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Exercise capacity in heart failure patients: relative importance of heart and skeletal muscle.

The knee extensor and the whole-body exercise capacities were measured in 11 chronic heart failure (CHF) patients and 11 healthy age- and sex-matched controls, and were related to ejection fraction and to biochemical and histochemical markers of the musculature. The CHF patients had a 39% lower maximal oxygen uptake measured on an ergometer cycle than the healthy controls (1.54 +/- 0.57 vs. 2.51 +/- 0.70 1 min-1, P < 0.001). The low exercise capacity was markedly related to the ejection fraction (r = 0.77, P < 0.001). The maximal strength of m. quadriceps femoris was 15% lower in the CHF patients than in the controls (P < 0.05). The cross-sectional area (CSA) of m. quadriceps femoris explained 55% (r = 0.74, P < 0.001) of the difference in strength between both groups. The endurance capacity of m. quadriceps femoris was 30% lower in CHF patients than in controls, partly as a result of the 25% lower capillary density (P < 0.05) and the 27% lower aerobic enzyme capacity (P < 0.05), as estimated by the citrate synthase activity, in the CHF patients. The citrate synthase activity correlated with the maximal oxygen uptake (r = 0.61, P < 0.05). Moreover, the ejection fraction, together with the CSA of m. quadriceps femoris, explained 75% (r = 0.86%, P < 0.01) of the difference in maximal oxygen uptake between CHF patients and controls. These results demonstrate that CHF patients have both a lower local and a lower whole-body work capacity than healthy controls. This is a function of a smaller leg muscle mass and a lower capillary density and mitochondrial enzyme capacity in the CHF patients; however, a lowered pump capacity of the heart is the factor which limits the exercise capacity the most.

Aged↗

Sildenafil increased exercise capacity during hypoxia at low altitudes and at Mount Everest base camp: a randomized, double-blind, placebo-controlled crossover trial.

BACKGROUND: Alveolar hypoxia causes pulmonary hypertension and enhanced right ventricular afterload, which may impair exercise tolerance. The phosphodiesterase-5 inhibitor sildenafil has been reported to cause pulmonary vasodilatation. OBJECTIVE: To investigate the effects of sildenafil on exercise capacity under conditions of hypoxic pulmonary hypertension. DESIGN: Randomized, double-blind, placebo-controlled crossover study. SETTING: University Hospital Giessen, Giessen, Germany, and the base camp on Mount Everest. PARTICIPANTS: 14 healthy mountaineers and trekkers. MEASUREMENTS: Systolic pulmonary artery pressure, cardiac output, and peripheral arterial oxygen saturation at rest and during assessment of maximum exercise capacity on cycle ergometry 1) while breathing a hypoxic gas mixture with 10% fraction of inspired oxygen at low altitude (Giessen) and 2) at high altitude (the Mount Everest base camp). INTERVENTION: Oral sildenafil, 50 mg, or placebo. RESULTS: At low altitude, acute hypoxia reduced arterial oxygen saturation to 72.0% (95% CI, 66.5% to 77.5%) at rest and 60.8% (CI, 56.0% to 64.5%) at maximum exercise capacity. Systolic pulmonary artery pressure increased from 30.5 mm Hg (CI, 26.0 to 35.0 mm Hg) at rest to 42.9 mm Hg (CI, 35.6 to 53.5 mm Hg) during exercise in participants taking placebo. Sildenafil, 50 mg, significantly increased arterial oxygen saturation during exercise (P = 0.005) and reduced systolic pulmonary artery pressure at rest (P < 0.001) and during exercise (P = 0.031). Of note, sildenafil increased maximum workload (172.5 W [CI, 147.5 to 200.0 W]) vs. 130.6 W [CI, 108.8 to 150.0 W]); P < 0.001) and maximum cardiac output (P < 0.001) compared with placebo. At high altitude, sildenafil had no effect on arterial oxygen saturation at rest and during exercise compared with placebo. However, sildenafil reduced systolic pulmonary artery pressure at rest (P = 0.003) and during exercise (P = 0.021) and increased maximum workload (P = 0.002) and cardiac output (P = 0.015). At high altitude, sildenafil exacerbated existing headache in 2 participants. LIMITATIONS: The study did not examine the effects of sildenafil on normoxic exercise tolerance. CONCLUSIONS: Sildenafil reduces hypoxic pulmonary hypertension at rest and during exercise while maintaining gas exchange and systemic blood pressure. To the authors' knowledge, sildenafil is the first drug shown to increase exercise capacity during severe hypoxia both at sea level and at high altitude.

