Aerobic exercise training can reverse age-related peripheral circulatory changes in healthy older men.

BACKGROUND: The age-related decline in maximal oxygen consumption is attenuated by habitual aerobic exercise. However, the relative effects of training on central and peripheral responses to exercise in older subjects are not known. The present study assessed the contribution of central and peripheral responses to the age-associated decline in peak oxygen consumption and compared the effect of exercise training in healthy older and younger subjects. METHODS AND RESULTS: Ten older and 13 younger men underwent invasive measurement of central and peripheral cardiovascular responses during an upright, staged cycle exercise test before and after a 3-month period of exercise training with cycle ergometry. At baseline, cardiac output and AV oxygen difference during exercise were significantly lower in older subjects. With training, the older and younger groups increased maximal oxygen consumption by 17.8% and 20.2%, respectively. Peak cardiac output was unchanged in both groups. Systemic AV oxygen difference increased 14.4% in the older group and 14.3% in the younger group and accounted for changes in peak oxygen consumption. Peak leg blood flow increased by 50% in older subjects, whereas the younger group showed no significant change. There was no change in peak leg oxygen extraction in the older group, but in the younger group, leg AV oxygen difference increased by 15.4%. CONCLUSIONS: These findings suggest that the age-related decline in maximal oxygen consumption results from a reversible deconditioning effect on the distribution of cardiac output to exercising muscle and an age-related reduction in cardiac output reserve.

Mechanism and significance of a decrease in ejection fraction during exercise in patients with coronary artery disease and left ventricular dysfunction at rest.

The purpose of this study was to determine whether an exercise-induced decrease in ejection fraction in patients with coronary artery disease and left ventricular dysfunction at rest represents ischemia or the nonspecific response of a compromised left ventricle to exercise stress. Accordingly, radionuclide ejection fraction responses of 246 patients with coronary artery disease and an ejection fraction at rest of less than 0.50 were compared with those of a "nonischemic" control group of 48 patients with idiopathic dilated cardiomyopathy and a similar degree of ventricular dysfunction. The significance of the ejection fraction response in the group with coronary artery disease was further examined by relating it to the angiographic extent of coronary artery disease, severity of angina, incidence of chest pain and electrocardiographic ST segment depression during exercise and long-term prognosis. The ejection fraction decreased by greater than or equal to 0.01 and greater than or equal to 0.05 during exercise in 48 and 28%, respectively, of the patients with coronary artery disease compared with only 8 and 2%, respectively, of the patients with cardiomyopathy. When exercise was limited by fatigue at a submaximal heart rate, the ejection fraction decreased in 25% of the patients with coronary artery disease but in none of the patients with cardiomyopathy. Patients with coronary artery disease whose ejection fraction decreased during exercise had a significantly higher incidence of three vessel disease, exercise-induced chest pain or ST depression and late mortality than did patients whose ejection fraction did not decrease. These relations were confirmed equally in subgroups of patients with moderate (ejection fraction 0.30 to 0.49) and severe (ejection fraction less than 0.30) left ventricular dysfunction. Thus, in patients with coronary artery disease and left ventricular dysfunction at rest, a decrease in ejection fraction during exercise is more likely to indicate ischemia than a nonspecific left ventricular response to exercise stress. In the individual patient, a decrease of 0.05 or greater, or a decrease during submaximal exercise, appears to be highly specific for ischemia. A decrease in ejection fraction identifies a subgroup of patients with a high prevalence of multivessel coronary artery disease and a high risk of death during long-term follow-up on medical therapy.

Exercise intolerance in patients with heart failure and preserved left ventricular systolic function: failure of the Frank-Starling mechanism.

