exercise considerations in hypertension, obesity, and
TRANSCRIPT
Exercise considerations in hypertension,
obesity, and dyslipidemia
John M. MacKnight, MDUniversity Physicians Clinic, University of Virginia Health System, Box 800671,
Charlottesville, VA 22908, USA
Sports medicine practitioners who care for a wide array of athletes and active
individuals will consistently face issues regarding chronic cardiovascular diseases
and their associated risk factors. Among these, hypertension, obesity, and dyslipide-
mia are common clinical conditions that may be encountered even amongst elite
caliber athletes. Consequently, those entrusted with the care of this active popu-
lation must recognize the presence of these disorders and feel comfortable with
their management in the face of continued sports or exercise participation. This
article reviews the pathophysiology of these conditions as they relate to athletes and
outlines the value of continued exercise in the management of each of these entities
while addressing the specific and unique treatment needs of active individuals.
Hypertension
Approximately 50 million Americans are hypertensive [1], and hypertension is
the most common cardiovascular condition in competitive athletes [2]. A
thorough understanding of the pathophysiology of the condition, especially as
it relates to the effects of exercise, is essential for anyone who cares for active
patients. With this understanding, physicians may ensure that active hyper-
tensives continue to exercise and compete while guarding against the devel-
opment of long-term complications.
Pathophysiology of hypertension
Hypertension is defined as blood pressure equal to or greater than 140/90 mm
Hg with or without antihypertensive medication use. Classification criteria for the
different stages of hypertension are provided in Table 1. Accurate, systematic,
0278-5919/03/$ – see front matter D 2003, Elsevier Science (USA). All rights reserved.
PII: S0278 -5919 (02 )00069 -8
E-mail address: [email protected]
Clin Sports Med 22 (2003) 101–121
and consistent blood pressure values are necessary to confirm the diagnosis. The
evaluation of the hypertensive athlete should then include a thorough personal
and family history, a physical examination with special attention to the cardio-
vascular system, kidneys, and thyroid, and appropriate laboratory and electro-
cardiographic tests, as listed below [2,3].
Components of a systematic evaluation for hypertension
Blood pressure measurement technique
Patient seated, with arm bared and back supported
No tobacco or caffeine within 30 minutes of measurement
Patient rests 5 minutes before measurement
Bladder of cuff encircles at least 80% of patient’s arm
Multiple readings, when necessary, are separated by 2 minutes each
and averaged
History
Symptoms of hypertension-related conditions (chest pain, dyspnea,
orthopnea, poor exercise tolerance)
Family history of hypertension and its comorbidities
Weight change
Type and intensity of exercise
Diet
Alcohol and tobacco use
Caffeine intake
Illicit drug use (eg, cocaine, amphetamines, anabolic-androgenic
steroids, erythropoietin)
Use of sympathomimetic agents (eg, nasal decongestants), non-
steroidal anti-inflammatories, or appetite suppressants or other
stimulants (eg, ephedrine, ma huang)
Table 1
Classification of blood pressure in adults [3]
Blood Pressure (mm Hg)
Category Systolic Diastolic
Optimal < 120 < 80
Normal < 130 < 85
High–normal * 130–139 85–89
Stage 1* HTN 140–159 90–99
Stage 2* HTN 160–179 100–109
Stage 3* HTN > 180 >110
Abbreviation: HTN = hypertension.
* Elevated systolic or diastolic pressure alone is sufficient to meet the criterion.
From Slattery ML, McDonald A, Bild DE, et al. Associations of body fat and its distributiom with
dietary intake, physical activity, alcohol, and smoking in blacks and whites. Am J Clin Nutr 1992;55:
943–9; with permission.
J.M. MacKnight / Clin Sports Med 22 (2003) 101–121102
Physical examination (for signs of end-organ damage or second-
ary causes)
S4 gallop
Arterial bruits, particularly renal
Peripheral pulses
Tachycardia
Hypertensive retinopathy
Exophthalmos
Thyroid abnormalities
Tremor
Diagnostic tests (in all hypertensive patients)
Complete blood count
Lipid profile
Serum electrolytes, glucose, blood urea nitrogen, and creatinine
Urinalysis for hematuria and proteinuria
Electrocardiogram
Ninety-five percent of these individuals will be diagnosed with ‘‘essential’’
hypertension where no identifiable cause can be found. Their elevated blood
pressure results from increases in total peripheral resistance mediated by plasma
epinephrine and norepinephrine [4] and the renin-angiotensin system. In the other
5% of cases, a secondary cause of hypertension, as listed below, may be implicated.
Secondary causes of hypertension
Androgen or growth hormone use
Coarctation of the aorta
Cushing’s disease
Erythropoietin use
Excessive alcohol intake
Hyperaldosteronism
Hyperthyroidism
Illicit drug use (eg, cocaine, ephedrine amphetamines)
Pheochromocytoma
Renal artery stenosis
Renal parenchymal disease
Vasoconstrictive drug use (eg, decongestants)
Physiologic blood pressure responses to exercise are addressed elsewhere in
this issue. Briefly, in contrast to normotensive athletes, hypertensive individuals,
with both dynamic and static exercise, generally demonstrate exercise-induced
increases in total peripheral resistance and impaired vasodilation, with a resultant
increase in myocardial oxygen consumption and exaggerated blood pressure
elevations [5]. Over time, these abnormal responses may lead to pathologic left
J.M. MacKnight / Clin Sports Med 22 (2003) 101–121 103
ventricular hypertrophy (LVH) with thickened, stiff, and poorly compliant
ventricular walls, particularly during cardiac filling in diastole. This impaired
filling response leads to diastolic dysfunction that may actually decrease cardiac
output during exercise and significantly impair performance and exercise capacity.
An altered vasodilatory response to exercise in hypertensive athletes may also
predispose to heat illness by impairing heat dissipation and potentially leading to
seriously elevated core body temperatures, excessive water loss, and hypokalemia.
Chronic pressure overload and microvascular trauma are the major pathophys-
iologic mechanisms for the development of hypertension-related end-organ
disease. Such complications include an increased annual incidence of cerebro-
vascular, retinovascular, peripheral arterial, and renal parenchymal diseases with
chronic blood pressure elevations above 160/95 mm Hg [6–8]. Sustained high
blood pressure also significantly raises the risk of coronary artery disease (CAD)
and LVH, with a resultant increase in cardiac morbidity and mortality, heart
failure, and sudden cardiac death.
The management of high blood pressure in active patients and athletes
should include exercise, lifestyle modifications, and, if blood pressure is still
inadequately controlled, medication. Nonpharmacologic therapy may be suf-
ficient for controlling blood pressure in borderline or mildly hypertensive
patients and should be used concomitantly even if medication is needed. One
of the most important messages for hypertensive active patients and athletes is
that exercise should be continued, because it is safe for most patients and helps
control blood pressure.
Relative postexercise hypotension [9] was first noted by Kaul [10] over 30 years
ago as a normal physiologic response to moderate-intensity dynamic exercise.
The largest absolute and relative blood pressure reductions are seen in hypertensive
subjects [9,11], with mildly hypertensive athletes deriving the greatest benefit,
as exercise reduces sympathetic neural activity, leading to lower heart rate and
cardiac output [4]. Maximal decreases of 18 mm to20 mmHg systolic and 7 mm to
9 mmHg diastolic have been reported among stage 1 hypertensives. This lowering
effect may persist for up to 16 hours after exercise, thus allowing stage 1 patients to
be normotensive for most of the day. [9,12–14].
Three prior meta-analyses have validated dynamic exercise as an effective
means of managing high blood pressure [15–17]. In an additional recent meta-
analysis of 54 studies investigating over 2400 patients, aerobic exercise over at
least 4 weeks of time was found to modestly reduce blood pressure in both
hypertensive and normotensive persons [18]. Overall, blood pressure was lowered
by 3.84 mm Hg systolic and 2.58 mm Hg diastolic, but hypertensive individuals
demonstrated even larger benefits, with systolic and diastolic lowering of 7 mm
and 6 mm Hg, respectively. These findings were independent of changes in body
weight. Given the results of these numerous studies, aerobic physical activity
should be considered an important component of both the prevention and
treatment of high blood pressure. This is also valuable information in light of
our increasing understanding of the beneficial effects of even small degrees of
blood pressure lowering on the risk for cardiovascular complications.