3',5'-Cyclic-GMP Phosphodiesterases↗

Mechanism of improvement in exercise capacity after the maze procedure combined with mitral valve surgery.

OBJECTIVE: To clarify the mechanism of improvement in exercise capacity after the maze procedure. DESIGN: Retrospective study. SETTING: Tertiary referral centre. PATIENTS: 26 patients (mean (SD) age 57 (9) years) with atrial fibrillation (AF) and mitral valve disease were studied with echocardiography and cardiopulmonary exercise testing before and after the maze procedure combined with mitral valve surgery. Of these, eight had persistent AF and 18 had restored sinus rhythm (SR) by the surgery. Six patients (mean (SD) age 59 (12) years) with AF undergoing mitral valve surgery without the maze procedure who had cardiopulmonary exercise testing before and after the surgery formed the control group. MAIN OUTCOME MEASURES: Echocardiographic parameters of atrial function were measured from transmitral flow recordings. Peak oxygen uptake (VO2) and the slope of the relation between VO2 and workload (ratio of DeltaVO2 to Delta work) were determined as indices of exercise capacity. RESULTS: The degree of improvements in peak VO2 and the ratio of DeltaVO2 to Delta work after the mitral valve surgery was comparable between the maze and control group. It was also comparable between patients with and those without successfully restored SR after the maze procedure. The degree of the increase in peak VO2 correlated with the change in left atrial diameter (r = -0.40, p = 0.047) but atrial contraction did not correlate with the increase. CONCLUSIONS: Improvement in exercise capacity may not be caused by restored SR and atrial contraction but may at least partly relate to the reduction of left atrial size and improvement of haemodynamic variables by the surgery.

Adult↗

Effect of cold air on exercise capacity in COPD: increase or decrease?

STUDY OBJECTIVE: To clarify the effect of cold air on exercise capacity in COPD. DESIGN: Cycle ergometer tests under different environmental conditions. SETTING: Pulmonary function laboratory and an environmental chamber at a university hospital. PARTICIPANTS: Eighteen patients with stable COPD; 14 completed the study. INTERVENTIONS: A preliminary cycle ergometer test followed by two incremental, symptom-limited cycle ergometer tests, one at 24 degrees C and the other at -20 degrees C. MEASUREMENTS: On the first study day: arterial blood gas analysis, 12 to 15 s maximal voluntary ventilation, maximal expiratory flow-volume curves before and 1 h after inhalation of 80 microg of ipratropium bromide, and diffusion capacity of the lung. During the exercise challenges: spirometric indices, minute ventilation (VE), oxygen consumption (VO2), carbon dioxide production (VCO2), facial skin temperature, and heart rate. The feeling of dyspnea was assessed with a visual analogue scale. RESULTS: The maximal work load was 87.5+/-7.3 W at -20 degrees C compared with 96.4+/-6.9 W at 24 degrees C (p<0.05). Accordingly, the exercise duration was shorter in the cold. Exercise dyspnea was more severe in the cold at equal work loads. The shortening of exercise duration induced by cold air correlated with the enhancement of exercise dyspnea. Furthermore, cold air cooled the facial skin and induced immediate bronchoconstriction. VE, VO2, VCO2, and heart rate did not differ between the warm and cold challenges. CONCLUSIONS: Cold air decreases exercise capacity in COPD, probably by increasing exercise dyspnea.

Adult↗

Relationship between left ventricular diastolic function at rest and exercise capacity in patients who have suffered a previous myocardial infarction.

