[Effect of stimulation of beta-2 adrenergic receptors on the exercise capacity and subjective exercise tolerance in patients with asthma].
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Exercise capacity in hypertrophic cardiomyopathy is thought to relate to elevated left atrial pressure as a consequence of impaired diastolic function, but this assumption has not previously been evaluated. Twenty-three patients with hypertrophic cardiomyopathy underwent hemodynamic assessment during symptom-limited maximal exercise with objective measurement of exercise capacity by respiratory gas analysis. Maximal oxygen consumption and anaerobic threshold were 28.1 +/- 7.5 and 21.5 +/- 6.1 ml/kg per min, respectively (the lower limit of reference range in our laboratory is 39 and 27 ml/kg per min, respectively). Maximal oxygen consumption was reduced in 11 of 13 patients who were in New York Heart Association functional class I and who denied limitation of exercise capacity and in all 10 patients who were in functional class II or III. Maximal oxygen consumption and anaerobic threshold were related to peak cardiac index (r = 0.650, p less than 0.001 and r = 0.459, p = 0.03, respectively) and to the increase in cardiac index on exercise (r = 0.677, p less than 0.001 and r = 0.509, p = 0.016, respectively), but not to cardiac index at rest, peak and rest pulmonary capillary wedge pressure, pulmonary capillary wedge pressure at an oxygen consumption of 15 ml/kg per min or the rise in pulmonary capillary wedge pressure on exercise. These findings are not consistent with the hypothesis that elevated left atrial pressure is the major determinant of exercise capacity in patients with hypertrophic cardiomyopathy and they suggest that, as in patients with chronic cardiac failure, other mechanisms should be considered.
OBJECTIVE: Exercise capacity has been used as a noninvasive parameter for predicting cardiovascular events. It has been demonstrated previously in NIDDM patients that several risk factors (i.e., obesity, smoking, hypertension, and African-American race) are associated with an impaired exercise capacity. We studied 265 male and 154 female NIDDM patients who underwent graded exercise testing with expired gas analyses to determine the possible influences of diabetic neuropathy, nephropathy, and retinopathy on exercise capacity. RESEARCH DESIGN AND METHODS: Univariate and multiple linear regression analyses were performed to determine the relationship between diabetic neuropathy, urinary albumin excretion (UAE), and retinopathy with respect to peak oxygen consumption (VO2). Neuropathy was assessed by neurological symptom and disability scores, autonomic function testing, and quantitative sensory exams involving thermal and vibratory sensation. Three categories of UAE were used: normal albuminuria (< 20 micrograms/min), microalbuminuria (20-200 micrograms/min), and overt albuminuria (> 200 micrograms/min). Retinopathy was assessed by stereoscopic fundus photographs. Multiple linear regression analyses were then performed controlling for age, sex, length of diagnosed diabetes, duration of hypertension, race and ethnicity, GHb, BMI, and smoking to determine whether there was an independent effect of these diabetic complications on exercise capacity. RESULTS: Univariate analyses revealed that the presence of diabetic retinopathy (P = 0.03), neuropathy (P = 0.002), microalbuminuria (P = 0.04), and overt albuminuria (P = 0.06) were associated with a lower peak VO2. Multiple linear regression analyses were performed to determine independent relationships with peak VO2. The results revealed that increasing retinopathy stage (Parameter estimate [PE] = -0.59 +/- 0.3 ml.kg-1.min-1; P = 0.026) and increasing UAE stage (PE = -0.62 +/- 0.3 ml.kg-1.min-1; P = 0.04) were associated with a decrease in peak VO2. CONCLUSIONS: In the present study of NIDDM subjects, a significant independent association was demonstrated between diabetic nephropathy and retinopathy with exercise capacity. These results were obtained controlling for age, sex, length of diagnosed diabetes, hypertension, race, and BMI. Thus the findings in this large NIDDM population without a history of coronary artery disease indicate a potential pathogenic relationship between microvascular disease and exercise capacity.
