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Hypertension in Athletes and Active Patients

Tailoring Treatment to the Patient

John M. MacKnight, MD

Internal Medicine Series Editor: Donald M. Christie Jr, MD

THE PHYSICIAN AND SPORTSMEDICINE - VOL 27 - NO. 4 - APRIL 99


In Brief: Understanding the hemodynamic responses to exercise in normotensive and hypertensive persons allows physicians to effectively treat hypertension in active people and athletes. If lifestyle modifications such as weight loss and moderation of sodium intake along with continued exercise are not effective, drug therapy can be added. Nonselective beta-blockers and diuretics may impair performance; cardioselective beta-1 blockers, ACE inhibitors, calcium channel blockers, and alpha-1 blockers are less likely to hinder exercise. Therapy tailored to the type and intensity of a patient's exercise and the stage of hypertension may allow him or her to participate safely without compromising performance.

Hypertension is one of the most common medical problems in today's patients and the most common cardiovascular condition in competitive athletes (1). Consequently, primary care physicians often manage hypertension in active patients and athletes. A thorough understanding of the pathophysiology of the condition, especially as it relates to the effects of exercise, can help physicians recommend the most effective pharmacologic and nonpharmacologic therapies. Skillful management of blood pressure can help hypertensive patients continue to exercise and compete safely, while guarding against the development of long-term complications.

Pathophysiology

About 95% of hypertensive individuals have essential hypertension that has no identifiable cause. These people seem to develop pathologic elevations in blood pressure because of an increase in total peripheral resistance, which is probably mediated by plasma epinephrine and norepinephrine (2) in conjunction with effects from the kidneys and the renin-angiotensin system. In the other 5% of cases, one of several secondary causes may be implicated (table 1).


Table 1. 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)


Chronic pressure overload and microvascular trauma are the major causes of hypertension's end-organ pathology. Sustained high blood pressure significantly raises the risk of coronary artery disease and left ventricular (LV) hypertrophy, with the consequent increased risk of cardiac morbidity and mortality, heart failure, and sudden cardiac death. Other hypertension-related disorders include cerebrovascular, retinovascular, peripheral arterial, and renal parenchymal diseases.

Hemodynamic Responses to Exercise

In normotensive people. Normal physiologic responses to exercise depend on whether the activity involves primarily dynamic or static exercise (table 2).


Table 2. Normal Hemodynamic Changes Related to Exercise

Hemodynamic Responses

Exercise Type Acute (During Exercise) Chronic

CO SV TPR HR VR SBP DBP       LVH LVF

Dynamic elevated elevated decreased elevated elevated elevated unaffected       eccentric normal
Static elevated unaffected unaffected elevated decreased greatly elevated elevated       concentric normal

CO = cardiac output
SV = stroke volume
TPR = total peripheral resistance
HR = heart rate
VR = venous return
SBP = systolic blood pressure
DBP = diastolic blood pressure
LVH = left ventricular hypertrophy
LVF = left ventricular function

In general, dynamic or isotonic exercise results in lower total peripheral resistance and greater systolic blood pressure (180 to 220 mm Hg) with little or no change in diastolic pressure. With increasing levels of cardiovascular conditioning, eccentric LV hypertrophy—manifested by a significant increase in LV diameter, lumen size, and mass—will develop without compromise in LV function (3).

Static or isometric exercise causes a rise in both systolic and diastolic pressures; systolic pressure may rise dramatically to more than twice baseline levels. In contrast to dynamic activity, however, static activity causes little or no change in total peripheral resistance. Over time, repetitive static exercise and the resultant marked increase in cardiac afterload lead to the development of concentric LV hypertrophy (3). As with dynamic exercise, LV diastolic function and cardiac output are preserved (4,5).

In hypertensive people. Dynamic and static exercise produce essentially the same hemodynamic responses in hypertensive persons, and these responses differ in some respects from those of normotensive individuals (table 3). The most important difference is that hypertensive patients generally demonstrate exercise-induced increases in total peripheral resistance. They also show increases in myocardial oxygen consumption, and impaired vasodilation with exercise may result in exaggerated blood pressure elevations (6).


Table 3. Differences in Hemodynamic Responses to Dynamic Exercise in Normotensive and Chronically Hypertensive Persons

Blood Pressure Status Hemodynamic Responses

Acute Chronic

CO TPR DBP LVH

Normotensive elevated decreased unaffected physiologic
Hypertensive decreased elevated unaffected or elevated pathologic

CO = cardiac output, TPR = total peripheral resistance, DBP = diastolic blood pressure, LVH = left ventricular hypertrophy

Over time, these abnormal responses may lead to pathologic LV hypertrophy, 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. The greater the degree of these abnormal responses to exercise, the greater the related pathologic hypertrophy and/or diastolic dysfunction.