J.M. MacKnight / Clin Sports Med 22 (2003) 101–121104
With respect to acceptable levels of activity in the face of hypertension,
moderate-intensity exercise, in keeping with current American College of Sports
Medicine (ACSM) guidelines [19], is safe for most hypertensive patients. Training
studies have shown that the acute effects of exercise on blood pressure are a low-
threshold phenomenon observed after energy expenditures requiring only 40%
maximal capacity [9,11,12] and after only three sessions of aerobic activity
[12,20,21]. Similarly, data from over 40 studies of low to moderate-intensity
endurance training (20 to 60 minutes at 40% to 70% of VO2max, or 50% to 70%
maximum age-predicted heart rate, 3 to 5 days per week) found effective decreases
in both systolic and diastolic blood pressures [19]. There is little evidence to
justify higher-intensity exercise (>70% VO2max) for lowering blood pressure
[22–30], as the beneficial effects of moderate-intensity exercise are equal or
superior to those of higher-intensity exercise [31]. This is an important consid-
eration in limiting the cardiovascular and musculoskeletal risks of exercise,
particularly in older patients.
Chronic exercise training produces greater blood pressure reductions than do
acute bouts of exercise [32]. Such a program should be at least 1 to 3 months in
duration to reach the stable stage, and training should be maintained indefinitely,
because the hypotensive effect persists only as long as regular endurance exercise
is maintained. Generally, maximum limits of blood pressure lowering are reached
after 3 months of training; no further blood pressure reduction occurs thereafter,
except in rare instances.
Most studies examining the different modes of exercise in the management of
hypertension have focused on walking, running, or cycling. Obviously, each
hypertensive athlete’s sporting activities must be assessed for relative value and
safety with respect to blood pressure management. Walking and running do not
cause a sustained increase in blood pressure and perhaps represent the most
suitable endurance exercises for hypertensive patients. Moderate swimming (30-
to 45-minute sessions, 3 days a week) can lower systolic but not diastolic blood
pressure at rest. Swimming can be an alternative exercise for patients who are
obese, have exercise-induced asthma, or have orthopedic injuries. Vigorous
activities done with rhythmic high force, such as sprinting or rowing, are generally
unsuitable for uncontrolled hypertensive patients. Downhill skiing can elevate
blood pressure, and mountain sports may exaggerate an elevated blood pressure
response from the cold and decreased partial pressure of oxygen. Even resistance
training (8 to 10 major-muscle-group exercises, two to three times per week),
especially circuit weight training [33,34], may help lower blood pressure when the
exercises are done at 40% to 50% of the patient’s one-repetition maximum [35].
Resistance training, however, is not recommended as the only approach to low-
ering blood pressure.
Despite their high level of exercise performance, athletes may also need to
correct poor lifestyle habits to obtain optimal blood pressure control. Interventions
that have proven to be beneficial include weight reduction, moderation of alcohol
and sodium intake, high potassium and increased calcium intake, and smoking
cessation [36]. No convincing data support the use of increased magnesium intake,
J.M. MacKnight / Clin Sports Med 22 (2003) 101–121 105
Table 2
A profile of common antihypertensive medications: mechanism of action, adverse effects, and effects on aerobic capacity
Class Agents Mechanism of action Adverse effects Effects on aerobic capacity
Angiotensin-converting
enzyme (ACE) inhibitors
Benazepril hydrochloride
Captopril
Enalapril maleate
Lisinopril
Quinapril hydrochloride
Prevent production of angiotensin II,
a potent vasoconstrictor
Cough, renal dysfunction,
hyperkalemia
None
Calcium channel blockers Amlodipine
Diltiazem hydrochloride
Isradipine
Verapamil hydrochloride
Decrease vascular smooth muscle
contractility; cause negative inotropic
and chronotropic effects on myocardium
Bradycardia, constipation,
peripheral edema; for
short-acting dihydropyridines,
increased cardiac mortality
None
Alpha-1-receptor blockers Doxazosin mesylate
Terazosin
Prazosin
Cause decreased vascular contractility
by blocking alpha-1 receptors in
smooth muscle
Orthostatic hypotension,
tachycardia
None
Central alpha-receptor
antagonists
Clonidine hydrochloride Act on CNS alpha-2 receptors to
block sympathetic stimulation
Many CNS effects, including
dry mouth, dizziness, sedation;
postexercise hypotension
None, but poor first-line
choice because of CNS
effects and risk of
postexercise hypotension
Beta-blockers*
Nonselective Propranolol hydrochloride
Nadolol
Block cardiac beta-receptors,
leading to decreased heart rate,
myocardial contractility,
Bradycardia, depression,
exacerbation of asthma,
and impotence
Decreased aerobic capacity
Cardioselective Atenolol
Metoprolol
Labetalol hydrochloride
Same as above (except labetalol has beta-1,
beta-2, and alpha-1 blocking activity)
Bradycardia, depression,
and impotence
None
Diuretics** Hydrochlorothiazide
Furosemide
Decrease circulatory volume Hypokalemia, hyponatremia,
volume depletion, dehydration
None directly, but adverse
effects are accentuated by
athletic activity
Angiotensin receptor
blockers
Losartan potassium
Valsartan
Block angiotensin II receptor site,
preventing vasoconstriction
Renal dysfunction, hyperkalemia.
(No cough, however.)
None
J.M.MacK
night/Clin
Sports
Med
22(2003)101–121
106
high-protein diets, other special dietary measures, relaxation techniques, or
biofeedback in the prevention or control of hypertension [19].
If other interventions fail to control blood pressure, pharmacologic therapy is
warranted. The goals are to (1) decrease elevated resting blood pressure, (2) lower
increases in systolic and diastolic blood pressure during exercise, and (3) preserve
central hemodynamics and exercise capacity [37]. The choice of pharmacologic
agents is especially important in active patients and athletes because inappropri-
ate medications can impair performance, whereas optimal choices can enhance it
by reducing elevated blood pressure at rest and thus limiting exercise-induced
hypertensive responses [2]. According to the Sixth Joint National Committee
report (JNC VI) on the management of hypertension, patients using beta-blockers
and diuretics to control uncomplicated hypertension have lower mortality rates
than those who use other medications [3]. The medications typically used in
treating hypertensive athletes are presented in Table 2.
In general, agents that decrease total peripheral resistance have the least effect
on exercise performance. All commonly used antihypertensive agents except for
nonselective beta-blockers and diuretics allow for essentially normal exercise
capacity. Noncardioselective beta-blockers (eg, propranolol, nadolol) are contra-
indicated in athletes because they significantly reduce maximal aerobic capacity.
Their potentially deleterious effects on performance, however, as well as those of
diuretics, must be weighed against the mortality benefit noted above. The
physician must also be sure that the use of a particular antihypertensive agent
is allowed by a sport’s governing body. Restrictions regarding the use of beta-
blockers and diuretics are included in Table 2.
Cardioselective beta-1 blockers without intrinsic sympathomimetic activity
(eg, atenolol, metoprolol tartrate) lead to the greatest reduction in exercise-
induced blood pressure and heart rate increases and have little effect on per-
formance. Thus, some authorities [37] consider these medications to be the best
choice for hypertensive athletes. Even the slightest performance decrement may
be unacceptable to elite athletes, however. Alternative agents that may be more
suitable choices for such athletes include angiotensin-converting enzyme (ACE)
inhibitors, angiotensin receptor blockers (ARB), calcium channel blockers, and
alpha-1 blockers. These alternative medications are well tolerated and have few
negative effects on exercise performance.
Recommendations for sports participation
The physician’s role in evaluating hypertensive athletes and managing
their condition is vital. Although athletes should not be exposed to undue
Notes to Table 2:
Abbreviation: CNS = central nervous system.
* Beta-blockers are banned by the International Olympic Committee (IOC) and the National
Collegiate Athletic Association (NCAA) for competitors in archery and riflery.
