EFFECTS OF EXERCISE ON CARDIOVASCULAR
HEALTH
Exercise as an intervention for treatment and management of coronary heart disease and many of its associated comorbidities (e.g., diabetes, obesity, hypertension, dyslipidemia) remains one of the most effective, yet poorly used treatments. This chapter outlines the current evidence supporting an active lifestyle, active exercise training, and their impact on various measures of cardiovascular health. It reviews the available data for patients with heart failure, which constitutes one of the largest groups of patients cared for with chronic heart disease, resulting in heavy health care resource utilization. The chapter reviews the evolving wearable and mHealth technologies that may affect our ability to recommend and monitor exercise in the future and may suggest further directions for research.
FIG 4.1 Effects of Exercise on Cardiovascular Health: Primary Prevention.
Numerous terms are used in the literature in reference to exercise and
physical activity. In this chapter, we use these terms as they are commonly
defined. Physical activity is any bodily movement produced by contraction of
skeletal muscle that increases energy expenditure above the basal level.
Physical activity is generally categorized by mode, intensity, and purpose.
Leisure activities are considered to be physical activities performed by a
person that are not required as essential activities of daily living and are
performed at the discretion of the person. Leisure activities include sports
participation, exercise conditioning or training, and recreational activities,
such as going for a walk, dancing, and gardening. Exercise is a subcategory of
physical activity that is “planned, structured, and repetitive” and generally
has a purpose to improve or maintain some aspect of physical fitness. Physical
fitness is defined in many ways, but an accepted definition is “the ability to
carry out daily tasks with vigor and alertness, without undue fatigue and with
ample energy to enjoy leisure-time pursuits and meet unforeseen emergencies.”
There are many components to fitness, both performance and health related.
Health-related fitness consists of cardiorespiratory fitness, muscle strength
and endurance, body composition, flexibility, and balance. Because of the
explosion of technology and mobile communications resulting in >1 billion
smartphones and >165 million tablets shipped annually worldwide, there are
now novel, evolving platforms for health-care monitoring and delivery, and a
new vocabulary related to this technology. The WHO defines mobile health
(mHealth) as “medical and public health practice supported by mobile devices
such as mobile phones, patient monitoring devices, personal digital assistants
and other
PRIMARY PREVENTION
High levels of sedentary activity in adults are prevalent according to
the 2015 National Health Interview Survey. One in three adults does not engage
in leisure-time physical activity. Inactivity increases with age, in women, with Hispanic and black
adults providing a large potential pool of the public to target for activity
interventions to reduce CVD risk. There is a strong inverse relationship
between physical activity and the risk of coronary disease and death. Across
studies, there is an estimated 30% risk reduction in all-cause mortality,
comparing the most physically active subjects with the least active subjects.
Similar CV benefit from fitness also exists in both sexes and across different
races and ethnic groups (Fig. 4.1). The inverse dose response relation for total volume of
physical activity is curvilinear, meaning that those with the lowest physical activity levels have the largest risk
reduction with increased physical activity. Studies in men support a role for
physical activity in reducing the risk of mortality. In nonsmoking, retired
men, ages 61 to 81 years, who had other risk factors controlled, the distance
walked daily at baseline inversely predicted the risk for all-cause mortality
during a 12-year follow-up. Of 10,269 Harvard alumni born between 1893 and
1932, those individuals who began moderately vigorous sports between 1960 and
1977 had a reduced risk of all-cause and CHD-related death over an average of 9
years of observation compared with
those who did not increase sports participation. This finding was independent of the effects of lower BP or
lifestyle behaviors related to low cardiac risk, such as cessation of smoking
and maintenance of lean body mass. Data on the leisure-time physical activity
levels of men participating in the Multiple Risk Factor Intervention Trial
(MRFIT) supported a reduction of risk for all-cause and CHD-related fatalities
when leisure time was spent doing moderate or high (compared with low) levels
of physical activity. The effect was retained when confounding factors,
including baseline risk factors and MRFIT intervention group assignments, were
controlled. Mortality rates for the high and moderate physical activity groups
were similar. The Lipid Research Clinics Mortality Follow-up Study found that men
with a lower level of physical fitness, as indicated by heart rate (HR) during
phase 2 (sub-maximal exercise) of the Bruce Treadmill Test, were at
significantly higher risk for death due to CV causes within 8.5 years compared
with men who were physically fit.
