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Sumatriptan reduces exercise capacity in healthy males: a peripheral effect of 5-hydroxytryptamine agonism?

5-Hydroxytryptamine (5-HT; serotonin) has been implicated in the perception of exercise-induced fatigue. Sumatriptan is a selective 5-HT(1B/D) receptor agonist which does not cross the blood-brain barrier. The aim of the present study was to determine the effect of sumatriptan on exercise capacity. Ten healthy male subjects (mean age 28.4+/-10.8 years) performed a maximal treadmill exercise test according to the Bruce protocol with expired gas analysis on two occasions. Either 6 mg of sumatriptan or placebo was administered subcutaneously in a randomized, double-blind, placebo-controlled, cross-over design. Exercise time was greater after placebo compared with sumatriptan [914 and 879 s respectively; 95% confidence interval (CI) of difference 12.1 s, 59.1 s; P = 0.008]. There was no significant effect on peak oxygen consumption (placebo, 50.6+/-6.3 ml.min(-1).kg(-1); sumatriptan, 51.7+/-7.6 ml.min(-1).kg(-1)). Sumatriptan administration resulted in decreases in both heart rate (sumatriptan, 188+/-14 beats/min, placebo, 196+/-12 beats/min; 95% CI of difference 12.6, 2.6; P = 0.008) and respiratory exchange ratio (sumatriptan, 1.23+/-0.06; placebo, 1.26+/-0.07; 95% CI of difference 0.05, 0.01; P = 0.01) at peak exercise. There were no significant differences in blood pressure, heart rate or submaximal oxygen consumption between sumatriptan and placebo treatments at any stage of exercise. Thus sumatriptan reduces maximal exercise capacity in normal males. The failure to demonstrate any haemodynamic or cardiorespiratory effect suggests that sumatriptan enhances perception of fatigue by a peripheral mechanism affecting 5-HT modulation.

Adult↗

Comparison of doxazosin and atenolol in mild hypertension, and effects on exercise capacity, hemodynamics and left ventricular function.

The effects of once-daily therapy with doxazosin (1 to 8 mg/day) on exercise capacity, left ventricular performance and hemodynamics (radionuclide ventriculography) were compared with those of atenolol (50 to 100 mg/day) and placebo in a randomized, double-blind crossover trial in 16 patients (9 men) with mild hypertension. Both medications controlled blood pressure (BP) to a similar degree (mean BP was 150 +/- 12, 137 +/- 17 and 141 +/- 14 mm Hg for placebo, atenolol and doxazosin, respectively) but by different mechanisms. Changes during maximal semierect bicycle exercise were similar to those seen at rest. Doxazosin decreased total peripheral resistance and maintained cardiac output, whereas atenolol decreased cardiac output. Exercise capacity (136 +/- 56 watts with placebo) was maintained by doxazosin (135 +/- 56 watts) but decreased with atenolol (122 +/- 55 watts). Compared with atenolol, doxazosin slightly increased the left ventricular ejection fraction at rest and during exercise. The significance of this study is in the choice of a first-line antihypertensive agent. Both are once-a-day medications that control BP. However, doxazosin does so by improving the abnormal physiology of essential hypertension and, consequently, does not adversely affect exercise performance.

Antihypertensive Agents↗

Hemoglobin-based oxygen carrier preserves submaximal exercise capacity in humans.