An impaired vasodilatory response in hypertensive athletes may also make exercising in hot environments dangerous. If the body cannot dissipate heat properly, seriously elevated core temperatures, excessive water loss, and hypokalemia can result.

Diagnosis and Classification

The accurate diagnosis of hypertension depends on a comprehensive, systematic evaluation (table 4) (1,7). The main items include careful measurements of blood pressure; a thorough personal and family history; a physical examination with special attention to the cardiovascular system, kidneys, and thyroid; and appropriate laboratory and electrocardiographic tests.


Table 4. 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), nonsteroidal anti-inflammatories, or appetite suppressants or other stimulants (eg, ephedrine, ma huang)

Physical Examination (for Signs of End-organ Damage or Secondary 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


Once the diagnosis has been confirmed, the physician should use the diagnostic classifications of hypertension recommended by the Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VI) (7) (table 5) as the basis for selecting a treatment program and advising each patient about the appropriate type and level of sports participation.


Table 5. Classification of Blood Pressure in Adults (7)

Blood Pressure (mm Hg)

Category Systolic Diastolic

Optimal <120 <80
Normal <130 <85
High-normal* 130-139 85-89
Stage 1* HT 140-159 90-99
Stage 2* HT 160-179 100-109
Stage 3* HT >180 >110

*Elevated systolic or diastolic pressure alone is sufficient to meet the criterion; HT = hypertension.

Management

Several approaches can be helpful in controlling high blood pressure in active patients and athletes, including exercise, other lifestyle modifications, and medication. Nonpharmacologic therapy may be sufficient for controlling blood pressure in borderline or mildly hypertensive patients and should be used concomitantly even if medication is needed.

Exercise. 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. Patients who receive the most benefit are mildly hypertensive athletes, probably because exercise reduces sympathetic neural activity, leading to lower heart rate and cardiac output (2).

Moderate-intensity exercise in keeping with current American College of Sports Medicine (ACSM) guidelines (8) should be safe for most hypertensive patients and may contribute to blood pressure control. Data from over 40 studies indicate that low- to moderate-intensity endurance training (20 to 60 minutes at 40% to 70% of VO2 max 3 to 5 days per week) decreases systolic and diastolic blood pressures by about 10 mm Hg (8). The beneficial effects of moderate-intensity exercise on blood pressure are equal or superior to those of higher-intensity exercise (9), an important consideration in limiting the cardiovascular and musculoskeletal risks of exercise, particularly in older patients.

Even resistance training (8 to 10 major-muscle-group exercises two to three times per week), especially circuit weight training (10,11), may help lower blood pressure when the exercises are done at 40% to 50% of the patient's one-repetition maximum (12). However, resistance training is not recommended as the only approach to lowering blood pressure.

Lifestyle modifications. Even patients who exercise may also need to correct poor lifestyle habits to obtain optimal blood pressure control. Interventions that have proven to be beneficial are weight reduction if appropriate, moderation of alcohol and sodium intake, high potassium and increased calcium intake, and smoking cessation (13).

No convincing data support the use of increased magnesium intake, high-protein diets, other special dietary measures, relaxation techniques, or biofeedback in the prevention or control of hypertension (8).

Medication. 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 work capacity (14). The choice of pharmacologic agents is especially important in active patients and athletes because inappropriate medications can impair performance, while optimal choices can enhance it by reducing elevated blood pressure at rest and thus limiting exercise-induced hypertensive responses (1). The medications typically used in treating hypertensive athletes are presented in table 6.


Table 6. 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
Nifedipine
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

*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.

CNS = central nervous system


In general, agents that decrease total peripheral resistance affect exercise performance the least. All commonly used antihypertensive agents, except for nonselective beta-blockers and diuretics, allow for essentially normal exercise capacity.

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 performance. Thus, some authorities (14) consider these medications to be the best choice for hypertensive athletes. However, even the slightest performance decrement may be unacceptable to elite athletes, so other agents may be more suitable choices, such as angiotensin-converting enzyme (ACE) inhibitors, calcium channel blockers, and alpha-1 blockers. Since these medications are well tolerated and have few negative effects on exercise performance, they may be appropriate for hypertensive athletes, even though they are more expensive than beta-blockers.

Noncardioselective beta-blockers (eg, propranolol, nadolol) are contraindicated in athletes, since they significantly reduce maximal aerobic capacity. However, their potentially deleterious effects on performance, as well as those of diuretics, must be weighed against data cited in the JNC VI report (7). These data, derived from a cross section of patients and not particularly from athletes and very active people, show that those who use beta-blockers and diuretics to control uncomplicated hypertension have lower mortality rates than those who use other medications.