OBJECTIVES: We sought to define the prognostic implications of the extent and severity of exercise echocardiographic abnormalities in patients with good exercise capacity. BACKGROUND; The exercise capacity of patients with known or suspected coronary artery disease (CAD) is of prognostic importance, as is the extent of exercise-related left ventricular (LV) hypoperfusion or dysfunction. METHODS: We examined the outcomes of 1,874 patients with known or suspected CAD (mean age 64 +/- 10 years, 64% men) who had good exercise capacity (> or = 5 metabolic equivalents [METs] for women, > or = 7 METs for men) but abnormal exercise echocardiograms and analyzed the potential association between clinical, exercise and echocardiographic variables and subsequent cardiac events. RESULTS: Multivariate predictors of time to cardiac death or nonfatal myocardial infarction (MI) were diabetes mellitus (risk ratio [RR] 1.88; 95% confidence interval [CI] 1.2 to 3.0), history of MI (RR 2.44; 95% CI 1.6 to 3.6) and an increase or no change in LV end-systolic size in response to exercise (RR 1.61; 95% CI 1.1 to 2.5). Using echocardiographic variables that were of incremental prognostic value, we were able to stratify the cardiac risk of the study population; cardiac death or nonfatal MI rate per person-year of follow-up was 1.6% for patients who had a decrease in LV end-systolic size in response to exercise (n = 1,330) and 1.2% for patients who did not have any severely abnormal LV segments immediately after exercise (n = 868). CONCLUSIONS: In patients with good exercise capacity, echocardiographic descriptors of the extent and severity of exercise-related LV dysfunction were of independent and incremental prognostic value. Stratification of patients into low- and higher risk subgroups was possible using these exercise echocardiographic characteristics.
We evaluated 12 patients with stable chronic airflow obstruction (CAO) and no clinical evidence of left ventricular disease to determine the effects of oral digoxin on exercise capacity (VO2 max) and on right ventricular pump function during exercise. In this randomized, double blind, placebo controlled, cross-over study, patients performed exercise tests and underwent measurement of ejection fractions after two weeks of therapy with oral digoxin (0.25 mg/day) and after two weeks of placebo. Incremental upright exercise testing to a symptom-limited maximum was performed on a cycle ergometer. Right and left ventricular ejection fractions (RVEF, LVEF) were obtained in the supine position at rest and at approximately 75 percent of the maximum workload by gated equilibrium radionuclide angiography. All patients had abnormal right ventricular function, manifested either by a low resting RVEF (less than 45 percent) or a subnormal response to exercise (less than 5 percent increase). The small increases in RVEF with digoxin (mean +/- SE) at rest (44 +/- 5 vs 41 +/- 4 percent) and during exercise (46 +/- 4 vs 44 +/- 3 percent) did not achieve statistical significance. With digoxin, small increases in exercise duration (10.0 +/- 1.5 vs 9.0 +/- 1.4 min), maximum workload achieved (48 +/- 6 vs 42 +/- 5 W), VO2 max (0.85 +/- 0.06 vs 0.81 +/- 0.06 L/min), and oxygen-pulse (O2-P) (6.6 +/- 0.5 vs 6.3 +/- 0.4 ml/beat) occurred. Only the increase in O2-P was significant (p less than 0.05). From this study we conclude that digoxin does not significantly improve exercise capacity in severe chronic airflow obstruction with impaired right ventricular function, nor does it improve RVEF either at rest or during supine submaximal exercise.
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BACKGROUND: Mitral regurgitation (MR) is known as one of the most frequent causes of heart failure and sudden death. In spite of increasing prevalence of MR, there have been no available data on cardiac determinants of exercise capacity in patients with chronic MR. HYPOTHESIS: This study aimed to investigate cardiac determinants of exercise capacity in patients with chronic MR. METHODS: We consecutively enrolled 32 patients (11 men, mean age: 44 +/- 14 years) who had greater than moderate MR with normal left ventricular (LV) systolic function (LV ejection fraction >50%). Conventional echocardiographic indices and parameters measured by Doppler tissue imaging at septal side of mitral annulus were obtained before exercise. Mitral regurgitation fraction, forward stroke volume, pulmonary venous flow velocities, and systolic pulmonary artery pressure (sPAP) were also obtained with standard methods. RESULTS: Left ventricular ejection fraction was 61 +/- 6% and MR fraction was 48 +/- 13%. All patients finished a symptom-limited treadmill exercise test with a peak heart rate of >85% of predicted maximum heart rate. Mean exercise time was 9.95 +/- 2.17 min, corresponding to 11 +/- 2 metabolic equivalents. Among pre-exercise echocardiographic variables, only early diastolic mitral annulus velocity (E') and pulmonary venous reversal flow velocity (PVa) showed a significant correlation with exercise time (r = 0.44, p = 0.011, and r = -0.40, p = 0.040, respectively), which persisted after multivariate analysis (p = 0.011 and 0.038, respectively). Other parameters such as systolic mitral annulus velocity, resting and postexercise sPAP, forward stroke volume, LV size, LV ejection fraction, left atrial size, and regurgitant fraction showed no significant correlation. CONCLUSIONS: Left ventricular diastolic function is an important determinant of exercise capacity in patients with chronic MR. Both E' and PVa, accepted surrogate estimates for LV diastolic function, may be useful for identifying patients with chronic MR and with poor exercise capacity.
