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PubMed1985

Improvement in exercise capacity and associated changes in hemodynamics and left ventricular function after the addition of metoprolol to nifedipine in patients with stable exertional angina.

In 10 men with stable exertional angina, the changes in exercise capacity, hemodynamics, and left ventricular (LV) function were measured after 20 mg sublingual nifedipine (N) and again after adding 100 mg oral metoprolol (M). Nifedipine alone did not significantly improve exercise workloads (+18%) and duration (+21%), but the addition of metoprolol increased both parameters by a further 37 and 32%, respectively (both p less than 0.005 vs. N). After nifedipine the onset of angina was slightly delayed (5.14 +/- 2.41 min placebo (P), 6.00 +/- 2.31 min N, p less than 0.1) and occurred at higher workloads (36 +/- 17 W P, 43 +/- 8 W N, p less than 0.1). After the addition of metoprolol, the onset of angina was delayed substantially more (9.57 +/- 2.22 min, p less than 0.001 vs. P and N) and occurred at much higher workloads (62 +/- 20 W, p less than 0.001 vs. P and N). At rest (R) and during exercise (E), nifedipine decreased systemic vascular resistance (-36% R, -27% E, both p less than 0.001) and mean arterial pressure (-18% R, -21% E, both p less than 0.001), and increased heart rate (+15% R, +11% E, both p less than 0.001), Pulmonary artery wedge pressure on exercise increased less (22 +/- 7 mmHg P, 13 +/- 5 mmHg N, p less than 0.001). After adding metoprolol, the major change was a reduced heart rate (-25% vs. N at R and E, both p less than 0.001), and arterial pressure was unaltered. Pulmonary artery wedge pressure on exercise increased to 18 +/- 5 mmHg (p less than 0.05 vs. N). Exercise LV ejection fraction and volume did not change significantly after adding metoprolol despite marked improvement in angina. In this acute exercise study in patients with stable exertional angina, metoprolol added to nifedipine markedly improved exercise capacity by preventing the increase in heart rate seen with nifedipine. In our patients with relatively normal LV function at rest, the combination was safe and produced no deleterious effects on LV function.

Administration, Oral↗

PubMed1999

Addition of angiotensin II receptor blockade to maximal angiotensin-converting enzyme inhibition improves exercise capacity in patients with severe congestive heart failure.

BACKGROUND: Incomplete suppression of the renin-angiotensin system during long-term ACE inhibition may contribute to symptomatic deterioration in patients with severe congestive heart failure (CHF). Combined angiotensin II type I (AT1) receptor blockade and ACE inhibition more completely suppresses the activated renin-angiotensin system than either intervention alone in sodium-depleted normal individuals. Whether AT1 receptor blockade with losartan improves exercise capacity in patients with severe CHF already treated with ACE inhibitors is unknown. METHODS AND RESULTS: Thirty-three patients with severe CHF despite treatment with maximally recommended or tolerated doses of ACE inhibitors were randomized 1:1 to receive 50 mg/d losartan or placebo for 6 months in addition to standard therapy in a multicenter, double-blind trial. Peak aerobic capacity (V(O2)) during symptom-limited treadmill exercise and NYHA functional class were determined at baseline and after 3 and 6 months of double-blind therapy. Peak V(O2) at baseline and after 3 and 6 months were 13.5+/-0.6, 15.1+/-1.0, and 15.7+/-1.1 mL. kg-1. min-1, respectively, in patients receiving losartan and 14.1+/-0.6, 14.3+/-0.9, and 13.6+/-1.1 mL. kg-1. min-1, respectively, in patients receiving placebo (P<0.02 for treatment group-by-time interaction). Functional class improved by at least one NYHA class in 9 of 16 patients receiving losartan and 1 of 17 patients receiving placebo. CONCLUSIONS: Losartan enhances peak exercise capacity and alleviates symptoms in patients with CHF who are severely symptomatic despite treatment with maximally recommended or tolerated doses of ACE inhibitors.

Adult↗

PubMed2002

Effects of the angiotensin-converting enzyme inhibitor alacepril on exercise capacity and neurohormonal factors in patients with mild-to-moderate heart failure.

