Severity of heart failure and dosage of angiotensin converting enzyme inhibitors.
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Biomedical subjects
Publications and source records attributed to A L Clark.
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BACKGROUND: We have shown previously that transient right ventricular restriction after tetralogy of Fallot repair prolongs postoperative course. This is a prospective study of right ventricular diastolic performance in late follow-up patients. METHODS AND RESULTS: We studied biventricular function, using Doppler echocardiographic examination. Pulmonary arterial, tricuspid, and mitral valves and superior vena cava Doppler spectrals were obtained in 41 patients (mean age, 28.8 years), 15 to 35 years (mean, 23.6) after complete repair of tetralogy of Fallot. Patients were considered to have evidence of right ventricular restriction if antegrade diastolic flow was detected in the main pulmonary artery, coinciding with atrial systole (A wave), throughout the respiratory cycle. Exercise function was measured by graded treadmill testing with respiratory mass spectrometry. Three patients were excluded because of pulmonary outflow obstruction (Doppler gradient > 40 mm Hg) or residual intracardiac shunts. Of the 38 patients, 37 were in sinus rhythm. Twenty (52.6%) had definite evidence of restriction with an A wave in the pulmonary artery, augmented during inspiration. In all 20 cases, there was superior vena caval flow reversal with atrial systole. Both inspiratory and expiratory transtricuspid E-wave deceleration time was significantly shorter in the restrictive group (P < .003 and P < .03, respectively). All patients had Doppler evidence of pulmonary regurgitation, but its duration was shorter in the restrictive group (P < .01) during inspiration. Cardiothoracic ratio was significantly lower in the restrictive group (P < .01), suggesting less severe pulmonary regurgitation. Both restrictive and nonrestrictive groups had reduced exercise MVO2 compared with healthy age- and sex-matched control subjects, but those with restrictive physiology had significantly better maximum oxygen uptake than the nonrestrictive group (P < .001). CONCLUSIONS: Isolated right ventricular restriction late after tetralogy of Fallot repair is common. Although it reflects abnormal hemodynamics, the A wave contributes to forward pulmonary arterial flow and shortens the duration of pulmonary regurgitation. Consequently, there is less cardiomegaly and improved exercise performance in those patients.
BACKGROUND: The exercise limitation of patients with chronic heart failure is associated with an increased ventilatory response during exercise. This is thought to be due, at least in part, to excessive dead space ventilation. METHODS: To assess ventilation perfusion matching, 20 patients with chronic heart failure and eight controls with asymptomatic left ventricular dysfunction underwent symptom limited treadmill exercise with arterial blood sampling. Metabolic gas exchange was determined by expired gas analysis. Fractional dead space ventilation and the alveolar arterial oxygen difference were derived. RESULTS: There was a fall in fractional dead space ventilation (0.43 to 0.28; P < 0.001), more marked in the controls (peak dead space fraction 0.19 (controls), 0.32 (patients); P = 0.002). There was a rise in alveolar arterial difference in all patients (1.59 to 2.55 kPa; P = 0.006) with no difference between patients and controls. Arterial carbon dioxide tension fell during exercise (4.89 to 4.63 kPa; P < 0.001), with no difference between patients and controls. There was no significant change in arterial oxygen tension. CONCLUSIONS: The fall in arterial carbon dioxide was the same in both patients and controls. The modest increase in alveolar-arterial oxygen difference tension was the same in both groups, which, coupled with the stable arterial oxygen tension makes it unlikely that a primary change in ventilation-perfusion matching is the cause of increased ventilatory response to exercise in chronic heart failure.
OBJECTIVE: Our purpose was to study the influence of intravenous immunoglobulin on pregnancy outcome. STUDY DESIGN: Pregnancy outcomes were evaluated in five patients with 17 unsuccessful previous pregnancies. Each patient received 400 mg/kg immunoglobulin for 5 days monthly beginning in the first or early second trimester. Four patients with previous thromboembolic events were treated with concomitant heparin prophylaxis. Four patients received 81 mg of aspirin daily. RESULTS: Short- and long-term decreases of anticardiolipin immunoglobulin G were noted in three patients. Four patients were delivered of healthy infants at term, one at 32 weeks' gestation with a diagnosis of fetal distress. Neither preeclampsia nor fetal intrauterine growth retardation were observed. The immunoglobulin therapy was not associated with major side effects. Significant placental histologic anomalies were not identified. CONCLUSIONS: The observations suggest that immunoglobulin therapy may improve pregnancy outcomes beyond that observed with heparin and aspirin. A prospective trial is encouraged.