The same benefits from physical activity accrue for women. In women,
higher physical activity level was related to an improved health outcome in
several longitudinal studies. The Iowa Women’s Health Study observed 40,417
postmenopausal women for 7 years; moderate and vigorous exercise were
associated with a reduced risk of death. This reduction of risk was present for
all-cause mortality and specifically for deaths resulting from CV and
respiratory causes.
Women who increase their frequency of
activity from rarely or never to ≥4 times per week also have a reduced risk of
death. The Women’s Health Initiative (73,743 postmenopausal women) and the
Nurses’ Health Study (72,488 women aged 40–65 years) assigned subjects into
quintiles based on energy expenditure. Age-adjusted risk decreased
incrementally from the lowest to the highest energy expenditure group, was
statistically significant when other CV risk factors were controlled, and was
similar in white and black women. In addition, energy expenditure from vigorous
exercise or walking and time spent walking were linked to a lowered risk for
the development of CHD. This inverse relation between CHD risk and activity
level was observed in groups of women with other high-risk factors, including
smokers and women with high cholesterol levels, although it was not observed in
hypertensive women. In one study of postmenopausal women, the odds ratios for
nonfatal MI, adjusted for confounding factors, decreased across the second,
third, and fourth highest quartiles of energy expenditure compared with the
lowest quartile. Exercise equivalent to 30 to 45 minutes of walking 3 days/week
decreased the risk for MI by 50%.
Studies show that in black and white men and women, lack of exercise is
associated with a higher risk of 5-year all-cause mortality, independent of
age, male sex, low income, BP, or a number of CV measures (left ventricular
[LV] ejection fraction, abnormal ECG) or other physiological measures (e.g.,
glucose level, creatinine level). A community-based study of older adults (aged
65 years or older) with no history of heart disease showed that walking at
least 4 hours weekly significantly reduced the risk of hospitalization due to
CV disease events during the subsequent 4 to 5 years.
The epidemic of obesity in the United States has significantly affected
the development of CHD, hypertension, diabetes, and other athero- sclerosis
risk factors. In 2011 to 2014, it was estimated that approximately 69% of the
adult population aged older than 20 years was overweight or obese with a body
mass index (BMI) of ≥25 kg/m2. The prevalence of obesity differs
across racial/ethnic and socioeconomic groups. Native Americans, African
Americans, Hispanics, and Pacific Islanders have significantly higher BMIs
compared with whites and Asian Americans. There is also a significant
sex–ethnicity interaction. African American women have a much higher prevalence
of obesity (BMI >30 kg/m2) (57%) compared with Hispanic (46%) and
white (38%) women. This holds true
for men as well, although the prevalence is lower (38%, 39%, and 34%, respectively). The total
estimated costs in 2008 related to obesity were $147 billion USD. There is a
dose–response relationship between physical activity and weight loss, but in
general, successful weight loss and maintenance is a complex issue, which
includes caloric restriction, in addition to increased physical activity.
Several studies have shown that anthropometric measures (BMI, waist
circumference, waist-to-hip ratio) are associated with CHD risk factors and/or
adverse events. The increased risk is partially explained by the milieu of
insulin resistance, inflammation, and other atherosclerotic risk factors
associated with obesity. Although weight loss is important and improves CV risk
factors, the direct benefit of weight reduction alone on CV risk is not clear.
However, physical activity reduces CV risk. A study of women being evaluated
for suspected myocardial ischemia found that measures of increased BMI, waist
circumference, waist-to-hip ratio, and waist- to-height ratio were not
independently associated with coronary artery disease (CAD) or adverse CV
events. Lower levels of self-reported physical fitness scores were associated
with higher prevalence of CHD risk factors and angiographic CAD, and higher
risk of adverse events during follow- up, independent of other risk factors.
This supports the findings that fitness may be more important than overweight
or obesity in women and men.
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| FIG 4.2 Secondary Prevention. |
SECONDARY PREVENTION
Recent studies have conclusively demonstrated that exercise and fitness are as beneficial for patients with an
established diagnosis of CHD as for those who do not have known CHD (Fig. 4.2).