Invasive cardiopulmonary exercise testing was performed in 7 patients who presented with congestive heart failure, normal left ventricular ejection fraction and no significant coronary or valvular heart disease and in 10 age-matched normal subjects. Compared with the normal subjects, patients demonstrates severe exercise intolerance with a 48% reduction in peak oxygen consumption (11.6 +/- 4.0 versus 22.7 +/- 6.1 ml/kg per min; p less than 0.001), primarily due to a 41% reduction in peak cardiac index (4.2 +/- 1.4 versus 7.1 +/- 1.1 liters/min per m2; p less than 0.001). In patients compared with normal subjects, peak left ventricular stroke volume index (34 +/- 9 versus 46 +/- 7 ml/min per m2; p less than 0.01) and end-diastolic volume index (56 +/- 14 versus 68 +/- 12 ml/min per m2; p less than 0.08) were reduced, whereas peak ejection fraction and end-systolic volume index were not different. In patients, the change in end-diastolic volume index during exercise correlated strongly with the change in stroke volume index (r = 0.97; p less than 0.0001) and cardiac index (r = 0.80; p less than 0.03). Pulmonary wedge pressure was markedly increased at peak exercise in patients compared with normal subjects (25.7 +/- 9.1 versus 7.1 +/- 4.4 mm Hg; p less than 0.0001). Patients demonstrated a shift of the left ventricular end-diastolic pressure-volume relation upward and to the left at rest. Increases in left ventricular filling pressure during exercise were not accompanied by increases in end-diastolic volume, indicating a limitation to left ventricular filling.(ABSTRACT TRUNCATED AT 250 WORDS)

Age-related alterations of Doppler left ventricular filling indexes in normal subjects are independent of left ventricular mass, heart rate, contractility and loading conditions.

The purpose of this study was to determine whether age-related alterations in Doppler diastolic filling indexes occur independent of cardiovascular disease and confounding physiologic variables. Ten old (62 to 73 years) and 10 young (21 to 32 years) healthy male volunteers were rigorously screened for cardiovascular disease and underwent comprehensive Doppler echocardiography, radionuclide ventriculography and invasive measurements of right heart and left atrial pressures. There were no differences between the two groups in the physiologic variables of left ventricular mass, volumes, ejection fraction, end-systolic wall stress, left atrial size, heart rate and right atrial, pulmonary artery, pulmonary capillary wedge and systemic arterial pressures. However, there were marked differences in Doppler left ventricular filling indexes. Compared with the young group, the old group had reduced peak early diastolic flow velocity (56 +/- 13 vs. 82 +/- 12 cm/s, p = 0.0002) and increased atrial diastolic flow velocity (59 +/- 14 vs. 43 +/- 10 cm/s, p = 0.009) and had a peak atrial/early flow velocity (A/E) ratio twice that of the young group (1.09 +/- 0.29 vs. 0.54 +/- 0.15, p less than 0.0001). Similar results were obtained for the time-velocity integrals of the peaks. Subjects in the old group also had a markedly reduced peak filling rate (274 +/- 62 vs. 448 +/- 152 ml/s, p = 0.004). In univariate and multivariate regression analyses, peak early and atrial flow velocities were not related to any of the physiologic variables measured once age was accounted for, although peak filling rate, a volumetric measure flow, was related to body surface area as well as age.(ABSTRACT TRUNCATED AT 250 WORDS)

Value and limitation of biplane rest and exercise radionuclide angiography for assessing individual bypass grafts: a prospective study.

