Ute Goebbels

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.

Effect of Exercise Training on Myocardial Remodeling in Patients With Reduced Left Ventricular Function After Myocardial Infarction Application of Magnetic Resonance Imaging

BACKGROUND There are conflicting reports on the effects of training on the remodeling process in post-myocardial infarction patients with ventricular damage. METHODS AND RESULTS Twenty-five patients with reduced ventricular function (mean ejection fraction, 32.3+/-6%) after an anteroseptal or inferolateral myocardial infarction were randomized to an exercise group (n=12) or a control group (n=13). Patients in the exercise group resided in a rehabilitation center for 2 months and underwent a training program consisting of two 1-hour sessions of walking daily, along with four monitored 45-minute sessions of stationary cycling weekly. Before and after the study period, maximal exercise testing and cardiac MRI were performed. Oxygen uptake increased 26% at maximal exercise (19.7+/-3 to 23.9+/-5, P<.05) and 39% at the lactate threshold (P<.01) in the exercise group, whereas control values did not change. No differences were observed within or between groups in MRI measures of end-diastolic (187+/-47 pre versus 196+/-35 mL post in the exercise group and 179+/-52 pre versus 180+/-51 mL post in the control group), end-systolic volume (118+/-41 pre versus 121+/-33 mL post in the exercise group and 119+/-54 pre versus 116+/-56 mL post in the control group), or ejection fraction (38.0+/-9 pre versus 38.2+/-10% post in the exercise group and 37.0+/-10 pre versus 38.3+/-13% post in the control group). Myocardial wall thickness measurements at end diastole and end systole and their difference in 80 myocardial segments determined by MRI yielded no significant interactions between groups. When myocardial wall thickness measurements were classified by infarct or noninfarct areas, no differences were observed between groups over the study period. CONCLUSIONS A high-intensity, 2-month residential cardiac rehabilitation program resulted in substantial increases in exercise capacity among patients with reduced left ventricular function. In contrast to some recent reports, the training program had no deleterious effects on left ventricular volume, function, or wall thickness regardless of infarct area.

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.

Exercise training and myocardial remodeling in patients with reduced ventricular function: One-year follow-up with magnetic resonance imaging

BACKGROUND Exercise training is now an accepted therapeutic intervention in patients with reduced ventricular function after a myocardial infarction. However, there are conflicting reports on the effects of training on the remodeling process of the heart, and previous studies have only assessed short-term effects of training. METHODS AND RESULTS Twenty-five patients with reduced ventricular function after myocardial infarction were randomly assigned to an intensive 2-month exercise training program or to a control group (control group: n = 13, aged 55 +/- 7 years, ejection fraction 33.3% +/- 6%; exercise group: n = 12, aged 56 +/- 5 years, ejection fraction 31.5% +/- 7%) and followed up for 1 year. Measures of left ventricular size, function, and wall thickness in the infarct and noninfarct areas were made by magnetic resonance imaging at baseline, after the 2-month training period, and 1 year later. Maximal oxygen uptake increased in the trained group, from 19.7 +/- 3 mL/kg per minute at baseline to 25.1 +/- 5 and 24.2 +/- 5 mL/kg per minute after 2 months and 1 year, respectively (P <.05 vs baseline for both), whereas the control group did not change significantly. Ejection fraction, end-diastolic volumes, and end-systolic volumes did not change at any measurement point throughout the study period in either the trained or control groups. Myocardial wall thickness measurements at end-diastole and end-systole and their differences determined by magnetic resonance imaging yielded no significant interactions between groups. When myocardial wall thickness measurements were classified by infarct or noninfarct areas, no differences were observed between groups over the study period. CONCLUSIONS Intensive exercise training in patients with reduced ventricular function resulted in a significant improvement in exercise capacity after 2 months, and this improvement was sustained over 1 year. In contrast to some recent reports, training had no deleterious effects on left ventricular volume, function, or wall thickness regardless of infarct area.

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.

Influence of exercise training on blood viscosity in patients with coronary artery disease and impaired left ventricular function

Exercise training has recently become an accepted therapeutic modality in chronic heart failure after myocardial infarction. Because the therapeutic mechanism behind it is controversial and not well understood, we analyzed the influence of exercise training on blood viscosity. Twenty-five patients with chronic heart failure (ejection fraction < 40%) after myocardial infarction were randomly assigned to either an 8-week intensive exercise program at a residential rehabilitation center or 8 weeks of sedentary life at home. Exercise consisted of two 1-hour walking sessions per day and four intensive bicycle ergometer training sessions of 40 minutes at 70% to 80% peak exercise capacity per week. Whole blood viscosity, viscosity at standardized hematocrit of 45% (P45) at high and low shear rates, and plasma viscosity were measured in a Couette-type viscometer before, during, and at the end of the study period. Exercise training, which significantly increased maximal cardiac output and oxygen uptake, did not change plasma viscosity, whole blood viscosity, and P45 significantly. Sedentary controls, however, had a higher whole blood viscosity and P45 after 8 weeks. No statistical difference was found, however, between the two groups. We conclude that blood rheology remains unaffected by exercise training in patients with chronic heart failure. The improvement of blood viscosity remains an interesting therapeutic option for the symptoms of these patients, which must be achieved by methods other than exercise training.

Effects of exercise training on limb blood flow in patients with reduced ventricular function

BACKGROUND Among the factors that contribute to limiting exercise tolerance in chronic heart failure are reduced peripheral blood flow and impaired vasodilatory capacity. Exercise training improves vasodilatory capacity in normal subjects, but controlled studies of exercise training evaluating upper and lower limb blood flow rates have not been performed in patients with reduced ventricular function. Improved vasodilatory capacity could help explain how training increases exercise capacity in these patients. METHODS Twenty patients (mean age 55 +/- 6 years) with reduced left ventricular function (mean ejection fraction 32% +/- 6%) after a myocardial infarction were randomized to a 2-month high-intensity residential rehabilitation program or to a control group and were monitored over the subsequent year. Both groups were treated according to current practice with angiotensin-converting enzyme inhibition therapy. Training began 1 month after myocardial infarction. Baseline and postischemic flow rates were measured by plethysmography in both the upper and lower limbs 1 month, 3 months, and 1 year after the infarction. Peak oxygen uptake (VO2) and cardiac output were measured before and after training, and peak VO2 was determined again after 1 year. RESULTS After 2 months of training peak VO2 increased 25%, VO2 at the lactate threshold increased 40%, and maximal cardiac output increased from 12.1 +/- 1.6 L/min to 13.9 +/- 2.4 L/min in the exercise group (all p < 0.05), whereas no differences were observed in the control group. At the 1-year follow-up no further increases in peak VO2 were noted in either group, but the higher value persisted in the trained group. However, changes in limb flow rates were poorly related to changes in both peak VO2 and maximal cardiac output. Improvements in baseline and postischemic flow rates occurred mainly in the lower limbs and were observed in the two groups to a similar degree. CONCLUSION Exercise training is highly effective in improving exercise capacity in patients with reduced ventricular function after myocardial infarction. These improvements parallel an increase in maximal cardiac output, but they are unrelated to vasodilatory capacity. In patients with reduced ventricular function after myocardial infarction, lower limb vasodilatory capacity improves gradually over the subsequent year, and these improvements occur irrespective of exercise training.