Central adaptations to exercise training in patients with chronic heart failure.
Read an Interview with Prof. Pantaleo Giannuzzi, editor of the European Journal for Cardiovascular Prevention and Rehabilitation, on adaptations to exercise training in patients with chronic heart failure.
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Q&A with Prof. Pantaleo Giannuzzi, Salvatore Maugeri Foundation IRCCS, Scientific Institute for Clinical Care and Research in Veruno (No), Italy
Editor of the European Journal for Cardiovascular Prevention and Rehabilitation
By Andrea Massa
How safe or well-advised is to set an aerobic training program for chronic heart failure patients?
No clinical or hemodynamic deteriorations have been demonstrated in stable heart failure patients in spite of long-term exercise. Indeed, on the basis of the available literature, a central effect of aerobic training in CHF patients cannot be denied. Such an effect is due to training-induced adaptations of the main cardiac output determinants, that is, heart rate and stroke volume. Still parameters are influenced by several factors whose response to aerobic training may vary among different individuals.
Nevertheless, the existence of a central response to aerobic training in CHF patients is meaningful. Data presented by our Institute (Scientific Institute for Clinical Care and Research in collaboration with colleagues A.Mezzani and U.Corra) unequivocally confirms both the safety and the central morpho-functional benefits, setting the stage for an even more widespread use of this non-pharmacologic intervention in the everyday clinical practice. Such study was conducted in the pre-beta-blockers era though, so the possibility to extend our conclusions to patients on beta-blocking therapy still needs to be verified.
Aerobic training is already a well-established non-pharmacologic treatment for CHF patients in stable clinical conditions. How are your assumptions different from the prevalent scientific literature?
In normal subjects, aerobic training significantly increases peak effort ventilation, cardiac output, peripheral blood flow, and skeletal muscle oxygen extraction. However, in CHF patients the increase of peak VO2 observed after a period of aerobic training is currently attributed more to peripheral (skeletal muscle) than to central (heart) adaptations, therefore leaving central effects of training quite neglected. That’s why in a recent review we assessed particularly the existence or the absence of significant central adaptations to aerobic training in patients with CHF due to left ventricular systolic dysfunction.
Still, today we are facing some methodological limitations in considering the cardiac output response to aerobic training in CHF patients, isn’t this the case?
Yes, unfortunately the gold standard for cardiac output measurement is yet today the right heart catheterization with thermo-dilution technique, an invasive procedure with inherent risks and problems of compliance on the part of the patients. Few studies focused on cardiac output response have shown a significant increase at peak effort after a period of training with respect to pre-training values. Furthermore, subanalysis of a leading study (Hambrecht et al.) has shown that central adaptations to aerobic training are also demonstrable in patients with severe CHF. The problem is that failure to demonstrate a significant improvement in peak cardiac output is often associated with a weaker study design and a lower training intensity. In any case, a recent meta-analysis has substantiated the effect of aerobic training on peak cardiac output, showing a training-induced significant mean increment of 2.5 l/min (equal to 21% of the pre-trainingvalue) in a total of 104 CHF patients.
We shouldn’t forget that all the data mentioned has been collected during the pre-beta-blockers era, again still open to debate. However, some studies have demonstrated an improvement of peak VO2 after aerobic training in patients on beta-blockers similar to that of patients off these drugs. If one assumes that beta-blockers are not expected to significantly modify peripheral oxygen extraction, the linear relationship between relative changes in cardiac output and peak VO2 should also be preserved in beta-blocked patients.
Professor, you previously mentioned some effects of aerobic training on peak cardiac output. What is the response of stroke volume?
Unlike peak cardiac output, this is not easily identifiable from current literature. We noticed a wide array of individual responses to aerobic training of the several stroke volume determinants, as already evaluated in many papers. However, most of these works measured such parameters at rest instead of at peak effort. Given that resting hemodynamic indexes are known to correlate poorly with the response to aerobic training in CHF patients, we consider such a lack of a peak effort evaluation a serious conceptual flaw.
Are there any consequences for the left ventricular end-diastolic volume?
