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Patients with high baseline exercise capacity benefit from cardiac rehabilitation and exercise training programs.

Despite the well-proven benefits of cardiac rehabilitation and exercise training, no data are available on the benefits of this therapy in patients with preserved baseline exercise capacity. Therefore we assessed data before and after phase II cardiac rehabilitation and exercise programs at two large teaching institutions to determine the benefits in 163 patients with high baseline exercise capacity (> or = 6 estimated [mean 8.8 +/- 2.4] metabolic equivalents [METs]) compared with 125 patients with low baseline functional capacity (< 6 estimated [mean 4.6 +/- 0.8] METs). After cardiac rehabilitation and exercise training, patients with high baseline exercise capacity had significant improvements in triglyceride (-10%; p < 0.05), high-density lipoprotein cholesterol (+7%; p < 0.001), and low-density lipoprotein cholesterol (-4%; p = 0.09) levels; low-density lipoprotein/high-density lipoprotein ratio (-10%; p < 0.01); body mass index (-1.5%; (p < 0.001); percent body fat (-6%; p < 0.0001); and exercise capacity (+22%; p < 0.0001). Patients with high baseline exercise capacity had less relative improvement in exercise capacity (p < 0.0001) after cardiac rehabilitation but had greater relative improvement in low-density lipoprotein cholesterol level (p < 0.05) and low-density lipoprotein/high-density lipoprotein ratio (p < 0.05) than did patients with low baseline exercise capacity. These data demonstrate the benefits of cardiac rehabilitation and exercise training in patients with preserved exercise capacity and support routine referral of these patients to these programs after major cardiac events.

Adult↗

[Comparison of exercise capacity evaluated by cardiopulmonary exercise test and hemodynamic parameters in patients with atrial septal defect].

We evaluated the maximal exercise tolerance using cardiopulmonary exercise testing, and investigated the relation of the hemodynamic parameters such as mean pulmonary artery pressure (PAm) and pulmonic-to-systemic flow ratio (Qp/Qs) to exercise tolerance in 18 adult patients consecutively. All the patients had atrial septal defect (ASD). Maximal oxygen uptake (VO2 max) averaged only 21.6 +/- 5.6 ml/min/kg and 63.5 +/- 16.2% of the predicted values (VO2max). And anaerobic threshold averaged 12.5 +/- 2.3 ml/min/kg and 56.7 +/- 12.4% of the predicted values. There were 2 patients who had marked pulmonary hypertension (PH, PAm more than 44 mmHg). Maximal exercise tolerance of these patients was severely impaired, and %VO2max was only 45.9% and 46.2% respectively. In patients without PH (PAm less than 20 mmHg), however %VO2 max ranged widely from 100.3 to 44.7% and PAm correlated with %VO2max weakly (r = -0.53, p less than 0.05). But there was a significant inverse relationship between Qp/Qs and %VO2max(r = -0.85, p less than 0.01). In 16 patients without PH, maximal O2-pulse during exercise was also inversely correlated with Qp/Qs (r = -0.76, p less than 0.01). The relation between PAm and %VO2max suggests that afterload on the right ventricle may be an important determinant of exercise capacity in patients with PH. And the relation between Qp/Qs and %VO2max or Qp/Qs and % maximal O2-pulse suggests that Qp/Qs may also be a very important determinant factor of exercise capacity in patients without PH.

Adult↗

Effect of risk factors on exercise capacity in NIDDM.