This prospective study evaluated the ability of serial biplane rest and exercise radionuclide angiography to predict the status of individual coronary bypass grafts in 20 patients 2 to 6 months after surgery. The preoperative coronary angiogram was used to assign vessels to 10 regions of distribution on the radionuclide angiogram. Predictions of graft adequacy for individual vessels were based on a detailed assessment of rest and exercise wall motion in their regions of supply. Of 59 grafts, 38 were judged adequate (patent with less than 75% stenosis) and 21 inadequate by postoperative catheterization. Radionuclide prediction of graft status was possible for 32 of the 59 grafts, including 19 of 24 left anterior descending, 7 of 19 circumflex and 6 of 16 right coronary artery grafts. The status of the remaining 27 grafts could not be assessed because of normal wall motion in their region of supply both pre- and postoperatively (22 vessels) or because a region of supply was not represented on the biplane radionuclide angiogram (5 vessels). Of the 32 predictions made, 25 (78%) were correct, including 13 (93%) of 14 predictions of graft adequacy and 12 (67%) of 18 predictions of graft inadequacy. The single incorrect prediction of graft adequacy resulted from improved exercise wall motion in a region supplied by a graft judged as having a 75% anastomotic stenosis. Most incorrect predictions of graft inadequacy were due to new septal or other rest wall motion abnormalities postoperatively. The comparison of pre- and postoperative studies was essential to maintain the predictive ability of the test. Thus, a detailed analysis of regional wall motion by rest and exercise radionuclide angiography can be used to predict the status of individual coronary artery bypass grafts. Reliable predictions can be made for most successful anterior descending grafts, and may permit cardiac catheterization to be deferred in certain cases. However, the method is limited by the need to perform preoperative exercise studies, by the low number of right and circumflex coronary artery grafts that can be evaluated and by the poor specificity of predictions of graft failure.

Chronic stable angina monotherapy. Nifedipine versus propranolol.

A placebo-controlled, double-blind, crossover study was conducted to determine the effects of nifedipine (60 to 90 mg per day) monotherapy and propranolol (240 mg per day) monotherapy on symptoms, angina threshold, and cardiac function in patients with chronic stable angina. Following a two-week placebo period, patients were randomly assigned to receive either nifedipine or propranolol for a five-week treatment period, after which they crossed over to the alternative regimen. All 21 patients were men with chronic stable angina pectoris, 13 of whom had symptoms both at rest and on exertion. New York Heart Association functional class improved in patients taking either nifedipine or propranolol, and nitroglycerin consumption decreased with both treatments compared with placebo. Nifedipine significantly delayed the onset of chest pain and 1 mm of ST-segment depression during bicycle exercise; increases with propranolol were smaller and not statistically significant. Nine patients had a preferential clinical response to nifedipine compared with six patients to propranolol; this was unrelated to the presence or absence of pain at rest or to any baseline hemodynamic finding. Nifedipine and propranolol were equally effective in relieving exertional ischemia as shown by improvement in radionuclide ejection fraction at identical work loads. Exercise wall motion, assessed by a semiquantitative wall motion score, also improved with both drugs. Propranolol treatment decreased exercise cardiac output by 14 percent (p = 0.01) through its effect on heart rate. In contrast, nifedipine treatment had no effect on cardiac output. Thus, nifedipine is more effective on several measurements than propranolol when administered as single drug therapy in stable angina and has the advantage of preserving cardiac output during exercise.

The ventilatory threshold: quantitative analysis of reproducibility and relation to arterial lactate concentration in normal subjects and in patients with chronic congestive heart failure.

The present study evaluates optimal ventilatory criteria and exercise protocols for determining the ventilatory threshold, and assesses the day-to-day reproducibility of the ventilatory threshold and its relation to peak oxygen uptake VO2 and blood lactate concentration in normal subjects and patients with stable chronic congestive heart failure (CHF). Eighteen normal subjects and 18 patients underwent rapid (1-minute stage) and gradual (3-minute stage) bicycle exercise tests on consecutive days. The ventilatory threshold was determined from computer-generated printouts of expired gas variables measured breath by breath. Interobserver variability of ventilatory threshold was small in both normal (0.66 +/- 0.85 ml/min/kg) and CHF patients (0.50 +/- 0.46 ml/min/kg). Variability in the normal subjects was lower for the rapid exercise protocol (0.66 +/- 0.85 ml/min/kg) than the gradual protocol (1.72 +/- 1.63 ml/min/kg) (p less than 0.05), but both protocols produced similar results in the CHF group. Day-to-day reproducibility of ventilatory threshold was high (r = 0.91, standard error of the estimate 1.74 ml/min/kg) and was similar to that of peak VO2 (r = 0.95, standard error of the estimate 3.31 ml/min/kg). The use of co-plotted ventilatory equivalents for oxygen and carbon dioxide yielded ventilatory threshold values comparable to values obtained by using multiple parameters (r = 0.94, p less than 0.0001). Although the ventilatory threshold did not predict a precise lactate level for individual subjects, the lactate increment at the ventilatory threshold occurred within a narrow range in both normal subjects and patients with CHF; the increase was 7.5 +/- 4.5 mg/dl and 7.7 +/- 4.1 mg/dl, respectively, indicating a relation to initial increases in blood lactate.

