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Thematic Units Arrhythmias and Electrophysiology Basic Research Bioengineering and Medical Informatics Cardiac Surgical Intensive Care Cardiomyopathies Cardiovascular Nursing Cardiovascular Pharmacology Cardiovascular Surgery Chagas Disease Echocardiography Epidemiology and Cardiovascular Prevention Heart Failure Hemodynamics - Cardiovascular Interventions High Blood Pressure Ischemic Heart Disease Nuclear Cardiology Pediatric Cardiology Peripheral and Cerebral Vascular Diseases Sports Cardiology Transdisciplinary Cardiology and Mental Health in Cardiology

Prescription of Physical Activity in Patients with Compensated Chronic Heart Failure

Cardiac insufficiency, or heart failure, is no longer considered, pure and simply, a heart disease. Rather, it is a complex syndrome, which involves multiple systems and compensatory neurohumoral mechanisms. The peripheral manifestations of the disease, such as endothelial dysfunction, skeletal muscle changes, abnormal blood flow, and the chemoreflex control of breathing [1,2], are the best elements to determine the symptoms which generate effort intolerance. The Framingham Heart Study

[3] shows that the prevalence of cardiac insufficiency between the ages of 65 and 74 is estimated at 4.5%, with a survival rate of less than 40% within the 5 subsequent years. The 40-year follow-up of over 9,000 patients in this study demonstrated that heart failure is one of the major causes of hospitalization nowadays, its numbers verifying that it accounted for 10 new cases in each group of 1,000 individuals in their 70’s and 25 new cases in each group of individuals in their 80’s. In Brazil, heart failure accounted for 4% of all hospital admissions and 31% of hospital admissions due to cardiovascular problems, in 2002 [4]. The prognosis of heart failure becomes more somber with the evolution of neurohumoral action, of the inflammatory process, of the progressive activation of the renin-angiotensin-aldosterone system (RAAS), and of the sympathetic nervous system (SNS).

Dyspnea and fatigue during physical activity constitute the main clinical symptoms of heart failure [5], which prompts the patient to cease the physical effort much too early. This, in turn, causes a restriction in one’s daily activities which ultimately diminishes the individual’s physical capacity and worsens his/her quality of life [6]. These symptoms are due to a complex physiopathological response to ventricular dysfunction and ensuing reduction of oxygen delivery to tissue.

Recent studies show tenuous correlation between the hemodynamic variables and exercise capacity [7]; an immediate increase in aerobic competence with improved heart performance [8] or with pharmacological increase of muscle blood flow [9] was not detected. On the other hand, they do point toward intrinsic changes in peripheral muscles [10, 11] and a neurohormonal interaction between the periphery and the heart [12]; furthermore, cardiac pump function is impaired, and all these interactions are determinant to the reduction of functional capacity in individuals suffering from heart failure.

Compensatory mechanisms are unleashed to maintain the perfusion of vital organs and stabilize the heart’s performance in face of a cardiac injury, regardless of the causal agent. The continuous reoccurrence of these processes, even if initially beneficial, triggers a series of undesirable side effects, such as ventricular remodeling, which is characterized by alterations in the geometry and mechanical efficiency of the heart [13]. Further, there occur changes in gene expression, progressive apoptosis, and worsening of myocardial function [14]. Cardiac debt and augmented systemic vascular resistance (SVR) stimulate the sympathetic nervous system. Other changes include an increase in cardiac frequency, energy consumption of the myocardium, systemic vasoconstriction, and activation of the renin-angiotensin-aldosterone system (RAAS). Angiotensin II and aldosterone act upon cardiovascular remodeling and arterial flexibility [15].