Exercise capacity has been used as a noninvasive parameter for predicting cardiovascular events. It is known that diabetic patients have an impaired exercise capacity when compared with nondiabetic age-matched control subjects, but the risk factors associated with this impairment have not been thoroughly analyzed. A total of 453 male and female NIDDM patients who underwent graded exercise testing with expired gas analysis were studied to determine the possible influences of demographic and cardiac risk factors on exercise capacity. Univariate and multiple linear regression analyses were performed on baseline patient characteristics with respect to peak oxygen consumption (VO2). In the regression analyses, African-American race was strongly associated with a decrease in peak VO2; the difference in means between African-Americans and other subjects for men was -2.50 ml.kg-1.min-1 (-4.28, -0.07, 95% CI) (P < 0.006) and for women was -2.96 ml.kg-1.min-1 (-4.45, -1.47) (P < 0.0002). Univariate analyses revealed that African-American subjects had increased prevalence, longer duration, and higher systolic and diastolic hypertension than the non-Hispanic and Hispanic whites. Other independent predictors of peak VO2 (reported as change in peak VO2 in milliliters per kilogram per minute) were BMI (men: -0.39 kg/m2 [-0.52, -0.29], P < 0.0001; women: -0.39 kg/m2 [-0.48, -0.31], P < 0.0001), age (men: -0.16/year [-0.23, -0.09], P < 0.0001; women: -0.17/year [-0.24, -0.11], P < 0.0001), baseline resting systolic blood pressure (men: -0.03/mmHg [-0.06, -0.01], P < 0.05; women: -0.03/mmHg (-0.06, -0.01)f1p4< 0.05), and pack-years smoking (men: -0.04/pack-years [-0.04, -0.01], P < 0.01; women: -0.04/pack-years [-0.07, -0.01], P < 0.0001). Thus, in this large NIDDM study, weight loss, smoking cessation, and aggressive blood pressure control, particularly in African-Americans with NIDDM, would appear to be important in improving exercise capacity and potentially improving the increased cardiovascular mortality associated with an impaired exercise capacity.

Adult↗

[Exercise capacity after heart valve replacement].

Exercise capacity following heart-valve replacement is dependent on how close to normal the artificial device can restore valve function, to what degree a preoperative impaired myocardial function and/or an increased pulmonary vascular resistance is normalized. The postoperative functional result can be determined by the subjective improvement of the patient, his functional capacity, exercise capacity, the central hemodynamics at rest and during exercise, and the systolic and diastolic function of the left and right ventricular myocardium. The subjective improvement of individual symptoms is obviously dependent on the degree of postoperative normalization of hemodynamics, especially of pressures in the pulmonary circulation. Subjective improvement can be objectified by comparing the functional capacities before and after surgery. Post-operative normalization of central hemodynamics and myocardial function does not happen immediately but within 3 to more than 12 months. A 12-month period can generally be expected in patients with mitral stenosis and increased pulmonary vascular resistance (> 400 dyn.sec.cm-5) prior to surgery. In patients with mitral and aortic regurgitation as well as with aortic stenosis and preoperative decrease of their left ventricular ejection fraction during exercise, continuous improvement of left ventricular pump function also may need up to 12 months. Physiological hemodynamic conditions generally are not restored by valve replacement. All prostheses are stenotic to forward blood flow because of the obstruction created by the narrowing of the valve area by sewing cuff and valve poppet. This may result in a hemodynamically important stenosis, especially after atrio-ventricular valve implantation, and may limit subjective and functional improvement. Exercise capacity after aortic valve replacement depends mainly on whether or not myocardial damage persists postoperatively. A workload of 1.5 w/kg body weight (BW) has been performed by 100% of patients aged 45 to 55 years with prostheses implanted for aortic stenosis. The significant lower exercise capacity all patients with valve replacement for aortic regurgitation have experienced (0.4 w/kg BW) indicates that a substantial number of these patients has irreversible myocardial damage prior to surgery. The workload experienced by patients with mitral valve prostheses varies between 0.4 and 2.0 w/kg BW (mitral stenosis) and 0.3-2.3 w/kg BW (mitral regurgitation), respectively. To objectify the functional result of heart-valve replacement, hemodynamic-metabolic measurements of functional improvement, determination of left, eventually also of right-ventricular function by echocardiography and additional invasive measurements of the central hemodynamics and myocardial pump function parameters at rest and during exercise might be necessary.

Adult↗

Effects of enalapril on the exercise capacity and neurohumoral factors during exercise in patients with chronic heart failure.