During exercise patients with chronic left heart failure ventilate more than normal individuals at the same workload; the ratio of minute ventilation to minute production of carbon dioxide (VE/VCO2) is increased. The relation between increased VE/VCO2, severity of heart failure, and exercise capacity has not been defined. VE/VCO2 was measured in 47 patients with chronic left heart failure (New York Heart Association grades II and III) and in 1009 healthy controls. Exercise capacity was assessed by peak oxygen consumption (VO2max) during progressive exercise. In the controls VO2max ranged from 25 to 93 ml/kg/min; VE/VCO2 was 17-36 and did not correlate with VO2max. In chronic left heart failure the VO2max ranged from 9 to 29 ml/kg/min; VE/VCO2 was 22-42 and correlated strongly with VO2max. End tidal carbon dioxide and respiratory rate at peak exercise were similar in the controls and patients with chronic left heart failure. The increase in VE/VCO2 on exercise in chronic left heart failure indicates increased physiological dead space, presumably caused by a ventilation-perfusion mismatch. In the controls and patients with chronic left heart failure the relation of VE/VCO2 to VO2max was curvilinear with a threshold of VO2max below which VE/VCO2 started to rise above the normal range. This point of inflection may be explained by the existence of a critical level of cardiac function necessary to perfuse adequately all lung zones on exercise.
Oxygen supplementation may improve exercise tolerance and the physiological response to exercise in cystic fibrosis (CF) patients. Elevated barometric pressure at low altitude is a simple means of increasing the quantity of inspired oxygen. Our objectives were to examine the effect of natural oxygen enrichment (at the Dead Sea, 396 m below sea level) on exercise capacity, and the physiological responses to maximal and submaximal exercise in CF patients. Patients were tested twice: at sea level (barometric pressure, 754 +/- 6 mmHg, mean +/- SD), and at the Dead Sea (barometric pressure, 791 +/- 3 mmHg), in a randomized crossover design. We studied 14 CF patients (6 females, 8 males), aged 15-45 years, with moderate to severe lung disease (mean forced expired volume in 1 sec = 50.0 +/- 11.2% predicted). Tests at each site included resting spirometry, anthropometry, a graded submaximal exercise test, a maximal exercise test on a treadmill, and a 6-min walk test. Tests were performed in identical order at both sites. Tests at the Dead Sea were performed 72 hr after arrival. No differences between sites were observed in lung function at rest. Peak oxygen consumption was significantly improved at the Dead Sea compared with sea level (1.68 +/- 0.73 vs. 1.57 +/- 0.74 l/min, respectively, P = 0.05), along with an improvement in the ventilatory equivalent for oxygen (41.2 +/- 6.3 vs. 46.1 +/- 7.1, respectively, P < 0.05). During submaximal exercise, blood oxygen saturation improved at the Dead Sea compared with sea level at all exercise intensities (P < 0.05). In conclusion, these results suggest that even a brief stay at the Dead Sea area may have physiological benefits for CF patients with moderate to severe lung disease.