The physician must also be sure that use of an antihypertensive agent is allowed by a sport's governing body. Restrictions regarding the use of beta-blockers and diuretics are included in table 6.

Recommendations for Sports Participation

The physician's role in evaluating hypertensive athletes and managing their condition is vital. While athletes should not be exposed to undue risks, physicians should also beware giving 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 (6,1). Further, no increase in sudden death has been seen in hypertensive competitive athletes who are younger than 35 years (15,16). In addition, resistance training has not been associated with increased morbidity in hypertensive individuals (8), despite the elevated blood pressure that static exercise can cause.

Keeping these findings in mind, physicians may use the JNC VI staging system for hypertension (see table 5) as a framework for making exercise recommendations that are based on the degree of hypertension and the presence or absence of complicating factors.

Stages 1 and 2. Patients who are in these stages may participate fully in dynamic and static sports if there is no evidence of end-organ damage, including heart disease (1). For those who have mild hypertension (a resting diastolic pressure of 90 to 105 mm Hg and systolic pressure of less than 160 mm Hg), physical activities should be primarily dynamic. Some authors (12) 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. Examples of suitable sports include walking, 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) (14). Blood pressure should be checked every 2 to 4 months to ensure that it remains in an acceptable range.

Stage 3. Patients who have a resting diastolic pressure above 110 to 115 mm Hg should discontinue exercise until blood pressure is well-controlled, especially if they are involved in high static or isometric sports (14). 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 (1). 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 the progression of hypertension or of sudden death (15-17).

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 (1). Again, high static or isometric sports and dynamic exercise of more than moderate intensity should most likely be avoided.

Managed Participation

Hypertensive patients whose blood pressure is skillfully managed can exercise and compete athletically without compromising performance. The foundation of effective management includes an understanding of exercise-associated hemodynamics, the physiologic demands of particular sports, and the ways that lifestyle modification, exercise, and antihypertensive medication may be used to treat each patient. Physicians who build their treatment program on these elements can help athletes exercise safely at the highest possible level.

References

  1. Kaplan NM, Deveraux RB, Miller HS Jr: 26th Bethesda conference: recommendations for determining eligibility for competition in athletes with cardiovascular abnormalities. Task Force 4: systemic hypertension. Med Sci Sports Exerc 1994;26(10):S268-S270
  2. Duncan JJ, Farr JE, Upton SJ, et al: The effects of aerobic exercise on plasma catecholamines and blood pressure in patients with mild essential hypertension. JAMA 1985;254(18):2609-2613
  3. Shapiro LM: Morphologic consequences of systematic training. Cardiol Clin 1992;10(2):219-226
  4. Effron MB: Effects of resistive training on left ventricular function. Med Sci Sports Exerc 1989;21(6):694-697
  5. Fleck SJ: Cardiovascular adaptations to resistance training. Med Sci Sports Exerc 1988;20(5 suppl):S146-S151
  6. Pickering TG: Pathophysiology of exercise hypertension. Herz 1987;12(2):119-124
  7. 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):2413-2446
  8. American College of Sports Medicine Position Stand: Physical activity, physical fitness, and hypertension. Med Sci Sports Exerc 1993;25(10):i-x
  9. Arroll B, Beaglehole R: Does physical activity lower blood pressure: a critical review of the clinical trials. J Clin Epidemiol 1992;45(5):439-447
  10. 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):147-151
  11. Harris KA, Holly RG: Physiological response to circuit weight training in borderline hypertensive subjects. Med Sci Sports Exerc 1987;19(3):246-252
  12. Tanji JL: Exercise and the hypertensive athlete. Clin Sports Med 1992;11(2):291-302
  13. Kaplan N: Clinical Hypertension, ed 5. Baltimore, Williams & Wilkins, 1990, pp 3-5, 17, 138, 149-153, 165-171
  14. Klaus D: Management of hypertension in actively exercising patients: implications for drug selection. Drugs 1989;37(2):212-218
  15. Maron BJ, Epstein SE, Roberts WC: Causes of sudden death in competitive athletes. J Am Coll Cardiol 1986;7(1):204-214
  16. 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
  17. 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

Dr MacKnight and Dr Christie are board certified in internal medicine and hold certificates of added qualifications in sports medicine. Dr MacKnight is an assistant professor of clinical internal medicine and sports medicine at the University of Virginia Health Sciences Center in Charlottesville and a member of the American Medical Society for Sports Medicine (AMSSM). Dr Christie is medical director of Northeast Sportsmedicine at St. Mary's Regional Medical Center in Lewiston, Maine. He is a board member of the AMSSM and The Physician and Sportsmedicine. Address correspondence to John M. MacKnight, MD, Box 263-95, University of Virginia Health Sciences Center, Charlottesville, VA 22908; address e-mail correspondence to [email protected].


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