Paul Dubach

Effect of High Intensity Exercise Training on Central Hemodynamic Responses to Exercise in Men With Reduced Left Ventricular Function

OBJECTIVES The aim of this study was to evaluate the effects of high intensity exercise training on left ventricular function and hemodynamic responses to exercise in patients with reduced ventricular function. BACKGROUND Results of studies on central hemodynamic adaptations to exercise training in patients with chronic heart failure have been contradictory, and some research has suggested that training causes further myocardial damage in these patients after a myocardial infarction. METHODS Twenty-five men with left ventricular dysfunction after a myocardial infarction or coronary artery bypass graft surgery were randomized to an exercise training group (mean age +/- SD 56 +/- 5 years, mean ejection fraction [EF] 32 +/- 7%, n = 12) or a control group (mean age 55 +/- 7 years, mean EF 33 +/- 6%, n = 13). Patients in the exercise group performed 2 h of walking daily and four weekly sessions of high intensity monitored stationary cycling (40 min at 70% to 80% peak capacity) at a residential rehabilitation center for a period of 2 months. Ventilatory gas exchange and upright hemodynamic measurements (rest and peak exercise cardiac output; pulmonary artery, wedge and mean arterial pressures; and systemic vascular resistance) were performed before and after the study period. RESULTS Maximal oxygen uptake (VO2max) increased by 23% after 1 month of training, and by an additional 6% after month 2. The increase in VO2max in the trained group paralleled an increase in maximal cardiac output (12.0 +/- 1.8 liters/min before training vs. 13.7 +/- 2.5 liters/min after training, p < 0.05), but maximal cardiac output did not change in the control group. Neither stroke volume nor hemodynamic pressures at rest or during exercise differed within or between groups. Rest left ventricular mass, volumes and EF determined by magnetic resonance imaging were unchanged in both groups. CONCLUSIONS High intensity exercise training in patients with reduced left ventricular function results in substantial increases in VO2max by way of an increase in maximal cardiac output combined with a widening of maximal arteriovenous oxygen difference, but not changes in contractility. Training did not worsen hemodynamic status or cause further myocardial damage.

Exercise-induced hypotension in a male population. Criteria, causes, and prognosis.

The objective of this study was to demonstrate the causes, optimal definition, and predictive value of exercise-induced hypotension occurring during treadmill testing. This study included all patients referred for clinical reasons to the Long Beach Veterans Administration Medical Center treadmill laboratory and then followed for a 2-year period for cardiac events. The population consisted of 2,036 patients who underwent testing from April 4, 1984, to May 7, 1987, 131 of whom exhibited exercise-induced hypotension (6.4%). We found that exercise-induced hypotension is usually related to myocardial ischemia or myocardial infarction, is best defined as a drop in systolic blood pressure during exercise below the standing preexercise value, and indicates a significantly increased risk for cardiac events (3.2-fold, p less than 0.005). This increased risk was not found in those having no previous myocardial infarction or no signs or symptoms of ischemia during the exercise test, and the increased risk was also not found in those undergoing a treadmill test within 3 weeks after a myocardial infarction. Exercise-induced hypotension appeared to be reversed by revascularization procedures, but confirmation of a beneficial effect on survival requires a randomized trial. The clinical importance of this study is that we have demonstrated that a drop in systolic blood pressure below standing preexercise values during treadmill testing indicates an increased risk for cardiac events except in certain subsets of patients.

Exercise-induced silent ischemia: age, diabetes mellitus, previous myocardial infarction and prognosis

The purposes of this study were 1) to determine the prognosis of silent ischemia in an unselected group of patients referred for exercise testing, and 2) to assess whether age or the presence of myocardial infarction or diabetes mellitus influences the prevalence of silent myocardial ischemia during exercise testing. The design was retrospective, with a 2 year mean follow-up period. The study group consisted of 1,747 predominantly male in-patients and outpatients referred for exercise testing at a 1,200 bed Veterans Administration hospital. The main result was that the mortality rate was significantly greater (p = 0.02) among patients with abnormal ST segment depression than in patients without ST depression. The presence or absence of angina pectoris during exercise testing was not significantly related to death. The prevalence of silent ischemia was not significantly different among patients categorized according to myocardial infarction or diabetes mellitus status, but was directly related to age. It is concluded that, in patients with an ischemic ST response to exercise testing, the presence or absence of angina pectoris during the test does not alter the risk of death. The prevalence of silent ischemia during exercise testing is not statistically different among patients with recent, past or no myocardial infarction or with insulin-dependent or noninsulin-dependent diabetes mellitus.