In subjects with higher levels of physical activity, there is a 20% to 35%
lower risk for CVD, CHD, and stroke compared with those with the lowest levels
of activity. In a large study of men with established heart disease, regular
light to moderate activity (such as 4 hours/week of moderate to heavy gardening
or 40 min/day of walking) was associated with reduced risk of all-cause and CV
mortality compared with a sedentary lifestyle. Another large study assessed
health status and physical fitness in men during two medical examinations
scheduled approximately 5 years apart. Men who were unfit at both examinations
(baseline and 5 years later) had the highest subsequent 5-year death rate
(122/10,000 man-years). The death rate was substantially lower in initially
unfit men who improved their fitness (68/10,000 man-years) and was lowest in
the group who maintained their fitness from the first to the second examination
(40/10,000 man-years). The mortality risk decreased approximately 8% for each
minute that the maximal treadmill exercise time at the second examination
exceeded the baseline treadmill time. These results were retained when subjects
were stratified by health status, demon-strating that unhealthy and initially
healthy individuals benefited from exercise fitness.
Exercise intervention experiments have documented better health and
survival even in patients who have experienced an MI. In one randomized study,
patients were enrolled in a rehabilitation program of three 30-minute periods
of exercise weekly, whereas other patients— matched by age, sex, coronary risk
factors, site and level of cardiac damage, and acute-phase complications—served
as control subjects. At 9 years after the initial MI, the rate of death caused
by acute MI and the frequency of angina pectoris were lower in the treatment
group. In the National Exercise and Heart Disease Project, male post-MI patients
were randomly assigned to a 3-year program of supervised regular vigorous
exercise (jogging, cycling, or swimming) or to regular care not involving an
exercise program. Subjects were reevaluated at 3, 5, 10, 15, and 19 years to
determine total and CV-related mortality. A moderate advantage of the treatment
versus control condition in reducing the risk of all-cause and CV death was
seen at the first follow-up time point but diminished and eventually
reversed as the time since baseline
increased. This may indicate that the benefits of an intensive exercise program
are time-limited or may be related to several other factors (see later
discussion). Each metabolic equivalent unit by which the work capacity of the
participant increased from the outset to the completion of the 3-year program
resulted in an incremental reduction in total and CV-related mortality, which
suggested that increasing exercise fitness did promote survival. Failure to
observe a long-term benefit in the treatment group versus the control group
might have resulted from crossover between the two groups during the protracted
follow-up period, improvements in medical therapy (routine use of statins),
and/ or revascularization approaches.
A large meta-analysis of 10 randomized clinical trials of post-MI
patients showed that cardiac rehabilitation (CR) with exercise reduced
all-cause mortality by 24% and CV death by 25% versus that of control subjects.
However, the risk of nonfatal recurrent MI did not differ between groups.
Exercise training plays an important role in post-MI rehabilitation. Significant increases in functional
capacity (10%–60%) and reductions of myocardial work at standardized exercise
workloads (10%–25%) have been observed after 12 weeks of post-MI CR. The
Exercise in Left Ventricular Dysfunction Trial demonstrated that exercise
training after an MI might also improve ventricular remodeling and LV function.
The American Heart Association (AHA) guidelines on physical activity in
secondary prevention after MI, bypass surgery, or clinical ischemia recommend
that the maximal benefit occurs when an exercise–CR program is initiated at
supervised facilities where symptoms, HR, and BP can be monitored. A
symptom-limited exercise test is essential for all participants before starting
an exercise program.
Limiting Coronary Atherosclerotic Progression
Several randomized intervention studies evaluated the influence of
exercise training on progression of coronary atherosclerosis. In one study,
patients with a history of stable angina were randomized to receive a
behavioral intervention (≥2 hours/week of intensive exercise group training
sessions, at least 20 min/day of exercise, and a low-fat, low-cholesterol diet)
or usual care. After 1 year, 32% of the treatment group versus 9% of the control
group had regression in atherosclerotic coronary lesions, and conversely, 48%
of the control group versus 23% of the treatment group had progression of
lesions. These differences were statistically significant. Other changes in the
treatment group included reductions in weight, total cholesterol, and
triglyceride levels, and increases in high-density lipoprotein cholesterol
(HDL-C) levels, work capacity, and myocardial oxygen consumption.