Stroke volume increases by similar mechanisms during upright exercise in normal men and women.

To define the effects of gender on stroke volume control during upright exercise in normal subjects, we examined central hemodynamics in 34 men and 27 women during staged bicycle ergometry. Central hemodynamics were assessed by right-sided cardiac catheterization and simultaneous radionuclide angiography. Left ventricular end-diastolic and end-systolic volumes were calculated from the stroke volume (by direct Fick) and the corresponding left ventricular ejection fraction. Men were larger than women (1.85 +/- 0.11 vs 1.65 +/- 0.13 m2, p less than 0.001) but groups were matched for age (39 +/- 12 vs 36 +/- 9 years, p = 0.27). Oxygen consumption at peak exercise was higher in men than in women (2.51 +/- 0.50 vs 1.74 +/- 0.30 liters/min, p less than 0.001) but was not different when adjusted for body weight (31.5 +/- 8.1 vs 28.4 +/- 6.4 ml/kg/min, p = 0.14), indicating similar levels of overall fitness in the 2 groups. At rest and during submaximal and maximal exercise, stroke volume and left ventricular end-diastolic and end-systolic volumes were higher in men than in women, but there were no intergroup differences in stroke volume index, left ventricular ejection fraction, and left ventricular end-diastolic or end-systolic volume indexes. Comparison of derived regression equations of cardiac index, stroke volume index and left ventricular end-diastolic and end-systolic volume indexes revealed no differences in the time course or magnitude of changes with respect to oxygen consumption, expressed as percentage of peak oxygen consumption, in the 2 groups.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Comparison of nifedipine alone with propranolol alone for stable angina pectoris including hemodynamics at rest and during exercise.

The effects of nifedipine (60 to 90 mg/day) and propranolol (240 mg/day) on symptoms, angina threshold and cardiac function were compared in a placebo-controlled, double-blind, crossover study. Five-week treatment periods with nifedipine and propranolol were compared with 2 weeks of placebo treatment in 21 men with chronic stable angina pectoris, 13 of whom had symptoms both at rest and on exertion. Compared with placebo, New York Heart Association functional class improved in patients equally with nifedipine (p = 0.001) and propranolol (p = 0.006). Frequency of chest pain decreased with nifedipine (p = 0.001) and propranolol (p = 0.01), and nitroglycerin consumption similarly decreased with both treatments. Nifedipine significantly delayed the onset of chest pain (p = 0.01) and 1 mm of ST-segment depression (p = 0.002) during bicycle exercise; smaller increases with propranolol were not statistically significant. A preferential clinical response to nifedipine (9 patients) or propranolol (6 patients) was unrelated to the presence or absence of pain at rest or to any baseline hemodynamic finding. Nifedipine and propranolol were equally effective in relieving exertional ischemia as shown by improvements in ejection fraction at identical workloads, from 0.48 +/- 0.11 to 0.58 +/- 0.12 (p less than 0.001) and 0.56 +/- 0.14 (p less than 0.001), respectively. Exercise wall motion, assessed by a semiquantitative wall motion score, also improved with both drugs. Propranolol treatment decreased exercise cardiac output by 14% (p = 0.01) through its effect on heart rate. In contrast, nifedipine treatment had no effect on cardiac output.(ABSTRACT TRUNCATED AT 250 WORDS)

Determinants of variable exercise performance among patients with severe left ventricular dysfunction.