High concentrations of norepinephrine and angiotensin II boost the release of arginine vasopressin in

Argentine-Brazilian Symposium on Exercise, Ergometry and Rehabilitation

Almir Sergio Ferraz *

1. Coordinator of the Cardiopulmonary Laboratory of the Cardiovascular Rehabilitation Section of The Dante Pazzanese

Institute of Cardiology 2. Director of the Exercise Labotory of the Institute of Cardiology

of São Paulo, 3. Phylosofer Doctor in Cardiology from the Medical School of the

University of São Paulo, Brasil

Ferraz A. - Prescription of Physical Activity in Patients with Compensated Chronic Heart Failure

5th. Internacional Congres of Cardiology on the Internet

the neurohypophysis and stimulate the production of endothelin in the vascular endothelium, which are additional causes of hypertrophic remodeling, apoptosis, and deterioration of cardiac function. Chronic ß-adrenergic stimulation leads to an increase of proinflammatory cytokines, such as interleukin-1 and interleukin-6, to endothelin, and tumor necrosis factor-α (TNF-α) [16], which cause myocardial inflammation, an increase of nitric oxide synthesis, skeletal muscle myopathy, and activity of phosphatase protein 2A in the muscle, a regulator of muscle apoptosis [17,18] . On the other hand, the actual cause of structural, metabolic, and functional damage to the muscle as a whole remains unknown. Krankel et al [18] recently identified 24 regulatory genes of skeletal muscle dysfunction in an experimental model in rats with induced heart failure.

In comparison to normal controls, the skeletal muscle microscopy of individuals suffering from heart failure revealed decreased capillary density, atrophy, remodeling, predominantly with muscle fiber type II instead of type I, which have high oxidant properties; and fewer mitochondria per cell. An ultrastructural morphometric analysis further revealed reduction in volume, mass, and surface of mitochondrial cristae. Reduction in the activity of cytochrome c oxidase, creatine kinase (CK), and other oxidant enzymes in this organelle have been detected through histochemical analysis [19, 20]. These alterations, similar to those observed in physical deconditioning due to inactivity, compromise cellular respiration and lead to early anaerobic metabolism during exercise. The increase in carbon

dioxide ( CO2) production resulting from metabolic acidosis stimulates respiratory control centers and

they, in turn, increase minute ventilation (VE); this results in dyspnea, muscular fatigue, and effort intolerance [21, 22]. As for respiratory muscles, the cytokines and other catabolism byproducts also contribute to jeopardize the ventilation/perfusion relation, causing excessive respiratory effort and dyspnea [23].

Up until a few decades ago, physical activity was not recommended for individuals with chronic heart failure because it was believed it worsened cardiac function. Towards the end of the 1970s, Lee e cols. [24] put forth the safety and benefits of physical training on individuals with ventricular dysfunction. These findings were later corroborated by Conn e cols in 1982 [25]. In 1990, Coats e cols [26] observedimprovement in both aerobic power and heart failure symptoms with the regular practice of exercises, thus putting in check the recommendation that patients should rest as part of the treatment of the illness. These results were confirmed in subsequent, randomized trials.

A recent review in the existing literature encompassed 29 studies and 1,126 individuals with primary and secondary heart failure, NYHA classes II or III and left ventricular ejection fraction (LVEF) less than 40%. They were underwent 23 aerobic training programs and 6 muscular resistance training programs. The analysis of the results verified improvements in HRQoL, VO2max, distance on the 6-

minute walk test, work capacity measured in Watts, and duration of physical activity [27].

Rehabilitation through physical activity improves NYHA classification of heart failure patients, exercise tolerance and even left ventricular function [28]. Systolic volume may present slight increase [29] and improvement of cardiac debt and cardiac index have been attributed to the reversion of chronotropic incompetence and higher diastolic filling [30, 31, 32]. Giannuzzi et cols. [33] suggest the attenuation of left ventricular remodeling in post-myocardial-infarction patients who underwent physical conditioning programs for a long period.

Regular physical exercises have direct impact on the neuroendocrine and autonomic nervous systems in cases of heart failure. Reduction a sympathetic activity and changes in the renin-angiotensin axis cause smaller liberation of norepinephrine, improved RR variability and chronotropic response during effort [26, 34, 35]. A reduction in peripheral vascular resistance, associated to endothelial dysfunction correction, attenuates cardiovascular remodeling and enhances muscular blood flow [36, 37].

