than in group A as well as oxygen uptake (p<0.01). Higher QoL correlated positively with peak VO2 only in group B (r=0.56, p<0.05).
                Physical training improves QoL in men with CHF, but only progressive/increasing workload seems to markedly improve oxygen uptake. Improvement of QoL is related to psychological well-being and physical complaints associated with CHF. Physiological benefits of exercise training for heart failure (HF) patients have been demonstrated, however little is known about the effects of training on the symptoms of fatigue and dyspnea.
                The purpose of this study was to examine HF symptoms of fatigue and dyspnea in response to a 24-week exercise training intervention.
                This pilot study was a randomized, two-group repeated measures design. Fifteen subjects in the intervention group completed a combination of aerobic and resistance training three times per week in a standard cardiac rehabilitation setting. The control group consisted of 6 subjects who were instructed not to begin any formal exercise program during the 24-week intervention.
                Subjects (19 males and 2 females) had a mean age of 66.2+/-10.2 years and mean ejection fraction (EF) of 28.4+/-7.4%. Non-parametric Friedman Analysis of Variance by Ranks showed the exercise group significantly decreased sensory fatigue (Piper Fatigue Scale) over time (chi(2)=6.49, p=.04) while the control group did not change (chi(2)=0.93, p=.63). Dyspnea showed a non-significant decrease over time for the exercise group (chi(2)=4.16, p=.13) while the control group showed a decrease from baseline to 12 weeks but an increase to above baseline values by week 24 (chi(2)=0.18, p=.91).
                These results provide support for the beneficial effects of exercise training on symptoms of fatigue and dyspnea in HF patients. Larger studies to evaluate symptom response to exercise are needed. Although there are limited clinical data to support the use of exercise training as a means to reduce mortality and morbidity in patients with heart failure, current guidelines state that exercise is beneficial.
                The objective of this trial is to determine whether exercise training reduces all-cause mortality or all-cause hospitalization for patients with left ventricular systolic dysfunction and heart failure symptoms. After undergoing baseline assessments to determine whether they can safely exercise, patients are randomized to either usual care or exercise training. Patients in the exercise training arm attend 36 supervised facility-based exercise training sessions. Exercise modalities are cycling or walking. After completing 18 sessions, patients initiate home-based exercise and then transition to solely home-based exercise after completing all 36 sessions. Patients return for facility-based training every 3 months to reinforce their exercise training program. Patients are followed for up to 4 years. Physiologic, quality-of-life, and economic end points that characterize the effect of exercise training in this patient population will be measured at baseline and at intervals throughout the trial. Blood samples will be collected to examine biomarkers such as brain natriuretic peptide, tumor necrosis factor, and C-reactive protein.
                Because of its relatively low cost, high availability, and ease of use, exercise training is an intervention that could be accessible to most patients with heart failure. The HF-ACTION trial is designed to definitively assess the effect of exercise training on the clinically relevant end points of mortality, hospitalization, and quality of life in patients with heart failure. To determine the short- and long-term effects of an intensive, concentrated rehabilitation programme in patients with chronic heart failure.
                Randomized controlled trial, with one-month and six-year evaluations.
                Residential rehabilitation centre in Switzerland.
                Fifty patients with chronic heart failure, randomized to exercise or control groups.
                A rehabilitation programme lasting one month, including educational sessions, a low-fat diet, and 2 hours of individually prescribed exercise daily.
                Exercise test responses, health outcomes and physical activity patterns.
                Peak Vo(2) increased 21.4% in the exercise group during the rehabilitation programme (P<0.05), whereas peak Vo(2) did not change among controls. After the six-year follow-up period, peak Vo(2) was only slightly higher than that at baseline in the trained group (7%, NS), while peak Vo(2) among controls was unchanged. During long-term follow-up, 9 and 12 patients died in the exercise and control groups, respectively (P = 0.63). At six years, physical activity patterns tended to be higher in the exercise group; the mean energy expenditure values over the last year were 2,704 +/- 1,970 and 2,085 +/- 1,522 kcal/week during recreational activities for the exercise and control groups, respectively. However, both groups were more active compared to energy expenditure prior to their cardiac event (P<0.001).