Stress-induced myocardial ischemia also decreased from the intervention, which
was presumably attributable to enhanced myocardial perfusion. At the 6-year
follow-up, the progression of CAD was significantly slowed in the treatment
group compared with the control group. Retrospective analysis of exercise
intensity and angiographic data revealed that eliciting a regression of
coronary stenosis necessitated expenditure of at least 2200 kcal/week
(equivalent to 5–6 hours of exercise).
In the Stanford Coronary Risk Intervention Project, patients received a
behavioral risk reduction intervention or usual care. Intervention programs
were similar to those in the aforementioned studies, but smoking cessation and
pharmacological treatment of lipid profiles (according to established treatment
guidelines) were added. Evaluation at 4 years after baseline revealed that the
risk reduction intervention significantly improved levels of low-density
lipoprotein cholesterol (LDL-C), apolipoprotein B, HDL-C, triglycerides, body
weight, exercise capacity, cholesterol, and intake of dietary fat. These
positive changes were not seen in the control group. The rate of coronary
stenosis pro- gression and the number of hospitalizations were also lower for
the intervention group, although each group experienced the same number of
deaths.
The Lifestyle Heart Trial used an intervention program to transform
lifestyle behaviors, including a low-fat vegetarian diet, aerobic exercise,
stress management training, smoking cessation, and group psychosocial support.
Follow-up angiograms at 1 and 5 years after baseline showed an average relative
decrease in stenosis of 4.5% and 7.9%. Conversely, individuals in the control
group showed a 5.4% and 27.8% average relative worsening of stenosis. The
5-year risk of adverse cardiac events was also significantly greater in the
control group.
Based on these findings, it is apparent that programs that introduce
intensive measures to alter coronary risk–promoting behaviors, especially via
exercise training and cholesterol reduction, can limit or even reverse the
progression of coronary stenosis. Although the associated changes in coronary
diameter were relatively small and therefore unlikely by themselves to explain
the accompanying improvements in myocardial
perfusion, improvements in vascular tone and reduction in
the risk of plaque rupture might have contributed to the observed outcomes.
PHYSIOLOGY OF EXERCISE EFFECTS ON CARDIOVASCULAR HEALTH
Oxygen Supply and Demand
Ventilatory oxygen uptake is increased by exercise training via enhanced
maximum cardiac output (blood volume ejected by the heart per minute, which
determines the amount of blood delivered to exercising muscles) and the
capacity of the muscles to extract and use oxygen from blood. Increased
exercise capacity, in turn, favorably affects hemodynamic, hormonal, metabolic,
neurological, and respiratory function. Exercise training reduces the
myocardial oxygen demand associated with a given level of work, as represented
by a decrease in the product of HR times systolic arterial BP, and allows
persons with CHD to attain a higher level of physical work before reaching the
threshold at which an inadequate oxygen level results in myocardial ischemia (Box 4.1).
Lipids
Exercise training regimens in general all favorably alter lipid and car-
bohydrate metabolism. The positive effect of a low-saturated fat, low-
cholesterol diet on blood lipoprotein levels is enhanced by a strict regular
exercise regimen in overweight adults. Training also influences adipose tissue
relocation, which is believed to be important in lowering CV risk. Intense
endurance training also enhances insulin sensitivity and has a highly salutary
effect on fibrinogen levels in healthy older men. The beneficial effects of
exercise on lipids are at least part of the benefits that result in primary and
secondary prevention of heart disease in the studies reviewed here. Kraus and
colleagues examined the effects of graded exercise on serum cholesterol in sedentary
and overweight adults with hyperlipidemia who completed a 6-month protocol.
Com- paring the three treatment exercise programs—high-amount, high- intensity
exercise; low-amount, high-intensity exercise; and low-amount,
moderate-intensity exercise—with control groups, all of the exercising groups
showed improvements in plasma lipoprotein levels, including a decrease in very
low-density lipoprotein cholesterol triglycerides and an increase in the size
of LDL-C particles. Increased HDL-C levels and particle size occurred only in
the high-amount, high-intensity group; the largest improvements in LDL-C
measures were also seen only in this group. These effects were independent of
weight loss, and higher amounts of exercise were associated with greater benefits
in lipoproteins. A recent
meta-analysis supported the findings that volume of exercise exposure was the primary determinant of
HDL-C change.