To assess whether left ventricular (LV) diastolic function is a determinant of exercise capacity in patients who have suffered a previous myocardial infarction (MI), we investigated the relationship between maximum exercise duration and resting LV diastolic function in 65 MI patients. Each patient underwent both a symptom-limited exercise test and LV biplane angiography with simultaneous high-fidelity pressure measurements. LV relaxation was assessed by the time constants (T1/e and T1/2) of isovolumic pressure decay, and LV diastolic distensibility was assessed by the LV end-diastolic volume (V) index-pressure (P) ratio. The time constants of relaxation did not correlate with maximum exercise capacity (r = -0.19 for T1/e, NS; r = - 0.17 for T1/2, NS). LV diastolic distensibility also did not correlate with exercise capacity (r = - 0.08, NS). These results suggest that the resting LV diastolic dysfunction is unlikely to be the principal cause of exercise intolerance in MI patients without congestive heart failure.

Adult↗

Acute and chronic effects of surgical thromboendarterectomy on exercise capacity and ventilatory efficiency in patients with chronic thromboembolic pulmonary hypertension.

OBJECTIVE: To assess acute and chronic effects of surgical thromboendarterectomy on exercise capacity and ventilatory efficiency in patients with chronic thromboembolic pulmonary hypertension (CTEPH). DESIGN: Cardiopulmonary exercise testing was performed in 20 patients with CTEPH before thromboendarterectomy (baseline), one month after (early phase), and four months after (late phase). Peak oxygen uptake (peak VO(2)) and the ventilatory response to carbon dioxide production (VE-VCO(2) slope) were measured for assessment of exercise capacity and ventilatory efficiency. Right heart catheterisation was performed in all patients before and one month after surgery. RESULTS: Baseline peak VO(2) decreased and VE-VCO(2) slope increased along with the increase in pulmonary vascular resistance in patients with CTEPH. After thromboendarterectomy, the VE-VCO(2) slope decreased greatly from baseline to the early phase (mean (SD), 50 (9) to 37 (7), p < 0.05) and reached a steady level thereafter. In contrast, a continued increase in peak VO(2) was noted from the early to the late phase (16.9 (4.1) to 21.1 (5.0) ml/kg/min, p < 0.05). The decrease in the VE-VCO(2) slope from baseline to the early phase, but not the increase in peak VO(2), correlated strongly with the decrease in pulmonary vascular resistance after surgery (r = 0.75, p < 0.01). CONCLUSIONS: Thromboendarterectomy may cause an immediate improvement in ventilatory efficiency, possibly through its beneficial haemodynamic effects. In contrast, exercise capacity may continue to improve towards the late phase, reflecting peripheral adaptation to exercise.

Acute Disease↗

The effect of acute branched-chain amino acid supplementation on prolonged exercise capacity in a warm environment.

Eight males were recruited to examine the effect of branched-chain amino acid (BCAA) supplementation on exercise capacity in a glycogen-depleted state in a warm environment. Following a exercise and dietary regimen designed to reduce glycogen availability, subjects returned to the laboratory the following morning and remained seated for 2 h, before cycling to volitional exhaustion at 50% VO2 peak in a warm environment [30.0 (0.2) degrees C; mean (SD)]. Four 250 ml aliquots of a 12 g l(-1) BCAA solution or placebo were ingested at 30 min intervals prior to exercise, with an additional 150 ml consumed every 15 min throughout exercise. BCAA ingestion had no effect on exercise capacity [placebo 103.9 (26.9) min; BCAA 111.0 (29.2) min; P = 0.129). No difference in heart rate (P = 0.345), core temperature (P = 0.628), or weighted mean skin temperature (P = 0.114) was apparent between trials. Ingestion of the BCAA solution produced a marked increase in plasma BCAA immediately prior to exercise [+ 1126 (158) micromol l(-1); P < 0.001) with this difference maintained throughout. Consequently, a significant reduction in the plasma concentration ratio of free tryptophan to BCAA was observed during the BCAA trial when compared to the placebo (P < 0.001). Plasma ammonia concentration was significantly elevated during exercise throughout the BCAA trial (P < 0.001), with no change from rest apparent during the placebo trial (P = 0.608). Blood glucose (P = 0.114) and lactate (P = 0.836) concentrations were not different between trials. Ingestion of a BCAA solution prior to, and during, prolonged exercise in glycogen-depleted subjects did not influence exercise capacity in a warm environment.

Adult↗

Exercise capacity and muscle structure in kidney recipient and twin donor.