There is an impressive list of benefits to skeletal muscle, such as an increase of muscle fiber type I, enhancement of phosphocreatine resynthesis, and an increase of adenosine diphosphate, intracellular pH, and phosphate to phosphocreatine ratio [38, 39, 40]. These effects retard the beginning of metabolic acidosis and reduce ventilatory abnormalities through the action of ergoreceptors,

diminishing minute volume ( E) in submaximal workload and normalization of ventilatory equivalent

ratio for CO2 ( E/ CO2). Among other things, physical activity restores structural and functional

changes of peripheral muscle in HF, reduces the incidence of cytokines in the muscles, increases antiapoptotic factors and cytochrome c oxidase activity [41], delays catabolic process, improves ventilation/perfusion ratio, exercise tolerance and quality of life of patients suffering from heart failure [42, 43].

The clinical manifestations of heart failure, and more specifically in relation to effort intolerance, may be accentuated by a peripheral component associated to myocardial dysfunction. The physical condition of the patients suffering from cardiac insufficiency is determined by the sum of primary myocardial injury and skeletal muscle abnormality, which resulted in the Muscle Hypothesis put forth by Clark et al. [13, 44]. (Picture 1).



The functional capacity of these patients is evaluated by effort tolerance, peak VO2, and oxygen

consumption at the moment of anaerobic ventilatory threshold, which corresponds to the level of the exercise that accompanies the majority of the activities of HF patients [45, 46].

No relationship between dysfunction evaluated at rest and exercise capacity was observed in left ventricular systolic dysfunction. This may be influenced by changes in peripheral oxygen extraction and it has been demonstrated that the functional limitation in these patients may predominantly be due to the reduction of peripheral extraction of oxygen with a smaller participation of central factors

[47,48]. Numerous research studies were published in the last decade and they demonstrated that effort limitation on heart failure patients is related to qualitative and quantitative changes in skeletal muscle, which may have reasonable reversibility through regular physical activity [49, 50].

In heart failure there is greater activation of arterial and cardiopulmonary baroreflex, which aim at the preservation of arterial blood pressure. There is an increase in sympathetic activity at rest and during physical training, elevation in heart rate, reduction in heart rate variability, and improvement in sympathetic vasoconstriction tonicity. Continuous physical activity leads to an increase in parasympathetic activity, characterized by lower heart rate at rest and during submaximal exercises [51].

Neurohormonal system stimulation is classified as one of the main markers present in heart failure. This is characterized by high levels of plasma noradrenaline in the patients. A study recently conducted by Roveda et al [48] demonstrated muscle nerve sympathetic activity, measured directly from the peroneal nerve, increases progressively from the healthy individual to the patient with left ventricular dysfunction, and from those to the ones who presented advanced heart failure, with a reduction of renal and muscle blood flow.

The activation of the renin-angiotensin-aldosterone system has been attributed to low renal perfusion pressure. There is an increase in vasopressin levels and liberation of natriuretic peptides. These physiopathological changes facilitate vasoconstriction and expansion of plasma volume, thus contributing to preserve cardiac debt and systemic arterial blood pressure and reducing vasodilation capacity. Chronic physical activity seems to reduce the levels of angiotensin II, aldosterone, vasopressin, and natriuretic peptides [52]. Some mechanisms account for the reduction of vasodilation capacity in chronic heart failure: a) hardening of the arteries due to elevated levels of salt and water along the walls of the arteries, which accounts for one-third of vasodilation capacity; b) chronic vascular deconditioning; c) endothelial dysfunction, caused by the reduction in the production of nitric oxide. On the other hand, physical activity restores vasodilation capacity in patients who suffer from heart failure, which in turn improves endothelial synthesis of nitric oxide. This vasodilating effect is not limited to the limb trained and its benefits last systemically for an average of up to six months after the end of the training program [45]. These morphofunctional changes interfere with the

reduction of exercise tolerance and reduction of O2 at peak of effort and anaerobic threshold [49]

(Picture 2). Regular physical activity improves mitochondrial oxidating capacity which reverts, at least

Picture 1: Factors that influence functional capacity.



partially, the abnormalities in skeletal muscle fiber [50] (Picture 3).