The effects of enalapril on exercise capacity and neurohumoral factors during exercise were evaluated in 10 patients with heart failure. Echocardiograms and exercise testing with expired gas analysis were performed before and after enalapril. Blood samples were obtained before and after exercise. Both ejection fraction and percent fractional shortening increased with enalapril (p < 0.05). The anaerobic threshold and peak VO2 did not change with enalapril. Epinephrine and norepinephrine levels at peak exercise decreased with enalapril (p < 0.1). Plasma renin both at rest and at peak exercise increased with enalapril (p < 0.1). Angiotensin II was lower after enalapril both at rest and at peak exercise (p < 0.1 and p < 0.05, respectively). Aldosterone was lower after enalapril both at rest and at peak exercise (p < 0.05). Atrial natriuretic peptide (ANP) was lower after enalapril both at rest and at peak exercise. There was no significant correlations between peak VO2 and changes in neurohumoral factors before and after enalapril during exercise. In conclusion, neurohumoral changes with enalapril occurred during exercise even if exercise capacity did not improve. Moreover, the improvement of cardiac function at rest and neurohumoral factors with enalapril did not lead to a change of exercise capacity.

Aged↗

Humidity influences exercise capacity in subjects with exercise-induced bronchoconstriction (EIB).

RATIONALE: Exercise-induced bronchoconstriction (EIB) increases in cold and dry air and decreases in humid air in subjects with asthma. Few reports have reported on the effect of humid environment upon exercise capacity in subjects with EIB. OBJECTIVE: The primary aim of the present study was to examine the effect of changing the humidity of the environmental air upon exercise capacity measured by peak oxygen uptake (V O2 peak), peak ventilation (V Epeak) and peak running speed (V peak) and secondarily to assess the influence of environmental humidity upon EIB in subjects suffering from EIB. METHODS: Twenty subjects (10-45 years old, male/female:13/7) with diagnosed EIB performed exercise testing under standardised, regular environmental conditions, 20.2 degrees C (+/- 1.1) and 40% (+/- 3.3) relative humidity [mean (+/- SD)], and under standardised humid environmental conditions; 19.9 degrees C (+/- 1.0) and 95% (+/- 1.7) relative humidity in random order on separate days. Lung function was measured before and 1, 3, 6, 10 and 15 min after exercise. Heart rate (HR), oxygen uptake (V O2), respiratory gas exchange ratio (RER), breathing frequency (BF) and minute ventilation (V E) were measured during exercise. RESULTS: V O2 peak and V peak increased significantly from 40% to 95% relative humidity of the environmental air, 4.5% and 5.9%, respectively (P = 0.001). HRpeak increased significantly in the humid environment, while BF(peak) decreased significantly. RERpeak and V Epeak did not change significantly. Post-exercise reduction in FEV1 (DeltaFEV1) and FEF50 (forced expiratory flow at 50% of FVC) (DeltaFEF50) significantly decreased after exercise in a humid environment as compared to regular conditions, DeltaFEV1: 12% (7,17) vs. 24% (19,29) [mean (95% confidence intervals)], respectively, DeltaFEF50: 20% (12,29) vs. 38% (30,46), respectively (P < 0.001). CONCLUSION: Exercise capacity (V O2 peak and V peak) markedly improved during exercise in humid air in subjects with EIB, whereas EIB was reduced to the half.

Adolescent↗

Prognosis of patients with good exercise capacity and mildly abnormal exercise echocardiography results: identification of an at-risk subgroup.

BACKGROUND: Patients with good exercise capacity and mildly abnormal exercise echocardiography results have a favorable overall prognosis. OBJECTIVE: We sought to define subgroups that might be at higher risk. METHODS: We examined outcomes of 868 patients (women, > or = 5 metabolic equivalents; men, > or = 7 metabolic equivalents) with mild rest- or exercise-induced wall-motion abnormalities and evaluated potential predictors of time to cardiac death or nonfatal myocardial infarction (MI). RESULTS: Mean age was 64 +/- 10 years; 477 patients (55%) were men. Mean follow-up was 3.1 +/- 1.5 years; cardiac event rate was 1.2% per person-year. A history of MI was the only significant predictor (risk ratio, 3.9; 95% confidence interval, 1.9-7.8; P = .0001), with 1-, 3-, and 5-year event-free survival of 98.5% +/- 1.1%, 92.6% +/- 2.6%, and 83.3% +/- 5.1%, respectively (event rate, 3.4%). CONCLUSIONS: Patients with a history of MI have a higher annual cardiac event rate and may benefit from reevaluation, whereas no history of MI connotes a favorable prognosis.