1. Alacepril is a long-acting, sulphydryl-containing angiotensin-converting enzyme inhibitor. Data are limited regarding the effects of alacepril on exercise tolerance in patients with chronic heart failure (CHF). The aim of the present study was to determine the effects of chronic alacepril treatment on exercise capacity and neurohormones in patients with CHF. 2. The effects of 12 weeks treatment with alacepril on clinical, echocardiographic and cardiopulmonary exercise variables were studied in 18 CHF patients (mean age: 63 +/- 2 years; New York Heart Association (NYHA) class I n = 6, class II n = 10, class III n = 2) in a cross-over fashion. Resting levels of plasma noradrenaline, renin-angiotensin system activity and natriuretic peptides were evaluated. 3. Treatment with alacepril significantly improved NYHA functional class and decreased cardiothoracic ratio (60.1 +/- 2.0 vs 58.1 +/- 1.9% for baseline vs alacepril, respectively; P < 0.01). Cardiac dimensions by echocardiogram were decreased after alacepril therapy. Peak Vo2 (17.7 +/- 1.2 vs 19.5 +/- 1.3 mL/min per kg; P < 0.01) and anaerobic threshold (11.7 +/- 0.6 vs 13.2 +/- 0.9 mL/min per kg; P < 0.01) increased with alacepril treatment. Plasma noradrenaline and plasma angiotensin II levels were not altered, but plasma aldosterone (77.7 +/- 13.5 vs 51.7 +/- 9.7 pg/mL; P < 0.01), atrial natriuretic peptide (ANP; 86.5 +/- 20.3 vs 43.6 +/- 7.6 pg/mL; P < 0.05) and brain natriuretic peptide (BNP; 222.7 +/- 59.3 vs 117.7 +/- 34.3 pg/mL; P < 0.05) levels decreased after alacepril treatment. 4. These results suggest that treatment with alacepril improves functional status and exercise capacity in patients with mild-to-moderate CHF. Neurohormones were favourably influenced by alacepril therapy, with significant decreases in plasma aldosterone, ANP and BNP levels.

Aged↗

PubMed1990

Acute increase in exercise capacity with milrinone: lack of correlation with resting hemodynamic responses.

1. The acute administration of milrinone, a positive inotropic vasodilator agent, improves resting hemodynamic function and maximal and submaximal metabolic responses to exercise in patients with severe congestive heart failure. 2. To determine whether the improvement in exercise capacity induced by milrinone administration can be predicted by its acute positive inotropic and/or vasodilator effects at rest, milrinone was administered intravenously (progressive doses of 12.5 to 75 microns/kg) to 15 patients with heart failure (functional classes III and IV, New York Heart Association) at rest, and during maximal upright exercise testing on a cycle ergometer. Serum drug levels were matched for the resting and exercise tests. Drug administration for exercise tests was placebo-controlled and double-blind. 3. At rest, milrinone administration caused substantial decreases in right atrial pressure (-53%), left ventricular end-diastolic pressure (-30%), and systemic vascular resistance (-35%); and increases in cardiac index (+59%), peak positive dP/dt (+20%) and stroke work index (+51%). Administration of milrinone during exercise resulted in a 15% increase in peak oxygen uptake and a 16% increase in anaerobic threshold. However, none of the changes in resting hemodynamic function correlated significantly in magnitude with the changes in peak oxygen uptake and anaerobic threshold. 4. Thus, the acute improvement in exercise capacity that occurs with milrinone is not predicted by the positive inotropic or vasodilator effects of the drug at rest.

Anaerobic Threshold↗

PubMed2006

Influence of autonomic nervous dysfunction characterizing effect of diabetes mellitus on heart rate response and exercise capacity in patients undergoing cardiac rehabilitation for acute myocardial infarction.

