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876

FOCUSED REVIEW

Exercise, Cardiovascular Disease, and Chronic Heart Failure


Reed Humphrey, PhD, PT, Matthew N. Bartels, MD, MPH
ABSTRACT. Humphrey R, Bartels MN. Exercise, cardio- Emerging evidence indicates that relatively intensive modi-
vascular disease, and chronic heart failure. Arch Phys Med fication of lifestyle may slow or reverse CAD. 14-17 The ben
Rehabil 2001;82 Suppl I:S76-81. of exercise in lowering CAD have confounded the contribu-
7fits
tions of dietary changes and lipid-lowering agents. The ran-
In addition to patients with coronary artery disease, high-risk domized trial by Niebauer et aP7 of 113 male patients revealed
patients with severe congestive heart failure can benefit from that after 6 years of risk factor intervention, only improv.ed
rehabilitation. Traditionally, such patients were excluded from physical work capacity independently contributed to angio-
rehabilitation, but resistive exercise, higher-intensity programs, graphic evidence of regression in CAD lesions, It is important
and interval training have now been safely conducted. Emerg- to note that exercise caloric expenditure in the Niebauer
ing data indicate that exercise training results in a number of group's study was about 1800kcal/wk, or nearly 4 hours of
improved physiologic and psychologic indices, including neu- moderate physical exercise, well below the threshold of most
ral control, quality of life, exercise tolerance, ventricular func- supervised exercise intervention programs.
tion, skeletal muscle physiology, peripheral blood flow, and
endothelial function. This review explores these beneficial out- CHRONIC HEART FAILURE
comes through an assessment of therapeutic approaches, with Cardiac rehabilitation now includes higher risk patients,
special emphasis on the unique clinical characteristics of pa- such as those with severe congestive heart failure (CHF). The
tients with congestive heart failure. prevalence of CHF is increasing worldwide, as indicated by the
Overall Article Objective: To describe the benefits and the 116% increase in CHF mortality between 1929 and 1995. 18
evolving role of cardiac rehabilitation for patients with con- Experience gained through treating CAD patients can be ap-
gestive heart failure. plied to patients with severe CHF, especially those with ejec-
Key Words: Coronary disease; Heart-assist devices; Heart
tion fractions less than 30%, who have traditionally been
failure, congestive; Exercise; Rehabilitaton excluded from rehabilitation. Despite a 6- to 9-times higher
2001 by the American Academy ofPhysical Medicine and
occurrence of sudden cardiac death in patients with severe CHF
Rehabilitation when compared with less severely ill CHF patients, emerging
evidence demonstrates that exercise intervention is safe and
VER THE PAST 30 years, the effectiveness of rehabili-
O tation for patients with coronary heart disease (CAD) has
been established.' In addition to traditional exercise, cardiac
effective in severe CHF.19,20
Risk-stratification models exist for patients with severe
CHF, but they are based on clinical characteristics-t-P and
rehabilitation now includes risk factor modification and patient annual cardiovascular mortality risk, not on the risk of an
education. Recent literature has emphasized a variety of posi- exercise-induced event. The American Heart Association pro-
tive outcomes from secondary prevention programs, including vides a risk-stratification model that is based on exercise event
improved exercise tolerance, skeletal muscle strength, psycho- risk,23 and this model is useful in making decisions regarding
logic status, and quality of life.>? Combined exercise and risk supervision of exercise assessment and training. Although
intervention programs have important implications for reduced strongly associated with mortality, left ventricular dysfunction
health care costs and hospitalization.s-? Yet, despite this vol- in severe heart failure is poorly related to exercise performance
ume of evidence, cardiac rehabilitation is often underutilized, as measured by oxygen consumption.>'
especially for women. I Exercise does not worsen left ventricular performance in
Cardiac rehabilitation for CAD patients reduces mortality by CHF. The data of Belardinelli et apo suggest reduced mortality
as much as 25% in comparison with CAD patients not enrolled after exercise training. Moreover, emerging data indicate that
in such programs.tv'! Moreover, mortality rates are lower in exercise training is safe and that it results in improved physi-
CAD patients who receive multifactorial interventions than in ologic and psychologic indices, including neural control,2s,26
those exposed to exercise only.'> Although the efficacy of quality of life,27,28 exercise tolerance,29-31 left ventricular func-
cardiac rehabilitation in reducing morbidity is less clear, it is tion,32,33 skeletal muscle physiology.w> peripheral blood flow,
important to stress that exercise training does not increase and endothelial function. 36-38 Additionally, resistive exer-
morbidity. 1 Exercise intervention has been shown to be safe, cise 39,40 and higher-intensity programs, including interval train-
with a low rate of nonfatal cardiovascular events.'> In any case, ing,3R,41-43 have been safely conducted and are recommended as
cardiac rehabilitation improves function and quality of life. therapeutic options for CHF patients, including the elderly.s-
Improved fitness is attained by a combination of central
(cardiac output) and peripheral (arterovenous oxygen differ-
ence) adaptation, the latter being of fundamental importance
From the Department of Physical Therapy, Virginia Commonwealth University, because stroke volume and ejection fraction are reduced in the
Richmond, VA (Humphrey); and Department of Rehabilitation Medicine, Columbia presence of CHF. A lowering of myocardial oxygen demands
University, New York, NY (Bartels),
Accepted November I, 2000.
at equivalent workloads is achieved through improvement in
No commercial party having a direct financial interest in the results of the research peripheral circulation, oxygen extraction, and utilization in
supporting this article has or will confer a benefit upon the authorts) or upon any trained muscle. Increased oxidative capacity associated with
organization with which the author(s) is/are associated. skeletal muscle adaptation allows improved extraction and use
Address correspondence to Reed Humphrey, PhD, PT, Dept of Physical Therapy,
Virginia Commonwealth University, PO Box 980224, Richmond, VA 23298.
of available oxygen to resynthesize adenosine triphosphate
0003-9993/01/8203-6664$35.0010 (ATP), delaying the exercise-limiting fatigue associated with
doi: 1O.1053/apmr.2001.22445 excess accumulation of blood lactate. In addition, a training-