Aged↗

Exercise capacity and mortality among men referred for exercise testing.

BACKGROUND: Exercise capacity is known to be an important prognostic factor in patients with cardiovascular disease, but it is uncertain whether it predicts mortality equally well among healthy persons. There is also uncertainty regarding the predictive power of exercise capacity relative to other clinical and exercise-test variables. METHODS: We studied a total of 6213 consecutive men referred for treadmill exercise testing for clinical reasons during a mean (+/-SD) of 6.2+/-3.7 years of follow-up. Subjects were classified into two groups: 3679 had an abnormal exercise-test result or a history of cardiovascular disease, or both, and 2534 had a normal exercise-test result and no history of cardiovascular disease. Overall mortality was the end point. RESULTS: There were a total of 1256 deaths during the follow-up period, resulting in an average annual mortality of 2.6 percent. Men who died were older than those who survived and had a lower maximal heart rate, lower maximal systolic and diastolic blood pressure, and lower exercise capacity. After adjustment for age, the peak exercise capacity measured in metabolic equivalents (MET) was the strongest predictor of the risk of death among both normal subjects and those with cardiovascular disease. Absolute peak exercise capacity was a stronger predictor of the risk of death than the percentage of the age-predicted value achieved, and there was no interaction between the use or nonuse of beta-blockade and the predictive power of exercise capacity. Each 1-MET increase in exercise capacity conferred a 12 percent improvement in survival. CONCLUSIONS: Exercise capacity is a more powerful predictor of mortality among men than other established risk factors for cardiovascular disease.

Adrenergic beta-Antagonists↗

[Significance of exercise capacity in cardiology].

Exercise capacity is reduced in many patients with cardiovascular disease. In post-acute myocardial infarction, ischemic heart disease and heart failure patients, exercise capacity has a strong independent prognostic impact. Even in subjects without history of heart disease, the lower the cardiorespiratory fitness the higher is the risk for cardiovascular events and mortality. With appropriate physical activity, exercise capacity is improved in most individuals. Improvement of functional capacity is associated with improvement of survival.

Angina, Unstable↗

Effects of arotinolol on exercise capacity and humoral factors during exercise in normal subjects.

A placebo-controlled, double-blind crossover study was undertaken in 10 normal subjects to examine the effects of arotinolol (10 mg bid), a nonselective beta blocker with alpha-blocking activity, on exercise capacity and hormone levels during exercise after a 2-week treatment period. Maximal oxygen uptake (VO2 max) and blood lactic acid concentration (LA) were measured during progressive exercise testing. An exercise intensity equivalent to 4 mmol/l of LA was used for the constant workload exercise test. Humoral factors were measured after 20 minutes of constant workload exercise. The administration of arotinolol significantly decreased systolic blood pressure and heart rate at rest and during exercise, but diastolic blood pressure did not change. No significant difference was found between arotinolol and placebo with regard to VO2 max and maximal workload. Plasma renin activity (PRA), aldosterone (PAC), and norepinephrine (NE) levels at rest and during exercise did not differ between the two treatments. In contrast, plasma epinephrine (EN) levels at rest and during exercise were significantly greater with arotinolol. Atrial natriuretic peptide (ANP) at rest did not differ between the two treatments. However, exercise caused a significant increase in ANP after arotinolol treatment. These findings suggest that arotinolol decreases blood pressure and heart rate without affecting exercise capacity.

Adrenergic beta-Antagonists↗

Exercise capacity and impact of exercise training in patients after a Fontan procedure: a review.