OBJECTIVE: The objective of this study was to evaluate the exercise capacity of subjects given an autologous transfusion or a polymerized bovine hemoglobin solution to define the pharmacodynamics and pharmacokinetics of a new hemoglobin-based oxygen carrier (HBOC-201). METHODS: Six normal healthy male subjects (ages 25 to 45 years) participated in this randomized, single-blind, two-way crossover study, which took place at Upjohn Research Clinics in Kalamazoo, Mich. A radial artery catheter was inserted in each subject before serial cardiac output and pulmonary function tests and phlebotomy of 15% blood volume (750 ml plus another 250 ml for study laboratories yields 1000 ml, or about 150 gm human hemoglobin). This was followed by isovolemic hemodilution with Ringer's lactate plus an autologous blood transfusion (or HBOC-201) and 1 week later 45 gm bovine hemoglobin of HBOC-201 (or autologous transfusion). Bicycle exercise stress tests to anaerobic threshold (approximately 65% of predicted maximum aerobic capacity) were done before phlebotomy and at approximately 45 minutes after the autologous transfusion or HBOC-201 infusion. RESULTS: Subjects had similar exercise and diffusion capacity but lower lactate levels (for up to 24 hours) during HBOC-201 (which paralleled plasma HBOC-201 levels) than during autologous transfusion periods. Oxygen use (uptake) and carbon dioxide production at rest were greater during the HBOC-201 infusion than during the autologous transfusion period. The half-life of HBOC-201 was about 23 hours. CONCLUSIONS: Exercise capacity and diffusion capacity were similar after HBOC-201 and autologous transfusion. HBOC-201 resulted in greater oxygen (or uptake) and carbon dioxide production and lower lactate levels compared with autologous transfusion. Under the conditions of the study, the physiologic effects of 1 gm bovine hemoglobin of HBOC-201 were similar to 3 gm human hemoglobin from autologous transfusion.

Adult↗

[The acute and chronic effects of bunazosin on exercise capacity estimated by the anaerobic threshold in patients with chronic congestive heart failure].

To study the effect of bunazosin on exercise capacity in patients with congestive heart failure (NYHA II-III), anaerobic thresholds (AT, VO2, ml/min/kg) were measured before (control) and after initial 1 = 2mg administration of bunazosin (acute phase; N = 14) and after two weeks of bunazosin therapy (3mg/day, 1mg t. i. d., chronic phase; N = 6). AT were determined by Wasserman's V-slope method during ergometer exercise test with a ramp loading (10 watt/min). AT increased significantly from control during both acute (14.2 +/- 2.7 to 16.9 +/- 3.6 ml/min/kg p < 0.005) and chronic (13.6 +/- 2.5 to 16.7 +/- 1.0 p < 0.05) phase. Additionally, work (watt) attained at AT increased significantly from control during both acute (33.6 +/- 19.2 to 52.6 +/- 30.2 p < 0.005) and chronic (35.8 +/- 25 to 49.3 +/- 15 p < 0.05) phase. Pressure-rate-products (PRP, x 10(2) mmHg/min) at AT increased significantly from control during the acute phase (119 +/- 35 to 240 +/- 50 p < 0.005) alone. In the chronic phase, PRP decreased significantly at the work level equal to AT during control (from 207 +/- 41 to 187 +/- 39 p < 0.05). These data suggest that bunazosin has favorable acute and chronic effects on exercise capacity in patients with congestive heart failure.

Adult↗

Influence of creatine monohydrate ingestion on muscle metabolites and intense exercise capacity in individuals with multiple sclerosis.

OBJECTIVE: To evaluate the effectiveness of ingesting creatine monohydrate in elevating intramuscular creatine stores and improving exercise capacity in individuals with multiple sclerosis (MS). DESIGN: Randomized, double-blind, placebo-controlled, pre-posttrial. SETTING: A university-based exercise physiology laboratory. PARTICIPANTS: Sixteen individuals with relapsing-remitting MS (median Expanded Disability Status Scale score, 4.75; range, 1.5-6.0). INTERVENTION: Eight individuals with MS were randomized to the creatine group (20g/d of creatine monohydrate for 5d), and 8 others were randomized to the placebo group. Needle biopsies were performed on the vastus lateralis at rest before and after treatment. Subjects performed 3 bouts of 30 maximal knee extensions and flexions at 180 degrees /s with 1 minute of recovery between bouts before and after treatment. MAIN OUTCOME MEASURES: Intramuscular total creatine, phosphocreatine, free creatine, and total work output. RESULTS: Creatine ingestion did not significantly elevate intramuscular total creatine, phosphocreatine, or free creatine or improve total work production. CONCLUSION: Creatine ingestion had no significant effect on muscle creatine stores or high-intensity exercise capacity in individuals with MS.

Adult↗

Factors affecting the exercise capacity of pediatric patients with aortic regurgitation.