Influence of high-intensity exercise training on the ventilatory response to exercise in patients with reduced ventricular function.

BACKGROUND Exercise training increases exercise capacity in patients with reduced ventricular function in part through improved skeletal muscle metabolism, but the effect training might have on abnormal ventilatory and gas exchange responses to exercise has not been clearly defined. METHODS Twenty-five male patients with reduced ventricular function after a myocardial infarction were randomized to either a 2-month high-intensity residential exercise training program or to a control group. Before and after the study period, upright exercise testing was performed with measurements of ventilatory gas exchange, lactate, arterial blood gases, cardiac output, and pulmonary artery and wedge pressures. RESULTS In the exercise group, peak VO2 and VO2 at the lactate threshold increased 29 and 39%, respectively, whereas no increases were observed among controls. Maximal cardiac output increased only in the exercise group (1.7 L x min(-1), P < 0.05), and no changes in rest or peak exercise pulmonary pressures were observed in either group. At baseline, modest inverse relationships were observed between pulmonary wedge pressure and peak VO2 both at rest (r = -0.56, P < 0.05) and peak exercise (r = -0.43, P < 0.05). Maximal VE/VCO2 was inversely related to maximal cardiac output (r = -0.72, P < 0.001). Training did not have a significant effect on these relationships. Training lowered VE/VO2, heart rate, and blood lactate levels at matched work rates throughout exercise and tended to lower maximal Vd/Vt. The slope of the relationship between VE and VCO2 was reduced after training in the exercise group (0.33 pre vs 0.27 post, P < 0.01), whereas control patients did not differ. CONCLUSIONS Exercise training among patients with reduced left ventricular function results in a systematic improvement in the ventilatory response to exercise. Training increased maximal cardiac output, tended to lower Vd/Vt, and markedly improved the efficiency of ventilation. Peak VO2 and ventilatory responses to exercise were only modestly related to pulmonary vascular pressures, and training had no effect on the relationships between exercise capacity, ventilatory responses, and pulmonary pressures.

Does the rest electrocardiogram after myocardial infarction determine the predictive value of exercise-induced st depression? A 2 year follow-up study in a veteran population

The failure of exercise-induced ST segment depression to consistently predict prognosis in patients after myocardial infarction could be a result of population differences and the rest electrocardiogram (ECG). These hypotheses were tested by studying 198 veterans who survived a myocardial infarction, underwent a submaximal predischarge treadmill exercise test and were followed up for cardiac events for 2 years. During the 2 years, 29 deaths, 19 reinfarctions and 28 revascularization procedures were documented. The prevalence of death or reinfarction was two times higher in patients who had exercise-induced ST depression than in patients who did not. However, in the 55 patients without Q waves, the risk increased to 11 times for an abnormal ST response. These findings suggest that exercise-induced ST depression only predicts high risk in patients after myocardial infarction whose ECG at rest does not exhibit Q waves and that differences in the prevalence of rest ECG patterns are the most likely explanation for the failure of agreement among prior studies.

Maintenance of exercise capacity and physical activity patterns 2 years after cardiac rehabilitation.