                Six years after participation in a residential rehabilitation programme, patients with chronic heart failure had slightly better outcomes than control subjects, maintained exercise capacity and engaged in activities that exceed the minimal amount recommended by guidelines for cardiovascular health. Exercise training in heart failure patients improves exercise capacity, physical function, and quality-of-life. Prior studies indicate a rapid loss of these effects following termination of the training. We wanted to assess any sustained post-training effects on patients global assessment of change in quality-of-life (PGACQoL) and physical function.
                Fifty-four stable heart failure patients were randomised to exercise or control. The 4-month exercise programme consisted of bicycle training at 80% of maximal intensity three times/week, and 49 patients completed the active study period. At 10 months (6 months post training) 37 patients were assessed regarding PGACQoL, habitual physical activity, and dyspnea-fatigue-index.
                Both post-training patients (n=17) and controls (n=20) deteriorated PGACQoL during the 6-month extended follow-up, although insignificantly. However, post-training patients improved PGACQoL slightly but significantly from baseline to 10 months (P=0.006), differing significantly (P=0.023) from controls who were unchanged. Regarding dyspnea-fatigue-index, post-training patients were largely unchanged and controls deteriorated insignificantly, during the extended follow-up as well as from baseline to 10 months. Both groups decreased physical activity insignificantly during the extended follow-up, and from baseline to 10 months post-training patients tended to decrease whereas controls significantly (P=0.007) decreased physical activity.
                There was no important sustained benefit 6 months after termination of an exercise training programme in heart failure patients. A small, probably clinically insignificant sustained improvement in PGACQoL was seen in post-training patients. Controls significantly decreased the habitual physical activity over 10 months and post-training patients showed a similar trend. Exercise training obviously has to be continuing to result in sustained benefit. The purpose of this study was to examine the effects of exercise training on functional capacity in patients with heart failure.
                One hundred eighty-one patients in New York Heart Association class I to III, with ejection fraction <40% and 6-minute walk distance <500 meters, were recruited into a randomized, controlled, single-blind trial comparing 3 months of supervised training, then 9 months of home-based training with usual care.
                There was a significant increase in 6-minute walk distance at 3 and 12 months but no between-group differences. Incremental peak oxygen uptake increased in the exercise group compared with the control group at 3 months (0.104 +/- 0.026 L/min vs 0.025 +/- 0.023 L/min; P =.026) and 12 months (0.154 +/- 0.074 L/min vs 0.024 +/- 0.027 L/min; P =.081). Compared with the control group, significant increases were observed in the exercise group for arm and leg strength. No significant changes were observed in cardiac function or quality of life. Adherence to exercise was good during supervised training but reduced during home-based training.
                Exercise training improves peak oxygen uptake and strength during supervised training. Over the final 9 months of the study, there was little further improvement, suggesting that some supervision is required for these patients. There were no adverse effects on cardiac function or clinical events. To assess the benefit of exercise training in patients with heart failure caused by left ventricular systolic dysfunction and to further describe the physiologic changes associated with exercise training in these patients.
                Randomized, controlled trial.
                Urban outpatient clinic.
                40 men with compensated heart failure who were receiving standard medical therapy were randomly assigned to an exercise-training group or to a control group that did not exercise. Fifteen of the 21 patients assigned to exercise training and 14 of the 19 patients assigned to the control group completed the study.
                Patients assigned to exercise training participated in a program of three exercise sessions per week for 24 weeks.
                Symptom-limited exercise tests with gas exchange analysis done just before randomization, at week 12, and at week 24.
                At week 24, the following changes (mean +/- SE) were seen in patients in the exercise group and patients in the control group, respectively; exercise duration, 2.8 +/- 0.6 minutes and 0.5 +/- 0.5 minutes; peak oxygen consumption (VO2), 231 +/- 54 L/min and 58 +/- 38 L/min; peak ventilation, 12 +/- 3 L/min and -4 +/- 3 L/min; peak heart rate, 10 +/- 4 beats/min and -2 +/- 4 beats/min; and peak power output, 20 +/- 6 W and 2 +/- 5 W. Differences between the increases occurring in the exercise group and the changes occurring in the control group were significant (P < 0.05). Among patients in the exercise group, 85% of the increase in peak VO2 occurred by week 12, and 46% of the increase in peak VO2 was caused by the increase in peak heart rate.