Mechanisms that link exercise with an improved lipoprotein profile may
include increased lipoprotein lipase activity and reduced hepatic lipase
activity, leading to HDL-C increases and decreased conversion of
cardioprotective HDL2 into smaller HDL3 particles.
Exercise reduces the conversion of HDL-C into LDL-C and very low-density
lipoprotein cholesterol by decreasing serum concentrations of cholesterol ester
transfer protein. It increases the conversion of HDL3 to HDL2
by increasing levels of serum lecithin cholesterol acyltransferase. LDL-C does
not seem to be as responsive to exercise training as HDL-C and triglycerides.
Triglyceride levels are consistently and robustly affected in direct
correlation to the total amount of exercise, similar to those changes seen in
HDL-C (10–20 metabolic equivalent tasks—hours per week), although some reports
suggest that women are more resistant to changes in triglycerides with exercise
than men.
Metabolic Syndrome and Diabetes
MS is a cluster of metabolic risk factors that promote development of
atherosclerotic CVD. Risk factors include atherogenic dyslipidemia,
hypertension, elevated blood glucose, central adiposity, and proinflammatory
and prothrombotic markers. Prospective studies have demonstrated a twofold
increase in the relative risk of atherosclerotic events, and for those without
diabetes, a fivefold increase in the risk for developing diabetes. There are
several groups who have defined MS. The two most widely cited are the Adult
Treatment Panel III (ATP III) and WHO criteria. The ATP III criteria for
diagnosis of MS is the presence of any three of the following criteria: (1)
waist circumference >40 inches in
men and >35 inches in women, (2) triglycerides >150 mg/ dL or drug
treatment, (3) low HDL-C or drug treatment (<40 mg/dL in men; <50 mg/dL
in women), (4) elevated BP or drug treatment (>130/85 mm Hg), and (5)
fasting glucose >100 mg/dL or drug treatment. The WHO defines MS as insulin
resistance, identified by one of the following: (1) type 2 diabetes, (2)
impaired fasting glucose, (3)
impaired glucose tolerance, (4) or for those with normal fasting glucose levels
(<6.1 mmol/L), glucose uptake below the lowest quartile for the background
population being investigated under hyperinsulinemic, euglycemic conditions;
plus any two of the following: (1) anti- hypertensive medication and/or high BP
(≥140 mm Hg systolic or >90 mm Hg
diastolic), (2) plasma triglycerides >150 mg/dL, (3) HDL cholesterol <35
mg/dL in men or <39 mg/dL in women, (4) BMI >30 kg/ m2 and/or
waist-to-hip ratio >0.9 in men and >0.85 in women, (5) urinary albumin excretion rate >20 µg/min or
albumin-to-creatinine ratio >3.4 mg/mmol.
Regular physical activity is associated with a 30% to 40% lower risk for
developing MS. There is an inverse dose–response association between level of
activity and risk. The minimal amount of activity necessary to prevent MS
ranges from 120 to 180 minutes of activity per week. These findings are
consistent for both men and women. There have been no prospective trials to
examine exercise training as a treatment to reverse MS.
Currently, it is estimated that 23.4 million Americans have been
diagnosed with diabetes and that another 7.6 million are undiagnosed, and 81.6
million adults have prediabetes (fasting blood glucose of 100 to <126
mg/dL). There were 1.7 million new cases of diabetes diagnosed in 2012.
Although mortality rates have declined in women and men with and without
diabetes, the rates of CVD mortality are still twofold higher for those with
diabetes compared with those without diabetes. Numerous large-cohort studies
have demonstrated the benefit of physical activity in preventing type 2
diabetes. In the Nurses’ Health Study, walking
and vigorous activity were associated with a decreased risk for diabetes, with greater physical activity providing the most
benefit. The estimate across studies is a 30% to 40% lower risk for developing
type 2 diabetes for those with moderate levels of activity. The benefits are
seen for both men and women, as well as young and old and for different
races/ethnic groups. The data indicate that at least 120 to 150 minutes of
moderate to vigorous physical activity are needed to significantly lower risk
for diabetes.