Picture 2: VO2 at the anaerobic threshold and muscle mass of the thighs: CHF

patients: r = 0.39 P = 0.02 One may notice that the more athrofied the skeletal muscle mass, the lower the

oxygen consumption at the anaerobic threshold level.Source: Vivaqua RC et al Arq Bras Cardiol 2003; 81 (6):576

Picture 3a: In A (initial biopsy), fibers with a less intense coloration may be observed inSDH enzyme.



Patients with chronic heart failure experience inequality in ventilation perfusion relation with an increase of physiological dead space. Consequently, there is a disproportionate increase of ventilation, and peripheral desaturation with diminished respiratory efficiency during effort may occur. Regular physical activity, with the inclusion of breathing exercises, helps equalize ventilatory parameters, improving dyspnea and favorably influencing effort tolerance. The dyspnea observed in patients in a less severe state, without edema, has been more clearly associated to lack of physical activity and metabolic abnormalities of locomotor skeletal muscle than pulmonary congestion [46]. The ventilatory benefits observed during effort are partially due to a retardation of lactate blood buildup, obtained through the increase of anaerobic threshold values in cardiopulmonary test, the patients displaying lesser limitation in performing daily activities [53].

Prescription of Physical Activity to Patients with Chronic Heart Failure Before starting a physical activity program, heart failure patients must have been clinically stable for a period no lesser than thirty days; moreover, they must undergo an exercise test, preferably one with a direct analysis of the gases exhaled. This evaluation will allow for an individual customization of the different metabolic phases during physical effort. That way it is possible to optimize an individual determination of ventilatory thresholds, from which the metabolic and hemodynamic quantification of physical activities for these patients will be established. Should ergospirometry not be available, an ergonomic test with progressive and continuous loads should be conducted, and only interrupted in the event of signs or symptoms [54,55,56]. An ECG is recommended so that left ventricular function may be assessed. Patients who display lesser tolerance to effort, early ischemic response, ejection

fraction below 30% and higher E/ CO2 values must be followed up more closely, for they constitute

a higher risk group. The constant monitoring of blood pressure and heart rate with the aid of a heart rate monitor is advisable. The intensity of the physical activity must be always individualized and progress gradually, in particular with patients with exacerbated exercise intolerance. Warm-up (before the exercise) and cool down (after the exercise) periods must be prolonged – average of 10 and 15 minutes, respectively – chiefly to observe possible arrhythmias. In table 1 there is a physical training scheme for patients suffering from heart failure at the Dante Pazzanese Institute of Cardiology. (Table 1)

Picture 3b: In B (final biopsy), it is possible to note more stained fibers, especially on its periphery. The darker stains represent an increase in SDH enzyme within the

mitochondria. Source: Ferraz AS et al Eur Heart J 2003;24(suppl):183. Optical Microscopy for the histology of stained Vastus Lateralis muscle fiber for the

activity of oxidative succinate dehydrogenase (SDH) in a patient with HF



The initial intensity recommended for aerobic physical activity is 80% of the heart rate corresponding

to the O2 measured at anaerobic threshold, and may reach 100% by the end of the first month. Another model used at InCor at FMUSP-HC recommends that the intensity for the physical activity be

kept between 40% and 60% of the heart rate of O2 attained at peak effort, in the conventional ergometric test, or the average heart rate measured ventilatory threshold and less 10% of the one obtained at respiratory compensation point [57], when the cardiopulmonary effort test is chosen, even in the likelihood that the patient may be on medication which could interfere with chronotropism (Table 2, Pictures 4 and 5).

Table1: Physical training program for patients with heart failure

Table 2: Male, 38 years, suffering from dilated cardiomyopathy, class II (NYHA). Behavior of hemodynamic, ventilatory and metabolic variables observed every 15 seconds during cardiopulmonary test. VE/VO2 and VE/VCO2 = oxygen and carbon

dioxide ventilatory equivalents, respectively, VO2/kg = oxygen consumption per

ml/Kg/minute, RQ = respiratory quotient (VCO2/VO2), VO2/HR = oxygen pulse in

ml/beat, RR = respiratory rate per minute e VE = minute ventilation. Note the drop in VO2 and VO2/HR after 5:15 minutes, which suggests an abrupt reduction in cardiac

debt.