                Exercise training does not appear to be contraindicated in patients with compensated heart failure. Exercise training improved exercise tolerance, as measured by increases in peak VO2, exercise duration, and power output. This improved exercise tolerance was caused in part by an increase in peak heart rate. Exercise programs for patients with heart failure have often enrolled and evaluated relatively healthy, young patients. They also have not measured the impact of exercise performance on daily activities and quality of life.
                We investigated the impact of a 6-month supervised and graded exercise program in 33 elderly patients with moderate to severe heart failure randomized to usual care or an exercise program. Six of 17 patients did not tolerate the exercise program. Of those who did, peak oxygen consumption increased by 2.4 +/- 2.8 mL/kg/min (P < .05) and 6-minute walk increased by 194 ft (P < .05). However, outpatient energy expenditure did not increase, as measured by either the doubly labeled water technique or Caltrac accelerometer. Perceived quality of life also did not improve, as measured by the Medical Outcomes Study, Functional Status Assessment, or Minnesota Living With Heart Failure questionnaires.
                Elderly patients with severe heart failure can safely exercise, with an improvement in peak exercise tolerance. However, not all patients will benefit, and daily energy expenditure and quality of life do not improve to the same extent as peak exercise. The effects of exercise training (ET) on left ventricular (LV) remodeling in chronic heart failure are not definitively established, and the safety of ET in these patients is still debated.
                This multicenter study investigated the long-term effect of moderate ET on LV remodeling, work capacity, and quality of life (QoL) in 90 patients with stable chronic heart failure caused by LV systolic dysfunction, randomized to a 6-month ET program (T, n=45) or a control group (C, n=45). All patients underwent resting echocardiography, a cardiopulmonary exercise test, 6-minute walking test, and QoL assessment at entry and after 6 months. At entry, end-diastolic (EDV) and end-systolic (ESV) volume, ejection fraction, work capacity, peak o2, and walking distance were similar in the 2 groups. After 6 months, LV volumes diminished in T (EDV, from 142+/-26 to 135+/-26 mL/m2, P<0.006; ESV, from 107+/-24 to 97+/-24 mL/m2, P<0.05) but increased in C (EDV, from 147+/-41 to 156+/-42 mL/m2, P<0.01; ESV, from 110+/-34 to 118+/-34 mL/m2, P<0.01). Ejection fraction improved in T (P<0.001) but was unchanged in C (P=NS). Significant improvement in work capacity (P<0.001), peak VO2 (P<0.006), walking distance (P<0.001), and QoL (P<0.01) was observed in T but not in C (P=NS). T showed a trend toward fewer (P=0.05) hospital readmissions for worsening dyspnea in the absence of other adverse cardiac events.
                In stable chronic heart failure, long-term moderate ET has no detrimental effect on LV volumes and function; rather, it attenuates abnormal remodeling. Furthermore, ET is safe and effective in improving exercise tolerance and QoL. The aim of this study was to determine the effects of a home-based exercise program on clinical outcomes. Exercise training improves exercise capacity in patients with heart failure (HF) but the long-term effects on clinical outcomes remain unknown.
                We randomized 173 patients with systolic HF to control (n = 87) or home-based exercise (n = 86). The primary end point was a composite of all-cause hospitalizations, emergency department admissions, urgent transplantation, and death at 12 months. Functional performance (as assessed by cardiopulmonary exercise testing and the 6-minute walk test), quality of life, and psychological states were measured at baseline, 3 months, and 6 months.
                There was no significant difference between experimental and control groups in the combined clinical end point at 12 months and in functional status, quality of life, or psychological states over 6 months. Patients in the exercise group had a lower incidence of multiple (2 or more) hospitalizations compared with the control group: 12.8% versus 26.6%, respectively (P = .018).