** Diuretics are banned by the IOC and NCAA; in addition to being used in rapid weight loss,
they have been implicated in attempts to enhance the renal clearance of anabolic steroids.
J.M. MacKnight / Clin Sports Med 22 (2003) 101–121 107
risks, physicians should be cautious not to give recommendations for sports
participation that are more conservative than is consistent with scientific
evidence. For example, hypertensive people who exercise are not at increased
risk for hemorrhagic stroke or sudden cardiac death [2,5]. In addition, resistance
training has not been associated with increased morbidity in hypertensive indi-
viduals [19] despite the significantly elevated blood pressure that static exercise
may cause.
Keeping these findings in mind, physicians may use the JNC VI staging sys-
tem for hypertension (see Table 1) as a framework for making exercise recom-
mendations that are based on the degree of hypertension and the presence or
absence of complicating factors.
Stages 1 and 2
Patients may participate fully in dynamic and static sports if there is no evi-
dence of end-organ damage, including heart disease [2]. For those with mild
hypertension (a resting diastolic pressure of 90 mm to 105 mm Hg and systolic
pressure of less than 160 mmHg), physical activities should be primarily dynamic.
Some authors have suggested that strength training and high-static and high-
intensity activities, though not absolutely restricted, should be avoided until better
blood pressure control is obtained [35]. Examples of suitable sports include walk-
ing, hiking, jogging, cycling, swimming, softball, volleyball, and cross-country
skiing. Sports to avoid include rowing, diving, tennis, competitive ball sports, and
strenuous physical training (above 80% of maximum age-predicted heart rate)
[37]. Blood pressure should be checked every 2 to 4 months to ensure that it re-
mains in an acceptable range.
Stage 3
Patients who have a resting diastolic pressure above 110 mm to 115 mm Hg
should discontinue exercise until blood pressure is well-controlled, especially if
they are involved in high static or isometric sports [37]. Because activities such as
boxing, cycling, rowing, bodybuilding, weight lifting, wrestling, and gymnastics
have a static component, they should be avoided until acceptable blood pressure
levels are established [2]. Although prudence would suggest that all types of
exercise be limited until blood pressure is controlled, strenuous dynamic exercise,
even among severely hypertensive patients, has never been shown to increase the
risk of progression of hypertension or sudden death [38–40].
Hypertension with complications
For patients who have conditions such as pathologic LV hypertrophy,
hypertensive nephropathy or retinopathy, or peripheral vascular disease, the type
and severity of the condition and the nature of the sport determine the patient’s
ability to participate safely [2]. Again, high static or isometric sports and dynamic
exercise of more than moderate intensity should likely be avoided.
J.M. MacKnight / Clin Sports Med 22 (2003) 101–121108
Obesity
Obesity and overweight have become increasing health concerns worldwide
over the last several decades. Few sports medicine practitioners will encounter
frankly obese athletes competing at elite levels. Much more commonly, the sports
medicine physician may play a vital role in the creation of exercise and diet
strategies for the management of overweight athletes at lower skill levels or obese
patients from the general population. As the complications of obesity become
more apparent, there are few more important tasks that must be assumed than to
advocate the establishment and maintenance of healthful weight.
The most widely used measure of relative body size is the body mass index
(BMI), which is determined by weight in kilograms divided by height in meters
squared (kg/m2). BMI is age- and sex-dependent but independent of ethnicity [41].
Per current National Institutes of Health (NIH) guidelines [42], ideal BMI is less
than 19 to 25. ‘‘Overweight’’ is defined as a BMI 25 to 29.9, and ‘‘obese’’
corresponds to a BMI greater than 30. The prevalence of obesity has risen more
than 50% within the past 10 to 15 years, with nearly half of adult Americans now
classified as overweight or obese by these criteria [43]. Rates of obesity are even
higher in non-Hispanic black women and Mexican-American women. Alarm-
ingly, the numbers of Americans whose BMIs classify them as overweight or
obese are rising in both categories.
Although much attention has been paid to this growing problem, there is much
that is unknown regarding the causative factors. What is understood is that the
determination of body weight is a complex process with neural, humoral,
metabolic, and psychological contributing features [44]. It is likely that elements
of both ‘‘nature’’ and ‘‘nurture’’ play roles in a unique interaction of genotypic
versus environmental factors [45,46]. One common theory implicates genetic
metabolic programming that favors a tendency toward obesity. Although genetic
predispositions do determine resting metabolic rate (RMR) [47,48], the available
data have failed to show that low RMR is a major factor in the etiology of human
obesity [49–51]. A societal theory for the high prevalence of obesity in the United
States. is a positive energy balance (and resultant weight gain) that results from the
promotion and increasing acceptance of a high dietary energy intake and, at a
variety of levels, the discouragement of regular physical activity.
At the cellular level, obese patients demonstrate disordered metabolic re-
sponses of adipose tissue to insulin and to catecholamines. Insulin normally stim-
ulates lipoprotein lipase (LPL) activity to control triglyceride metabolism and fat
deposition. In obese patients, the hormonal control of adipocyte triglyceride
turnover is altered and is most marked in patients with central obesity [52]. There
is resistance to insulin stimulation of LPL and abnormal hepatic sensitive lipase
(HSL) activity as well. Alterations in catecholamine-induced lipolysis lead to
enhanced activity in visceral fat but decreased activity in subcutaneous fat [53],
leading in turn to abnormal fat deposition and further weight gain.
Whether activity is actively discouraged or not, data at this point support the
notion that our society as a whole is becoming less active. According to the
J.M. MacKnight / Clin Sports Med 22 (2003) 101–121 109
Behavioral Risk Factor Survey (BRFSS) [54], 64% of high school students
reported vigorous (hard or very hard) activity for at least 20 minutes on 3 or
more days per week. Boys were more active than girls, and whites were more
active than blacks or Hispanics. Unfortunately, physical activity declined with
higher grade in school, especially in girls. Among adults, only 28% of men and
women achieve moderate or vigorous levels of physical activity. Twenty-seven
percent of men and 31% of women report no regular physical activity at all outside
of work. Although fewer than 20% of college graduates reported being inactive,
nearly half of the high school educated population is inactive. These are disturbing
trends with rising consequences.
The degree to which lack of regular physical activity creates or promotes
obesity remains in debate. There are substantial data to suggest that differences in
the amount of individual physical activity do contribute to differences in body
weight and body fatness and may play a role in whether obesity develops. When
evaluating cross-sectional and population-based studies, there emerges an inverse
relationship between level of physical activity and indices of obesity, such as
BMI [55–57]. Similarly, cohort studies have revealed that high levels of physical
activity do appear protective against obesity [57,58]. Although there are no
prospective studies that have looked at this issue, there is overwhelming indirect
evidence via observational studies that declining amounts of physical activity
have contributed importantly to a rising prevalence of overweight and obesity.
Taken in total, these data support a relationship between the level of physical
activity and body fatness. This should not be surprising, in light of the fact that
exercise is one of the most potent physiologic stimuli for lipolysis, with a higher
rate of fat metabolism during exercise in trained individuals than that reported
during either critical illness [59] or starvation [60]. With adaptation to chronic
endurance aerobic activity, muscle develops a higher oxidative enzyme activity
and is better equipped to burn fat through the use of free fatty acids as the energy
substrate instead of glycogen stores. Activation of HSL is also increased [61].
Many significant medical conditions have been linked either directly or indi-
rectly to obesity. The exact correlations between obesity and a number of these
conditions remain unclear. Obesity-related sedentary behaviors and associated
poor dietary habits may exert independent effects on health that are difficult to
discern from obesity alone. Nevertheless, from the standpoint of identification and
management of these conditions, they can at a minimum be safely viewed as
obesity-associated.