After a successful Fontan procedure, children and adolescents should improve their exercise capacity. However, several studies have shown that these children have a reduced maximal oxygen consumption compared with healthy children. The lower exercise performance in these patients was mainly explained by a reduced cardiorespiratory functional capacity. However, it has recently been reported that the lower exercise performance may also be related to altered skeletal muscle function. Moreover, exercise training had a beneficial impact on several parameters related to exercise tolerance in these patients. The main studies supporting these observations are reviewed, with a focus on the physiological adaptation and limitation of the exercise performance as well as the benefits of exercise training in patients after a Fontan procedure.

Adaptation, Physiological↗

Effect of warming of exercising legs on exercise capacity in patients with impaired exercise tolerance.

OBJECTIVE: The purpose of this study was to determine whether warming of exercising legs improves exercise capacity in patients with cardiac disease and low exercise tolerance. BACKGROUND: Exercising muscle temperature reflects both muscle metabolic rate and muscle blood flow. Increase in muscle temperature in exercising legs is impaired in patients with chronic heart failure. We hypothesized that the mechanisms responsible for impairment of temperature increase in exercising muscle might be related to those responsible for low exercise tolerance. METHODS: We studied 17 patients with cardiac disease whose anaerobic threshold (AT) ranged from 6.6 to 14.8 ml/kg/min (mean 11.2 +/- 1.9 SD). Subjects performed symptom-limited sitting cycle ergometer exercise with or without warming of the thighs. Both thighs were warmed by use of hot packs fixed by supporters. To determine the effect of the supporters themselves on AT and peak VO2, the same ergometer exercise was performed by 7 patients with or without supporters. Peak VO2 and AT were determined by concomitant respiratory gas monitoring. RESULTS: 1) Warming of the thighs increased deep temperature in the thighs (1.0 approximately 2.8 degrees C). 2) AT and peak VO2 were significantly improved in the warming exercise compared with the non-warming exercise (p < 0.01, p < 0.01). 3) There was no significant difference in AT or peak VO2 between the exercise with and without supporters. CONCLUSION: The findings of this study indicate that warming of exercising legs improves exercise capacity in patients with cardiac disease and low exercise tolerance.

Aged↗

Exercise capacity and biochemical profile during exercise in patients with glycogen storage disease type I.

Glycogen storage disease type I (GSD-I) is an inherited disorder of carbohydrate metabolism. Hepatic glucose-6-phosphatase is deficient, leading to impaired gluconeogenesis and glycogenolysis. Patients prevent fasting hypoglycemia by frequent feeds of low glycemic index foods. Normal muscle does not contain glucose-6-phosphatase, and GSD-I is usually classified as a hepatic glycogenosis. However, clinical experience has suggested that patients have decreased cardiovascular fitness, but this had not been formally investigated. This paper reports the results of maximal treadmill cardiopulmonary exercise testing in adult patients with GSD-I. It documents a major reduction in exercise capacity in these patients and demonstrates biochemical aspects of exercise that are different from those of normal controls. All patients showed a reduction in exercise capacity, but there was a wide range of exercise tolerance. Additional work needs to address whether improved adherence to or intensification of therapy in adulthood will ameliorate exercise intolerance.

Adolescent↗

Long-term antihypertensive therapy with beta-blockers: submaximal exercise capacity and metabolic effects during exercise.

The effects of long-term (6 months) antihypertensive treatment with three different types of beta-blockers (propranolol, nonselective without ISA; pindolol, nonselective with ISA; metoprolol, beta 1-selective without ISA) on submaximal exercise capacity and metabolic variables during submaximal endurance exercise were studied in seven subjects with essential hypertension. Exercise tests were performed on a bicycle ergometer at 70% of estimated VO2 max. Similar reductions of resting and exercise blood pressure and exercise heart rate were obtained with the three beta-blockers. Exercise time was significantly reduced by all three beta-blockers during chronic antihypertensive therapy. The reduction tended to be more pronounced after 5-6 months of treatment than after 1 week (P = 0.06). During exercise, the plasma glycerol and nonesterified fatty acid concentrations were reduced. Plasma glucose concentration was reduced at the end of the exercise test during propranolol treatment only. Plasma lactate concentrations tended to be increased, but the difference was significant during pindolol treatment only. Oxygen uptake tended to decrease and respiratory exchange ratio to increase. Plasma potassium concentrations during exercise were significantly increased with all three beta-blockers. The effects on the metabolic variables during exercise were similar after 1 week and during long-term (20/24 weeks) beta-blocker treatment. The study shows that submaximal endurance exercise capacity is impaired in patients with essential hypertension on beta-blocker therapy and that the impairment is maintained during long-term antihypertensive beta-blocker treatment.