BACKGROUND The benefits of exercise training for postmyocardial infarction and postcoronary artery bypass surgery patients are well established, but little is known about the effects of rehabilitation in the months or years following the program. The purpose of this study was to assess exercise capacity, blood lipids, and physical activity patterns 2 years after completing a concentrated residential rehabilitation program in Switzerland. METHODS Seventy-eight patients (86% males, mean age = 56 +/- 10, mean ejection fraction = 64% +/- 12%) were referred to a residential rehabilitation program after a myocardial infarction or coronary artery bypass surgery between January 2001 and June 2001. Patients lived at the center for 1 month, during which time they underwent educational sessions, consumed a low-fat diet, and exercised 2 hours daily. Two years after completing the program, patients returned to the hospital and underwent a maximal exercise test, an assessment of recent and adulthood physical activity patterns, and evaluation of blood lipids. RESULTS During the 2-year follow-up period, there were 5 deaths, and 70 of the remaining 73 patients returned for repeat testing. Mean exercise capacity increased 27% during the rehabilitation program (P < .01). Gains in exercise capacity during rehabilitation were maintained after the follow-up period; mean exercise capacity after 2 years was 34% higher compared with that at baseline (P < .01). At the 2-year evaluation, patients were expending a mean of 3127 +/- 1689 kcals/wk during recreational activities compared with 977 +/- 842 kcals/wk during adulthood prior to their cardiac event (P < .001). Between the completion of rehabilitation and the 2-year follow-up, total cholesterol, total cholesterol/high-density lipoprotein ratio, and triglycerides increased significantly. CONCLUSIONS Two years after a cardiac event and participation in a concentrated residential rehabilitation program, patients maintained their exercise capacity and engaged in physical activities that exceed the levels recommended by guidelines for cardiovascular health. These observations suggest that a relatively intensive rehabilitation program provided a catalyst to maintain physical activity patterns and exercise tolerance in the 2 years following a cardiac event.

Exercise capacity, physical activity patterns and outcomes six years after cardiac rehabilitation in patients with heart failure

Objective: To determine the short- and long-term effects of an intensive, concentrated rehabilitation programme in patients with chronic heart failure. Design: Randomized controlled trial, with one-month and six-year evaluations. Setting: Residential rehabilitation centre in Switzerland. Subjects: Fifty patients with chronic heart failure, randomized to exercise or control groups. Interventions: A rehabilitation programme lasting one month, including educational sessions, a low-fat diet, and 2 hours of individually prescribed exercise daily. Main measures: Exercise test responses, health outcomes and physical activity patterns. Results: Peak Vo2 increased 21.4% in the exercise group during the rehabilitation programme (P<0.05), whereas peak Vo2 did not change among controls. After the six-year follow-up period, peak Vo2 was only slightly higher than that at baseline in the trained group (7%, NS), while peak Vo2 among controls was unchanged. During long-term follow-up, 9 and 12 patients died in the exercise and control groups, respectively (P = 0.63). At six years, physical activity patterns tended to be higher in the exercise group; the mean energy expenditure values over the last year were 2704 ± 1970 and 2085 ± 1522 kcal/week during recreational activities for the exercise and control groups, respectively. However, both groups were more active compared to energy expenditure prior to their cardiac event (P<0.001). Conclusions: Six years after participation in a residential rehabilitation programme, patients with chronic heart failure had slightly better outcomes than control subjects, maintained exercise capacity and engaged in activities that exceed the minimal amount recommended by guidelines for cardiovascular health.

Use of the exercise test to predict prognosis after coronary artery bypass grafting

The objective of this study was to predict the prognosis of patients who become symptomatic after having undergone coronary artery bypass grafting (CABG) using clinical and exercise test responses. A retrospective analysis was performed of all veterans referred for clinical indications to a Veterans Administration Medical Center for a treadmill test after having undergone CABG. Of 2,044 patients who were exercise tested from April 1984 to May 1987, 296 had previously undergone CABG. Clinical data considered included age, sex, medication and symptom status, history of myocardial infarction, type of myocardial infarction and time from CABG. The exercise test responses considered were MET level, maximal heart rate, maximal systolic blood pressure, chest pain pattern and ST-segment response. During a 2-year follow-up after exercise testing, there were 15 deaths, 11 nonfatal myocardial infarctions, 6 repeat CABGs and 3 percutaneous transluminal coronary angioplasties. Although MET level and maximal heart rate were significantly related to prognosis and no patient who exceeded 8 METs died, the predictive power of these exercise test responses was low and ST-segment depression was not predictive at all. The inability of the exercise electrocardiogram to predict cardiac events in patients after CABG requires the use of other methods of testing to identify those who need invasive studies and intervention.