The relation between bicycle exercise performance and determinants of central and peripheral cardiovascular function was assessed in 17 patients with class II to III heart failure and in 9 normal subjects. Proportional changes in oxygen consumption (VO2) from rest (R) to maximal exercise (Ex), or Mets, were used as an objective measure of the exercise capacity or functional reserve of the cardiovascular system. Left ventricular ejection fraction (EF) and proportional changes in end-diastolic volume, stroke volume, and cardiac output were determined from appropriate count data by equilibrium radionuclide angiography. Proportional changes in arteriovenous oxygen difference (A-VO2) were derived from the equation Ex/R A-VO2 = Ex/R VO2 divided by Ex/R CO, where CO = count output. Each subject exercised to an anaerobic endpoint. Maximal VO2 was significantly lower in patients than in normal subjects. Because Ex/R A-VO2 was comparable in normal subjects and patients, the lower exercise performance in patients resulted from a reduced count output response. The reduced CO response in patients resulted from failure of the ejection fraction to increase or from an attenuated heart rate response, or both. Exercise performance was variable in both groups. Multivariable analysis in the patient group identified changes in heart rate, count output, and A-VO2 with exercise as important predictors of Mets, but found no relation between Mets and changes in ejection fraction or stroke counts during exercise. Similarly, multiple regression analyses between Mets and determinants of cardiovascular function demonstrated significant correlations with Ex/R heart rate, Ex/R count output, and Ex/R A-VO2 in both groups. In patients, EF at rest ranged from 0.09 to 0.36, but it did not correlate with Mets, nor did changes in ejection fraction, stroke counts, or end-diastolic counts during exercise. The variable exercise performance among patients with severe left ventricular dysfunction was determined predominantly by a variable heart rate and A-VO2 response and not by rest or exercise indexes of left ventricular function.

Comparison of high-dose and medium-dose propranolol in the relief of exercise-induced myocardial ischemia.

The effects of medium-dose (160 mg/day) and high-dose (480 mg/day) oral propranolol were compared in 22 patients who had typical angina pectoris and objective evidence of myocardial ischemia during exercise. Left ventricular (LV) ejection fraction (EF) and wall motion score (WMS) (an index of regional LV dysfunction) were assessed by radionuclide angiography both at rest and during exercise to the pretreatment maximum work load. Functional class improved in 11 of the 22 patients during medium-dose propranolol therapy. Medium-dose propranolol reduced mean resting heart rate from 71 to 55 beats/min, exercise heart rate from 122 to 93 beats/min, and exercise systolic blood pressure from 183 to 162 mm Hg (p less than 0.001 for each). The incidences of exercise-induced chest pain and S-T segment depression were reduced from 19 to 9 patients (p less than 0.001), and from 20 to 10 patients (p = 0.002), respectively. Medium-dose propranolol had no effect on mean EF or WMS at rest, but improved function in ischemic regions during exercise; WMS decreased (p = 0.001), and mean exercise EF increased from 0.51 to 0.56 (p = 0.025). Compared with the medium dose, high-dose propranolol improved functional class in 3 additional patients, and further reduced mean resting heart rate (from 55 to 52 beats/min, p = 0.001) and mean exercise heart rate (from 93 to 86 beats/min, p = 0.001). Exercise-induced chest pain and S-T segment depression were abolished in a further 7 and 6 patients, respectively. Exercise EF and WMS improved further in several patients, but the changes were not statistically significant for the group (p = 0.095 and 0.082, respectively). Thus, in patients with coronary artery disease and exercise-induced ischemia, propranolol reduced heart rate and blood pressure and the incidence of exercise-induced chest pain, electrocardiographic changes, and ischemic LV dysfunction. Although most of these effects were seen with medium-dose propranolol, higher doses provided additional relief of chest pain and S-T segment depression, and further improved global and regional LV function in several patients.