Arch Phys Med Rehabil Vol 82, Suppl 1, March 2001


EXERCISE, CARDIOVASCULAR DISEASE, AND CHRONIC HEART FAILURE, Humphrey S77

Table 1: Potential Changes Due to Exercise Training workload-induced ischemia. Clearly, the integrity of the coro-
for Patients With CHF nary blood supply and the consequent degree of exercise-
Increases or provides improvements in: induced ischemia significantly influence the exercise profile for
Measures of oxygen transport and endurance, including peak CHF patients. Since the myocardial demand associated with
oxygen consumption, ventilatory anaerobic threshold, peak the ischemic threshold may vary for an individual patient,
cardiac output, physical work capacity, and submaxlrnal exercise identification of this threshold from exercise assessment is
endurance essential for setting the safe upper limit of exercise. Through
Leg blood flow and arterial oxygen content exercise, the metabolic equivalent (MET) level at which the
Skeletal muscle aerobic enzyme activity, phosphocreatine, and heart rate is at anaerobic threshold increases, along with the
ATP resynthesis mean arterial pressure (or rate-pressure product). This im-
Muscle fiber size and skeletal muscle strength and endurance provement in exercise capacity increases the range of func-
Parasympathetic nervous system activity tional activities in which the patient may safely engage, and it
Respiratory muscle function may be sufficient to permit return to work or a substantial
Spontaneous daily activity and indices of quality of life increase in the range of tolerance of avocational activities.
Decreases in: Although left ventricular ejection fraction alone does not
Symptoms of dyspnea, fatigue, and weakness correlate well with oxygen uptake, normal right ventricular and
Submaximal exercise ventilation, carbon dioxide, and respiratory mitral valve function are important for optimal physical per-
exchange ratio formance in the presence of CRF. Additionally, patients with a
Neurohormonal activation and sympathetic nervous system low left ventricular ejection fraction increase their exercise
activity capacity less with exercise training than do those with better
Resting and submaximal exercise heart rate and blood lactate myocardial function. If cardiac function were the sole limiting
level factor, a stronger association between exercise tolerance and
Ventricular arrhythmias left ventricular ejection fraction would be expected. The poor
New York Heart Association functional class correlation emphasizes the importance of training in skeletal
Morbidity and mortality in patients with coronary artery disease muscle adaptation in severe CHF. For patients with severely
impaired cardiac output, the adaptation of skeletal muscle
Adapted from Squires RW. Exercise prescription for the high-risk through exercise training can often compensate for central
cardiac patient. Champaign (lL): Human Kinetics; 1998. p 149-51.49 cardiac dysfunction.
Reprinted with permission.
Approaches to Exercise Intervention for Patients
With Severe CHF
induced increase in blood volume and improved shunting of Because of the profound exercise-induced fatigue experi-
blood to skeletal muscle during exercise result in improved enced by most CHF patients, the patient must be carefully
delivery of oxygen. prepared for exercise. Defining cardiac and noncardiac limita-
Improved central adaptation is also reported with exercise tions to exercise is critical. Exercise programs must be com-
training in CRF. A higher rate-pressure product at the onset of plemented by optimal pharmacologic measures, nutritional
ischemia has been observed.v as has reduction in exercise support, dyspnea management (supplemental oxygen, mobili-
ischemia as assessed by radionuclide technology.w'? Central zation of secretions), hemoglobin stabilization, and pain man-
adaptation mechanisms have been postulated in explanation, agement.
including decreased blood viscosity and/or improved collateral Assessment of body mechanics is important in the selection
coronary circulation,48.49 but these mechanisms remain un- of appropriate exercise modalities to lessen dyspnea or fatigue.
proven. Squires'? has provided an extensive compilation of Since recumbent or sernirecumbent exercise may lead to de-
evidence-based benefits of exercise training for severe CHF creased diaphragmatic excursion, lower lung volumes, in-
patients, as summarized in table 1. creased venous return, and pulmonary edema, it is important to
maintain adequate body pcsition.P-" Cahalin" has suggested
FUNCTIONAL IMPROVEMENT AND APPLIED that the best approach for CHF patients may be progression of
EXERCISE PHYSIOLOGY IN SEVERE body position to achieve consistently upright posture during
HEART FAILURE exercise. CHF patients often benefit from ventilatory breathing
A primary outcome of exercise training is improved func- exercises (pursed-lip breathing, inspiratory muscle training,
tional reserve for safe participation in vocational and avoca- diaphragmatic breathing, inhibition of accessory muscles) be-
tional activities. The ability to sustain activity is a function of cause they decrease dependency on accessory muscles and the
oxygen consumption, cardiac output, oxygen transport, and the associated higher oxygen cost of ventilation.52 53
extraction of oxygen by active skeletal muscle, as described in Not all CHF patients are appropriate candidates for exercise
the previous section. Improving functional reserve for activity training. Patients should be able to speak without signs or
is dependent on improving aerobic capacity. This is accom- symptoms of dyspnea (speak comfortably with a respiratory
plished through exercise training to increase both peak oxygen rate of less than 30 breaths/min); have no more than moderate
consumption and the fatigue-limiting anaerobic threshold, with fatigue by subjective clinical impression; have rales present in
a lower relative oxygen cost and associated myocardial de- less than half of the lungs; and, for invasively monitored
mand. Activities that were at or slightly above the anaerobic patients, have a cardiac index of more than 2L1min/m2 and a
threshold become feasible after training, which is vitally im- central venous pressure of less than 12mmHg.s2
portant for patients with severe CHF, who have lower peak CHF patients who are hospitalized for inotropic support of
oxygen consumption values as a result of diminished cardiac an exacerbation and patients with severe heart failure who are
output. taking intravenous inotropes while awaiting heart transplanta-
Improved fitness from exercise training results in a critical tion have been involved in rehabilitation programs.52 Exercise
reduction in heart rate and blood pressure for any specific to maintain and improve function can safely be prepared in this
activity. This improves the range of safety in patients with setting, with close monitoring.