Effects of exercise training on myocardial energy metabolism and ventricular function assessed by quantitative phosphorus-31 magnetic resonance spectroscopy and magnetic resonance imaging in dilated cardiomyopathy.

OBJECTIVES The present study investigated changes in cardiac energy metabolism and function in patients with dilated cardiomyopathy (DCM) before and after exercise training (ET) with phosphorus-31 magnetic resonance spectroscopy (MRS) in combination with magnetic resonance imaging (MRI). BACKGROUND Exercise training might have a beneficial role on myocardial function and oxidative metabolism in DCM, but it is unclear whether the additional load on the failing heart leads to deterioration of cardiac energy metabolism. METHODS Twenty-four patients were randomized to an exercise (age 53 +/- 12 years) or a control (age 56 +/- 6 years) group. Supervised ET was performed for 2 months, followed by 6 months of self-regulated training. At baseline and 2 and 8 months, maximal exercise testing along with quantitative MRS and MRI studies were performed. RESULTS The effectiveness of ET was demonstrated by a 17% increase in peak oxygen uptake (p < 0.05). Exercise training improved left ventricular (LV) end-systolic volume (p < 0.05) and LV ejection fraction (30 +/- 15% vs. 37 +/- 15%; p < 0.01) but not right ventricular parameters. The improvement in cardiac function was not accompanied by changes in cardiac high-energy phosphate concentrations; phosphocreatine, adenosine triphosphate, and the phosphocreatine/adenosine triphosphate ratio were all unchanged after training. CONCLUSIONS The observation that LV function improved and LV energy metabolism remained unchanged suggests that the beneficial effect of ET on LV function is achieved without adversely affecting metabolism. These findings lend further support for the use of ET as an adjunct therapy in DCM.

Influence of intensive physical training on urinary nitrate elimination and plasma endothelin-1 levels in patients with congestive heart failure

BACKGROUND Congestive heart failure (CHF) is associated with increased peripheral vascular resistance. Exercise-induced shear stress may release endothelial relaxing factors, such as nitric oxide (NO), and inhibit the production of vasoconstrictors such as endothelin-1 (ET-1) thereby modulating vascular tone. We examined the effect of intensive training on ET-1 plasma concentrations and NO-metabolite elimination in patients with CHF after acute myocardial infarction. METHODS Seventeen patients with CHF after a myocardial infarction were randomized to an exercise group (n = 9), who performed physical training for 8 weeks, or a control group (n = 8) who received usual care. A physical examination, pulmonary function test, and a maximum exercise test were performed, and 24-hour urinary nitrate elimination and ET-1 in plasma were determined before and at the end of the study period. RESULTS Maximal oxygen uptake remained unchanged in controls (17.9 +/- 1.4 to 18.1 +/- 1.5 mL/(kg min) but increased in the exercise group (from 20.4 +/- 0.75 to 26.7 +/- 1.4 mL/(kg min). After 8 weeks the urinary nitrate elimination in controls was significantly decreased (1.25 +/- 0.20 to 1.03 +/- 0.22 mmol/24 hours; P < 0.001), while it was unchanged in the exercise group (1.26 +/- 0.23 to 1.39 +/- 0.28; P = 0.71). Plasma ET-1 levels did not change after 8 weeks (7.87 +/- 0.62 versus 7.57 +/- 0.75 and 7.13 +/- 0.6 versus 7.35 +/- 0.7 pg/mL for control and exercise groups, respectively). CONCLUSION In patients with CHF after acute myocardial infarction nitrate elimination decreases over the subsequent 2 months. This trend was reversed by training. Because nitrate elimination mirrors endogenous NO production, these results suggest that training may positively influence endothelial vasodilator function.