An impaired exercise capacity is common in hypertensive patients (pts) and factors affecting exercise capacity are not completely elucidated. The aim of the study was to investigate factors influencing exercise capacity in hypertensive pts Studied group consisted of 41 pts (18 males, 23 females) mean age 54.2 +/- 11.9 with essential hypertension and without coronary artery disease. Each patient underwent an echocardiographic examination followed by treadmill exercise test. Echocardiographic assessment comprised estimation of left ventricular (LV) mass index (LVMI), pattern of LV geometry, ejection fraction (LVEF), fractional shortening (LVFS), peak and integral velocities of early (E, Ei) and late (A, Ai) transmitral flow, deceleration time of E wave (DT), isovolumic relaxation time (IVRT), duration of A wave (A-dur), total ejection isovolume index (TEI), E (ETT) and A (ATT) wave transit time to the LV outflow tract, flow propagation velocity of E wave (EP), peak and integral velocities of systolic (S, Si), diastolic (D, Di) and atrial reversal (AR, ARi) pulmonary venous flow, duration of AR wave (AR-dur), acceleration (SAT) and deceleration (SDT) of systolic pulmonary venous flow, systolic forward fraction of pulmonary venous flow (SFF). Exercise capacity was assessed by exercise time and total workload expressed in MET. Significant correlations were found for MET and: age (r = -0.49, p < 0.001), A (r = -0.62, p < 0.001), E/A ratio (r = 0.55, p < 0.004), Di (r = 0.55), p < 0.004), ARi (r = -0.38, p < 0.01), SFF (r = 0.46, p < 0.002). Exercise time correlated with A (r = -0.61, p < 0.001), E/A ratio (r = 0.41, p < 0.04), Di (r = 0.51, p < 0.009), ARi (r = -0.35, p < 0.02), SFF (r = -0.51, p < 0.008), S/D ratio (r = -0.47, p < 0.01). Other investigated parameters did not correlate with both MET and exercise time. By stepwise multiple linear regression analysis Di and ARi were the only determinants of MET (multiple r = 0.85, p < 0.0001) whereas A and Di turn out to be the only independent predictors of exercise time (multiple r = 0.76, p < 0.0004). In hypertensive pts: 1. diastolic function of LV is a principle determinant of exercise capacity, 2. integral velocity of diastolic and atrial reversal pulmonary venous flow and peak velocity of late transmitral flow are the best predictors of exercise tolerance.
BACKGROUND: It is known that left ventricular systolic function at rest does not correlate well with exercise capacity of patients with heart failure. However, the contribution of left ventricular diastolic dysfunction, especially during exercise, to exercise capacity of cardiac patients remains to be determined. OBJECTIVE: To determine the impact of left ventricular systolic and diastolic function during exercise on exercise capacity of patients with left ventricular dysfunction after myocardial infarction. METHODS: A symptom-limited exercise test was performed with measurements for hemodynamics and uptake of oxygen (Vo2) of 26 men who had previously suffered myocardial infarction. These patients were divided into two groups according to their peak Vo2 (group 1 with peak Vo2 > or = 16 ml/kg per min, n= 13; and group 2 with peak Vo2 < 16 ml/kg per min, n= 13). Pulmonary arterial pressure, left ventricular and systemic arterial pressure, and cardiac output were measured at rest and during exercise. RESULTS: At rest, there was no difference between the two groups in terms of hemodynamic parameters except for minimal dP/dt, minimal left ventricular pressure (LVP) and time constant for decay of left ventricular pressure (tau). During peak exercise, cardiac output, left ventricular end-diastolic pressure (EDP), minimal dP/dt, minimal LVP, and tau for the two groups were significantly different. Furthermore, peak Vo2 was significantly correlated with T, minimal LVP, minimal dP/dt, EDP, and maximal dP/dt during peak exercise for the whole group of patients. CONCLUSION: Left ventricular diastolic function during exercise, i.e. diastolic reserve, may be an important determinant of exercise capacity of patients with left ventricular dysfunction after myocardial infarction.