Exercise capacity and muscle function are known to be abnormal in patients with renal disease. We present a case study in which we studied a kidney transplant recipient who received a kidney from his identical twin. Testing included maximal exercise testing with measurement of oxygen uptake (VO2max), isokinetic muscle function testing, body composition analysis using dual energy X-ray absorptiometry (DEXA) imaging and quality of life using The Medical Outcomes Short Form (SF-36) questionnaire. Muscle biopsies were also analysed for fibre composition and size and ultrastructure. We found that the twin recipient had lower values for VO2max, muscle strength, muscle mass and quality of life scales (physical domains) compared with the twin donor. Muscle fibre composition was identical in the twins, however, muscle fibres size was reduced in the twin donor in Type I, and Type IIA fibre types. The twin recipient also showed lower fibre density (volume percentage) and greater intrafibrillar space than the donor. The twins were both sedentary, thus we conclude that the low exercise capacity and abnormalities observed in the recipient are characteristics of renal failure, and not the result of physical deconditioning, nor was it related to prednisone therapy, which may negatively affect muscle function.

Absorptiometry, Photon↗

Plasma levels of atrial natriuretic peptide and of other vasoconstricting hormones in patients with chronic heart failure: relationship to exercise capacity.

We investigated the relationship between exercise capacity and the level of neurohormonal activation at rest and during exercise in patients with various degrees of severity of chronic heart failure. We performed exercise testing with measurements of peak oxygen consumption (pVo2) and blood sampling at rest and at peak exercise in eight patients with moderate heart failure (pVo2 = 17 +/- 0.4 ml/kg/min) (mean +/- S.E.M.) and eight patients with severe CHF (pVo2 = 9 +/- 1 ml/kg/min). None of the patients was taking angiotensin converting enzyme inhibitors or beta-blockers. Plasma levels of atrial natriuretic peptide, cGMP, arginine-vasopressin, renin, angiotensin II, epinephrine and norepinephrine increased significantly (P < 0.01), from rest to peak exercise, in all patients. Among all the studied neurohormonal factors, only atrial natriuretic peptide levels at rest as well as at peak exercise, in patients with severe heart failure were correlated significantly to pVo2 (r = -0.77, P = 0.04; r = -0.85, P = 0.01, respectively) and to exercise duration (r = -0.72, P = 0.05; r = -0.79; P = 0.03, respectively). The relationship between plasma levels of atrial natriuretic peptide and of cGMP was shifted downward in the more severe patients suggesting the loss of biological activity of atrial natriuretic peptide.

Adult↗

Onset of blood lactate accumulation exercise capacity, skeletal muscle fibers and metabolism before and after coronary artery bypass grafting.

Male patients with effort angina were studied before (n = 7), 1 week, and 1 and 6 months (n = 6) after coronary artery bypass grafting (CABG) with 2 to 7 grafts. The test battery included graded exercise, which was performed until unbearable leg exertion or chest pain, or both, was present. Onsets of blood lactate accumulation, anginal pain, leg exertion and dyspnea were interpolated for either the lactate concentration 2 mmol X 1-1 or the ratings 2 on the Borg subjective intensity scale. Onsets of blood lactate accumulation and symptom-limited exercise capacity before surgery amounted to 58 and 100 W, respectively. The corresponding figures 6 months later were the same for onset of blood lactate accumulation, whereas symptom-limited exercise capacity had increased by 58%. Blood lactate was the same at rest and mild exercise (congruent to onset of blood lactate accumulation) but more than doubled at symptom-limited exercise capacity (peak blood lactate concentration). Muscle fiber typing showed a low figure for the slow twitch fiber proportion (35%), which was unchanged after 6 months. Fast twitch subtype C was elevated before (7%) but disappeared after surgery, and fast twitch subtype A percent increased correspondingly. The major muscle biochemical changes were in the glycogenolytic pathway and the lactate dehydrogenase enzyme system, which appeared to increase in a quantitative manner, but with an unchanged relative lactate dehydrogenase isozyme pattern. The increased symptom-limited exercise capacity was related to the increased glycogenolytic activity and peak blood lactate (i.e., increased "anaerobic power"). Whether the causative explanation was the relief from chest pain, i.e., a psychophysiologic feature or the biochemical changes that took place in the muscle could only be speculated on.