BACKGROUND: The aim of this study was to clarify the influence of sympathetic and parasympathetic nerve (SN and PN) dysfunction on the heart rate (HR) response to exercise and the exercise capacity of patients with acute myocardial infarction (AMI) and diabetes mellitus (DM). METHODS AND RESULTS: Fifty-two male patients who underwent cardiopulmonary exercise testing (CPX) 1 month after onset of AMI were divided into 2 groups: (DM (+) group, n=20; DM (-) group, n=32). HR, peak oxygen uptake (VO2peak), and plasma norepinephrine (NE) levels were measured during CPX. The high-frequency power (HF) was analyzed by HR variability. The DeltaHR/logDeltaNE obtained from changes of HR and NE from rest to peak exercise and HR change from baseline to the minimum HF (DeltaHRHF) were calculated as parameters of HR response derived from SN and PN activities, respectively. DeltaHR, VO2peak, DeltaHR/logDeltaNE, and DeltaHRHF were significantly lower in the DM (+) group than in the DM (-) group, and both of them showed positive correlations with VO2peak. CONCLUSION: An inadequate HR response to exercise is a major factor causing a decline of exercise capacity, which is derived from both of SN and PN dysfunction, in AMI patients with DM.

Autonomic Nervous System↗

PubMed1998

Improvement of exercise capacity by sarpogrelate as a result of augmented collateral circulation in patients with effort angina.

OBJECTIVES: The purpose of this study was to evaluate whether a serotonin blocker, sarpogrelate, improves exercise capacity as a result of vasodilation of coronary collateral channels in patients with effort angina. BACKGROUND: Serotonin has been reported to decrease coronary collateral blood flow by collateral vasoconstriction in a canine model, suggesting that platelet activation in feeding coronary arteries of the collateral network has the potential to cause collateral vasoconstriction. METHODS: The subjects consisted of 22 patients with effort angina and reproducible ischemic threshold (group A, 11 patients with thrombolysis in myocardial infarction (TIMI) grade 2 or 3 flow of the ischemia-related coronary artery and Rentrop's collateral index 0 or 1; group B, 11 patients with TIMI grade 0 or 1 flow and Rentrop's collateral index 2 or 3). We repeated the symptom-limited treadmill exercise test using the Balke-Ware protocol and exercise tetrofosmin myocardial perfusion scintigraphy with and without pretreatment with 200 mg orally administered sarpogrelate. Each exercise test was performed at 9:00 a.m. on different days. The order of tests with and without sarpogrelate was randomized. RESULTS: In group A, sarpogrelate increased neither exercise time at 0.1 mV ST depression nor double product at 0.1 mV ST depression. In contrast, in group B sarpogrelate increased the exercise duration at 0.1 mV ST depression from 181+/-112 (SD) to 248+/-131 s (p < 0.05) and also increased the double product at 0.1 mV ST depression by 21% (p < 0.01). The severity score using myocardial perfusion scintigraphy at the same workload was significantly (p < 0.01) decreased by 37% in group B, but not in group A (11%), due to the sarpogrelate treatment. CONCLUSIONS: Sarpogrelate augments flow reserve of the collateral circulation and improves exercise capacity in anginal patients with well-developed collaterals. These findings indicate that a serotonin blocker, sarpogrelate, is useful not only as an antiplatelet drugs, but as an antianginal drug.

Aged↗

PubMed2005

Aerobic exercise capacity in normal adolescents and those with type 1 diabetes mellitus.

OBJECTIVE: To compare the aerobic exercise capacity between normal adolescents and those with type 1 diabetes mellitus (T1DM). METHODS: An experimental group with 72 individuals diagnosed with T1DM aged 9--20, time from diagnosis 4.9 +/- 3.6 yr, without clinical cardiopulmonary disease or anemia and a control group (C) with 46 healthy individuals aged 10--18, matched by age, weight, height, body mass index, and lean and fat mass (kg), underwent an incremental aerobic exercising test on a motorized treadmill, where gas exchange variables - peak pulmonary ventilation (VE), peak oxygen consumption (VO(2)), and carbon dioxide production (CO(2)) - as well as their heart rate (HR) and time to exhaustion were recorded. RESULTS: Body mass composition had no significant difference between experimental and control groups, and male and female subjects had similar exercising performances. The mean of hemoglobin A1c in the control group was 5.2+/- 0.9% and in the diabetic group 8.1+/- 2.2%; p=0.000. The patients with T1DM showed lower levels of aerobic capacity than the control group. Their respective values for each variable were as follows: (i) maximal VO(2) (T1DM: 41.57+/-7.68 vs. C: 51.12+/- 9.94 mL/kg/min; p< 0.001) and (ii) maximal VE (T1DM: 76.39+/-19.93 vs. C: 96.90 +/- 25.72 mL/kg/min; p< 0.001). Patients with T1DM also had an earlier time to exhaustion (T1DM: 8.75+/-1.60 vs. 10.82+/-1.44 min). CONCLUSIONS: Adolescent patients with T1DM showed a reduced aerobic exercising capacity when compared to healthy peers matched to anthropometric conditions. This potential condition should be taken into consideration by the time of evaluation of the aerobic performance of these patients with glycemic control level.