Type 2 diabetes is associated with reduced exercise capacity, which is
associated with cardiac and hemodynamic abnormalities. Exercise increases the
activity of mitochondrial enzymes, which improves muscle energetics. Even
modest levels of exercise increase insulin sensitivity and reduce visceral
adipose tissue and plasma triglycerides. Women with diabetes who exercise
moderately or vigorously for at least 4 hours/ week have a 40% lower risk of
developing coronary disease than those with lower exercise levels. Low physical
activity in men with diabetes is an independent predictor for CHD. Several
cohort studies have shown that CV fitness and physical activity levels are
inversely correlated with mortality and/or CVD event rates in subjects with
type 2 diabetes. In the Nurses’ Health Study of 5000 diabetic women followed
for 14 years, the relative risk for CV events decreased progressively with
increasing weekly volume of moderate to vigorous activity. This relationship
remained after adjusting for smoking, BMI, and other CV risk factors.
Maintaining a habitual exercise routine can lower systolic BP by as much
as 5 to 15 mm Hg in patients with essential hypertension; mean reductions of 4
to 5 mm Hg systolic pressure and 3 to 5 mm Hg diastolic pressure are widely
reported. Just as perseverance with an exercise program elicits a hypotensive
response, detraining is associated with an increase in BP toward the
pre-exercise level. Reductions in circulating norepinephrine level, plasma
volume, and cardiac index parallel the reduction in BP and are probably
involved in the antihypertensive con- sequences of exercise. Reduced systemic
vascular resistance resulting from decreased sympathetic activity probably also
affects BP.
The recommended targets for BP control have undergone revisions since the publication of the Eighth Joint National Committee (JNC-8). However, because of the change in methodology for review, sponsoring of the oversight group midway through the guideline development process, and recent publication of the results of the Systolic Blood Pressure Intervention Trial (SPRINT), the current recommended BP targets have been subjected to intense criticism and have resulted in confusion for patients. The guidelines were updated in the fall of 2017. Normal blood pressure is now defined to be <120/80. The previous threshold of >140/90 is now considered stage 2 hypertension.
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ROLE OF EXERCISE TRAINING IN HEART FAILURE
Heart failure (HF) is a growing problem in the industrialized world and
has reached epidemic proportions in the United States. Although the central
effects of HF are pulmonary and peripheral vascular congestion, many patients
believe that exercise limitation is the most troubling feature. Traditional
therapies, such as angiotensin-converting enzyme inhibitors, β-blockers,
spironolactone, and most recently, neprilysin inhibitors combined with
angiotensin receptor blockers show impressive reductions in mortality with somewhat
less significant improvement in functional capacity. Hence, there is a need for
therapies targeted at improving functional capacity. Exercise training was once
prohibited in HF patients out of concern for patient safety. However, it is now
recognized as a therapeutic option for improving functional capacity in
patients with HF (Fig. 4.3), with the most recent full revision of the American
College of College/American Heart Association (ACC/AHA) HF guidelines made in
2013, which provided a class I recommendation (level of evidence A) for exercise training (or regular physical
activity) as being “safe and effective for patients with heart failure who are
able to participate to improve functional status.”
In HF, mechanical function and functional capacity do not always have a
direct correlation. LV ejection fraction is a poor index of exercise capacity
in patients with chronic HF; therefore other factors must con- tribute to
exercise intolerance in HF. The physiological mechanisms for exercise intolerance
in HF, albeit incompletely understood, help to explain the potential benefits
of exercise training.
Among the factors contributing to exercise limitation are impaired LV
systolic and diastolic function, baroreflex desensitization, sympathetic
nervous system activation, impaired vasodilator capacity, skeletal muscle
abnormalities, and abnormalities of pulmonary function. The emerging data on
diastolic dysfunction indicates that this pathology results in disabling
symptoms and activity intolerance, and has been labeled HF with preserved
ejection fraction (HFpEF). Skeletal muscle abnormalities in patients with HF
include atrophy of highly oxidative, fatigue-resistant (type I) muscle fibers;
increased glycolytic, less fatigue-resistant (type II) muscle fibers; decreased mitochondrial oxidative enzyme
concentration and activity; reduced mitochondrial volume and density; and
reduced muscle bulk and strength. As HF progresses, patients become more
physically limited because of pulmonary congestion and therefore reduce
physical activity, causing a downward spiral in which cardiac limitation
aggravates skeletal muscle deconditioning. The increases in circulating
cytokines, part of the HF syndrome, further worsen muscle atrophy. Reduced peak
skeletal muscle blood flow with exercise limitation also reduces shear stress
and thereby depletes tissue vasodilator reserve.