Angina Pectoris↗

Exercise capacity and systolic and diastolic ventricular function after recovery from acute dilated cardiomyopathy.

OBJECTIVES: This study was undertaken to determine whether abnormalities in exercise capacity or ventricular function persist after recovery from acute dilated cardiomyopathy. BACKGROUND: Persistent ventricular structural abnormalities could cause abnormalities in exercise capacity or ventricular function. METHODS: The results of rest and exercise first-pass radionuclide ventriculography in 18 patients who were seen within 6 months of the onset of dilated cardiomyopathy and subsequently had a normal rest left ventricular ejection fraction were compared with those of age- and gender-matched control subjects. RESULTS: Patients were studied 144 +/- 34 (mean +/- SEM) days after the onset of left ventricular dysfunction at a time when heart failure symptoms had resolved. Patients with myocyte necrosis, as assessed by endomyocardial biopsy (n = 13) or antimyosin scintigraphy (n = 12), recovered more rapidly than did those without necrosis. Oxygen consumption both at peak exercise (17.7 +/- 1.2 vs. 26.1 +/- 1.5 ml/kg per min, p < 0.05) and at the anaerobic threshold (11.1 +/- 0.5 vs. 17.1 +/- 1.3 ml/kg per min, p < 0.05) was lower in the patients who had recovered from cardiomyopathy than in control subjects. Rest and exercise end-systolic and end-diastolic left ventricular volumes were greater in the patients than in the control subjects, although stroke volumes were similar. Left ventricular filling at rest was lower at diastolic filling intervals of 40% and 90%, and rest and exercise left ventricular early peak filling rate normalized for end-diastolic volume was slower in the patients than in the control subjects. At long-term follow-up of 1,082 +/- 206 days, two patients had a return of heart failure symptoms and a decrease in left ventricular ejection fraction. CONCLUSIONS: Despite the apparent normalization of rest left ventricular ejection fraction, patients who have recovered from dilated cardiomyopathy have abnormalities in aerobic exercise capacity and in left ventricular systolic and diastolic performance.

Acute Disease↗

Factors related to exercise capacity in asymptomatic middle-aged type 2 diabetic patients.

AIM: We aimed to look at the relationship between exercise capacity and metabolic variables in unselected consecutive asymptomatic middle-aged type 2 diabetic patients as a potential marker for undiagnosed coronary heart disease. METHOD: Ninety patients (49 +/- 6 years) were included in the study. All patients performed a treadmill exercise test using the Bruce protocol. According to achieved EC, patients were separated into three groups; Group I (n, 24) 8 > metabolic equivalents (METs) > or = 5, Group II (n, 54) 11 > METs > or = 8 and Group III (n, 12) METs > or = 11. RESULTS: Patients in group I are more likely to be of female gender and to have a family history of coronary heart disease (CHD) than in group III (P = 0.015, P = 0.009, respectively). When compared to group III, patients in group I had higher fasting insulin and fibrinogen levels (P = 0.049 and P = 0.01, respectively). Homeostasis model assessment for insulin resistance (HOMA-IR) index (P = 0.03) was also higher in group I than in group III. We found a significant negative correlation between achieved exercise capacity and age (r = -0.204, P = 0.048), fasting insulin (r = -0.209, P = 0.048), HOMA-IR (r = -0.204, P = 0.048) as well as fibrinogen (r = -0.301, P = 0.007). CONCLUSION: Reduced exercise capacity was associated with increased insulin resistance as assessed by HOMA-IR index in asymptomatic middle-aged type 2 diabetic patients.

Adult↗

Effects of blood transfusion on exercise capacity in patients with sickle-cell anemia.

Although sickle cells have increased intracellular viscosity, the viscosity of patient's blood is usually not increased, because of the low hematocrit typically found in such patients. When patients receive transfusions, their exercise capacity increases, but it is unclear whether the change is due primarily to increased hemoglobin concentration, or also reflects improved flow properties of the blood due to dilution of sickle cells with normal erythrocytes. To evaluate the relative importance of these two factors, submaximal exercise studies were performed before and after a series of transfusions. Exercise capacity improved and the patients were able to perform increased amounts of work at lower heart rates. Regression analyses indicated that the percent of sickle cells in patient's blood did not have a significant effect on exercise capacity after the transfusion-induced increase in hemoglobin concentration was taken into account. At the hematocrits typically found in patients, altered viscosity of blood due to the presence of sickle cells is much less important than hemoglobin concentration as a determinant of exercise capacity.