During the physical activity sessions, continuous medical supervision is mandatory. This is so due to the potential risks of angina, arterial hypotension, arrhythmias, or dyspnea. Trained professionals and emergency equipment for cardiorespiratory resuscitation must be easily accessible.

From our understanding, supervised physical training sessions should be performed at least 3 times a week, during 6 months. For stable patients non-supervised aerobic activity may be recommended for the remaining days, and should be controlled by the level of fatigue and training frequency previously established. The duration of the exercise must be gradually increased according to the patient’s tolerance. Endurance and resistance training might be optionally be applied along with aerobic training, ideally in the initial weeks. This yields excellent results, such as improved flexibility, muscle trophism, and muscle mass, notably in patients with sarcopenia [58].

The medical team that supervises the physical training sessions must be attentive to the symptoms and/or signs of cardiac decompensation in these patients during exercise, such as coughing, dyspnea, arterial hypotension, dizziness, cyanosis, angina, and arrhythmias.

Picture 4: Curves of oxygen uptake ( O2), carbon dioxide production ( CO2), minute

ventilation (VE) and heart rate (HR) during cardiopulmonary test on patient referred to in Table 2.

Note the drop of O2 and CO2 starting from the respiratory compensation point (RCP) or

threshold 2, which indicates reduction in cardiac debt. Exercise intensities in this case are banished

Picture 5: Oxygen pulse curve ( O2/HR), which is related to systolic volume. It

presents itself reduced throughout the whole activity, with a drop after threshold 2, or respiratory compensation point (RCP). Exercise prescription must be limited to threshold 1, or anaerobic threshold (AT), well before the area in which systolic volume decreases.



One of the most defined and visible effects of physical activity in these patients consists in the improvement of quality of life, due to better biomechanics with movement economy and consequent fatigue reduction, dyspnea, and optimization of psychological profile according to several studies

[51,59]. These benefits are mainly related to better vascular conductivity with partial recuperation of endothelial function [60], improved neurohumoral profile, and reduced inflammatory marker [61], which in turn result in a significant improvement of muscular oxidative capacity [50,62]. Picture 6 illustrates the reduction of the inflammatory marker, high-sensitivity C-reactive protein (hs-CRP), through supervised physical training for six months.

As for future clinical eventualities, regular physical training has been associated to lesser mortality and rehospitalization rates in a randomized controlled trial with 99 patients followed up for 14 months [63]. According to a recent meta-analysis in which 801 patients were followed up for 2 years, there were clear benefits over morbimortality. The authors concluded that the number needed to treat was that of 17 patients undergoing physical training to prevent one death in two years [64]. However, conclusive results about the effects of physical activity in extending one’s lifespan and quality of life of patients with heart failure are being expected for 2008 with the conclusion of a multicentric, randomized trial conducted by the National Institute of Health (NIH) in the United States. This study iscalled HF-ACTION (Heart Failure – A Controlled Trial Investigating Outcomes of Exercise Training) and will involve 5,000 patients with a 5-year follow up.

Physical Activity Program in Congestive Heart Failure In spite of the beneficial effects of physical activity on the cardiovascular system, it is a fact that during intense physical activities the relative risk of cardiovascular events is greater than in regular, daily activities [65]. However, there was no relationship between exercise and death in patients with heart failure during more than sixty thousand hours of exercise training, compared favorably with exercises in normal individuals and those with a heart condition [66]. Continuous and interval aerobic training, if associated to resistance exercises, improves functional capacity. Yet, studies of patients who performed only aerobic exercises verified an increase in oxygen uptake superior to that observed in studies in which the patients performed only resistance exercises [67].