                A home-based walking program that incorporated aerobic and resistance exercise did not result in improved clinical outcomes at 1-year follow-up in this cohort of patients with systolic HF. However, the exercise program resulted in reduced rehospitalization rates. The aim of this study was to assess the effects of regular physical exercise on local inflammatory parameters in the skeletal muscle of patients with chronic heart failure (CHF).
                Inflammatory activation with increased serum cytokine levels and expression of inducible nitric oxide synthase (iNOS) in the myocardium and peripheral skeletal muscles has been described in CHF.
                Twenty male patients with stable CHF (left ventricular ejection fraction 25 +/- 2%; age 54 +/- 2 years) were randomized to a training group (n = 10) or a control group (n = 10). At baseline and after six months, serum samples and vastus lateralis muscle biopsies were obtained. Serum tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and IL-1-beta levels were measured by enzyme-linked immunosorbent assay, local cytokine, and iNOS expression by real-time polymerase chain reaction.
                Exercise training improved peak oxygen uptake by 29% in the training group (from 20.3 +/- 1.0 to 26.1 +/- 1.5 ml/kg. min; p < 0.001 vs. control group). While serum levels of TNF-alpha, IL-6, and IL-1-beta remained unaffected by training, local skeletal muscle TNF-alpha decreased from 1.9 +/- 0.4 to 1.2 +/- 0.3 relative U (p < 0.05 for change vs. control group), IL-6 from 71.3 +/- 16.5 to 41.3 +/- 8.8 relative U (p < 0.05 vs. begin), and IL-1-beta from 2.7 +/- 1.1 to 1.4 +/- 0.6 relative U (p = 0.02 vs. control group). Exercise training also reduced local iNOS expression by 52% (from 6.3 +/- 1.2 to 3.0 +/- 1.0 relative U; p = 0.007 vs. control group).
                Exercise training significantly reduced the local expression of TNF-alpha, IL-1-beta, IL-6, and iNOS in the skeletal muscle of CHF patients. These local anti-inflammatory effects of exercise may attenuate the catabolic wasting process associated with the progression of CHF. Heart failure, a condition predominantly affecting the elderly, represents an ever-increasing clinical and financial burden for the NHS. Cardiac rehabilitation, a service that incorporates patient education, exercise training and lifestyle modification, requires further evaluation in heart failure management.
                The aim of this study was to determine whether a cardiac rehabilitation programme improved on the outcomes of an outpatient heart failure clinic (standard care) for patients, over 60 years of age, with chronic heart failure.
                Two hundred patients (60-89 years, 66% male) with New York Heart Association (NYHA) II or III heart failure confirmed by echocardiography were randomised. Both standard care and experimental groups attended clinic with a cardiologist and specialist nurse every 8 weeks. Interventions included exercise prescription, education, dietetics, occupational therapy and psychosocial counselling. The main outcome measures were functional status (NYHA, 6-min walk), health-related quality of life (MLHF and EuroQol) and hospital admissions.
                There were significant improvements in MLHF and EuroQol scores, NYHA classification and 6-min walking distance (meters) at 24 weeks between the groups (p<0.001). The experimental group had fewer admissions (11 vs. 33, p<0.01) and spent fewer days in hospital (41 vs. 187, p<0.001).
                Cardiac rehabilitation, already widely established in the UK, offers an effective model of care for older patients with heart failure. The purpose of this study was to determine the effects of systemic exercise training on endothelium-mediated arteriolar vasodilation of the lower limb and its relation to exercise capacity in chronic heart failure (CHF). Endothelial dysfunction is a key feature of CHF, contributing to increased peripheral vasoconstriction and impaired exercise capacity. Local handgrip exercise has previously been shown to enhance endothelium-dependent vasodilation in conduit and resistance vessels in CHF.