Resting left ventricular end-diastolic volume (LVEDV) has been shown not to change or even to be reduced after a period of aerobic training in CHF patients. A previously-quoted meta-analysis has shown a small but significant reduction in resting LVEDV. This effect, which parallels data from patients with asymptomatic left ventricular dysfunction, is at odds with the trend toward an enlargement of resting LVEDV after aerobic training described in normals, even with a large interindividual variability. The reasons for this anti-remodeling effect of aerobic training in CHF patients are not entirely understood. For instance, on patients with dilated cardiomyopathy of ischemic origin, training may improve blood flow supply to left ventricular areas of hibernating myocardium, ultimately leading to some degree of recovery of regional contractility and regression of unfavorable remodeling.
In any case, a series of studies from our group specifically aimed to evaluate the effects of aerobic training on left ventricular remodeling clearly and consistently demonstrated that regular aerobic exercise is not harmful in stable cardiac patients, but indeed exerts beneficial effects on the left ventricular remodeling process over a wide spectrum of clinical conditions and left ventricular systolic functions. As an increase in filling pressure is a major stimulus to unfavorable left ventricular remodeling, these findings are in agreement with those describing in CHF patients no training-induced changes of left ventricular end-diastolic pressure (evaluated invasively by pulmonary capillary wedge pressure) both at rest and submaximal and maximal effort, which seems to be true also in beta-blocked patients. Several mechanisms have been advocated to justify such a training-induced enhancement of diastolic function in CHF patients, such as an increased calcium uptake by the sarcoplasmic reticulum, an improved perfusion of myocardium, more efficient myocardial bioenergetics, and a reduction of left ventricular diastolic asynchrony.
In addition to heart rate, left ventricular dimensions, and preload, left ventricular compliance is another important determinant of LVEDV, both at rest and peak effort.
As already pointed out for cardiac output and heart rate adaptations to aerobic training, available data about LVEDV still refer mainly to non-beta-blocked patients.
Have you also evaluated the adaptations of left ventricular ejection fraction in CHF patients to a period of aerobic training?
Many authors have evaluated such adaptations in CHF patients, finding unchanged or significantly increased LVEF values. The data confirms from a functional standpoint the absence of deleterious effects.
The training-induced increase of LVEF observed by some authors has been ascribed to both contractility and afterload changes, which have been well described in patients who don’t have chronic heart failure. For instance, one study (Belardinelli et al.) has hypothesized an augmented contractile reserve after training in ischemic CHF patients, as demonstrated by an LVEF increase in the absence of changes in diastolic blood pressure (afterload) and LVEDV (preload); as already indicated for LVEDV modifications, such a gain in left ventricular contractility may be due to improved perfusion of hibernating myocardium areas.
Training-induced afterload modifications have also been demonstrated at peak effort as a decrease of both total peripheral resistances or leg vascular resistance by some authors. These adaptations are likely due to a corrective effect of aerobic training on the endothelial dysfunction typical of CHF patients. Aortic stiffness/distensibility is another factor known to affect afterload and exercise capacity.
In conclusion, as far as beta-blocked CHF patients are concerned, resting LVEF has been shown to be unchanged or significantly increased after a period of aerobic training but more data is needed for a proper assessment.
What’s the future scenario in respect of aerobic exercise for CHF patients?
Case studies on small groups of patients have highlighted that regular aerobic exercise of moderate intensity is sufficient to keep cardiovascular risks in check. Such exercise, in presence of non-ischemic cardiomyopathy, can possibly induce a reverse remodeling, even though this has yet to be fully demonstrated.
European Journal for Cardiovascular Prevention and Rehabilitation
The journal embraces all the scientific, clinical, and public health disciplines that address the causes and prevention of cardiovascular disease, as well as cardiovascular rehabilitation and exercise physiology. It provides a common clinical forum for all physicians and other health professionals who address cardiovascular prevention and rehabilitation in everyday practice. It provides an avenue for reports of the European Heart Network, national heart foundations, non-governmental and governmental organizations, and the European Union. Learn more
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