Pulmonary abnormalities are also common in HF, including reduced lung
volumes and respiratory muscle strength and endurance; increased airway
resistance with reduced flow rates; reduced diffusion capacity as a result of
alveolar edema; and increased ventilatory drive, minute ventilation,
respiratory rate, and dead space-to-tidal volume ratio. The effects of training
on these ventilatory abnormalities in patients with HF include reduction in
minute ventilation, reduced perceived sense of dyspnea, and improved
respiratory muscle function.
The well-documented, abnormal activation of neurohormones in chronic HF
is associated with a poor prognosis. An exercise training program can correct
the increased plasma levels of angiotensin II, aldosterone, arginine
vasopressin, and atrial natriuretic peptide in chronic HF to near-control
values. Decreased HR variability, which is markedly abnormal in patients with
HF, is a further marker of sympathetic activation. A physical conditioning
program can improve HR variability and endothelial dysfunction in patients with
chronic HF.
Clinical trials of exercise training in HF show improvements in exercise
time, functional capacity, and peak oxygen consumption. Exercise training seems
to be safe and generally well tolerated in patients with HF with a reduced
ejection fraction and HFpEF. One randomized trial found a reduction in cardiac
events, an improvement in Minnesota Living with Heart Failure scores, and, most
importantly, an improved survival rate in patients with HF who were randomized
to exercise training. The HF-ACTION (Heart Failure–A Controlled Trial
Investigating Outcomes of Exercise Training) study was sponsored by the National
Institutes of Health and designed to test the hypothesis that patients with LV
systolic dysfunction and New York Heart Association functional class II to IV
symptoms who underwent exercise training in addition to usual care would have a
20% lower rate of death and hospitalization over 2 years compared with usual
care. The results showed a balanced randomization of 2331 patients to exercise
or usual care. Exercise consisted of a 36-week supervised training program
followed by a home- based program. The mean follow-up was 2.5 years. The rates
of all-cause mortality and all-cause hospitalizations combined were not
significantly different between the two groups. Using a prespecified adjustment
for prognostic factors, there was a
significant reduction in the composite primary outcome by 11% (hazard ratio:
0.89; 95% confidence interval [CI]: 0.81–0.99; P = 0.03), and a
composite of CV mortality–HF hospitalizations were reduced by 15% (hazard
ratio: 0.85; 95% CI: 0.74–0.99; P = 0.03). Importantly, there were no
differences in adverse events between the two groups, indicating that exercise
training in this population was safe. There was also a statistically
significant improvement in quality of life in the exercise training group. The
findings of HF-ACTION offer good evidence for recommending exercise as a safe
but modestly effective treatment for patients with HF.
Exercise training in patients with HF is best initiated within a
traditional phase II (outpatient) CR program. Patients should be prescreened by
a cardiologist to assess the clinical risk for training initiation. Most
patients with New York Heart Association functional class II to IV symptoms can
exercise safely; however, patients with unstable symptoms, recent MI, unstable
angina, severe aortic stenosis, uncontrolled arrhythmias, significant
hypotension (systolic BP <85 mm Hg), or acute myo- carditis should be
excluded. Chronotropic response may be blunted in patients with HF, so the
level of perceived exertion and dyspnea should be used as a termination point
and should be no higher than 11 to 14 on the Borg scale (light to somewhat
difficult exertion). Patients with HF
require prolonged warm-up and cool-down periods compared with healthy
individuals and should avoid resistance training initially. Patients also
should be counseled to avoid exercise after meals. The usual recommended
activities, walking and cycling, arm ergometry (e.g., using arm motion, instead
of leg motion, to peddle an upright stationary bicycle), and rowing, are well
suited for individuals whose walking or cycling
is limited by arthritis or conditions other than CV fatigue.