                Twenty patients were prospectively randomized to a training group (n=10, left ventricular ejection fraction [LVEF] 24+/-4%) or a control group (n=10, LVEF 23+/-3%). At baseline and after 6 months, peak flow velocity was measured in the left femoral artery using a Doppler wire; vessel diameter was determined by quantitative angiography. Peripheral blood flow was calculated from average peak velocity (APV) and arterial cross-sectional area. After exercise training, nitroglycerin-induced endothelium-independent vasodilation remained unaltered (271% versus 281%, P=NS). Peripheral blood flow improved significantly in response to 90 microg/min acetylcholine by 203% (from 152+/-79 to 461+/-104 mL/min, P<0.05 versus control group) and the inhibiting effect of L-NMMA increased by 174% (from -46+/-25 to -126+/-19 mL/min, P<0.05 versus control group). Peak oxygen uptake increased by 26% (P<0.01 versus control group). The increase in peak oxygen uptake was correlated with the endothelium-dependent change in peripheral blood flow (r=0.64, P<0. 005).
                Regular physical exercise improves both basal endothelial nitric oxide (NO) formation and agonist-mediated endothelium-dependent vasodilation of the skeletal muscle vasculature in patients with CHF. The correction of endothelium dysfunction is associated with a significant increase in exercise capacity. To assess the physiological and psychosocial effects of exercise training in chronic heart failure.
                Twenty-six men with heart failure (New York Heart Association functional classes II and III) aged 52.5 (SD 9.8) years, were studied.
                The subjects were randomized either to rehabilitation group (Group A: 16 patients), participating in a 6-month exercise training program, or to control group (Group B: 10 patients). A psychosocial assessment, which included affective (Beck Depression Inventory and Hospital Anxiety and Depression Scale), quality of life (Quality of Life Index, Minnesota Living with Heart Failure Questionnaire and the Scale of Life Satisfaction) and personality (Eysenck Personality Questionnaire) parameters, was performed at the beginning and the end of the study.
                After training VO2 peak increased by 36% and exercise time by 35%, p < 0.05. A significant decrease in anxiety and depression was also observed. Moreover, trained patients demonstrated a significant improvement in quality of life. No significant correlations were found between deltaVO2 peak and all psychosocial parameter gains. However, the more depressed patients showed the largest physiological responses.
                An exercise rehabilitation program in patients with chronic heart failure is useful for improving their work capacity and psychosocial status. Improvements in psychological status seem to be independent of the aerobic gains. Physical training is a well-known complementary treatment for chronic heart failure (CHF); however, many aspects require further studies. One of them is the impact on remodeling of the left ventricle (LV). The purpose of this study was to evaluate the effect of 6 months of training on LV, exercise capacity and safety issues in patients with ischemic CHF.
                Fifty patients (mean age 60.1+/-9.2 years) with ischemic CHF, New York Heart Association (NYHA) classification class II and III and left ventricular ejection fraction (LVEF) <or=35% were randomized into groups: undergoing 6-month training (25 patients) and not trained (25 patients). In both groups at baseline and at 6 months a cardiopulmonary exercise test and magnetic resonance imaging (MRI) with evaluation of LV were performed. Training was limited by the achievement of 80% of the predicted heart rate at VO2peak achieved at the baseline cardiopulmonary exercise test.
                All patients completed the 6-month observation. No serious adverse events were found in either group. Exercise capacity improved only in the trained group (VO2peak increased by 31%). At 6 months in the trained group there was a tendency towards an improvement in some LV parameters: ejection fraction, end-diastolic volume and wall motion score index (WMSI), whereas an opposite trend was seen in the controls (P<0.05, P<0.05 and P<0.01 for comparison of LVEFs, end-diastolic volumes and WMSIs, respectively).
                Six-month training in ischemic CHF patients is a safe modality. Training improves exercise capacity. There was no negative impact on LV morphology, and a trend towards improvement of functional parameters on MRI may suggest an anti-remodeling effect of training in patients with ischemic CHF. The present study was designed to evaluate the effect of an ambulatory training program on ultrastructural morphology and the oxidative capacity of skeletal muscle and its relation to central and peripheral hemodynamic variables in patients with chronic heart failure.
                Clinical evidence supports the hypothesis that exercise intolerance in patients with chronic heart failure is not only a consequence of low cardiac output, but is also a result of alterations in oxidative metabolism of skeletal muscle.