Adolescent↗

PubMed2002

[Impairment of ventilatory parameters and exercise capacity in patients with pulmonary hypertension and chronic heart insufficiency].

BACKGROUND AND OBJECTIVE: Chronic heart failure often coincides with secondary pulmonary hypertension. In this study the influence of pulmonary hypertension on exercise capacity and ventilatory parameters in patients with chronic heart failure was examined. PATIENTS AND METHODS: 21 patients with chronic heart failure (six women, 15 men, mean age 55 +/- 10 years) and a left ventricular ejection fraction of 25 % +/- 5 % were studied by right heart catheterization, bodyplethysmography including carbonmonoxide diffusion testing and spiroergometry. Seven patients suffered from ischemic and 14 patients from dilative cardiomyopathy. Pulmonary hypertension (defined as pulmonary artery mean pressure > 25 mmHg) was found in ten patients. RESULTS: Patients with pulmonary hypertension showed a reduced vital capacity (75 % +/- 20 % of normal values vs. 93 % +/- 14 % of normal values, p < 0.001), a lower forced expiratory volume in one second (FEV1 68 % +/- 21 % of normal values vs. 91 % +/- 15 % of normal values, p < 0.001), and a reduced carbonmonoxide-diffusing capacity (58 % +/- 21 % vs. 77 % +/- 21 %, p < 0.001) compared to patients without pulmonary hypertension. Mean expiratory flow at 25 % and 75 % of the exspiration time was lower in patients with pulmonary hypertension (30 % +/- 13 % vs. 50 % +/- 29 % and 62 % +/- 25 % vs. 81 % +/- 20 %, each p < 0.05). In patients with pulmonary hypertension, the flow-volume diagram characteristically showed signs of "small airway disease". Spiroergometry revealed a significantly lower maximum oxygen-uptake (12.5 +/- 2.1 vs. 15.2 +/- 4.1 ml/min/kg, p < 0.05), oxygen-uptake at the anaerobic threshold (9.7 +/- 1.6 vs. 12.0 +/- 3.0 ml/min/kg, p < 0.05), carbon dioxide ventilatory efficiency (EqCO2 38 +/- 9 vs. 31 +/- 3, p < 0.05) and ventilatory reserve (39 % +/- 22 % vs 51 % +/- 21 %, p < 0.05) in patients with pulmonary hypertension. CONCLUSION: In patients with chronic heart failure the presence of pulmonary hypertension leads to a reduction of exercise capacity and impaired ventilatory parameters. Lung functional testing reveals bronchial obstruction, "small airway disease" and a reduced ventilatory efficiency.

Cardiac Catheterization↗

PubMed2002

[Cardiopulmonary exercise capacity in adult patients with atrial septal defect].

