Exercise considerations in hypertension, obesity, and

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,

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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.


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,


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.


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.


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


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%


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


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


[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


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.

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