BACKGROUND: The exercise limitation of patients with chronic heart failure may be due in part to an inability to increase heart rate as normal, a limitation sometimes referred to as chronotropic incompetence. This may be due to down regulation of beta receptors. METHODS: Fifty-seven patients with chronic heart failure and 14 age-matched controls underwent symptom limited treadmill exercise tests with metabolic gas exchange measurements. Heart rate and blood pressure responses were also recorded. RESULTS: Peak oxygen consumption was reduced in the heart failure patients (19.6 (S.D. +/- 7.6) vs. 35.0 (+/- 9.9); P < 0.001). Heart rate at peak exercise (r = 0.47, P < 0.001), and change in heart rate from rest to peak exercise (r = 0.59; P < 0.001) and rate pressure product at peak exercise (r = 0.56, P < 0.001) all correlated with peak oxygen consumption. The percentage of predicted maximal heart rate at peak exercise correlated poorly with peak oxygen consumption (r = 0.29; P > 0.05). Peak systolic and diastolic blood pressures did not correlate with peak oxygen consumption. Sixteen patients had chronotropic incompetence. There was no significant difference between this group and those without chronotropic incompetence in the intensity of exercise performed, underlying diagnosis, drug therapy or prevalence of atrial fibrillation. There was a trend towards shorter exercise times in the incompetent group (430 (+/- 251) vs. 545 (+/- 216) s; P = 0.08) compared to the other patients. CONCLUSIONS: Chronotropic incompetence was seen in < 30% of patients with chronic heart failure. However, there are few differences between the group with chronotropic incompetence and the group without. Chronotropic incompetence is thus unlikely to be a major factor limiting exercise capacity in unselected patients with chronic heart failure and is likely to be the major factor limiting exercise in a much smaller proportion of patients.
The pathogenesis of the limiting symptoms in patients with chronic heart failure, shortness of breath and fatigue on exercise, are poorly understood. We analysed data from 222 incremental symptom limited exercise tests to determine whether there were differences between patients stopped by breathlessness or fatigue. One hundred and sixty patients were stopped by breathlessness and 62 by fatigue. There was no differences between the two groups in underlying diagnosis or in exercise performance (peak oxygen consumption 15.66 (+/- 5.62) ml.kg-1.min-1 in the fatigue group, 15.13 (+/- 4.64) in the breathless group). The ventilatory response as assessed by ventilatory response to carbon dioxide production (VE/VCO2 slope) was not different between the two groups (2.61 (+/- 0.96) in the fatigue group, 3.03 (+/- 1.23) in the breathless group: P = ns). There were no differences between the two groups in left ventricular dimensions, left ventricular ejection fraction or left ventricular end-diastolic pressure. The limiting symptoms of breathlessness and fatigue in chronic heart failure are two sides of the same coin. Any pathophysiological explanation of exercise limitation in chronic heart failure must unify these two symptoms.