UNLABELLED: The aim of the study was to evaluate cardiopulmonary exercise capacity (WTS) in adult patients with atrial septal defect (ASD). After excluding 10 patients with additional cardiac, pulmonary or muscle diseases, 53 patients with ASD (Gr-ASD; mean age 37.8 +/- 14.9 years; 35 women, 19 men) were enrolled in our study. In addition, we evaluated 22 healthy age and gender matched control subjects (Gr-K; mean age 36.6 +/- 14.9 years; 13 women, 9 men). First, all subjects underwent resting spirometry and forced vital capacity--(FVC; % of predicted value), one-second forced expiratory volume--(FEV1; % of predicted value) and FEV1/FVC (%) were determined. Then each subject performed a symptom-limited, incremental exercise test (modo Bruce). We evaluated the following parameters of resting metabolism: respiratory rate--(RR; L/min), minute ventilation--(VE; L/min), tidal volume--(Vt; L), oxygen uptake--(VO2; ml/kg/min), end-tidal carbon dioxide pressure--(PET CO2; mmHg), end tidal oxygen pressure--(PET O2; mmHg), ventilatory equivalent for carbon dioxide--(VE/VCO2) and ventilatory equivalent for oxygen--(VE/VO2). The following exercise parameters were analysed: peak oxygen uptake--(VO2 peak; ml/kg/min), VO2 peak expressed as % of predicted value--(VO2 %N), anaerobic threshold--(AT; % VO2 max), ventilatory equivalent for carbon dioxide--(VE/VCO2), end-tidal carbon dioxide pressure--(PET CO2; mmHg), O2 pulse, time of exercise--(T; min) and time to AT--(TAT; min). In addition, we performed a subgroup analysis for ASD patients below and > or = 40 years of age. All values were expressed as mean +/- SD. RESULTS: Although there was no significant difference in FVC, FEV1, FEV1/FVC, VO2, VE, Vt, RR between ASD patients and controls, the ASD patients aged 40 or older showed significantly lower FEV1/FVC and significantly higher RR. Expiratory gas exchange analysis showed significant differences between the ASD patients and controls (higher VE/VCO2, VE/VO2, PET CO2, and lower PET O2 respectively). Moreover, VO2 peak, VO2%N, AT, PET CO2 and O2 pulse were significantly lower while VE/VCO2 was significantly higher in ASD patients than in normal subjects. On average, VO2%N in ASD patients was only 61% of the predicted value for age and sex. Total time of exercise and time to AT were significantly shorter in ASD patients as well. CONCLUSIONS: WTS allows appropriate evaluation of cardiopulmonary capacity in ASD patients, though the mechanisms underlying ventilatory and hemodynamic abnormalities are still not fully understood. Adult patients with ASD reveal ventilatory abnormalities with an age-related trend towards deterioration. Cardiopulmonary exercise capacity in adults with ASD is markedly reduced in comparison with healthy population and deteriorates with age. WTS complements echocardiographic and hemodynamic evaluation of patients with ASD, and is helpful in indicating patients for ASD closure and their follow up.

Adult↗

PubMed1994

Contribution of specific skeletal muscle metabolic abnormalities to limitation of exercise capacity in patients with chronic heart failure: a phosphorus 31 nuclear magnetic resonance study.

Several studies of phosphorus 31 (31P) magnetic resonance spectroscopy (MRS) have demonstrated the presence of skeletal muscle metabolic abnormalities during exercise in patients with chronic heart failure (CHF). We studied the contribution of these abnormalities to the limitation of exercise capacity in CHF. In 25 patients (age 57 +/- 2 years, left ventricular ejection fraction [LVEF] 28% +/- 1.6%, peak oxygen consumption (VO2) 16 +/- 1.2 ml/kg/mm) (mean +/- SEM), we studied the calf muscle at rest and during plantar flexion with 31P MRS. The phosphocreatine (PCr) depletion rate was significantly negatively correlated to peak VO2 (r = -0.62, p = 0.001) but not to LVEF. Muscle pH was correlated with the inorganic phosphorus (Pi)/PCr ratio (r = -0.69, p = 0.0001) and with the PCr/adenosine triphosphate beta (ATP beta) ratio (which negatively relates to adenosine diphosphate [ADP] concentration) (r = 0.65, p = 0.00001). Although muscle ATP (ATP/sum of phosphorus [sigma P] remained stable, in 8 patients ATP/sigma P decreased significantly (-15% +/- 4%, p = 0.0002). In this ATP-depleted group, peak VO2 was significantly lower than that of the nondepleted group and PCr depletion more rapid, whereas LVEF did not differ. Skeletal muscle metabolic abnormalities in CHF contribute markedly to the alteration of exercise capacity. Rapid PCr depletion and muscle acidosis are the most relevant abnormalities. ATP depletion and excessive increase in ADP during exercise may contribute further to exercise limitation specifically in patients with more marked CHF.

Adenosine Diphosphate↗

PubMed1995

Benefit of selective respiratory muscle training on exercise capacity in patients with chronic congestive heart failure.