Exercise capacity in patients with end-stage renal disease (ESRD) remains impaired despite correction of anemia. Carnitine insufficiency may contribute to impaired exercise and functional capacities in patients with ESRD. Two randomized placebo-controlled trials were conducted to test whether intravenous L-carnitine improves exercise capacity (assessed by maximal rate of oxygen consumption [VO(2max)]) and quality of life (measured by the Kidney Disease Questionnaire [KDQ]) in patients with ESRD. In study A, patients were administered L-carnitine, 20 mg/kg (n = 28), or placebo (n = 28) intravenously at the conclusion of each thrice-weekly dialysis session for 24 weeks. In study B, a dose-ranging study, patients were administered intravenous L-carnitine, 10 mg/kg (n = 32), 20 mg/kg (n = 30), or 40 mg/kg (n = 32), or placebo (n = 33) as in study A. The prospective primary statistical analysis evaluated changes in VO(2max) in each study and specified that changes in the KDQ were assessed only in the combined populations. L-Carnitine supplementation increased plasma carnitine concentrations, but did not affect VO(2max) in either study. Because change in VO(2max) showed significant heterogeneity, a secondary analysis using a mixture of linear models approach on the combined study populations was performed. L-Carnitine therapy (combined all doses) was associated with a statistically significant smaller deterioration in VO(2max) (-0.88 +/- 0.26 versus -0.05 +/- 0.19 mL/kg/min, placebo versus L-carnitine, respectively; P = 0.009). L-Carnitine significantly improved the fatigue domain of the KDQ after 12 (P = 0.01) and 24 weeks (P = 0.03) of treatment compared with placebo using the primary analysis but did not significantly affect the total score (P = 0.10) or other domains of the instrument (P > 0.11). Carnitine was well tolerated, and no drug-related adverse effects were identified. Intravenous L-carnitine treatment increased plasma carnitine concentrations, improved patient-assessed fatigue, and may prevent the decline in peak exercise capacity in hemodialysis patients. VO(2max) in the primary analysis and other assessed end points were unaffected by carnitine therapy.
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This study was conducted to evaluate the numerical changes and the recovery process in exercise capacity over time, and to establish new criteria that will objectively evaluate the recovery in exercise capacity after lung surgery using an expired gas analysis incorporating an exercise test. The subjects consisted of 47 patients that underwent curative resection (only lobectomy) for lung cancer in the four years from 1989 to 1992 that were able to undergo expired gas analysis incorporating an exercise test before and after surgery. The expired gas analysis were performed within one week prior to surgery and over a period from 14 to 449 days after surgery, maximum oxygen consumption (VO2max) and anaerobic threshold (AT) measured, and the VO2max/m2 and AT/m2 were calculated as an index by dividing by the body surface area (m2). In addition, in order to examine the changes in exercise capacity after surgery, the presurgical values were used as 100, and the rate of change after surgery found. These rate were divided into the following measuring times, and the postsurgical changes over time analyzed. The postsurgical measuring times were divided into five groups from 14-30 days (n = 11), from 31-90 days (n = 25), from 91-180 days (n = 8), from 181-270 days (n = 19), and greater than 271 days (n = 8) after surgery.(ABSTRACT TRUNCATED AT 250 WORDS)
Exercise intolerance is common in hemodialysis (HD) and renal transplant (RTx) patients. Aim of the study was to assess to what extent exercise capacity and skeletal muscle strength of RTx patients differ from HD patients and healthy controls and to elucidate potential determinants of exercise capacity in RTx patients. Exercise capacity, muscle strength, lean body mass (LBM) and physical activity level (PAL) were measured by cycle-ergometry, isokinetic dynamometry, DEXA and Baecke Questionnaire, respectively, in 35 RTx, 16 HD and 21 controls. VO2peak and muscle strength of the RTx patients were significantly lower compared to controls (p<0.01), but not different compared to HD patients. In RTx patients, strength (p<0.001), PAL (p=0.001) and age (p=0.045) were significant predictors of VO2peak. Muscle strength was related to LBM (p=0.001) and age (p=0.001), whereas gender (p<0.001) and renal function (p=0.01) turned out to be significant predictors of LBM. No effects of corticosteroids were observed. Exercise capacity and muscle strength seem equally reduced in RTx and HD patients compared to controls. In RTx patients, muscle strength and PAL are highly related to exercise capacity. Renal function appears to be a significant predictor of LBM, and through the LBM, of muscle strength and exercise capacity.