                Twenty-two patients were prospectively randomized either to a training group (mean [+/-SD] ejection fraction 26 +/- 9%, n = 12) participating in an ambulatory training program or to a physically inactive control group (ejection fraction 27 +/- 10%, n = 10). At baseline and after 6 months, patients underwent symptom-limited bicycle exercise testing, and central and peripheral hemodynamic variables were measured. Percutaneous needle biopsy samples of the vastus lateralis muscle were obtained at baseline and after 6 months. The ultrastructure of skeletal muscle was analyzed by ultrastructural morphometry.
                After 6 months, patients in the training group achieved an increase in oxygen uptake at the ventilatory threshold of 23% (from 0.86 +/- 0.2 to 1.07 +/- 0.2 liters/min, p < 0.01 vs. control group) and at peak exercise of 31% (from 1.49 +/- 0.4 to 1.95 +/- 0.4 liters/min, p < 0.01 vs. control group). There was no significant change in oxygen uptake at the ventilatory threshold and at peak exercise in the control group. The total volume density of mitochondria and volume density of cytochrome c oxidase-positive mitochondria increased significantly by 19% (from 4.7 +/- 1.5 to 5.6 +/- 1.5 vol%, p < 0.05 vs. control group) and by 41% (from 2.2 +/- 1.0 to 3.1 +/- 1.0 vol%, p < 0.05 vs. control group) after 6 months of regular physical exercise. Cardiac output at rest and at submaximal exercise remained unchanged but increased during maximal symptom-limited exercise from 11.9 +/- 4.0 to 14.1 +/- 3.3 liters/min in the training group (p < 0.05 vs. baseline; p = NS vs. control group). Peak leg oxygen consumption increased significantly by 45% (from 510 +/- 172 to 740 +/- 254 ml/min, p < 0.01 vs. control group). Changes in cytochrome c oxidase-positive mitochondria were significantly related to changes in oxygen uptake at the ventilatory threshold (r = 0.82, p < 0.0001) and at peak exercise (r = 0.87, p < 0.0001).
                Regular physical training increases maximal exercise tolerance and delays anaerobic metabolism during submaximal exercise in patients with stable chronic heart failure. Improved functional capacity is closely linked to an exercise-induced increase in the oxidative capacity of skeletal muscle. Exercise training in patients with chronic heart failure improves work capacity by enhancing endothelial function and skeletal muscle aerobic metabolism, but effects on central hemodynamic function are not well established.
                To evaluate the effects of exercise training on left ventricular (LV) function and hemodynamic response to exercise in patients with stable chronic heart failure.
                Prospective randomized trial conducted in 1994-1999.
                University department of cardiology/outpatient clinic in Germany.
                Consecutive sample of 73 men aged 70 years or younger with chronic heart failure (with LV ejection fraction of approximately 0.27).
                Patients were randomly assigned to 2 weeks of in-hospital ergometer exercise for 10 minutes 4 to 6 times per day, followed by 6 months of home-based ergometer exercise training for 20 minutes per day at 70% of peak oxygen uptake (n=36) or to no intervention (control group; n=37).
                Ergospirometry with measurement of central hemodynamics by thermodilution at rest and during exercise; echocardiographic determination of LV diameters and volumes, at baseline and 6-month follow-up, for the exercise training vs control groups.
                After 6 months, patients in the exercise training group had statistically significant improvements compared with controls in New York Heart Association functional class, maximal ventilation, exercise time, and exercise capacity as well as decreased resting heart rate and increased stroke volume at rest. In the exercise training group, an increase from baseline to 6-month follow-up was observed in mean (SD) resting LV ejection fraction (0.30 [0.08] vs 0.35 [0.09]; P=.003). Mean (SD) total peripheral resistance (TPR) during peak exercise was reduced by 157 (306) dyne/s/cm(-5) in the exercise training group vs an increase of 43 (148) dyne/s/cm(-5) in the control group (P=.003), with a concomitant increase in mean (SD) stroke volume of 14 (22) mL vs 1 (19) mL in the control group (P=.03). There was a small but significant reduction in mean (SD) LV end diastolic diameter of 4 (6) mm vs an increase of 1 (4) mm in the control group (P<.001). Changes from baseline in resting TPR for both groups were correlated with changes in stroke volume (r=-0.76; P<.001) and in LV end diastolic diameter (r=0.45; P<.001).