Physiologic basis for the age-related decline in aerobic work capacity.

To determine the physiologic mechanisms of the decline in aerobic work performance with age, a cross-sectional study was performed. Twenty-four sedentary male volunteers, aged 20 to 50 years, underwent right-sided cardiac catheterization, arterial cannulation, radionuclide angiography and expired gas analysis for detailed evaluation of central and peripheral cardiovascular function during submaximal and maximal exercise. Habitual physical activity level varied but was well matched across the age range. Over the 3-decade age range studied, there was no detectable change in cardiovascular function at rest. When peak exercise variables were examined, an age-related 25% decrease in O2 consumption was noted (r = -0.43, p = 0.04); this was associated with a 25% decrease in peak cardiac index (r = -0.54, p = 0.01) and a 20% decrease in peak heart rate (r = -0.63, p = 0.002). In addition, there was an age-related increase in calculated systemic and pulmonary vascular resistances and an increase in left ventricular ejection time. No age relation was seen for exercise stroke volume index, end-diastolic volume index, end-systolic volume index, pulmonary artery wedge pressure, ejection fraction or arteriovenous O2 difference. These results indicate that the age-related decline in aerobic work performance among men aged 20 to 50 years results primarily from a reduced exercise heart rate in older subjects rather than from a reduction in stroke volume or peripheral O2 utilization.

Value of radionuclide angiography for predicting specific cardiac events after acute myocardial infarction.

The value of rest and exercise radionuclide angiography (RNA) for predicting specific events including death, recurrent acute myocardial infarction (AMI), coronary care unit readmission for unstable chest pain, and medically refractory angina after AMI was studied in 106 consecutive survivors of AMI. Analysis of the RNA variables using the Cox proportional hazards regression model yielded significant associations of the time to death with ejection fraction at rest and during exercise (X2 = 11.1 and 14.0, respectively). Both variables added significant prognostic information to the clinical assessment (X2 = 4.3 and 5.7, respectively). The change in ejection fraction from rest to exercise predicted the time to coronary artery bypass grafting for medically refractory angina before (X2 = 21.0) and after (X2 = 13.2) adjustment for the clinical descriptors, but did not predict death or other non-fatal events. Significant correlations were found between RNA variables and a variety of clinical descriptors previously reported to have prognostic significance. Clinical and RNA variables that are measures of left ventricular function were predictive of subsequent mortality, whereas those that reflect residual potentially ischemic myocardium were predictive of subsequent nonfatal ischemic events. Rest and exercise RNA after AMI provides significant prognostic information regarding specific events during follow-up independent of that provided by clinical assessment.

A brief self-administered questionnaire to determine functional capacity (the Duke Activity Status Index).

To develop a brief, self-administered questionnaire that accurately measures functional capacity and assesses aspects of quality of life, 50 subjects undergoing exercise testing with measurement of peak oxygen uptake were studied. All subjects were questioned about their ability to perform a variety of common activities by an interviewer blinded to exercise test findings. A 12-item scale (the Duke Activity Status Index) was then developed that correlated well with peak oxygen uptake (Spearman correlation coefficient 0.80). To test this new index, an independent group of 50 subjects completed a self-administered questionnaire to determine functional capacity and underwent exercise testing with measurement of peak oxygen uptake. The Duke Activity Status Index correlated significantly (p less than 0.0001) with peak oxygen uptake (Spearman correlation coefficient 0.58) in this independent sample. The Duke Activity Status Index is a valid measure of functional capacity that can be obtained by self-administered questionnaire.

Doppler left ventricular diastolic filling abnormalities in aortic stenosis and their relation to hemodynamic parameters.