Although exercise testing is commonly employed to identify adult aortic regurgitation (AR) patients with early left ventricular (LV) dysfunction, the role and value of exercise testing in the management of pediatric AR patients have not been established. The purposes of this study were to evaluate the cardiorespiratory response to exercise of pediatric patients with chronic AR, examine the relation between exercise function and baseline echocardiographic measurements, and identify factors related to diminished exercise capacity (EC). The study group consisted of 26 patients aged 8 to 21 years (mean 14.4 +/- 3.7) with moderate or severe AR referred for exercise physiology testing. All patients underwent a baseline echocardiographic study and a symptom-limited, progressive cycle ergometer exercise test. LV diastolic dimension averaged 120 +/- 12% predicted, systolic dimension 112 +/- 20% predicted, shortening fraction 0.41 +/- 0.07, end-systolic wall stress 65 +/- 23 g/cm(2), and regurgitant fraction 38 +/- 16%. The average EC was 88 +/- 28% (56-143) predicted. No statistically significant correlation was found between EC and any of the echocardiographic parameters studied. Nine patients had EC < 75% predicted. These individuals did not differ from patients with higher EC with regard to any of the echocardiographic parameters or with regard to peak heart rate, blood pressure, respiratory exchange ratio, and incidence of ectopy or ST depression. However, the oxygen pulse at peak exercise (an index proportional to forward stroke volume at peak exercise) was significantly depressed among patients with EC < 75% predicted (77 +/- 6 vs. 106 +/- 16% predicted, p <. 0001). In conclusion, most pediatric patients with moderate or severe AR compensate well for their valve disease, maintain normal forward stroke volume during exercise, and have normal EC. However, a subset of AR patients have diminished EC secondary to an inability to augment forward stroke volume appropriately. These patients cannot be identified on the basis of resting echocardiographic studies. Timely identification of these patients, through formal exercise physiology testing, may have important clinical implications.

Adolescent↗

Skeletal muscle lactate accumulation and creatine phosphate depletion during heavy exercise in congestive heart failure. Cause of limited exercise capacity?

OBJECTIVE: To study the mechanisms of limited exercise capacity and skeletal muscle energy production in male patients with congestive heart failure. DESIGN: Muscle biopsy study. PATIENTS: Skeletal muscle metabolic response to maximal bicycle exercise was studied in 10 patients with chronic congestive heart failure (ejection fraction 0.22 +/- 0.05; peak oxygen consumption, VO2 15.1 +/- 4.9 ml.min-1.kg-1) and in nine healthy subjects (peak VO2 33.5 +/- 6.7 ml.min-1.kg-1). Activities of skeletal muscle enzymes were measured from the vastus lateralis muscle of 48 patients (ejection fraction 0.24 +/- 0.06, peak VO2 17.4 +/- 5.4 ml.min-1.kg-1) and 36 healthy subjects (peak VO2 38.3 +/- 8.4 ml.min-1.kg-1). RESULTS: Although blood lactate levels were lower in patients than in healthy subjects (2.2 +/- 0.3 vs 5.2 +/- 0.6 mmol.l-1; P < 0.001) at peak exercise (96 +/- 11 W for patients and 273 +/- 14 W for controls), skeletal muscle lactate was similarly elevated (25.6 +/- 3.2 vs 22.7 +/- 2.7 mmol.kg-1) and creatine phosphate was equally depressed (P < 0.02) to low levels (7.0 +/- 1.9 vs 6.7 +/- 0.9 mmol.kg-1). The muscle ATP decreased by 21% (P < 0.05) and 8% (P < 0.01) in the patients and controls, respectively. Activities of rate limiting enzymes of the citric acid cycle (alpha-ketoglutarate dehydrogenase) and oxidation of free fatty acids (carnitine palmitoyltransferase II) were 48% and 21% lower than in controls, but the mean phosphofructokinase activity was unchanged in congestive heart failure. CONCLUSIONS: It seems that the main limiting factor of exercise performance during heavy exercise is the same in congestive heart failure and healthy subjects, a high rate of skeletal muscle lactate accumulation and high-energy phosphate depletion. In congestive heart failure, the low activity of aerobic enzymes is likely to impair energy production and lead to lactate acidosis at low workloads.

Adenosine Triphosphate↗

Diltiazem improves cardiac function and exercise capacity in patients with idiopathic dilated cardiomyopathy. Results of the Diltiazem in Dilated Cardiomyopathy Trial.