Exercising in a swimming pool or a sauna are not indicated for patients with heart failure [68]. Nevertheless, in certain centers such as HC-FMUSP, patients with HF have carried out physical activities in a heated swimming pool and have not presented side effects when under programmed physical activity [69]. The sauna has also been tolerated and patients have shown improvements both in hemodynamics and endothelial function; furthermore, there has been a reduction in neurohormonal function as well [70].

Picture 6: Patients with advanced nonischemic dilated cardiomyopathy optimized with pharmacological treatment. A = this group underwent a six-month, supervised physical

training with na average reduction of 52% of high-sensitivity C-reactive protein (hs-CRP)concentration. B = control group. Source: Ferraz AS et al Circulation 2004;17

(suppl):793-4



Training programs conducted at home under indirect supervision have also been encouraged for patients with heart failure. Just as in the formal supervised program, home-based programs seem to be safe and effective in reducing symptoms and improving quality of life of patients with HF [71].

As for the most appropriate intensity of exercises for heart failure patients, the issue is controversial. Some authors, such as Dubach et al [30], stand for high intensities, which aim at changing central hemodynamic parameters.

Conversely, most programs use low to moderate intensity levels, remaining between 60% and 70% of

peak O2 [72] . We have recently conducted a prospective randomized trial which included maximum

functional capacity (peak O2) and submaximal (AT), peripheral muscle biopsy, neurohormonal

measurement, autonomic balance and inflammatory markers, and a questionnaire pertaining to quality of life. We evaluated all the data in two supervised physical training programs: a) high intensity (close to respiratory compensation point – RCP or Threshold II). Training prescription was around 88% of peak VO2, i.e., in an area of great metabolic acidosis; b) low intensity (close to

anaerobic threshold – AT or threshold I). This corresponds to 67% of peak VO2, before the beginning

of metabolic acidosis, as shown in picture 7.

The programs lasted for 24 weeks, with 45-minute sessions three times a week. The vastus lateralis muscle biopsy revealed that in both training approaches there occurred an increase in oxidative capacity of the skeletal muscle, as well as an increase of peak VO2 equivalents [50].

On the other hand, only in the low intensity group was it verified a significant improvement of VO2 at

the anaerobic threshold, of the Minnesota Living with Heart Failure (MLHF) score, and of ventilatory efficiency as evaluated by oxygen and carbon dioxide ventilatory equivalents; moreover, there was improvement B-type natriuretic peptide (BNP) [73]. Pictures 8 and 9 illustrate some of the improvements attributed to low intensity exercises.

Picture 7: Training in low intensity group (BI) at 67% of peak VO2 (VO2p), limited by the anaerobic threshold (AT) and the high intensity group (AI) at 88% of peak VO2, limited by the respiratory compensation point (RCP) in patients with HF. Points and

intervals delimitated graphically by the oxygen (VE/VO2) and carbon dioxide (VE/VCO2) ventilatory equivalents. PETCO2 = end-expiratory carbon dioxide. Time measured in

minutes. Source: Ferraz AS et al J Am Coll Cardiol. 2003; 41:182A



As for ventilatory efficiency, our hypothesis is that intense training leads to higher metabolic acidosis, which in turn causes a hyperstimulation of the peripheral muscle ergoreceptors. Via the central nervous system, they stimulate chemoreceptors of the ventilatory command, which results in the perpetuation of an inefficient ventilatory pattern. As for BNP, its secretion is related to the distention of the ventricular wall, and low intensity training could promote lesser parietal tension in the left ventricle and consequently reduce the discharge of BNP into the blood flow. Based on this date, our physical activity prescriptions take into account the heart rate during training and limited by AT, that is, exercises whose intensities are below the area of metabolic acidosis.

As for autonomic balance, regular exercises promote the reduction of sympathetic hyperstimulation and circulating catecholamines, thus resulting in increased heart rate variability [48, 74]. What is more, the use of beta blockers in the treatment of HF did not change the benefits resulting from physical training. Patients with stabilized HF under selective and nonselective beta blockers who underwent a physical training program also increased the tolerance to submaximal and peak exercise [75].