Doppler mitral flow indexes and their relation to invasively measured hemodynamic diastolic indexes were assessed in 13 patients with isolated aortic stenosis (AS), and compared to Doppler indexes in 10 normal subjects matched for age, heart rate, left ventricular (LV) ejection fraction and LV load. Patients with AS showed no difference in Doppler early filling (E) indexes, but demonstrated greater Doppler atrial filling (A) indexes in comparison to normal subjects: atrial velocity (89 +/- 31 vs 56 +/- 7 cm/s), atrial integral (11.4 +/- 4.8 vs 5.7 +/- 1.6 cm), A/E velocity (1.69 +/- 0.89 vs 1.06 +/- 0.26) and A/E integral (3.53 +/- 6.64 vs 0.81 +/- 0.27) (all p less than 0.05). Doppler indexes in patients with AS did not correlate with hemodynamic indexes of LV relaxation or chamber stiffness. Significant correlations were observed between Doppler and angiographic peak filling rates (r = 0.70) and between Doppler atrial filling velocity and LV end-diastolic volume (r = -0.66), LV end-diastolic pressure (r = -0.48) and LV ejection fraction (r = 0.53) (all p less than 0.05). These data indicate that, compared to matched normal subjects, most patients with AS have an increased atrial contribution to LV filling. However, in patients with decreased LV function, atrial function may also be depressed, as indicated by a decreased atrial contribution to LV filling, resulting in "normalization" of the Doppler mitral flow pattern.

Effects of exercise training on cardiorespiratory function in men and women older than 60 years of age.

This study reports the physiologic effects of up to 14 months of aerobic exercise in 101 older (greater than 60 years) men and women. After an extensive baseline physiologic assessment (Time 1), in which aerobic capacity and blood lipids were measured, subjects were randomized to an aerobic exercise condition (cycle ergometry, 3 times per week for 1 hour), nonaerobic yoga (2 times per week for 1 hour), or a waiting list nonexercise control group for 4 months, and then underwent a second (Time 2) assessment. At the completion of the second assessment, all remaining subjects completed 4 months of aerobic exercise and were reevaluated (Time 3). Subjects were given the option of participating in 6 additional months of supervised aerobic exercise, and all available subjects completed a fourth assessment (Time 4) 14 months after their initial baseline evaluation. Results indicated that subjects generally exhibited a 10 to 15% improvement in peak oxygen consumption after 4 months of aerobic exercise training, and a 1 to 6% improvement in aerobic power with additional aerobic exercise training. On the other hand, subjects, especially men, continued to have improvements in submaximal exercise performance (i.e., anaerobic threshold). In addition, aerobic exercise was associated with an improved lipid profile; subjects participating in aerobic exercise for up to 14 months exhibited increased levels of high-density lipoprotein cholesterol. Maintenance of regular aerobic exercise for an extended time interval is associated with greater cardiovascular benefits among older adults than has been reported previously.

Aerobic fitness, acute exercise and sleep in older men.

In the current study 12 aerobically fit and 12 sedentary older men underwent two nocturnal polysomnographic (PSG) studies. A control PSG was conducted following a day without aerobic activity, whereas a postexercise PSG study was conducted following an afternoon session of exhaustive aerobic exercise. In addition to deriving usual sleep parameters, a computer scoring program was used to count the number of individual electroencephalographic (EEG) slow waves in each PSG tracing. Multivariate and univariate analyses showed that the fit subjects had shorter sleep onset latencies, less wake time after onset, fewer discrete sleep episodes, fewer sleep stage shifts during the initial portion of the night, less stage 1 sleep, a higher sleep efficiency and more total slow waves during both PSGs than did the sedentary subjects. Although no main effects were found for the acute exercise challenge, post hoc analyses showed that high levels of body heating during exercise predicted increased sleep fragmentation for both fit and sedentary subjects. These findings provide initial support for the contention that exercise and fitness may have significant effects on the sleep of older men. However, results also suggest that high levels of body heating resulting from a single exercise challenge may have adverse effects. Implications of the study are discussed and suggestions for future research are provided.