BACKGROUND: Evidence is arising that calcium antagonists in idiopathic dilated cardiomyopathy (IDC) may have beneficial effects on virus-induced cardiopathology, alcohol toxicity, micro-circulatory disorders, and impaired calcium cycling, all possibly involved in the pathogenesis of the disease. Thus, the effect of adjunct diltiazem (60 to 90 mg TID) on standard treatment was investigated. METHODS AND RESULTS: The Diltiazem in Dilated Cardiomyopathy (DiDi) trial was a randomized, double-blind, placebo-controlled, multicenter trial of 186 patients (92 receiving diltiazem, 94 receiving placebo) with IDC diagnosed by coronary angiography, catheterization of the left side of the heart, and a left ventricular ejection fraction of < 0.50 (mean, 0.34 +/- 0.11). The effect of adjunct diltiazem treatment on transplant listing-free survival, hemodynamics, exercise capacity, and subjective status was investigated. During the 24-month study period, 33 patients dropped out of the study; 153 patients finished the study protocol. Twenty-seven patients died or had a listing for heart transplantation: 16 in the placebo group and 11 in the diltiazem group. The transplant listing-free survival rate was 85% for diltiazem and 80% for placebo recipients (P = .444). After 24 months, only diltiazem significantly increased cardiac index at rest (P = .01) and under a workload (P = .02), systolic and diastolic pressures (P = .003 and P = .004), stroke volume index (P = .003), and stroke work index (P = .000) and decreased both pulmonary artery pressure under workload (P = .007) and heart rate (P = .001). Diltiazem also increased exercise capacity (P = .002) and subjective well-being (P = .01). Adverse reactions were minor and evenly distributed in both groups, except for an increase in the PQ interval in the diltiazem group. CONCLUSIONS: In patients with IDC, the adjunct therapy of diltiazem improves cardiac function, exercise capacity, and subjective status without deleterious effects on transplant listing-free survival.

Calcium Channel Blockers↗

Acetazolamide reduces exercise capacity and increases leg fatigue under hypoxic conditions.

Acetazolamide (Acz) is used at altitude to prevent acute mountain sickness, but its effect on exercise capacity under hypoxic conditions is uncertain. Nine healthy men completed this double-blind, randomized, crossover study. All subjects underwent incremental exercise to exhaustion with an inspired O(2) fraction of 0.13, hypoxic ventilatory responses, and hypercapnic ventilatory responses after Acz (500 mg twice daily for 5 doses) and placebo. Maximum power of 203 +/- 38 (SD) W on Acz was less than the placebo value of 225 +/- 40 W (P < 0.01). At peak exercise, arterialized capillary pH was lower and Po(2) higher on Acz (P < 0.01). Ventilation was 118.6 +/- 20.0 l/min at the maximal power on Acz and 102.4 +/- 20.7 l/min at the same power on placebo (P < 0.02), and Borg score for leg fatigue was increased on Acz (P < 0.02), with no difference in Borg score for dyspnea. Hypercapnic ventilatory response on Acz was greater (P < 0.02), whereas hypoxic ventilatory response was unchanged. During hypoxic exercise, Acz reduced exercise capacity associated with increased perception of leg fatigue. Despite increased ventilation, dyspnea was not increased.

Acetazolamide↗

Skeletal muscle endurance training improves peripheral oxidative capacity, exercise tolerance, and health-related quality of life in women with chronic congestive heart failure secondary to either ischemic cardiomyopathy or idiopathic dilated cardiomyopathy.