Exercise intensity should be at the minimum level needed to produce a training effect but below the threshold
at which cardiac signs and symptoms develop. A baseline maximal oxygen
consumption (MVo2) study can be helpful in designing the exercise
prescription but is not mandatory. Target intensity should begin at 40% of the
MVo2 and progress to 75% of the MVo2 (roughly 70%–85% of
peak HR) over 4 to 6 weeks. Initially, the frequency of exercise generally
should be three times per week. MVo2 plateaus when the frequency of
exercise exceeds three to five sessions per week, and the injury rate increases
exponentially. In frail or high-risk individuals, two sessions per week may
also be effective for initial conditioning. The frequency of exercise should
eventually increase to five sessions per week.
Exercise sessions should begin with a 10- to 15-minute warm-up and end
with a 10- to 15-minute cool-down. The initial duration of exercise should be
10 to 20 minutes. Interval training may be required in markedly deconditioned
patients, with 2 to 6 minutes of exercise alternating with 1 to 2 minutes of
rest. Duration should increase gradually to 20 to 40 minutes per session. After
12 weeks, patients can proceed to unsupervised exercise and can consider light
to moderate resistance training.
CARDIAC REHABILITATION
CR is a comprehensive intervention program that includes prescribed
exercise, CV risk factor modification, education, counseling, and behavioral
intervention for patients with CVD. Based on strong evidence from randomized
clinical trials, it is recommended and reimbursable for patients with stable
angina pectoris, post-MI, coronary revascularization, heart transplantation, and valve surgery,
as well as HF. Despite this, the referral
of patients to CR and the enrollment of those referred remains low. The reasons
for this are multifactorial and include limited availability of programs for
the volume of patients who qualify, especially patients in rural areas,
frequency of visits requiring leave from work, transportation to sessions, lack
of full reimbursement depending on healthcare plan, in addition to other
financial or social issues. Telehealth programs and other mHealth applications
(wearables, Internet-based support groups) have been under evaluation as
potential solutions. The Million Hearts Program, as part of its second phase
initiative, is targeting better use of CR to 80% of eligible patients because
of the known risk reduction that can be achieved with these programs.
In 2007, the AHA and American Association of Cardiovascular and Pulmonary
Rehabilitation established the core components of CR to include the following,
which are all components of promoting cardiovascular health that have been
outlined in this chapter:
·
initial patient assessment
·
nutrition counseling
·
weight management
·
BP management
·
lipid management
·
diabetes management
·
tobacco cessation
·
psychosocial management
·
physical activity counseling and exercise
training
CR, in addition to promoting to physiological health, improves
psychological health. CR programs can help to identify and facilitate
management of psychological issues related to acute and chronic disease states
(e.g., anxiety and depression). The education regarding lifestyle changes
provides understanding and allows for mastery of skills for successful
self-management. There are also strong data that psychological benefits of
exercise include positive changes in mood; relief from tension, depression, and
anxiety; increased ability to cope with daily activities; and improved
cognitive function. These benefits bring about positive changes in
self-perception, well-being, self-confidence, and awareness, and may result in more health-promoting behaviors.
FUTURE DIRECTIONS
Increasing physical activity and exercise in patients at risk for and with CHD should be a primary intervention in all patients. The documented benefits for CV risk reduction, as well as reduction in the progression of (and in some cases normalization of) MS and type 2 diabetes, make this one of the most effective therapies in a practitioner’s arsenal. It must be noted that the obstacles to convincing a patient to engage in regular exercise are significant and begin with patient motivation. Further research is needed to learn more about dosing of exercise and physical activity, as well as better methods to improve subject compliance and adherence to prescribed exercise. In addition, public policy changes are necessary to alter aspects of our society that promote sedentary habits in children and adults, which contribute to obesity, diabetes, and CHD progression. The emergence of mHealth technology will provide new platforms to make exercise interventions more available to an almost limitless number of people, allow a mechanism for monitoring, and perhaps allow for more population-wide intervention strategies to improve CV health. The next decade will be an exciting time as this technology evolves and becomes more facile, accurate, accepted, and incorporated into everyone’s life.