Patients with chronic heart failure have an increased ventilatory response to exercise, and have metabolically abnormal skeletal muscle. It has been proposed that a neural signal to ventilation arising from exercising muscle may be heightened in chronic heart failure. Our objective was to detect evidence for such a signal in normal subjects by studying ventilatory behaviour during exercise with muscles in different metabolic states. Fifteen normal subjects undertook treadmill exercise both with and without cuffs inflated around each thigh to suprasystolic pressure. In a second experiment, a group of 11 normal subjects undertook cycle exercise using arms or legs at the same absolute work load. Metabolic gas exchange was measured using mass spectrometry with indicator gas dilution. The ventilatory response was greater at a given workload when subjects exercised with inflated cuffs. Oxygen consumption was reduced in keeping with the isolation of the exercising muscle bulk from the circulation. The ventilation/carbon dioxide output relationship was described by a linear regression function, but the slope of the relationship was increased by 25% from 20.9 (0.46) to 25.43 (0.73) (P < 0.001). Arm exercise at the same load as leg exercise resulted in unchanged oxygen consumption indicating that the same external work was being performed. There was an increase in ventilation at a given workload. The ventilation/carbon dioxide output slope was increased by 25% (from 21.9 (0.9) to 26.3 (0.8)) (P < 0.001). There is a signal to ventilation arising from exercising skeletal muscle which is enhanced by the ischaemia induced by cuff inflation during exercise. This signal appears to be neural.(ABSTRACT TRUNCATED AT 250 WORDS)
BACKGROUND: Adult patients with total correction of tetralogy of Fallot may have poor exercise capacity associated with impaired right heart function and in particular pulmonary regurgitation. The ventilatory responses to exercise were studied in a group of such patients to assess relations between ventilation, exercise capacity, and right ventricular function. METHODS: 30 patients (7 female) (aged 27.8 (6.0) years) and 30 (7 female) controls of a similar age range were studied prospectively. All underwent exercise testing with metabolic gas exchange to determine peak oxygen consumption (peak VO2), and (as indices of the ventilatory response) the slope of the relation between both respiratory rate (RR) and ventilation (VE) against carbon dioxide production (VCO2). Patients were studied with pulsed wave Doppler echocardiography to determine pulmonary arterial systolic and diastolic flow characteristics. Patients were defined as having restrictive right ventricular function where diastolic pulmonary forward flow was seen coincident with atrial systole. RESULTS: In the group with tetralogy of Fallot mean (SD) peak VO2 was 35.3 (7.5) ml/kg/min (93.6 (15.3) % of expected for age, weight, height and sex). The RR/VCO2 slope was steeper in the Fallot group (6.8 (2.6) v 9.6 (4.7), P < 0.02). Those with restrictive right ventricles achieved a higher peak VO2 than those without (82.5 (10.1) % v 100.9 (13.8), P < 0.001). In the Fallot group alone, there was an inverse relation between ventilatory response and peak VO2 (RR/VCO2 v peak VO2; r = -0.63, P = 0.003: VE/VCO2 v peak VO2; r = -0.62, P < 0.001). CONCLUSIONS: Many of these patients with repaired tetralogy of Fallot had near normal exercise capacity, but as exercise capacity decreased, the ventilatory response to exercise increased. This was not due to alterations in pulmonary function tests or to the effects of cardiac size causing decreased lung volume. It may be that the increased ventilatory rate at a given level of carbon dioxide production acts as a respiratory pump aiding right ventricular function.
BACKGROUND: Patients with chronic heart failure have an excessive ventilatory response to exercise, characterised by an increase in the slope of the relation between ventilation and carbon dioxide production (VE/VCO2 slope). Patients have an altered respiratory pattern with an increased respiratory rate (f) at a given tidal volume (VT), which may result in increased anatomical dead space ventilation. METHODS: The ventilatory responses in 88 patients with chronic heart failure and 43 age matched controls during maximal incremental treadmill exercise were analysed. Peak oxygen consumption (VO2), VE/VCO2 slope, and the slope of the relation between f and VT were derived. Anatomical dead space was estimated from a standard formula and anatomical dead space ventilation calculated. RESULTS: Peak VO2 was greater (mean (SD)) (33.2 (8.5) v 19.4 (6.7) ml/min/kg; P < 0.001) and the VE/VCO2 slope lower in the controls (25.96 (4.16) v 35.14 (9.80); P < 0.001). During matched submaximal exercise VT was higher (1.97 (0.92) v 1.68 (0.62) 1; P < 0.05) and flower in the controls (18.23 (6.48) v 24.28 (7.58); P < 0.001). At peak exercise there was no difference in f, but VT was higher in the controls (2.66 (0.97) v 1.90 (0.61) 1; P < 0.001). The VT/f slope was the same (0.04 (0.04)) in both groups. The intercept of the relation was greater for the control group (1.31 (1.28) v 0.59 (0.83); P < 0.001). Anatomical dead space ventilation was lower in the controls at submaximal work load (4.17 (1.56) v 5.58 (1.93) l/min; P < 0.001). At peak exercise anatomical dead space ventilation was the same in both groups, but was lower expressed as a percentage of total VE in the control group (9.8 (3.3) v 13.5 (4.0); P < 0.001). There were weak relations within the heart failure group alone between VT/f slope and peak VO2 and VE/VCO2 slope. CONCLUSIONS: The relation between anatomical dead space ventilation and VE/VCO2 slope is expected: as f increases, so do VE/VCO2 slope and anatomical dead space ventilation. The VT/f slope was the same in patients with chronic heart failure and controls, so change in respiratory pattern cannot explain the increase in VE/VCO2 slope. The stimulus causing the increased f has yet to be identified.