Weight gain during adult life is associated with an increased risk of heart disease
and death [62]. Indeed, most studies show an increase in mortality rate associated
with a BMI of 30 or more [42]. There exists a J-shaped relationship between BMI
and relative morbidity/mortality, with a primary concentration in the cardiovas-
cular diseases [63–70], presumably from the effects of obesity on cardiovascular
disease risk factors. In particular, the android fat distribution pattern with
prominent central/abdominal adipose deposition is now associated with a variety
of metabolic derangements, including dyslipidemia [71–73], hypertension [43],
hyperinsulinemia [74,75], and glucose intolerance/diabetes [68,76,77], with a 25%
J.M. MacKnight / Clin Sports Med 22 (2003) 101–121110
increase in diabetes risk for each additional unit of BMI over 22 kg/m2 [46,78].
Excess weight is also associated with increased risk for stroke, gall bladder disease,
sleep apnea and respiratory problems, and for a number of cancers, including
endometrial, breast, prostate, and colon cancer [46,79].
Similar associations have been found between increasing body weight and
increased risk for osteoarthritis(OA) [80,81]. Specifically, age, female sex, and
BMI are independent predictors of disabling knee OA [82]. Persons with a BMI
>30 have a markedly increased risk for knee OA compared with those with a
more modest BMI (25–29) [83]. As a result of increases in both cardiac preload
and afterload, obesity may create a hypertensive effect and may also predispose
to heat illness in athletes as a result of impaired heat exchange.
The value of regular exercise for the prevention or management of obesity
cannot be overstated. Each encounter with the obese patient should take into
consideration the information noted above with regard to rising prevalence and
increasing concern about obesity-associated morbidity. Substantial work in the
area of exercise physiology now allows for a focused approach to obesity
management based on predictable responses to the prescribed interventions.
Even modest reductions in body weight (5%–10%) will significantly improve
health. Overweight individuals can realize substantial improvements in a number
of health parameters by achieving the minimum public health recommendation
for physical activity and by improving their level of cardiorespiratory fitness [84–
87]. Indeed, regular exercise participation is known to improve the health of all
participants, regardless of size [42,85,88–93]. Being physically active and fit
reduces obesity-related chronic diseases and decreases risk for early death. In a
large observational study, unfit men of normal weight actually had a higher all-
cause mortality than men who were fit but overweight (BMI >27.8) [94].
Although a combination of cardiovascular fitness and at least modest weight loss
is the goal for almost all overweight or obese patients, the pursuit of fitness even
in the absence of substantial weight loss is clearly beneficial and should be
aggressively sought. Normalization of body weight is also not necessary to allow
exercise to improve the health of obese individuals with bodyweight-related
metabolic disorders such as diabetes [88]. In the athlete population, a multifaceted
approach including dietary measures and training alterations should be under-
taken to positively influence body composition, especially in athletes with a BMI
>30 kg/m2.
Advice to eat a healthful diet and increase physical activity to enhance overall
energy expenditure and assist with gradual weight loss is appropriate for almost
all individuals who are above a healthy weight [95,96]. Longer duration, low-
intensity training (at 30%–50% VO2max) favors the utilization of adipose tissue
over muscle glycogen and thus fosters weight loss [97]. Intermittent bouts of
exercise provide largely the same benefit as continuous for obtaining weight loss;
this may be advantageous for those who dislike continuous exercise or perceive
barriers to continuous exercise. Exercise goals for these patients should include
the progression of overweight adults to 200 to 300 minutes of exercise per week
or expenditure of >2000kcal/week [98]. They should be progressed to higher
J.M. MacKnight / Clin Sports Med 22 (2003) 101–121 111
levels of exercise gradually over time, and a variety of behavioral strategies
should be used to facilitate adoption of this level of exercise. Setting a reasonable
goal of a 5% to 10% reduction in weight is appropriate because many diseases
clinically improve with weight loss in this range [99]. Maintenance of a regular
exercise program may be one of the best predictors of long-term weight control
[100,101]; data increasingly show that those able to continue exercising are able
to maintain body weight loss for many years [92,93,100,102–105]. An excellent
example of the success of such an approach is the National Weight Control
Registry, which tracks patients with reduced body weight for at least 1 year.
These studied individuals have maintained a minimum weight loss of 13.6 kg for
an average of 5 years. Their success is largely due to consuming only 1800 kcal/
day and expending about 400 kcal/day [106].
The most widely accepted, safe, and accessible means of increasing physical
activity for weight control is walking. It appears clear from previous study that
low-intensity endurance activities are capable of producing beneficial metabolic
effects that are similar to those produced with high-intensity exercise. The
clinician should focus on improvements in the metabolic profile rather than on
weight loss alone, and a realistic goal of 0.5 to 1 pound per week of weight loss
should be set and actively sought. Little benefit has been derived from resistance
training for absolute weight loss [107–111].
By aggressively addressing overweight and obesity as major negative factors
for the overall health of our patients, sports medicine-oriented physicians may
foster vital changes in the management of this population. With obesity’s
associated comorbidities, few conditions should be viewed as more urgent in
their management.
Dyslipidemia
Dyslipidemia is a common clinical entity worldwide. Although experts now
largely view the ‘‘conservative’’ measures of diet, weight loss, and exercise as
adjuncts to powerful pharmacotherapy in the management of elevated lipids, data
do demonstrate a positive effect of exercise on the lipid profile. Even a single
exercise session has been shown to acutely reduce triglycerides (TG) and increase
high-density lipoprotein (HDL) cholesterol [32]. A number of physiologic
characteristics must be taken into consideration when assessing the potential
effects of exercise on elevated lipids. Key patient-related factors include the
baseline physical fitness of the subjects, subjects’ pre-exercise lipid levels, and the
intensity and duration of exercise performed [32]. Primary care physicians and
sports medicine practitioners should feel comfortable with the rationale for the use
and prescription of exercise activity for the control of dyslipidemic patients.
Similarly, it is also essential to feel comfortable managing elevated lipids in
athletes and highly active individuals in the face of continued participation.
The acute effects of exercise on lipids are greatest with respect to its HDL-
elevating properties. HDL has been found to increase 4% to 43% in various studies
J.M. MacKnight / Clin Sports Med 22 (2003) 101–121112
[112–122], and these changes have been seen in both moderately fit [114,122] and
highly trained [117] subjects. They have been reported after expenditures of 350
to 400 and 1000 kcal, respectively, in a single exercise session. A reduction in TG
also occurs 18 to 24 hours after an acute bout of exercise and persists for up to
72 hours [112–122]. This effect is greatest in those with the highest pre-exercise
TG values [115], and does not appear to require a threshold of exertion to be
demonstrated [116].
Single exercise sessions can also reduce postprandial lipemia, and in so doing,
reduce the risk of coronary artery disease (CAD). The magnitude of this risk
reduction is related to total energy expenditure rather than exercise intensity.
Acute reductions in total cholesterol are much more difficult, requiring very
prolonged exercise with a large amount of energy expenditure (>1100 kcal)
[117,123]. A number of studies, in fact, have shown no acute exercise-induced
change in plasma total cholesterol levels [124–130]. Low-density lipoprotein
(LDL) may also acutely decrease, but the changes are modest, with declines of
only 5% to 8% in hypercholesterolemic men [114,115,119]. No acute effects on
apolipoprotein subset levels have been demonstrated [123,131–135].
When evaluating the chronic effects of exercise, endurance athletes provide
the largest group for analysis. As a result of their high level of fitness, endurance
athletes have serum HDL cholesterol concentrations 10 to 20 mg/dL or 40% to
50% higher than their sedentary counterparts [120,136–138]. Their triglyceride
levels are 20% lower, and LDL cholesterol concentrations are approximately 5%
to 10% lower as well [120,136,137]. Untrained individuals are generally
incapable of the exertion required to foster these lipid adaptations, thus dem-
onstrating the importance of developing aerobic fitness to maximize the lipid-
lowering effect [32].
Our present understanding of the physiologic changes that occur in lipid
metabolism in the face of exercise supports the concept that frequent repetition of
isolated exercise sessions produces long-term adaptations in lipid metabolism.