Adolescent↗

How relevant are exercise capacity measures for evaluating treatment effects in chronic fatigue syndrome? Results from a prospective, multidisciplinary outcome study.

OBJECTIVE: To evaluate the outcome of a multidisciplinary treatment programme for patients with chronic fatigue syndrome, including health-related quality of life (HRQoL) and psychosocial variables, and exercise capacity measures. DESIGN: A six-month prospective outcome study. SETTING: University outpatient rehabilitation clinic; group setting. SUBJECTS: One hundred and sixteen women fulfilling chronic fatigue syndrome criteria. INTERVENTIONS: Cognitive behaviourally and graded exercise-based strategies; emphasis on adaptive lifestyle changes. MEASURES: Short Form General Health Survey (SF-36); Symptom Checklist (SCL-90); Causal Attribution List (CAL); Self-Efficacy Scale (SE); maximum progressive bicycle ergometer test with respiratory gas analysis; and isokinetic leg strength test, before and after treatment. RESULTS: The total group significantly improved on nearly all reported HRQoL/psychosocial variables. Changes in exercise capacity measures were rather modest and did not correlate or only weakly correlated with HRQoL/psychosocial variables. Subgroup analyses indicated that less fit patients improved significantly more on exercise capacity measures than their more fit counterparts. Patients who were fitter at baseline scored better on pretreatment HRQoL/psychosocial variables, but both subgroups improved similarly on these variables. CONCLUSIONS: Health-related quality of life and psychosocial functioning in patients with chronic fatigue syndrome improves after a six-month cognitive behaviourally and graded exercise-based multidisciplinary treatment programme. Increase in exercise capacity measures is not a necessary condition for reported improvements, except for less fit patients.

Adaptation, Psychological↗

Relation of the nine-minute self-powered treadmill test to maximal exercise capacity and skeletal muscle function in patients with congestive heart failure.

The 9-minute self-powered treadmill test has been employed to evaluate submaximal exercise capacity in heart failure patients, but its relation to maximal exercise capacity and to indexes of skeletal muscle function has not been well defined. Two protocols were utilized. The first evaluated the relation of the peak oxygen uptake (VO2) achieved on the self-powered treadmill to that during a symptom-limited treadmill protocol, and examined the reproducibility of this test. Thirteen patients (aged 62 +/- 2 years, in New York Heart Association class I to III [2.3 +/- 0.1], ejection fraction 23 +/- 2% [means +/- SEM]) and 10 age-matched sedentary controls were studied. The second protocol, which involved 18 patients (aged 65 +/- 2 years, in New York Heart Association class I to IV [2.4 +/- 0.1], ejection fraction 23 +/- 2%) and 10 age-matched controls evaluated the relation of performance on the self-powered treadmill to maximal systemic exercise capacity on a cycle ergometer and to indexes of skeletal muscle function. In the first protocol, the test was found to be highly reproducible. The proportion of self-powered treadmill to maximal treadmill peak VO2 did not differ significantly between patients and controls (95 +/- 5% vs 87 +/- 6%). In the second protocol, patients achieved a lower peak VO2 (15.6 +/- 1.1 vs 25.6 +/- 0.9 ml/kg/min, p < 0.001), walked a shorter distance on the self-powered treadmill (367 +/- 32 vs 667 +/- 28 m, p < 0.001), and exhibited less knee extensor work capacity (1,075 +/- 116 vs 1,390 +/- 110 ft-lbs, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Relation of systemic and local muscle exercise capacity to skeletal muscle characteristics in men with congestive heart failure.