BACKGROUND: Diminished respiratory muscle strength and endurance have been demonstrated in patients with heart failure. This may contribute to exertional dyspnea and reduced exercise capacity in these patients. The purpose of this study was to investigate whether selective respiratory muscle training could alleviate dyspnea and improve exercise performance in patients with chronic congestive heart failure. METHODS AND RESULTS: Fourteen patients with chronic heart failure (left ventricular ejection fraction, 22 +/- 9%) were enrolled in a supervised respiratory muscle training program. This consisted of three weekly sessions of isocapnic hyperpnea at maximal sustainable ventilatory capacity, resistive breathing, and strength training. Maximum sustainable ventilatory capacity, maximum voluntary ventilation, maximal inspiratory and expiratory pressures, peak VO2, and the 6-minute walk test were measured before (pre) and after (post) 3 months of training. Eight patients completed the training program. Respiratory muscle endurance was improved with training, as evidenced by increases in maximal sustainable ventilatory capacity (pre, 48.6 +/- 10.7 versus post, 76.9 +/- 14.5 L/min; P < .05) and in maximal voluntary ventilation (pre, 100 +/- 36 versus post, 115 +/- 39 L/min; P < .05). Respiratory muscle strength was also increased with training as maximal inspiratory (pre, 64 +/- 31 versus post, 78 +/- 33 cm, H2O; P < .01) and expiratory (pre, 94 +/- 30 versus post, 133 +/- 53 cm H2O; P < .001) pressures rose. Submaximal and maximal exercise capacity were significantly improved with selective respiratory muscle training as the 6-minute walk (pre, 1101 +/- 351 versus post, 1421 +/- 328 ft; P < .001) and peak exercise VO2 (pre, 11.4 +/- 3.3 versus post, 13.3 +/- 2.7 mL.kg-1.min-1; P < .05) both significantly increased. Dyspnea during activities of daily living was subjectively improved in the majority of trained patients. Dyspnea quantified by the Borg scale was significantly reduced during progressive isocapnic hypernea but not during bicycle exercise. No statistically significant improvement in maximal sustainable ventilatory capacity, maximum voluntary ventilation, maximal inspiratory or expiratory mouth pressures, 6-minute walk, or peak VO2 was observed in the 6 patients who did not complete the training program. CONCLUSIONS: Selective respiratory muscle training improves respiratory muscle endurance and strength, with an enhancement of submaximal and maximal exercise capacity in patients with heart failure. Dyspnea during activities of daily living was subjectively improved in the majority of trained patients.

Adult↗

PubMed2005

Rosiglitazone improves exercise capacity in individuals with type 2 diabetes.

OBJECTIVE: Although exercise is recommended as a cornerstone of treatment for type 2 diabetes, it is often poorly adopted by patients. We have noted that even in the absence of apparent cardiovascular disease, persons with type 2 diabetes have an impaired ability to carry out maximal exercise, and the impairment is correlated with insulin resistance and endothelial dysfunction. We hypothesized that administration of a thiazolidinedione (TZD) agent would improve exercise capacity in type 2 diabetes. RESEARCH DESIGN AND METHODS: Twenty participants with uncomplicated type 2 diabetes were randomly assigned in a double-blind study to receive either 4 mg/day of rosiglitazone or matching placebo after baseline measurements to assess endothelial function (brachial artery diameter by brachial ultrasound), maximal oxygen consumption (VO(2max)), oxygen uptake (VO(2)) kinetics, and insulin sensitivity by hyperinsulinemic-euglycemic clamp. Measurements were reassessed after 4 months of treatment. RESULTS: Participant groups did not differ at baseline in any measure. Rosiglitazone-treated participants (n = 10) had significantly improved VO(2max) (19.8 +/- 5.3 ml . kg(-1) . min(-1) before rosiglitazone vs. 21.2 +/- 5.1 ml . kg(-1) . min(-1) after rosiglitazone, P < 0.01), insulin sensitivity, and endothelial function. A change in VO(2max) correlated with improved insulin sensitivity measured by clamp (r = 0.68, P < 0.05) and with improved brachial artery diameter (r = 0.70, P < 0.05). Placebo-treated participants (n = 10) showed no changes in VO(2max) (19.4 +/- 5.2 ml . kg(-1) . min(-1) before rosiglitazone vs. 18.1 +/- 5.3 ml . kg(-1) . min(-1) after rosiglitazone, NS) or brachial artery diameter. CONCLUSIONS: This is the first known report showing that a TZD improved exercise function in type 2 diabetes. Whether this is due to the observed improvements in insulin sensitivity and/or endothelial function or to another action of the TZD class requires further exploration.