Endurance exercise reduces TG and increases HDL, and these effects are likely
related to total energy expenditure and to baseline TG concentration
[126,139,140]. Ferguson et al [117] found that lipoprotein lipase (LPL) activity
was increased in trained runners 24 hours after treadmill running at 70% VO2max
with an energy expenditure >1100 kcal. Such exercise is of sufficient volume and
intensity to deplete intramuscular triglyceride stores and increase LPL muscle
production and release, with a positive effect on lipid metabolism.
Exercise cessation studies confirm that higher HDL levels in very active
individuals are not due solely to acute exercise effects [32]. Rather, HDL responds
to aerobic training and increases by 2 to 8 mg/dL in a dose-dependent fashion, with
increased energy expenditure over time [126,141–143]. Wood et al [144] reported
that the beneficial effects of training on HDL elevation are seen at 12 weeks or
more and not seen at 10 weeks or less. Increased training volume predictably
yielded greater results [126,130,142,143,145,146]. Wood et al [147] also
combined caloric restriction and exercise training and found greater resultant
body composition and HDL changes. In the Health, Risk Factors, Exercise
J.M. MacKnight / Clin Sports Med 22 (2003) 101–121 113
Training andGenetics (HERITAGE) Family Study [148], 200menwere enrolled in
a 20-week endurance training program to study exercise effects on lipid metabol-
ism. A variety of triglyceride and HDL cholesterol patient subsets were followed.
Regular endurance exercise training was found to be particularly helpful in men
with low HDL cholesterol, elevated TGs, and central/abdominal obesity.
Data regarding the effects of chronic exercise on LDL and total cholesterol
lowering are less definitive. Prolonged exercise generally produces small reduc-
tions in LDL; the decrease in males has been shown to be approximately 8% [135].
The addition of physical activity to a modestly weight reducing, low-fat diet does
significantly enhance the LDL-lowering effect of the diet [149]. For a reduction in
plasma total cholesterol to occur with chronic exercise, a reduction in body
weight, body fat, or dietary fat must accompany the exercise training program.
In a meta-analysis by Halbert, et al [150], 31 trials were assessed, including
1833 previously sedentary hyperlipidemic and normolipidemic patients. Regular
aerobic exercise resulted in small but statistically significant decreases in TC,
LDL, TG and an increase in HDL. A comparison of intensities of training gave
inconsistent results, but more frequent exercise did not appear to result in greater
improvements in the lipid profile than exercise three times per week. The effects
of resistance training were also inconclusive in this study, although most data find
no consistent benefit from resistance training in lowering lipoprotein levels.
Of special note, in athletes with dyslipidemia severe enough to warrant therapy,
the use of statin lipid-lowering agents presents special concerns to the treating
physician. In addition to symptomatic muscle complaints that may arise with statin
use, these athletes may also develop asymptomatic elevations of creatine phos-
phokinase (CPK). Elevations in CPK may be further exacerbated by eccentric
exercise. Although elevations up to 21,000 U/L are generally tolerated without
sequelae, rarely athletes will develop frank rhabdomyolysis with vigorous exer-
cise. The risk for such a significant complication is raised by dehydration and the
concomitant use of statins with fibric acid derivatives, niacin, macrolide anti-
biotics, and azole derivative antifungals.
Few of the elite caliber athletes that sports medicine physicians care for have
significant dyslipidemia. Many of our patients who are attempting to manage one
if not several major risk factors for cardiovascular disease do suffer with
dyslipidemia, however, and are being counseled to exercise regularly. An
understanding of the response of lipids to both acute and chronic exercise is
essential to guiding patients toward appropriate decisions in the management of
dyslipidemia. Sport and exercise activities can be safely continued, as no large-
scale studies exist to suggest that patients with dyslipidemia are at increased risk
for adverse cardiovascular events as a result of their exercise activities.
References
[1] Wolz M, Cutler J, Roccella EJ, et al. Statement from the National High Blood Pressure
Education Program: prevalence of hypertension. Am J Hypertens 2000;13:103–4.
[2] Kaplan NM, Deveraux RB, Miller Jr HS. 26th Bethesda conference: recommendations for de-
J.M. MacKnight / Clin Sports Med 22 (2003) 101–121114
termining eligibility for competition in athletes with cardiovascular abnormalities. Task Force 4:
systemic hypertension. Med Sci Sports Exerc 1994;26:S268–70.
[3] The sixth report of the Joint National Committee on Prevention. Detection, Evaluation, and
Treatment of High Blood Pressure (JNC VI). Arch Intern Med 1997;157(21):2413–46.
[4] Duncan JJ, Farr JE, Upton SJ, et al. The effects of aerobic exercise on plasma catechol-
amines and blood pressure in patients with mild essential hypertension. JAMA 1985;254(18):
2609–13.
[5] Pickering TG. Pathophysiology of exercise hypertension. Herz 1987;12(2):119–24.
[6] He J, Whelton PK. Elevated systolic blood pressure and risk of cardiovascular and renal
disease: overview of evidence from observational epidemiologic studies and randomized con-
trolled trials. Am Heart J 1999;138:211–9.
[7] American Heart Association. 2000 Heart and stroke statistical update. Dallas (TX): American
Heart Association; 1999.
[8] Whelton PK, He J. Blood pressure reduction. In: Hennekens CH, Buring JE, Manson JE, et al,
editors. Clinical trials in cardiovascular disease. Philadelphia: WB Saunders; 1999. p. 341–60.
[9] Kenney MJ, Seals DR. Postexercise hypotension: key features, mechanisms, and clinical sig-
nificance. Hypertension 1993;22:653–64.
[10] Kaul J, Chrastek J, Adamirova J. The hypotensive effect of physical activity. In: Rabb W, editor.
Prevention of ischemic heart disease: principles and practice. Springfield (IL): Charles C Tho-
mas; 1966. p. 359–71.
[11] Hagberg JM, Brown MD. Does exercise training play a role in the treatment of essential
hypertension? J Cardiovasc Risk 1995;2:296–302.
[12] Pescatello LS, Fargo AE, Leach CN, et al. Short-term effect of dynamic exercise on arterial
blood pressure. Circulation 1991;83:1557–61.
[13] Pescatello LS, Miller BE, Danias PG, et al. Dynamic exercise normalizes resting blood pressure
in mildly hypertensive premenopausal women. Am Heart J 1999;138:916–21.
[14] Taylor-Tolbert NS, Dengel DR, Brown MD, et al. Ambulatory blood pressure after acute
exercise in older men with essential hypertension. Am J Hypertens 2000;13:44–51.
[15] Fagard RH. Physical activity in the prevention and treatment of hypertension in the obese. Med
Sci Sports Exerc 1991;31:S624–30.
[16] Fagard RH, Tipton CM. Physical activity, fitness and hypertension. In: Bouchard C, Shephard
RJ, Stephens T, editors. Physical activity, fitness and health. Champaign (IL): Human Kinetics;
1994. p. 633–55.
[17] Halbert JA, Silagy CA, Finucane P, et al. The effectiveness of exercise training in lowering
blood pressure: a meta-analysis of randomized controlled trials of 4 weeks or longer. J Hum
Hypertens 1997;11:641–9.
[18] Whelton SP, Chin A, Xin X, et al. Effect of aerobic exercise on blood pressure: a meta-analysis
of randomized, controlled trials. Ann Intern Med 2002;136:493–503.
[19] American College of Sports Medicine position stand. Physical activity, physical fitness, and
hypertension. Med Sci Sports Exerc 1993;25(10):i –x.
[20] Jennings GL, Deakin G, Korner P, et al. What is the dose-response relationship between
exercise training and blood pressure? Ann Med 1991;23:313–8.
[21] Meredith IT, Jennings GL, Esler MD, et al. Time-course of the antihypertensive and autonomic
effects of regular endurance exercise in human subjects. J Hypertens 1990;8:859–66.
[22] Braith RW, Pollock ML, Lowenthal DT, et al. Moderate- and high-intensity exercise lowers
blood pressure in normotensive subjects 60 to 79 years of age. Am J Cardiol 1994;73:1124–8.
[23] Cox KL, Puddey IB, Burke V, et al. Determinants of change in blood pressure during S.W.E.A.T.:
the sedentary women exercise adherence trial. Clin Exp Pharmacol Physiol 1996;23:567–9.