A muscle metaboreceptor (ergoreceptor) contribution to the hemodynamic and autonomic responses to exercise is well recognized, but a ventilatory component remains controversial. Control handgrips were compared with handgrips followed by 4-min regional circulatory occlusion of the exercising muscles to isolate the metaboreceptor role in blood pressure, autonomic tone (spectral analysis of R-R and blood pressure variability), and ventilatory responses to exercise in 11 normal subjects. Exercise responses were maintained after the effort by metaboreflex activation in systolic pressure (136.2 +/- 3.5 vs. 123.0 +/- 4.3 mmHg, P < 0.05), ventilation (19.0 +/- 2.6 vs. 8.5 +/- 0.4 l/min, P < 0.0005), and sympathetic discharge to the heart and circulation (elevated low-frequency components of R-R interval, 1,747.5 +/- 309.2 vs. 1,085.9 +/- 259.1 ms2, P < 0.05, and systolic pressure variability, 45.3 +/- 3.9 vs. 26.5 +/- 4.4 mmHg2, P < 0.005). We conclude that metaboreflex contributes to the sympathetic, hypertensive, and hyperpneic responses to exercise in normal subjects.
BACKGROUND: There are calls for the role of the practice nurse to be developed and extended. Before areas for further training and education can be identified, baseline data are needed on practice nurses' current activity and workload. AIM: A study was undertaken to analyse the activity of practice nurses in two large inner city general practices and to assess the skills mix of the nursing staff required to meet the needs of the practices. METHOD: The study practices had a combined list of 26,000 patients, 80% of patients attracting a deprivation allowance. Each practice employed three practice nurses. A nurse activity index with 45 codes was constructed to describe patient-nurse consultations. Activity codes were categorized into traditional treatment tasks, extended role tasks or diagnosis and management tasks. For eight months, practice nurses in practices Y and Z recorded activity index codes for each patient consultation. Practice Y also recorded the source of referral and the age and sex of the patient. RESULTS: There were 13,898 practice nurse consultations during the study period, equivalent to an annual nurse consultation rate of 0.8 per patient. Compared with the practice population as a whole, the patients attending the practice nurses in practice Y were older (mean age 43 years versus 37 years, P < 0.001). Those attending the practice nurses in practice Y were also more likely to be female (61% of consultations were with female patients compared with 50% of the practice population as a whole, P < 0.001). In practice Y, patients referred themselves to the practice nurse in 42% of consultations, 32% were follow-up consultations and in 25% of cases the patient had been referred by a doctor. The most common reasons for nurse consultation were blood tests (15% of procedures in practice Y and 18% in practice Z) and dressings (13% in both practices). Most procedures in practices Y and Z were in the traditional treatment category (61%), 26% were in the extended role category and 9% in the diagnosis and management category (3% coded 'other', 1% uncoded). Between practices, the greatest difference in recorded procedures was for asthma check ups (7% of procedures in practice Y compared with 2% in practice Z). CONCLUSION: This study describes the workload of practice nurses in two inner city practices over eight months. Other practices could use the activity index to make comparisons over time and between practices. Up to 60% of nurses' work in the study practices could be done by a nurse without extended training and up to 30% could be done by a health care assistant, but with some loss of quality. It is suggested that half the nursing hours available to a practice should be offered by a nurse with extended training in order to undertake and develop extended role tasks and diagnosis and management tasks.
The objective of this study was to investigate the existence of abnormalities of insulin sensitivity in patients with chronic heart failure. Glucose metabolism and insulin resistance were assessed in 10 male patients with severe, chronic heart failure and in 10 matched control subjects. Glucose, insulin and C-peptide concentration profiles were measured following a 0.5 g.kg-1 intravenous glucose tolerance test. Insulin sensitivity (inversely related to insulin resistance) was estimated by minimal modelling analysis of the glucose and insulin profiles. Heart failure patients had similar mean fasting plasma glucose concentration to controls but a significantly greater mean fasting plasma insulin concentration (P = 0.002) and C-peptide concentration (P = 0.02). Plasma glucose response profile was similar in the two groups but the incremental plasma insulin response profile of the heart failure group was significantly greater (P = 0.004). Mean insulin sensitivity was 73% lower in the heart failure patients (P = 0.003). These findings show that patients with severe chronic heart failure are hyperinsulinaemic and insulin resistant compared with a matched health group. This insulin resistance and hyperinsulinaemia may contribute to the progressive deterioration in myocardial function and associated clinical features of fatigue and reduced exercise tolerance seen in heart failure. Interventions designed to overcome or reduce insulin resistance warrant further investigation.