Arch Phys Med Rehabil Vol 82, Suppl 1, March 2001


878 EXERCISE, CARDIOVASCULAR DISEASE, AND CHRONIC HEART FAILURE, Humphrey

Conununity-based patients with stable CHF can be enrolled Dyspnea and Exercise
in outpatient cardiac rehabilitation programs. General exercise Altered pulmonary physiology in CHF plays a part in the
guidelines can be applied to these patients with individually observed symptomatic and physiologic limitations, particularly
designed programs that include 20 to 60 minutes of aerobic the respiratory factors that contribute to fatigue and dyspnea.
reconditioning, circuit weight training, and gentle resistive The model of decreased exercise tolerance because of dyspnea
exercises. Recent studies have suggested alternative formats of in CHF is based on the mechanism of decreased cardiac output
exercise training. Meyer et al54 have shown significant im- causing increased pulmonary vascular resistance and leading to
provement in exercise capacity for patients with severe heart interstitial and alveolar edema. This, then, impairs gas ex-
failure after only 3 weeks of high-intensity interval training. change and pulmonary compliance, and triggers J-fiber juxta-
They postulated that the improvement is associated with capillary receptors. The resulting stimulation of central nervous
greater reduction in venous return and left ventricular end
system receptors causes the subjective sensation of dyspnea.
diastolic pressure during interval work than during continuous
activity. Additionally, recent investigations suggest that endo- However, no clear correlation has been found between pulmo-
thelial function is enhanced by exercise programs approximat- nary wedge pressure or resting ejection fraction and dyspnea in
ing 60% to 70% exercise intensity.55.56 patients with CHF.55.56 Treatments that decrease filling pres-
While the work of Meyer and others has expanded the sures do not alter the symptoms of dyspnea or relieve the
options for exercise training in heart failure patients, higher- exaggerated ventilatory response. Measures of ventilatory pa-
intensity interval training does not facilitate weight manage- rameters reveal a better correlation. This constellation of find-
ment, which may be an important risk factor requiring modi- ings leads to the observation that peripheral and pulmonary
fication in many patients. The most effective reduction in body physiologic factors play prominent roles in dyspnea-induced
mass associated with exercise occurs when the weekly volume exercise intolerance.
of exercise exceeds 1200 to l500kcal. Interval training per- The pulmonary contribution to dyspnea lies partly in the
formed on alternate days with continuous exercise training may inability of the lungs in cardiac failure to acconunodate the
be the most pragmatic approach to optimizing training effect increased blood flow that accompanies a dynamic exercise
and weight control. response. With exercise, there is an increase in the disparity of
blood flow in the upper and lower lung fields, with a resultant
Role of Cardiovascular Exercise Testing in increase in ventilation-perfusion mismatch.s" There is in-
Rehabilitation in CHF creased physiologic dead space and an increased ratio of dead
The preferred protocol for cardiovascular exercise testing for space to tidal volume. 55.58 These changes in blood flow are
CHF patients is a modified ramped protocol of progressive chronic, and they contribute to parenchymal changes in the
exercise loads of 0.2 to 0.4 METS per 30-second stage. Patients lung, with the development of hypertrophy of the media in
with poor exercise tolerance should be tested with continuous small arteries, arterioles, and pulmonary veins, and interstitial