[24] Duncan JJ, Gordon NF, Scott CB. Women walking for health. JAMA 1991;266:3295–9.
[25] Fagard RH. Exercise characteristics and the blood pressure response to dynamic physical
training. Med Sci Sports Exerc 2001;33(Suppl 6):S484–92.
[26] Gettman LR, Pollock ML, Durstine JL, et al. Physiological responses of men to 1, 3, and 5 day
per week training programs. Res Q 1976;47:638–45.
J.M. MacKnight / Clin Sports Med 22 (2003) 101–121 115
[27] Jennings G, Nelson L, Nestel P, et al. The effects of changes in physical activity on major
cardiovascular risk factors, hemodynamics, sympathetic function, and glucose utilization in
man: a controlled study of four levels of activity. Circulation 1986;73:30–40.
[28] Moreira WD, Fuchs FD, Ribeiro JP, et al. The effects of two aerobic training intensities on
ambulatory blood pressure in hypertensive patients: results of a randomized trial. J Clin Epi-
demiol 1999;52:637–42.
[29] Nelson L, Esler MD, Jennings GL, et al. Effect of changing levels of physical activity on blood
pressure and haemodynamics in essential hypertension. Lancet 1986;2:473–6.
[30] Rogers MW, Probst MM, Gruber JJ, et al. Differential effects of exercise training intensity
on blood pressure and cardiovascular responses to stress in borderline hypertensive humans.
J Hypertens 1996;14:1369–75.
[31] Arroll B, Beaglehole R. Does physical activity lower blood pressure: a critical review of the
clinical trials. J Clin Epidemiol 1992;45(5):439–47.
[32] Thompson PD, Crouse SF, Goodpaster B, et al. The acute versus the chronic response to
exercise. Med Sci Sports Exerc 2001;33(6):S438–45.
[33] Hagberg JM, Ehsani AA, Goldring D, et al. Effect of weight training on blood pressure and
hemodynamics in hypertensive adolescents. J Pediatr 1984;104(1):147–51.
[34] Harris KA, Holly RG. Physiological response to circuit weight training in borderline hyper-
tensive subjects. Med Sci Sports Exerc 1987;19(3):246–52.
[35] Tanji JL. Exercise and the hypertensive athlete. Clin Sports Med 1992;11(2):291–302.
[36] Kaplan NM. Clinical Hypertension. 5th edition. Baltimore: Williams & Wilkins; 1990. p. 3–5,
17,138,149–53,165–71.
[37] Klaus D. Management of hypertension in actively exercising patients: implications for drug
selection. Drugs 1989;37(2):212–8.
[38] Maron BJ, Epstein SE, Roberts WC. Causes of sudden death in competitive athletes. J Am Coll
Cardiol 1986;7(1):204–14.
[39] Maron BJ, Shirani J, Mueller FO, et al. Cardiovascular causes of ‘‘athletic field’’ deaths:
analysis of sudden death in 84 competitive athletes, abstracted. Circulation 1993;88(suppl 1):
1–50.
[40] Sharper AG, Wannamethee G, Walker M. Physical activity, hypertension and risk of heart
attack in men without evidence of ischaemic heart disease. J Hum Hypertens 1994;8(1):3–10.
[41] Gallagher D, Visser M, Sepulveda D, et al. How useful is body mass index for comparison of
body fatness across age, sex, and ethnic groups? Am J Epidemiol 1996;143:228–39.
[42] National Heart, Lung, and Blood Institute Obesity Education Initiative Expert Panel. Clinical
guidelines on the identification, evaluation, and treatment of overweight and obesity in adults:
the evidence report. Obes Res 1998;6(Suppl):51S–209S.
[43] Flegal KM, Carroll MD, Kuczmarski RJ, et al. Overweight and obesity in the United States:
prevalence and trends, 1960–1994. Int J Obes 1998;22:39–47.
[44] Hill JO, Melanson EL. Overview of the determinants of overweight and obesity: current
evidence and research issues. Med Sci Sports Exerc 1999;31(11):S515–21.
[45] Bouchard C, Despres JP, Mauriege P. Genetic and nongenetic determinants of regional fat
distribution. Endocr Rev 1993;14:72–93.
[46] National Institutes of Health. Clinical guidelines on the identification, evaluation, and treatment
of overweight and obesity in adults—the evidence report. Obes Res 1998;2(Suppl):51S–209S.
[47] Bouchard C, Tremblay A, Nadeau A, et al. Genetic effect in resting and exercise metabolic
rates. Metabolism 1989;38:364–70.
[48] Rice T, Tremblay A, Deriaz O, et al. Genetic pleiotropy for resting metabolic rate with fat-free
mass and fat mass: the Quebec Family Study. Obes Res 1996;4:125–31.
[49] Goran MI, Carpenter WH, McGloin A, et al. Energy expenditure in children of lean and obese
parents. Am J Physiol 1995;268:E917–24.
[50] Seidell JC, Muller DC, Sorkin JD, et al. Fasting respiratory exchange ratio and resting meta-
bolic rate as predictors of weight gain: the Baltimore Longitudinal Study on Aging. Int J Obes
1992;16:667–74.
J.M. MacKnight / Clin Sports Med 22 (2003) 101–121116
[51] Weinsier RL, Nelson KM, Hensrud DD, et al. Metabolic predictors of obesity: contribution of
resting energy expenditure, thermic effect of food, and fuel utilization to four-year weight gain
of post-obese and never-obese women. J Clin Invest 1995;95:980–5.
[52] Poirier P, Despres JP. Exercise in weight management of obesity. Cardiol Clin 2001;19(3):
459–70.
[53] Coppack SW, Jensen MD, Miles JM. In vivo regulation of lipolysis in humans. J Lipid Res
1994;35:177–93.
[54] Anonymous. Prevalence of leisure-time physical activity among overweight adults—United
States, 1998. MMWR 2000;49:326–30.
[55] French SA, Jeffery RW, Forster JL, et al. Predictors of weight change over two years among a
population of working adults: the Healthy Worker Project. Int J Obes 1994;18:145–54.
[56] Slattery ML, McDonald A, Bild DE, et al. Associations of body fat and its distribution with
dietary intake, physical activity, alcohol, and smoking in blacks and whites. Am J Clin Nutr
1992;55:943–9.
[57] Williamson DF, Madans J, Anda RF. Recreational physical activity and ten-year weight change
in a US national cohort. Int J Obes 1993;17:279–86.
[58] Rissanen AM, Heliovaara M, Knekt P, et al. Determinants of weight gain and overweight in
adult Finns. Eur J Clin Nutr 1991;45:419–30.
[59] Klein S, Peters EJ, Shangraw RE, et al. Lipolytic response to metabolic stress in critically ill
patients. Crit Care Med 1991;19:776–9.
[60] Klein S, Wolfe RR. Carbohydrate restriction regulates the adaptive response to fasting. Am J
Physiol 1992;262:E631–6.
[61] Arner P. Impact of exercise on adipose tissue metabolism in humans. Int J Obes Relat Metab
Disord 1995;19(Suppl 4):S18–21.
[62] Bray GA. In defense of a body mass index of 25 as the cut-off point for defining overweight.
Obes Res 1998;6:461–2.
[63] Barrett-O’Connor EL. Obesity, atherosclerosis, and coronary artery disease. Ann Intern Med
1985;103:1010–9.
[64] Drenick EJ, Bale GS, Seltzer F, et al. Excessive mortality and causes of death in morbidly obese
men. JAMA 1980;243:443–5.
[65] Dyer AR, Elliott P. The INTERSALT study: relations of body mass index to blood pressure.
INTERSALT Cooperative Research Group. J Hum Hypertens 1989;3:299–308.
[66] Hoffmans MD, Kromhout D, De Lezenne Coulander C. The impact of body mass index of
78,612 18-year-old Dutch men on 32-year mortality from all causes. J Clin Epidemiol 1988;41:
749–56.
[67] Larsson B, Bjorntorp P, Tibblin G. The health consequences of moderate obesity. Int J Obes
1981;5:97–116.