Abnormalities of skeletal muscle rather than of haemodynamics may be important determinants of exercise capacity in chronic heart failure. We investigated an array of indicators of central haemodynamics and peripheral muscle function to establish which resting measurements predicted exercise performance. In 20 patients quadriceps strength, resting and peak leg blood flow and leg muscle cross sectional area were measured. In 18 patients average daytime blood pressure and pulse rate, haemodynamic variables at rest and during exercise, and autonomic activity were measured. There were correlations between peak oxygen consumption and quadriceps strength (0.65; P = 0.007), thigh muscle cross sectional area (r = 0.63; P = 0.004), and average daytime systolic blood pressure (r = 0.66; P < 0.01). There were no correlations with indices of peripheral blood flow, measures of haemodynamic function, or autonomic function. Quadriceps strength was the most important individual correlate of exercise tolerance (r = 0.73). With total muscle cross sectional area and left quadriceps strength also taken into consideration, 82% of the variation in peak oxygen consumption was explained. Of the haemodynamic variables, only average daytime systolic blood pressure predicted exercise performance. The resting variables that best predict exercise performance in chronic heart failure are measures of skeletal muscle function and bulk, and average daytime systolic blood pressure. These findings suggest that abnormalities in the periphery largely determine exercise performance in chronic heart failure, and that the ability of the heart to generate an adequate blood pressure response to daily activities is also predictive of functional status.
BACKGROUND: Measurement of variables of metabolic gas exchange during exercise is widely used to assess the severity of heart failure. The variables derived however, are potentially dependent on motivation of the patient and duration of exercise. METHODS: The data from exercise tests in 23 patients with exertional breathlessness were analysed to derive the following three common indices of exercise tolerance: anaerobic threshold, extrapolated maximum oxygen consumption, and the ventilation to carbon dioxide production slope. The data were reanalysed with the data points from the first 90% of subsequent exercise, the first 75%, and finally the data up to the point where a respiratory gas exchange ratio of 1 was reached. RESULTS: The mean (SEM) anaerobic threshold was lower when computed from 90% of the data points than from 100% (13.2 (1.0) ml/kg/min v 12.5 (1.0), p < 0.001) and lower still from 75% (11.4 (0.7), p = 0.006 v 90%). Extrapolated maximum oxygen consumption was unchanged when computed from 90% of the data, but higher when computed from 75% (25.4 (2.1) ml/kg/min at 100% v 28.6 (2.1) at 75%, p < 0.001). The slope of the ventilation to carbon dioxide production ratio became progressively shallower measured from 90% and 75% of eventual exercise: 32.3 (1.5) from 100% v 30.0 (1.5) from 90%, p < 0.001; and 28.3 from 75%, p < 0.001 v 90%. At a respiratory gas exchange ratio of 1, extrapolated oxygen consumption was unchanged from the final calculation, anaerobic threshold was lower than at 100% of exercise (11.8 (0.9), p = 0.005) and the ventilation to carbon dioxide production slope was shallower (27.5 (1.4), p < 0.001). CONCLUSIONS: Anaerobic threshold tends to overestimate severity of exercise limitation and extrapolated maximum oxygen consumption and the ventilation to carbon dioxide production slope tend to underestimate severity. Extrapolated maximum oxygen consumption is the most reliable of the three measures, and is independent of effort provided that patients are encouraged to exercise to the point where the respiratory gas exchange ratio exceeds 1.