protocols not exceeding 1 to 2 METS per 3 minute stage. fibrosis.w Additionally, these changes may be superimposed on
Criteria for test termination are consistent with traditional pulmonary parenchymal disease in CHF patients who have a
criteria for all cardiac patients, special attention being paid to history of tobacco use, further exaggerating the pathophysiol-
signs and symptoms associated with CHF, including dyspnea, ogy observed in heart failure.s?
weakness, and abnormal blood pressure responses, particularly Pulmonary compliance is also reduced in CHF, as a result of
hypotension with signs and/or symptoms of exertional intoler- increased vascular stiffness associated with fluid overload. This
ance. Less sophisticated exercise assessments, such as the decrease in compliance increases the work of breathing, con-
6-minute walk test, are useful in assessing exercise tolerance tributing to dyspnea at all levels of activity.s' In patients with
and monitoring progress during therapy. obstructive airway disease and CHF, treatment of the underly-
ing congestion and pulmonary edema has yielded an increase in
NEW FRONTIERS IN THE REHABILITATION forced expiratory volume in 1 second.s- Impaired diffusion
OFCHF capacity, which also contributes to dyspnea, does not respond
to treatment for heart failure.
In addition to the peripheral vascular and muscular adapta-
Nitric Oxide and Exercise tions discussed above, there is a direct effect on the respiratory
New understanding of the physiologic mechanisms underly- musculature in CHF. Maximal voluntary ventilation and max-
ing dyspnea in CHF has led to a new appreciation of the imal sustainable ventilatory capacity are lower in patients with
benefits of exercise training for these patients. The more we heart failure. 63.64 To treat these alterations in lung function,
comprehend this physiology, the clearer will the goals of selective respiratory muscle training has been tried in these
exercise in CHF become. Evidence shows that functional im- patients, such as inspiratory muscle training against resistance,
provement from cardiac rehabilitation in CHF patients is re- sustained (lOs) peak inspiratory and expiratory force genera-
lated to improved peripheral vascular resistance and muscle tion, and muscle endurance training with isocapneic hyperven-
metabolism, particularly the vascular flow of muscle tissue. tilation. Marked improvements in respiratory muscle strength,
The mechanisms of vascular dilation are partially associated maximal inspiratory and expiratory pressures, maximal volun-
with nitric oxide-mediated pathways. Measurement of urinary tary ventilation, and respiratory muscle endurance are reported
nitric oxide metabolites indicates that increasing systemic lev- when these exercises were performed 3 times weekly over 3
els of nitric oxide are reflected in improved vascular tone. This months. These improvements were accompanied by significant
improvement in vascular balance indicates exercise-induced gains in exercise capacity and decreases in subjective dys-
normalization in the physiology of patients with CHF. As more pnea.53 These interventions often are not included in cardiac
is learned about the role of nitric oxide and other vasoactive rehabilitation programs for CAD. Yet patients with CHF
substances in exercise training, there may be a role for inter- clearly could benefit from the addition of respiratory muscle
ventions to be tailored to favorably alter the balance of these training and careful assessment and treatment of any concom-
compounds.w itant pulmonary disease.

Arch Phys Med Rehabil Vol 82, Suppl 1, March 2001


EXERCISE, CARDIOVASCULAR DISEASE, AND CHRONIC HEART FAIL.URE, Humphrey 579

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