A recent study on patients with weak respiratory muscle was published by a group from the Laboratory of Exercise Physiopathology of Hospital das Clínicas in Porto Alegre. After a 12-week

Picture 8: After 6 months of physical training only with low intensity training was there

significant increase in oxygen uptake ( O2) at the submaximal level, that is, at the

anaerobic threshold (AT). Peak O2 shows corresponding increase in both intensities.

Picture 9: After 6 months of physical training only with low intensity training was there

significant reduction of the ventilatory ratio by carbon dioxide production (VE/ CO2) at rest, at anaerobic threshold (AT) and of peak exercise. This reduction represents an

improvement in ventilatory efficiency.



inspiratory muscle training, the authors demonstrated a boost in the order of 115% in maximum

inspiratory pressure; Besides, there was an increase of 17% in peak O2, which resulted in a

significant improvement of ventilatory response to exercise [76].

Hence, the incorporation of breathing exercises seems to unlock new possibilities to rehab programs, especially for patients with weak ventilatory muscle. Patients suffering from HF frequently complain of erectile dysfunction, which hinders their quality of life. A randomized trial published by Belardinelli et al submitted 59 male patients to a supervised aerobic physical training program. The intensity was

kept at 60% of peak O2 on a cycloergometer for a period of 8 weeks. The study revealed

improvement in sexual dysfunction as measured by the sexual performance score (SAP questionnaire)

and the increase of 18% in peak O2. The benefits were associated to the systemic effect of physical

activity on endothelial dysfunction with direct impact on the quality of penile erection [77]. Accordingly, regular physical training brings confirmed benefits with favorable systemic repercussions and must become part of the clinical treatment of patients with stable CHF and using optimized medication. Just as the clinical treatment yields evident central benefits, physical exercise promotes favorable peripheral adaptations, resulting in improved functional capacity and quality of life for these patients. Picture 10 illustrates the flow chart of evaluations and procedures for the recommendation of rehabilitation in HF.

(Click on image to enlarge)

Conclusion The mechanisms through which regular physical training improves effort tolerance and attenuates and/or partially reverts central and peripheral abnormalities associated to HF are still being deciphered. A myriad of randomized trials verify that exercises have a positive effect on the different, important variables which guide the lives of HF patients; they improve their quality of life, enhance functional capacity, blood flow to metabolically active peripheral muscle and the endothelial-dependent vasodilation, reduce indirect action of sympathetic activity, foster the reduction of plasma norepinephrine levels at rest, and ameliorate myocardial demand of oxygen (heart rate x systolic arterial blood pressure) during physical activity. Besides, there are other probable effects, such as the increase of cardiac debt due to augmented heart rate and peak systolic volume [78], and improved ejection fraction at rest. Likewise, resistance training leads to growth in size and number of mitochondria, growth in myosin heavy chain percentage in type 1 fibers and improvement in muscle strength and mass [79]. In addition, it fosters augmented capillary density, reduction of circulating inflammatory markers, and diminution of neuroendocrine hyperactivity. Some mechanistic gaps are yet to be investigated. It is still not known exactly how peak ejection fraction increase takes place, or how hemoglobin concentration and ventricular fibrillation threshold increase. Similarly, we still await definite answers about a possible decrease in mortality and long-range hospital readmission. Finally, while we wait for the huge HF-ACTION study on mortality, still other research studies are being conducted with the purpose of establishing the most suitable role for resistance and respiratory muscle training in aerobic training for these patients.

Furthermore, questions over the various pharmacological agents used in these patients’ therapeutic arsenal, some of which may lessen the physiological benefits attributed to performing exercise on a

Picture 10: Flow Chart of the Physical Training Program for Patients with Heart Failure



chronic basis.

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CV of the author - Doutor em Cardiologia pela Faculdade de Medicina da Universidade de São Paulo, Brasil. - Coordenador do Laboratório de avaliação cardiopulmonar da Seção de Reabilitação Cardiovascular do Instituto Dante Pazzanese de Cardiologia, Brasil. - Diretor da Divisão de Ergometria do Instituto de Cardiologia de São Paulo, Brasil

Publication: September 2007

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