BACKGROUND: Coexisting cardiorespiratory disease may contribute in individual cases to the increased ventilatory response to exercise in patients with chronic heart failure. OBJECTIVE: To characterise further the arterial blood gas response to exercise and to explore the possible uses of blood gas sampling in clinical practice in patients with chronic heart failure. METHODS: 37 patients with a primary diagnosis of chronic heart failure (age (range) 59 (45-80); left ventricular ejection fraction 24.5% (4%-44%)) underwent exercise testing with arterial blood gas analysis during exercise. RESULTS: In 34 patients there was a small fall in arterial carbon dioxide tension from a mean (SEM) of 4.9 (0.1) kPa at rest to 4.6 (0.1) kPa at peak exercise (p < 0.001). There was no significant change in arterial oxygen tension. During the recovery period arterial oxygen tension rose from 13.3 (0.3) kPa at peak exercise to 14.8 (0.3) kPa three minutes into recovery (p < 0.001). Arterial carbon dioxide tension was unchanged. In the remaining three patients there was considerable arterial hypoxaemia on exercise, from 10.4 kPa at rest to 7.7 kPa at peak exercise. All of these patients had an alternative diagnosis (patent foramen ovale with right to left shunt during exercise, pulmonary embolic disease, and clinically unsuspected obstructive airways disease). CONCLUSION: Patients with a presumptive diagnosis of chronic heart failure should undergo exercise testing with arterial blood gas analysis. Arterial hypoxaemia on exercise is rare in stable chronic heart failure. If hypoxia on exercise is detected, an alternative diagnosis should be sought.
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To evaluate possible autonomic nervous system (ANS) dysfunction in patients with chronic obstructive pulmonary disease (COPD) in the absence of any hypoxic neuronal damage, we studied 31 patients with COPD patients aged 31 to 68 years (55 +/- 10) and 32 age-matched healthy subjects (control). Respiratory function in the patients was as follows: FEV1 = 52 +/- 8 percent; PaO2 = 71 +/- 14 mm Hg; and PaCO2 = 40 +/- 10 mm Hg. The ANS was assessed by heart rate variability (HRV) in the time domain (SD of mean RR interval) and frequency domain (autoregressive spectral analysis recognizing low [LF] and high [HF] frequency components, vagal and sympathetic related, respectively). Patients and controls were evaluated at rest and during vagal (controlled breathing [CB]) and sympathetic (passive head-up tilt) maneuvers. Patients with COPD showed a depressed global HRV (rest SD = 34 +/- 20 ms vs 45 +/- 15 ms, p < 0.05; tilt SD = 28 +/- 14 ms vs 38 +/- 13, p < 0.01) with a predominant respiratory drive (rest HF = 44 +/- 28 vs 28 +/- 18, p < 0.05; tilt HF 42 +/- 28 vs 16 +/- 12, p < 0.01) as compared with normal subjects. In the control group, vagal and sympathetic responses were in opposite directions following a stimulus, whereas there was no significant HRV response in the COPD group. We conclude that patients with COPD have abnormalities of ANS function, with in particular a depressed HRV response to sympathetic and vagal stimuli.
BACKGROUND: In chronic heart failure, exercise training results in an improvement in exercise capacity and a reduction in the ventilatory response to exercise. The effects of a physical training programme on the ventilatory response in healthy persons is not known. METHODS: Metabolic gas exchange and ventilation were measured in 27 young healthy persons aged 31.4 +/- 7.6 years before and after a 19-week training programme of aerobic exercise; exercise was undertaken three times a week for 40 min. Ventilation, the slope of the relationship between ventilation and carbon dioxide production (VE-VCO2 slope) and the ventilatory equivalent for carbon dioxide were measured using respiratory mass spectroscopy. The peak expiratory flow rate in 1 s and forced vital capacity were also measured. RESULTS: Mean +/- SEM peak oxygen consumption increased from 39.5 +/- 1.5 to 45.4 +/- 1.7 ml/kg/min(P<0.001). Exercise time increased from 817 +/- 188 to 896 +/- 186 s (P<0.001). The respiratory exchange ratio at peak exercise was slightly lower after training: 1.30 +/- 0.02 compared with 1.36 +/- 0.03 (P = 0.02). Ventilation at equivalent stages of exercise was unchanged by training. The VE-VCO2 slope did not change (24.52 +/- 0.67 before training, 25.01 +/- 0.80 after training; NS). There was no change in the ventilatory equivalent for carbon dioxide either at rest (38.6 +/- 1.4 compared with 36.2 +/- 1.1; NS) or at its lowest point (23.3 +/- 0.6 compared with 22.9 +/- 3.2; NS). Neither exercise capacity nor the training response correlated with any of the measured ventilatory variables. CONCLUSION: In contrast to the situation in patients with chronic heart failure, there is no relationship between ventilatory variables and exercise capacity in healthy persons and no change in ventilatory performance as a result of physical training.