Despite reported benefits of exercise training in men with chronic congestive heart failure (CHF) and in both men and women with coronary artery disease, the effects of training in women with CHF have not been throughly investigated. Therefore, 16 women (62 +/- 10 years [mean +/- SD]) with stable, moderate, chronic CHF (left ventricular ejection fraction 28 +/- 8%) were studied in a randomized crossover trial with 8 weeks of knee extensor endurance training and 8 weeks of nontraining. The effects of the exercise-based rehabilitation were assessed in skeletal muscle metabolic capacity, exercise tolerance, and quality of life. The compliance rate in training was 98% and no adverse events occurred during the study period. Training increased the activity of citrate synthase (44%, p <0.0001) and lactate dehydrogenase (23%, p <0.002) in the trained muscles, and an improved oxidative capacity in relation to the glycolytic capacity (23%, p <0.002) was found. Peak oxygen uptake (14%, p <0.0005) and peak work rate (43%, p <0.0001) during incremental exercise increased, and blood lactate concentration during standardized submaximal exercise and during the recovery phase decreased (17%, p <0.05). The distance ambulated during 6 minutes (p <0.03), and the overall (p <0.01), physical (p <0.05), and psychosocial (p <0.03) health-related quality of life improved. Because the skeletal muscle endurance training improved peripheral oxidative capacity, exercise tolerance, and the health-related quality of life without any adverse events, this mode of training can be recommended for women with chronic heart failure.

Adult↗

Reduced exercise capacity in patients with tricuspid regurgitation after successful mitral valve replacement for rheumatic mitral valve disease.

OBJECTIVE: To determine how severe tricuspid regurgitation influences exercise capacity and functional state in patients who have undergone successful mitral valve replacement for rheumatic mitral valve disease. DESIGN: 9 patients in whom clinically significant tricuspid regurgitation developed late after mitral valve replacement were compared with 9 patients with no clinical evidence of tricuspid regurgitation. The two groups were matched for preoperative clinical and haemodynamic variables. Patients were assessed by conventional echocardiography, Doppler echocardiography, and a maximal treadmill exercise test in which expired gas was monitored by mass spectrometry. SETTING: University Hospital of Wales, Cardiff. SUBJECTS: 18 patients who had been reviewed regularly since mitral valve replacement. MAIN OUTCOME MEASURE: Objective indices of exercise performance including exercise duration, maximal oxygen consumption, anaerobic threshold, and ventilatory response to exercise. RESULTS: Mitral valve prosthetic function was normal in all patients and estimated pulmonary artery systolic pressure and left ventricular function were similar in the two groups. Right ventricular diameter (median (range) 5.0 (4.3-5.6) v 3.7 (3.0-5.4) cm, p less than 0.01) and the incidence of paradoxical septal motion (9/9 v 3/9, p less than 0.01) were greater in the group with severe tricuspid regurgitation. Exercise performance--assessed by exercise duration (6.3 (5.0-10.7) v 12.7 (7.2-16.0) min, p less than 0.01), maximum oxygen consumption (11.2 (7.3-17.8) v 17.7 (11.8-21.4) ml min-1 kg-1, p less than 0.01), and anaerobic threshold (8.3 (4.6-11.4) v 0.7 (7.3-15.5) ml min-1 kg-1, p less than 0.05)--was significantly reduced in the group with severe tricuspid regurgitation. The ventilatory response to exercise was greater in patients with tricuspid regurgitation (minute ventilation at the same minute carbon dioxide production (41.0 (29.9-59.5) v 33.6 (26.8-39.3) l/min, p less than 0.01). CONCLUSIONS: Clinically significant tricuspid regurgitation may develop late after successful mitral valve replacement and in the absence of residual pulmonary hypertension, prosthetic dysfunction, or significant left ventricular impairment. Patients in whom severe tricuspid regurgitation developed had a considerable reduction in exercise capacity caused by an impaired cardiac output response to exercise and therefore experienced a poor functional outcome. The extent to which this was attributable to the tricuspid regurgitation itself or alternatively to the consequences of right ventricular dysfunction was not clear and requires further investigation.

Aged↗

The effect of inspiratory resistive training on exercise capacity in optimally treated patients with severe chronic airflow limitation.

This study was designed to determine whether inspiratory resistive training could improve the exercise performance of patients with severe chronic airflow limitation who had already received optimum conventional therapy with bronchodilators and physiotherapy. Eighteen patients were studied. Ten patients were trained with an inspiratory resistance device for six weeks and eight patients used a placebo device. Psychological factors, likely to influence exercise capacity, were taken into account. Although there was no significant increase in maximum inspiratory pressure in the ten trained subjects, inspiratory muscle endurance was improved. Exercise performance, as assessed by progressive cycle exercise, stair climbing, 12 minute walking distance and treadmill walking did not change significantly in either group. It was concluded that inspiratory muscle training, using a currently available technique, produced no additional improvement in exercise capacity beyond that achieved by conventional bronchodilator and rehabilitation therapy.