Adrenergic beta-Antagonists↗

Forearm reactive hyperemic blood flow and arm-cranking exercise capacity in healthy and heart failure subjects.

BACKGROUND: The relationship between lower limbs maximal vasodilatory capacity and exercise capacity in congestive heart failure (CHF) and healthy subjects has been well-documented. However, the relationship between upper limbs maximal vasodilatory capacity and exercise is less well-established. METHODS AND RESULTS: Twelve patients with CHF, 16 age-matched normal subjects, and 11 very fit individuals underwent an arm-cranking exercise test using maximal oxygen uptake (arm VO(2max)) and measurements of peak forearm reactive hyperemic blood flow. Despite similar forearm strength, arm VO(2max) was significantly reduced in patients with CHF when compared to normal and very fit individuals (13.9 +/- 2.9, 23.5 +/- 4.8, and 36.4 +/- 8.5 mL/kg/min, respectively, P <.05). Similarly, peak reactive hyperemia was lower in CHF patients as compared to normal and very fit individuals (18.6 +/- 5.9, 24.3 +/- 5.8, and 41.1 +/- 8.1 mL/100 mL/min, respectively, P <.05). There was a strong relationship between peak reactive hyperemic blood flow and arm VO(2max) (r =.75; P <.001) in all subjects. CONCLUSIONS: These results suggest a significant relationship between forearm vasodilatory capacity and arm-cranking VO(2max) in CHF patients, sedentary, and very fit individuals.

Adult↗

[Evaluation of dynamic hyperinflation parameters and exercise capacity at maximal exercise in patients with COPD].

Hyperinflation is an important limiting factor for exercise performance in patients with chronic obstructive pulmonary disease (COPD). Hyperinflation can be determined by measuring residual volume (RV), functional residual capacity (FRC), and total lung capacity (TLC) at rest, and by measuring inspiratory capacity (IC) and end-expiratory lung volume (EELV) at maximal exercise. This study aimed to evaluate changes in hyperinflation parameters on maximal exercise in subjects with COPD. Patients with clinically stable COPD (n= 43) and healthy controls (n= 14) were included. Subjects performed pulmonary function tests and an incremental exercise test on cycle ergometry. Statistically significant differences (p< 0.05) were found regarding exercise test parameters including exercise duration, maximum oxygen uptake, breathing reserve, maximum minute ventilation, and breathing pattern between groups. There was significant increase in EELV (p< 0.05) and decrease in IC (p< 0.05) at maximum exercise when hyperinflation parameters were compared at baseline and maximum exercise. Our results showed that hyperinflation was evident at maximal exercise, although there were no hyperinflation findings at rest in subjects with COPD. We believe that in patients with COPD, it is better to evaluate hyperinflation at maximal exercise than at rest.

Exercise↗

Serial assessment of exercise capacity after heart transplantation.