Adipose Tissue↗

PubMed1988

Initial clinical experience with a minute ventilation sensing rate modulated pacemaker: improvements in exercise capacity and symptomatology.

A minute ventilation sensing rate modulated pacemaker was implanted in nine patients with bradycardia. Minute ventilation is sensed in this pacemaker by means of a standard bipolar pacing electrode. Compared with exercise in the constant rate ventricular pacing (VVI) mode at 1 month after pacemaker implantation, rate responsive pacing resulted in an improvement of exercise capacity of 33 +/- 5% (from 437 +/- 42 s in the VVI mode to 593 +/- 57 s in the rate modulated mode, P less than 0.01, Bruce protocol). This improvement was maintained in the seven patients in whom an exercise test was repeated at 3 months after implantation. The pacing rate was significantly correlated with oxygen consumption (r = 0.84 +/- 0.04) and measured minute ventilation (r = 0.76 +/- 0.06). Symptomatology in these patients was assessed by means of self-assessment questionnaires in a double blind, randomized cross-over study in which the pacemaker was alternatively programmed into the VVI and rate modulated modes. Significant improvements in "shortness of breath" and "energy during daily activities" were documented during rate modulated pacing and "palpitations" and "chest pain" were not worsened. Most patients preferred the rate modulated mode during the study. In conclusion, rate modulated pacing by sensing minute ventilation resulted in better exercise capacity and symptomatology. The pacing rate also showed good correlation with the individual's oxygen requirement.

Adult↗

PubMed2004

Effect of high-salt diet or chronic captopril treatment on exercise capacity in normotensive rats.

1. We investigated whether chronic suppression of the renin-angiotensin system, which is known to be associated with reductions in microvascular density and vasodilator responsiveness of skeletal muscle, could affect exercise capacity in normotensive rats. 2. Rats were placed on normal rat chow, normal rat chow with captopril (100 mg/kg per day) or a high-salt diet (HS; 4%) for 4 weeks. Following these interventions, rats with indwelling carotid artery catheters were submitted to stepwise increasing exercise on a motor treadmill at a speed of 10, 20 and 30 m/min for 4 min while blood lactate was measured. 3. Blood lactate after exercise at a speed of 20 m/min was significantly higher and the duration during which rats were able to run at a speed of 30 m/min was significantly shorter in captopril-treated rats and rats fed an HS diet compared with control rats. 4. We conclude that chronic treatment with captopril or HS diet could reduce the exercise capacity in inactive normotensive rats, probably through chronic inhibition of the renin-angiotensin system.

Animals↗

PubMed1999

Effect of terbutaline on exercise capacity and pulmonary function in patients with chronic obstructive pulmonary disease.

The objective of this study was to investigate the effects of a single dose of a beta2-agonist, terbutaline (Bricanyl Turbuhaler), on resting lung function and exercise capacity in patients with chronic obstructive lung disease. Using a double-blind, placebo-controlled, randomized crossover study and outpatients from a department of pulmonary medicine at a major inner-city hospital, we examined 26 individuals with chronic obstructive lung disease who met the criteria of 40% </= FEV1 </= 70% of predicted, FEV1/FVC </= 70%, and DeltaFEV1 </= 200 ml 20 min after inhalation of 1 mg of terbutaline. The patients inhaled 2.5 mg of terbutaline and matched placebo. At rest, terbutaline caused significant increases in DLCO, MVV12sec, and all spirometric indices derived from the flow-volume loop, the increases also being significantly larger than those after inhalation of 1 mg of terbutaline for FEV1, FVC, and PEF. The peak work rate was unchanged after terbutaline. Oxygen uptake, ventilation, and tidal volume at peak work rate increased significantly, whereas carbon dioxide elimination increased insignificantly. Cumulative oxygen uptake and carbon dioxide elimination during progressive exercise to exhaustion and 10 min of recovery were significantly higher after terbutaline. We concluded that despite significant improvements in resting lung function, inhalation of 2.5 mg of terbutaline did not increase exercise capacity, but it increased cumulative oxygen uptake and carbon dioxide elimination during exercise and recovery, presumably because of a thermogenic effect of terbutaline.