                In patients with stable chronic heart failure, exercise training is associated with reduction of peripheral resistance and results in small but significant improvements in stroke volume and reduction in cardiomegaly. JAMA. 2000. We sought to evaluate the effect of physical training on neurohormonal activation in patients with heart failure (HF).
                Patients with HF benefit from physical training. Chronic neurohormonal activation has detrimental effects on ventricular remodeling and prognosis of patients with HF.
                A total of 95 patients with HF were assigned randomly into two groups: 47 patients (group T) underwent a nine-month training program at 60% of the maximal oxygen uptake (VO2), whereas 48 patients did not (group C). The exercise load was adjusted during follow-up to achieve a progressive training effect. Plasma assay of B-type natriuretic peptide (BNP), amino-terminal pro-brain natriuretic peptide (NT-proBNP), norepinephrine, plasma renin activity, and aldosterone; quality-of-life questionnaire; echocardiogram; and cardiopulmonary stress test were performed upon enrollment and at the third and ninth month.
                A total of 85 patients completed the protocol (44 in group T, left ventricular ejection fraction [EF] 35 +/- 2%, mean +/- SEM; and 41 in group C, EF 32 +/- 2%, p = NS). At the ninth month, patients who underwent training showed an improvement in workload (+14%, p < 0.001), peak VO2 (+13%, p < 0.001), systolic function (EF +9%, p < 0.01), and quality of life. We noted that BNP, NT-proBNP, and norepinephrine values decreased after training (-34%, p < 0.01; -32%, p < 0.05; -26%, p < 0.01, respectively). Increase in peak VO2 with training correlated significantly with the decrease in both BNP/NT-proBNP level (p < 0.001 and p < 0.01, respectively). Patients who did not undergo training showed no changes.
                Clinical benefits after physical training in patients with HF are associated with blunting of adrenergic overactivity and of natriuretic peptide overexpression. It is still a matter of debate whether exercise training (ET) is a beneficial treatment in chronic heart failure (CHF).
                To determine whether long-term moderate ET improves functional capacity and quality of life in patients with CHF and whether these effects translate into a favorable outcome, 110 patients with stable CHF were initially recruited, and 99 (59+/-14 years of age; 88 men and 11 women) were randomized into 2 groups. One group (group T, n=50) underwent ET at 60% of peak &f1;O2, initially 3 times a week for 8 weeks, then twice a week for 1 year. Another group (group NT, n=49) did not exercise. At baseline and at months 2 and 14, all patients underwent a cardiopulmonary exercise test, while 74 patients (37 in group T and 37 in group NT) with ischemic heart disease underwent myocardial scintigraphy. Quality of life was assessed by questionnaire. Ninety-four patients completed the protocol (48 in group T and 46 in group NT). Changes were observed only in patients in group T. Both peak &f1;O2 and thallium activity score improved at 2 months (18% and 24%, respectively; P<0. 001 for both) and did not change further after 1 year. Quality of life also improved and paralleled peak VO2. Exercise training was associated both with lower mortality (n=9 versus n=20 for those with training versus those without; relative risk (RR)=0.37; 95% CI, 0.17 to 0.84; P=0.01) and hospital readmission for heart failure (5 versus 14; RR=0.29; 95% CI, 0.11 to 0.88; P=0.02). Independent predictors of events were ventilatory threshold at baseline (beta-coefficient=0.378) and posttraining thallium activity score (beta-coefficient -0.165).
                Long-term moderate ET determines a sustained improvement in functional capacity and quality of life in patients with CHF. This benefit seems to translate into a favorable outcome.
The previous version of this review showed that exercise training improved exercise capacity in the short term in patients with mild to moderate heart failure when compared to usual care. This updated review provides evidence that in a similar population of patients, exercise does not increase the risk of all-cause mortality and may reduce heart failure-related hospital admissions. Exercise training may offer important improvements in patients' health-related quality of life.