Oxygen deficit during exercise testing in heart failure. Relation to submaximal exercise tolerance.

Measurements of oxygen deficit during submaximal exercise were correlated with the anaerobic threshold (as measured by gas exchange analysis), peak work rate on a ramp protocol, and the ability to perform constant work rate exercise in 10 male patients with New York Heart Association class 2 congestive heart failure and 12 age- and gender-matched normal controls. All subjects performed a maximal ramp exercise test for measurement of the anaerobic threshold. In addition, several 15-min constant work rate exercise sessions were conducted to evaluate oxygen deficit, measured as the area between the "ideal" square curve of oxygen consumption at the onset of constant work rate exercise and the actual exponentially shaped curve. Since the oxygen deficit significantly correlated with the plateau oxygen consumption during the 25-W constant work rate exercise (r = 0.61, p = 0.002), the oxygen deficit was normalized by the rectangular area of 15-min oxygen consumption above baseline. This normalized value significantly correlated with the inverse of the anaerobic threshold (r = 0.81, p < 0.0001). The logarithm of the normalized oxygen deficit significantly correlated with the maximum ramp work rate (r = -0.86, p < 0.0001) and the highest constant work rate sustained for 15 min (r = -0.82, p < 0.0001). In addition, the time to reach plateau oxygen consumption for the 25-W exercise significantly correlated with the inverse of the anaerobic threshold (r = -0.78, p < 0.0001), the maximum ramp work rate (r = -0.76, p < 0.0001), and the highest constant work rate sustained for 15 min (r = -0.74, p < 0.0001). Thus, the oxygen deficit seen in patients with heart failure during constant work rate exercise results from abnormally slow oxygen uptake kinetics and correlates with exercise capacity as measured by anaerobic threshold (via gas exchange analysis) and maximal and submaximal exercise tolerance. Oxygen deficit warrants further evaluation as a submaximal index of functional capacity in patients with heart failure.

Allograft diastolic dysfunction and chronotropic incompetence limit cardiac output response to exercise two to six years after heart transplantation.

BACKGROUND: Because prolonged survival of heart transplant recipients is expected with the current immunosuppressive treatment, the functional capacity of these long-term survivors is of interest. Previous exercise studies showed no objective improvement in exercise tolerance several years after transplantation, but the extent to which chronotropic incompetence and allograft diastolic dysfunction observed early after transplantation may improve over time has not been defined. METHODS: Thirteen untrained heart transplant recipients without symptoms, between 27 and 70 months after transplantation, and 13 age-matched sedentary normal controls underwent maximal upright bicycle exercise testing with simultaneous hemodynamic, radionuclide, and expired gas measurements. RESULTS: Systolic function as measured by ejection fraction was supranormal at rest in the transplant group and normalized with exercise. Despite their maximal exercise effort, transplant recipients had a 60% reduction in their exercise capacity compared with nontransplant recipients. Peak oxygen consumption was similarly reduced by 52%. Cardiac output response to exercise was 43% lower in the transplant group because of a 78% reduction in heart rate reserve and an 18% reduction in maximal stroke volume. Ventricular volumes were similarly reduced after transplantation, but filling pressures remained normal, indicating allograft diastolic dysfunction. Despite the significantly reduced maximal cardiac output, maximal arteriovenous oxygen difference was 25% lower in the transplant recipients, suggesting a peripheral deficit in oxygen handling. CONCLUSIONS: Therefore, patients, 2 to 6 years after transplantation, continue to have a significant reduction in exercise tolerance as a result of a combination of severe chronotropic incompetence, limited stroke volume reserve caused by a reduced ventricular size and allograft diastolic dysfunction, and an abnormality in peripheral oxygen delivery or use. Efforts aimed at improving these factors may further enhance the functional capacity of these long-term survivors of heart transplantation.