BACKGROUND: Recent studies have demonstrated that exercise capacity is an independent predictor of mortality in women. Normative values of exercise capacity for age in women have not been well established. Our objectives were to construct a nomogram to permit determination of predicted exercise capacity for age in women and to assess the predictive value of the nomogram with respect to survival. METHODS: A total of 5721 asymptomatic women underwent a symptom-limited, maximal stress test. Exercise capacity was measured in metabolic equivalents (MET). Linear regression was used to estimate the mean MET achieved for age. A nomogram was established to allow the percentage of predicted exercise capacity to be estimated on the basis of age and the exercise capacity achieved. The nomogram was then used to determine the percentage of predicted exercise capacity for both the original cohort and a referral population of 4471 women with cardiovascular symptoms who underwent a symptom-limited stress test. Survival data were obtained for both cohorts, and Cox survival analysis was used to estimate the rates of death from any cause and from cardiac causes in each group. RESULTS: The linear regression equation for predicted exercise capacity (in MET) on the basis of age in the cohort of asymptomatic women was as follows: predicted MET = 14.7 - (0.13 x age). The risk of death among asymptomatic women whose exercise capacity was less than 85 percent of the predicted value for age was twice that among women whose exercise capacity was at least 85 percent of the age-predicted value (P<0.001). Results were similar in the cohort of symptomatic women. CONCLUSIONS: We have established a nomogram for predicted exercise capacity on the basis of age that is predictive of survival among both asymptomatic and symptomatic women. These findings could be incorporated into the interpretation of exercise stress tests, providing additional prognostic information for risk stratification.
BACKGROUND: Peak exercise capacity improves early after orthotopic cardiac transplantation. However, the physiological response to exercise remains abnormal, with a reduced rate of heart rate (HR) rise and reductions in peak exercise HR and the increment in HR from rest to peak exercise. This chronotropic incompetence is due in large part to cardiac denervation. If reinnervation occurs after transplantation, it might result in an improvement in both chronotropic responsiveness and maximal exercise capacity. We therefore hypothesized that the chronotropic response to exercise and maximal exercise capacity would improve with time after transplantation. METHODS AND RESULTS: Peak symptom-limited cardiopulmonary exercise tests performed in 57 clinically stable cardiac transplant recipients (mean age, 45 +/- 2 years) serially for up to 5 years after transplantation and in 33 control subjects without heart disease were analyzed retrospectively. Pretransplantation exercise tests were also performed in 41 patients an average of 4.7 +/- 0.6 months before transplantation. At 1 year after transplantation, peak oxygen consumption was 16.6 +/- 0.9 mL.kg-1.min-1, reflecting a 43% increase versus pretransplantation. Nevertheless, compared with control subjects, maximal exercise capacity and the HR response to exercise were subnormal in transplant recipients. There were no further increases in peak exercise capacity, peak exercise HR, or the peak increment in HR with exercise up to 5 years after transplantation. CONCLUSIONS: One year after cardiac transplantation, peak exercise capacity and chronotropic responsiveness are subnormal. There is no further improvement in peak exercise capacity or chronotropic responsiveness as late as 5 years after transplantation. These data indicate that with regard to chronotropic responsiveness, functionally significant cardiac reinnervation does not occur between the first and fifth years after transplantation.
A cross over study was performed in 16 cirrhotic patients with portal hypertension and oesophageal varices to assess the effects of propranolol and nitrates on the exercise capacity, respiratory minute volume and capillary oxygen saturation during exercise. All had normal peak expiratory flow rates, spirometry, chest X-ray, electrocardiography, ECHO cardiography, cardiac ejection fraction>55%, absent intra-pulmonary arterio-venous shunts (IPAVS) on contrast enhanced ECHO, and a haemoglobin>11 g/dl. Minute volume, capillary O(2) saturation and pulse rate, were measured during progressive exercise testing up to maximum exercise capacity. Testing was done on inclusion, after 1 month of treatment with propranolol (dose adequate for 25% reduction in resting pulse rate) and after another month of treatment with propranolol plus isosorbide dinitrate (ISDN). An age matched group of cirrhotics (n=9) (with no evidence of portal hypertension and had normal cardio respiratory functions as defined above) acted as controls. We observed a significant reduction in the minute volume at maximum exercise after both modes of treatment when compared to the pre-treatment values and the values of controls. There was a non-significant increase in capillary oxygen saturation. None of them had a reduction in exercise capacity after treatment. In conclusion, treatment with propranolol or a combination of propranolol and a nitrate dose not seem to impair exercise performance in patients who have hepatic cirrhosis with portal hypertension.