Administration, Inhalation↗

PubMed1999

Systolic and diastolic cardiac function time intervals and exercise capacity in women.

PURPOSE: To determine the relationship between exercise capacity and resting cardiac function time intervals in women. METHODS: The noninvasive method of seismocardiography was used to measure resting cardiac intervals in 12 female subjects. On the basis of maximal treadmill time (Bruce protocol), two groups were studied and categorized as long duration runners (LDR; N = 6) or short duration runners (SDR, N = 6). The following resting atrial and left ventricular (LV) cardiac function time intervals were determined: atrial systole, LV systole, LV diastole, LV isovolumetric contraction, LV isovolumetric relaxation, LV ejection, LV preejection, LV filling, LV rapid filling, and Tei index. RESULTS: Heart rate (HR) (65+/-3 vs 61+/-4 b x min(-1) for LDR and SDR, respectively; P = NS) and atrial systolic time (75+/-6 vs 81+/-5 ms for LDR and SDR, respectively; P = NS) were similar between groups. LV systole (348+/-15 vs 302+/-8 ms for LDR and SDR, respectively; P < 0.05) and LV ejection (297+/-13 vs 247+/-7 ms for LDR and SDR, respectively; P < 0.01) were longer in LDR, despite a similar LV isovolumetric contraction time. There was a general trend for a shortened LV diastole in LDR with a significantly shortened LV isovolumetric time in LDR (80+/-8 vs 107+/-8 ms for LDR and SDR, respectively; P < 0.05). LV preejection was shorter in LDR versus SDR (LDR; 114+/-6 vs SDR; 130+/-3 ms, P < 0.05), and the Tei index was less in LDR versus SDR. CONCLUSIONS: Independent of HR, increased treadmill time in young women is associated with greater resting systolic time intervals and decreased diastolic cardiac function time intervals.

Adult↗

PubMed1988

Exercise capacity prior to myocardial infarction relates inversely to enzyme activity during infarction.

Epidemiological studies suggest that myocardial infarction occurs less commonly in physically fit individuals, indicating an inverse relationship between fitness and coronary arterial disease. In this study, the exercise capacity measured prior to infarction, was related to enzyme activity during subsequent infarction. Out of 512 consecutive male patients with acute infarction 35 were found who had previously performed an eligible exercise test. The exercise capacity was inversely related to enzymic activity during the infarction.

Adult↗

PubMed1995

The effects of radiofrequency ablation versus medical therapy on the quality-of-life and exercise capacity in patients with accessory pathway-mediated supraventricular tachycardia: a treatment comparison study.

This study aims to evaluate the impact of transcatheter radiofrequency ablation on quality-of-life (QOL) and exercise capacity in patients with paroxysmal supraventricular tachycardia (SVT) on stable medical therapy and the extent of symptomatic benefits of this treatment in patients with SVT of different clinical severity. A total of 55 patients with SVT on stable medications for 3 months were randomly selected for either radiofrequency ablation treatment (46 patients) or continuation of medical therapy (medical control group, 9 patients). Severity of SVT was classified based on the frequency and duration of SVT episodes, hemodynamic disturbance, and the presence of preexcited atrial fibrillation during an episode. Treadmill exercise capacity (Bruce protocol) and QOL (questionnaire study and interview) were assessed before and at 3-month intervals for 1 year after the radiofrequency procedure and at 3 months in the medical control group. Thirty-six of 46 patients were successfully ablated in one session, and a QOL measure before and at 3 months after ablation in these patients showed an improvement in total scores for "General Health Questionnaire" (20.3 +/- 6.2 vs 16.9 +/- 5.3, P < 0.01), "Somatic Symptoms Inventory" (73.0 +/- 6.0 vs 76.1 +/- 4.1, P < 0.02), and "Sickness Impact Profile" (12.6 +/- 1.7 vs 4.9 +/- 3.9, P < 0.01). This improvement in QOL was progressive and sustained over a 1-year period. Major arrhythmia limitations, such as apprehension of strenuous activities and long distance travel, were alleviated after a successful procedure. The extent of improvement in QOL was significant for patients considered to have "mild" or "severe" arrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