Aged↗

Atrial septal defect in adults: cardiopulmonary exercise capacity before and 4 months and 10 years after defect closure.

OBJECTIVES: The purpose of the study was to evaluate the cardiopulmonary exercise capacity and ventilatory function in adults with atrial septal defect (ASD) preoperatively and 4 months and 10 years postoperatively. BACKGROUND: Only few data are available on cardiopulmonary exercise tolerance after ASD closure, but detailed knowledge might be helpful for indication for defect closure in certain patients. METHODS: The study was performed in adult patients (mean [+/-SD] age at operation 39.9 +/- 11.5 years; left-right shunt 9.6 +/- 5.6 liters/min; pulmonary/systemic flow ratio 2.8 +/- 1.2; mean pulmonary artery pressure 18.2 +/- 6.2 mm Hg). Cardiopulmonary exercise testing was performed with a bicycle ergometer. We determined peak oxygen uptake, anaerobic threshold, performance at anaerobic threshold and maximal performance in relation to these variables in a normal group. Ventilatory function at rest was expressed by vital capacity, maximal voluntary ventilation and forced expiratory volume in 1 s. RESULTS: Preoperatively, ventilatory function at rest was only moderately reduced to approximately 75% to 85%. Four months postoperatively we found no significant improvement, but 10 years postoperatively ventilatory function at rest was normalized. Preoperative cardiopulmonary exercise capacity was markedly reduced to 50% to 60%; early postoperatively it was only slightly higher, but late postoperatively exercise capacity significantly improved and was completely normalized. CONCLUSIONS: Although preoperative cardiopulmonary capacity in adult patients with nonrestrictive ASD was significantly decreased, some improvement was seen at 4 months postoperatively, with complete restitution to normal at 10 years after shunt closure.

Adult↗

Lack of effect of increased inspired oxygen concentrations on maximal exercise capacity or ventilation in stable heart failure.

Recent uncontrolled studies have suggested improved maximal exercise capacity and decreased exercise ventilation in heart failure after administration of increased inspired oxygen concentrations. To study the responses further, 16 patients performed staged, symptom-limited cycle ergometry with humidified 21% and 60% inspired oxygen concentrations using a randomized, double-blind, crossover study design. Serial measurements of minute ventilation, heart rate, blood pressure, leg blood flow, and arterial and venous lactate and oxygen content were obtained. Exercise time did not change between the 2 tests (595 +/- 179 seconds and 602 +/- 181 seconds for 21% and 60% oxygen concentrations, respectively). Similarly, measurements of the ventilatory response to exercise and of leg blood flow were not different between the 2 oxygen concentrations. Although hemoglobin oxygen saturation increased from 96.7 +/- 2.1% to 97.9 +/- 1.5% at rest, at both rest and maximal exercise there was no statistically significant difference in arterial or venous oxygen content. This study failed to demonstrate any physiologic or functional benefit from the administration of increased oxygen concentrations to patients with stable heart failure.

Adult↗

Effects of a muscle exercise program on exercise capacity in subjects with osteoarthritis.

Maximal aerobic power and muscle function have been shown to decrease with age and to be even lower in patients with osteoarthritis (OA). This study was designed to determine if subjects with OA who underwent only a muscle exercise program had improved exercise capacity and cardiovascular fitness. A maximal graded exercise test was given before and after 3 months of exercise (isometric, isotonic, and isometric force generated as a function of time contractions, three times a week). Maximal strength and the tension-time index improved significantly. Peak aerobic power increased from 15.99 +/- 3.96 mL.kg-1.min-1 to 20.34 +/- 3.29 mL.kg-1.min-1. On average, maximal walking speed increased from 2.0 +/- 0.6 mph to 2.4 +/- 0.7mph. Exercise time increased 22%, from 9.2 +/- 2.3 minutes to 11.2 +/- 2.7 minutes. There were significant reductions in submaximal heart rate (15b.min-1) and systolic blood pressure (15mmHg) after training. It would appear that the reduction in aerobic fitness of subjects with OA is secondary to their reduced muscle function. By improving muscle function, increases in exercise capacity and aerobic fitness occurred.