OBJECTIVES: The present study was undertaken to further characterize changes in skeletal muscle morphology and histochemistry in congestive heart failure and to determine the relation of these changes to abnormalities of systemic and local muscle exercise capacity. BACKGROUND: Abnormalities of skeletal muscle appear to play a role in the limitation of exercise capacity in congestive heart failure, but information on the changes in muscle morphology and biochemistry and their relation to alterations in muscle function is limited. METHODS: Eighteen men with predominantly mild to moderate congestive heart failure (mean +/- SEM New York Heart Association functional class 2.6 +/- 0.2, ejection fraction 24 +/- 2%) and eight age- and gender-matched sedentary control subjects underwent measurements of peak systemic oxygen consumption (VO2) during cycle ergometry, resistance to fatigue of the quadriceps femoris muscle group and biopsy of the vastus lateralis muscle. RESULTS: Peak VO2 and resistance to fatigue were lower in the patients with heart failure than in control subjects (15.7 +/- 1.2 vs. 25.1 +/- 1.5 ml/min-kg and 63 +/- 2% vs. 85 +/- 3%, respectively, both p < 0.001). Patients had a lower proportion of slow twitch, type I fibers than did control subjects (36 +/- 3% vs. 46 +/- 5%, p = 0.048) and a higher proportion of fast twitch, type IIab fibers (18 +/- 3% vs. 7 +/- 2%, p = 0.004). Fiber cross-sectional area was smaller, and single-fiber succinate dehydrogenase activity, a mitochondrial oxidative marker, was lower in patients (both p < or = 0.034). Likewise, the ratio of average fast twitch to slow twitch fiber cross-sectional area was lower in patients (0.780 +/- 0.06 vs. 1.05 +/- 0.08, p = 0.019). Peak VO2 was strongly related to integrated succinate dehydrogenase activity in patients (r = 0.896, p = 0.001). Peak VO2, resistance to fatigue and strength also correlated significantly with several measures of fiber size, especially of fast twitch fibers, in patients. None of the skeletal muscle characteristics examined correlated with exercise capacity in control subjects. CONCLUSIONS: These results indicate that congestive heart failure is associated with changes in the characteristics of skeletal muscle and local as well as systemic exercise performance. There are fewer slow twitch fibers, smaller fast twitch fibers and lower succinate dehydrogenase activity. The latter finding suggests that mitochondrial content of muscle is reduced in heart failure and that impaired aerobic-oxidative capacity may play a role in the limitation of systemic exercise capacity.

Aged↗

Diastolic and systolic function as predictors of exercise capacity after myocardial infarction in young Men.

We evaluated the power of measurements of left ventricular (LV) systolic and diastolic function for predicting exercise capacity in 97 young male survivors of a myocardial infarction. The patients were evaluated with M-mode echocardiography, a symptom-limited exercise test and coronary and LV angiography. In univariate analyses, maximum exercise workload was most closely related to the atrial emptying index, an index of diastolic function (r = 0.37, p < 0.005), but not to LV ejection fraction (r = 0.001, NS). This relationship was stronger in the 42 patients without signs of ischemia during exercise (r = 0.51, p < 0.005). Multivariate analyses indicated that the atrial emptying index (p < 0.005) provided independent contribution to the prediction of maximum exercise capacity. LV diastolic function but not LV systolic function was related to exercise capacity in young survivors of myocardial infarction.

Adult↗

Improvement in exercise capacity despite cardiac deteriora tion: nonivasive assessment of long-term therapy with amrinone in severe heart failure.

Seven patients with severe congestive heart failure (CHF) were treated with oral amrinone for a mean duration of 39 weeks (range 16 to 72). During the first week of therapy, exercise capacity as assessed on a treadmill using the Naughton protocol, increased substantially from 7.6 +/- 4.2 to 12.1 +/- 4.4 minutes (p less than 0.01). At an early period of follow-up (8 to 12 weeks), a further significant increase in exercise capacity to 14.7 +/- 5.0 minutes (p less than 0.05) was demonstrated, while at a later follow-up exercise capacity had decreased to 11.4 +/- 6.8 minutes (p less than 0.05). This was still significantly greater than prior to amrinone therapy (p less than 0.01). Left ventricular ejection fraction was increased from 14 +/- 4 to 19 +/- 4% (p less than 0.05) during the first week of therapy, but was not significantly different from control at the early and late periods of follow-up. Left ventricular end-diastolic dimension index increased from control value of 43 +/- 5 to 47 +/- 7 mm/m2 (p less than 0.01) at the late period of follow-up. Thus long-term amrinone therapy resulted in a substantial improvement in exercise capacity despite a slow, but progressive decline in cardiac performance.

Adult↗