[68] Lew EA, Garfinkel L. Variations in mortality by weight among 750,000 men and women.
J Chron Dis 1979;32:563–76.
[69] Sharper AG, Wannamethee SG, Walker M. Body weight: implications for the prevention of
coronary heart disease, stroke, and diabetes mellitus in a cohort study of middle aged men. BMJ
1997;314:1311–7.
[70] Willett WC, Browne ML, Bain C, et al. Relative weight and risk of breast cancer among
premenopausal women. Am J Epidemiol 1985;122:731–40.
[71] Ashley FW, Kannel WB. Relation of weight change to changes in atherogenic traits: the
Framingham Study. J Chron Dis 1974;27:103–14.
[72] Hershcopf RJ, Elahi D, Andres R, et al. Longitudinal changes in serum cholesterol in man: an
epidemiological search for an etiology. J Chron Dis 1982;35:101–14.
[73] Shekelle RB, Shryock AM, Paul O, et al. Diet, serum cholesterol, and death from coronary
heart disease: the Western Electric Study. N Engl J Med 1981;304:65–70.
[74] Haffner SM, Mitchell BD, Hazuda HP, et al. Greater influence of central distribution of adipose
tissue on incidence of non-insulin-dependent diabetes in women than men. Am J Clin Nutr
1991;53:1312–7.
J.M. MacKnight / Clin Sports Med 22 (2003) 101–121 117
[75] Van Hallie TB. Health implications of overweight and obesity in the United States. Ann Intern
Med 1985;103:983–8.
[76] Colditz GA, Willett WC, Stampfer MJ, et al. Weight as a risk factor for clinical diabetes in
women. Am J Epidemiol 1990;132:501–13.
[77] Kissebah AH, Krakower GR. Regional adiposity and morbidity. Physiol Rev 1994;74:
761–811.
[78] Colditz GA, Willett WC, Rotnitzky A, et al. Weight gain as a risk factor for clinical diabetes
mellitus in women. Ann Intern Med 1995;122:481–6.
[79] Calle EE, Thun MJ, Petrelli JM, et al. Body-mass index and mortality in a prospective cohort of
U.S. adults. N Engl J Med 1999;341:1097–105.
[80] Felson DT. Does excess weight cause osteoarthritis and, if so, why? Ann Rheum Dis 1996;55:
668–70.
[81] Hochberg MC, Lethbridge-Cejku M, Scott WW, et al. The association of body weight, body
fatness, and body fat distribution with osteoarthritis of the knee: data from the Baltimore
Longitudinal Study of Aging. J Rheumatol 1995;22:488–93.
[82] Eckel RH. Obesity in heart disease. Circulation 1997;96:3248–50.
[83] Anderson JJ, Felson DT. Factors associated with osteoarthritis of the knee in the first
National Health and Nutrition Examination Survey (NHANES I): evidence for an associ-
ation with overweight, race, and physical demands of work. Am J Epidemiol 1988;128:
179–89.
[84] Jakicic JM, Clark K, Coleman E, et al. ACSM position stand on the appropriate intervention
strategies for weight loss and prevention of weight regain for adults. Med Sci Sports Exerc
2001;33(12):2145–56.
[85] Barlow CE, Kohl III HW, Gibbons LW, et al. Physical activity, mortality, and obesity. Int J Obes
1995;19:S41–4.
[86] Lee CD, Jackson AS, Blair SN. US weight guidelines: is it also important to consider cardior-
espiratory fitness? Int J Obes 1998;22(Suppl 2):S2–7.
[87] Wei MJ, Kampert K, Barlow CE, et al. Relationship between low cardiorespiratory fitness and
mortality in normal-weight, overweight, and obese men. JAMA 1999;282:1547–53.
[88] Lamarche B, Despres JP, Pouliot MC, et al. Is body fat loss a determinant factor in the
improvement of carbohydrate and lipid metabolism following aerobic exercise training in obese
women? Metabolism 1992;41:1249–56.
[89] Miller WC, Lindeman AK. The role of diet and exercise in weight management. In: Dalton S,
editor. Overweight and weight management: the health professional’s guide to understanding
and practice. Gaithersburg (MD): Aspen Publishers; 1997. p. 405–38.
[90] National Heart, Lung, and Blood Institute. Clinical guidelines on the identification, evaluation,
and treatment of overweight and obesity in adults. Bethesda (MD): National Heart, Lung, and
Blood Institute; 1998.
[91] Shape Up America. American Obesity Association. Guidance for treatment of adult obesity.
Bethesda (MD): Shape Up America; 1996.
[92] Westerterp KR. Obesity and physical activity. Int J Obes 1999;23(Suppl 1):59–64.
[93] Wing R. Physical activity in the treatment of adulthood overweight and obesity: current
evidence and research issues. Med Sci Sports Exerc 1999;31(Suppl.):S547–52.
[94] Lee CD, Blair SN, Jackson AS. Cardiorespiratory fitness, body composition, and all-cause and
cardiovascular disease mortality in men. Am J Clin Nutr 1999;69:373–80.
[95] Miller WC. Effective diet and exercise treatments for overweight and recommendations for
intervention. Sports Med 2001;31(10):717–24.
[96] National Task Force on the Prevention and Treatment of Obesity. Overweight, obesity, and
health risk. Arch Intern Med 2000;160:898–904.
[97] Grubbs L. The critical role of exercise in weight control. Nurse Pract 1993;18:20–9.
[98] Jakicic JM, Winters C, Lang W, et al. Effects of intermittent exercise and use of home exercise
equipment on adherence, weight loss, and fitness in overweight women: a randomized trial.
JAMA 1999;282:1554–60.
J.M. MacKnight / Clin Sports Med 22 (2003) 101–121118
[99] Wadden TA. New goals of obesity treatment: a healthier weight and other ideals. Prim Psy-
chiatry 1998;5:45–54.
[100] Miller WC, Koceja DM, Hamilton EJ. A meta-analysis of the past 25 years of weight loss
research using diet, exercise, or diet plus exercise intervention. Int J Obes 1997;21:941–7.
[101] Pronk NP, Wing RR. Physical activity and long-term maintenance of weight loss. Obes Res
1994;2:587–99.
[102] Cowburn G, Hillsdon M, Hankey CR. Obesity management by lifestyle strategies. Br Med Bull
1997;53:389–408.
[103] Harris JE. The role of physical activity in the management of obesity. J Am Osteopath Assoc
1999;99(Suppl 4):S15–9.
[104] Rippe JM, Hess S. The role of physical activity in the prevention and management of obesity.
J Am Diet Assoc 1998;98(Suppl 2):S31–3.
[105] Votruba SB, Horvitz MA, Schoeller DA. The role of exercise in the treatment of obesity.
Nutrition 2000;16:179–88.
[106] Klem ML, Wing RR, McGuire MT, et al. A descriptive study of individuals successful at long-
term weight loss. Am J Clin Nutr 1997;66:239–46.
[107] Ballor DL, Katch VL, Becque MD, et al. Resistance weight training during caloric restriction
enhances lean body weight maintenance. Am J Clin Nutr 1988;47:19–25.
[108] Geliebter A, Maher MM, Gerace L, et al. Effects of strength or aerobic training on body
composition, resting metabolic rate, and peak oxygen consumption in obese dieting subjects.
Am J Clin Nutr 1997;66:557–63.
[109] Kraemer WJ, Volek JS, Clark KL, et al. Physiological adaptations to a weight-loss dietary
regimen and exercise programs in women. J Appl Physiol 1997;83:270–9.
[110] Kraemer WJ, Volek JS, Clark KL, et al. Influence of exercise training on physiological and
performance changes with weight loss in men. Med Sci Sports Exerc 1999;31:1320–9.
[111] Sweeney ME, Hill JO, Heller PA, et al. Severe vs moderate energy restriction with and without
exercise in the treatment of obesity: efficiency of weight loss. Am J Clin Nutr 1993;57:127–34.
[112] Bounds RG, Martin SE, Grandjean PW, et al. Diet and short term plasma lipoprotein-lipid
changes after exercise in trained men. Int J Sport Nutr Exerc Metab 2000;10:114–27.