Aged↗

Exercise capacity and prognosis in patients with chronic atrial fibrillation.

To evaluate the response of patients with chronic atrial fibrillation (AF) to exercise and to demonstrate if prognosis could be predicted, 200 male patients (64 +/- 1 years) with AF were identified retrospectively who underwent resting echocardiography and symptom-limited treadmill testing. They were classified by underlying disease into three subgroups: hypertension or no underlying disease (LONE; n = 102), ischemic heart disease (IHD; n = 45) and history of congestive heart failure or valvular disease (CHF-VD; n = 53). Maximal exercise capacities for LONE, IHD and CHF-VD were (mean +/- 1 SEM) 8.0 +/- 0.3, 6.4 +/- 0.4 and 6.0 +/- 0.3 metabolic equivalents, respectively (p < 0.01), and resting left ventricular ejection fractions were 61.7 +/- 1.6, 60.1 +/- 2.2 and 49.5 +/- 1.9%, respectively (p < 0.01). Stepwise multiple regression analysis demonstrated that, except for group classification (R2 = 0.13, p < 0.01), no clinical, exercise or morphologic variables could predict exercise capacity. After a mean 39.1-month follow-up (range 1-78), 17 of the 200 had died from cardiovascular causes. The rate of cardiac death using Kaplan-Meier survival analysis was significantly greater in CHF-VD patients (p < 0.01). However, Cox hazard function and Kaplan-Meier survival analysis demonstrated that neither echocardiographic measurements of cardiac size or function at rest, nor exercise or clinical variables were significant predictors of outcome. AF patients with a history of CHF and/or VD demonstrated a reduced exercise tolerance ad a worse prognosis than those without morphologic heart disease or those with IHD.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Dietary magnesium intake influences exercise capacity and hematologic parameters in rats.

The effects of feeding varying concentrations of dietary Mg (50, 100, 200, or 400 ppm) for 22 days on exercise capacity and hematologic parameters were investigated in male rats. Five-week-old male Osborne-Mendel rats fed diets containing 50 or 100 ppm Mg developed transitory priapism and hyperemia, signs of Mg deficiency. Based on a treadmill test, these rats showed a markedly lower exercise endurance capacity (four hours) than rats fed the higher levels of dietary Mg (six hours). They also showed a mild macrocytic anemia. Consumption of a mineral water containing 85 ppm Mg prevented these signs of Mg deficiency. These results show that a reduction in exercise capacity can be an early effect of Mg deficiency. Hematologic changes that occurred with Mg deficiency such as macrocytic anemia may be responsible, at least in part, for the depression of exercise observed in these rats. These data are important because they illustrate the potential significance of even a marginal deprivation of dietary magnesium.

Animals↗

Effect of a new transdermal therapeutic system containing nitroglycerin on exercise capacity in patients with angina pectoris.

In a double-blind, within-patient, randomized, placebo-controlled, acute study, the effects at rest and on exercise capacity of two doses of a new transdermal therapeutic system (TTS), releasing respectively 10 and 20 mg of nitroglycerin (NTG) over 24 hours, were assessed in 15 outpatients with stable exercise-induced angina pectoris. A symptom-limited exercise test was performed 4 and 24 hours after the application of each system. In comparison with placebo, both TTS-NTG doses induced a statistically significant (p less than 0.01) increase in total duration of exercise, in exercise duration to 1 mm ST segment depression, in maximal workload and in total work performed, at both 4 and 24 hours after dosing. Furthermore, both TTS-NTG doses induced a significant rise in the pressure-rate product, both 4 and 24 hours after dosing (p less than 0.01 and p less than 0.05, respectively). No statistical difference was found between the two doses of active drug in any of the above-mentioned evaluation parameters. The only unpleasant side effect was the typical nitrate headache, which occurred in 11 of 15 patients. In conclusion, a single application of TTS-NTG, 20 cm2 or 40 cm2, may improve exercise capacity over a 24-hour period in patients with stable exercise angina due to atherosclerotic heart disease.

Administration, Topical↗