BACKGROUND: Exercise capacity after heart transplantation is abnormal. This reduced exercise performance may in part be due to treatment with high-dose immunosuppressive therapy, deconditioning, graft rejection, or cardiac denervation. METHODS: To investigate whether exercise capacity significantly improves over time as immunosupression is lessened or whether reinnervation occurs, we measured peak exercise oxygen consumption in 60 patients 0.5 to 60 months after transplantation (age: 52 +/- 11 years; left ventricular ejection fraction: 56% +/- 10%) and in 14 healthy subjects (age: 44 +/- 8 years; p = Not significant). Resting hemodynamic measurements, left ventricular ejection fraction, and immunosuppressive therapy were recorded at the time of each of the patients' 116 exercise tests. Exercise test results were stratified into groups according to time after transplantation. RESULTS: Exercise capacity significantly improved after transplantation (pretransplantation peak exercise oxygen consumption: 9.9 +/- 4.3; posttransplantation: 16.6 +/- 4.0 ml/kg/min; p < 0.001). Patient groups after transplantation were without significance differences with regard to age, gender, left ventricular ejection fraction, resting hemodynamic measurements, antihypertensive regimen, and number of rejection episodes. For those patients exercising at 2 months compared with the patients exercising at 12 months, a significant increase was observed in peak exercise oxygen consumption (14.0 +/- 3.8 ml/kg/min at 2 +/- 2 months to 16.2 +/- 3.8 ml/kg/min at 12 +/- 2 months) and maximum heart rate (124 +/- 24 to 137 +/- 24 beats/min). No significant changes were found in peak exercise oxygen consumption or maximum heart rate after the first year after transplantation. Patients' exercise capacities as measured by peak exercise oxygen consumption remained abnormal (N1 peak exercise oxygen consumption: 35 +/- 11 ml/kg/min) despite significant reductions in steroid, azathioprine, and cyclosporine therapy. Peak exercise oxygen consumption was significantly correlated with maximal heart rate (r = 0.42) (p < 0.0001) but not with maximal blood pressure response, change in heart rate, left ventricular ejection fraction, or resting cardiac index (all p = Not significant). CONCLUSIONS: Exercise capacity is markedly improved after heart transplantation although it remains impaired compared with healthy individuals. Patients achieve their maximal exercise capacity by 1 year after transplantation. Subsequently, exercise capacity does not improve despite significant reductions in immunosuppressive agents. The lack of alteration in the heart rate response to exercise over time suggests that no significant functional reinnervation occurs.

Adult↗

Exercise capacity in adult African-Americans referred for exercise stress testing: is fitness affected by race?

STUDY OBJECTIVES: To determine the factors associated with exercise capacity. DESIGN: Retrospective evaluation of large stress-testing database. SETTING: Multispecialty tertiary care center. PATIENTS: A total of 5,069 consecutive patients who were referred for exercise stress testing. MEASUREMENTS: We compared levels of fitness in 641 African-Americans (52% male) with 4,428 whites (73% male), and performed univariate and multivariate analyses to determine the predictors of fitness (including race). RESULTS: Compared with African-American men (mean [+/- SD] age, 60 +/- 11 years), white men (mean age, 63 +/- 11 years) have significantly higher exercise capacity (10.7 +/- 3.5 vs 11.4 +/- 3.4 metabolic equivalents [METs], respectively; p < 0.001). The exercise capacity in African-American and white women was similar (8.5 +/- 2.9 vs 8.7 +/- 3.0 METs, respectively). However, body mass indexes (BMIs) were significantly higher in both African-American men (29.1 +/- 4.3 vs 28.2 +/- 4.3 kg/m(2), respectively; p < 0.001) and women (30.2 +/- 5.7 vs 27.9 +/- 5.5 kg/m(2), respectively; p < 0.0001) compared to their white counterparts, as was the prevalence of obesity (men, 44% vs 33%, respectively; women, 37% vs 27%, respectively; both p < 0.001). Although a model containing age, gender, BMI, and race only accounted for 32% of exercise capacity, all independently (p < 0.0001) predicted higher exercise capacity, as follows: younger age (r(2) = 0.14); male gender (r(2) = 0.12); BMI (r(2) = 0.06); and white race (r(2) = 0.004). CONCLUSIONS: In an adult population of individuals who were referred for exercise stress testing, African-Americans were more obese and had significantly lower exercise capacity than their white counterparts. Emphasis on weight reduction and increasing physical fitness is particularly needed for the prevention of cardiovascular diseases in African-Americans.

Black or African American↗