[113] Carlson LA, Mossfeldt F. Acute effects of prolonged, heavy exercise on the concentration of
plasma lipids and lipoproteins in man. Acta Physiol Scand 1964;62:51–9.
[114] Crouse SF, O’Brien BC, Grandjean PW, et al. Effects of training and a single session of exercise
on lipids and apolipoproteins in hypercholesterolemic men. J Appl Physiol 1997;83:2019–28.
[115] Crouse SF, O’Brien BC, Rohack JJ, et al. Changes in serum lipids and apolipoproteins after
exercise in men with high cholesterol: influence of intensity. J Appl Physiol 1995;79:279–86.
[116] Cullinane E, Siconolfi S, Saritelli A, et al. Acute decrease in serum triglycerides with exercise:
is there a threshold for an exercise effect? Metabolism 1982;31:844–7.
[117] Ferguson MA, Alderson NL, Trost S, et al. Effects of four different exercise volumes on
HDL-C and lipoprotein lipase. J Appl Physiol 1998;85(3):1169–74.
[118] Foger B, Wohlfarter T, Ritsch A, et al. Kinetics of lipids, apolipoproteins, and cholesteryl ester
transfer protein in plasma after a bicycle marathon. Metabolism 1994;43:633–9.
[119] Grandjean PW, Crouse SF, Rohack JJ. Influence of cholesterol status on blood lipid and lip-
oprotein enzyme responses to aerobic exercise. J Appl Physiol 2000;89:472–80.
[120] Sady SP, Cullinane EM, Saritelli A, et al. Elevated HDL cholesterol in endurance athletes is
related to enhanced plasma triglyceride clearance. Metabolism 1988;37:568–72.
[121] Thompson PD, Cullinane E, Henderson L, et al. Acute effects of prolonged exercise on serum
lipids. Metabolism 1980;29:662–5.
[122] Visich PS, Goss FL, Gordon PM, et al. Effects of exercise with varying energy expenditure on
high-density lipoprotein-cholesterol. Eur J Physiol 1996;72:242–8.
[123] Kantor MA, Cullinane EM, Herbert PN, et al. Acute increase in lipoprotein lipase following
prolonged exercise. Metabolism 1984;33(5):454–7.
[124] Holloszy JO, Skinner JS, Toro G, et al. Effects of a six month program of endurance exercise on
lipids of middle-age men. Am J Cardiol 1964;14:753–60.
J.M. MacKnight / Clin Sports Med 22 (2003) 101–121 119
[125] Huttunen JK, Lansimies E, Voutilainen E, et al. Effect of moderate physical exercise on serum
lipoproteins: a controlled clinical trial with special reference to serum high-density lipoproteins.
Circulation 1979;60(6):1220–9.
[126] Kokkinos PF, Holland JC, Narayan P, et al. Miles run per week and high-density lipoprotein
cholesterol levels in healthy, middle-aged men. Arch Intern Med 1995;155:415–20.
[127] Marti B, Suter E, Riesen WF, et al. Effects of long-term, self-monitored exercise on the serum
lipoprotein and apolipoprotein profile in middle-aged men. Atherosclerosis 1990;81:19–31.
[128] Seip RL, Mair K, Cole TG, et al. Exercise training decreases plasma cholesteryl ester transfer
protein. Arterioscler Thromb 1993;13:1359–67.
[129] Thompson PD, Yurgalevitch SM, Flynn MM, et al. Effect of prolonged exercise training
without weight loss on high-density lipoprotein metabolism in overweight men. Metabolism
1997;46:217–23.
[130] Wood PD, Haskell WL, Blair SN, et al. Increased exercise level and plasma lipoprotein con-
centrations: a one-year randomized, controlled study in sedentary middle-aged men. Metabolism
1983;32(1):31–9.
[131] Annuzzi G, Jansson E, Kaijser L, et al. Increased removal rate of exogenous trigylcerides after
prolonged exercise in men: time course and effects of exercise duration. Metabolism 1987;36(5):
438–43.
[132] Davis PG, Bartoli WP, Durstine JL. Effects of acute exercise intensity on plasma lipids and
apolipoproteins in trained runners. J Appl Physiol 1992;72(3):914–9.
[133] Durstine JL, Ferguson MA, Szymanski LM, et al. Effect of a single session of exercise on
lipoprotein(a). Med Sci Sports Exerc 1996;28(10):1277–81.
[134] Kleins L, Miller TD, Radam TE, et al. Acute physical exercise alters apolipoprotein E and C–III
concentrations of apo E-rich very low density lipoprotein fraction. Atherosclerosis 1992;97:
37–51.
[135] Sady SP, Thompson PD, Cullinane EM, et al. Prolonged exercise augments plasma triglyceride
clearance. JAMA 1986;256:2552–5.
[136] Thompson PD, Cullinane EM, Sady SP, et al. HDL metabolism in endurance athletes and
sedentary men. Circulation 1991;84:140–52.
[137] Thompson PD, Lazarus B, Cullinane E, et al. Exercise, diet or physical characteristics as
determinants of HDL-levels in endurance athletes. Atherosclerosis 1983;46:333–9.
[138] Wood PD, Haskell W, Klein H, et al. The distribution of plasma lipoproteins in middle-aged
male runners. Metabolism 1976;25:1249–57.
[139] Grandjean PW, Crouse SF, O’Brian BC, et al. The effects of menopausal status and exercise
training on serum lipids and the activities of intravascular enzymes related to lipid transport.
Metabolism 1998;47(4):377–83.
[140] Kokkinos PF, Narayan P, Colleran J. Effects of moderate intensity exercise on serum lipids in
African-American men with severe systemic hypertension. Am J Cardiol 1998;81:732–5.
[141] Durstine JL, Haskell WL. Effects of exercise training on plasma lipids and lipoproteins. Exerc
Sport Sci Rev 1994;22:447–521.
[142] Durstine JL, Pate RR, Sparling PB, et al. Lipid, lipoprotein, and iron status of elite women
distance runners. Int J Sports Med 1987;8:119–23.
[143] Williams PT. Relationship of distance run per week to coronary heart disease risk factors
in 8283 male runners: The National Runners’ Health Study. Arch Intern Med 1997;157:
191–8.
[144] Wood PD, Williams PT, Haskell WL, et al. Physical activity and high density lipoproteins.
In: Miller NE, Miller GJ, editors. Clinical and metabolic aspects of high-density lipoproteins.
Amsterdam: Elsevier; 1984. p. 133–65.
[145] Goodyear LJ, Fronsoe MS, Van Houten DR, et al. Increased HDL-cholesterol following eight
weeks of progressive training in female runners. Annals of Sports Medicine 1986;3:32–7.
[146] Tran ZV, Weltman A, Glass GV, et al. The effects of exercise on blood lipids and lipoproteins:
A meta-analysis of studies. Med Sci Sports Exerc 1983;15(5):393–402.
[147] Wood PD, Stefanick ML, Williams PT, et al. The effects on plasma lipoproteins of a prudent
J.M. MacKnight / Clin Sports Med 22 (2003) 101–121120
weight-reducing diet, with or without exercise, in overweight men and women. N Engl J Med
1991;325:461–6.
[148] Couillard C, Despres JP, Lamarche B, et al. Effects of endurance exercise training on plasma
HDL cholesterol levels depend on levels of triglycerides: evidence from men of the Health, Risk
Factors, Exercise Training and Genetics (HERITAGE) family study. Arterio Thromb & Vascular
Biol 2001;21(7):1226–32.
[149] Grundy SM, Blackburn G, Higgins M, et al. Physical activity in the prevention and treatment of
obesity and its comorbidities. Med Sci Sports Exerc 1999;31(Suppl 1):502–8.
[150] Halbert JA, Silagy CA, Finucane P, et al. Exercise training and blood lipids in hyperlipidemic
and normolipidemic adults: a meta-analysis of randomized, controlled trials. Euro J Clin Nu-
trition 1999;53(7):514–22.
J.M. MacKnight / Clin Sports Med 22 (2003) 101–121 121