Athletes and other physically active patients are usually thought to be free of cardiovascular disease and hypertension because of their apparently high level of fitness. Indeed, the overall prevalence of high blood pressure in these groups is approximately 50 percent lower than in the general population.1 However, the risk of hypertension is increased in some athletes and physically active patients, including blacks, the elderly, persons who are obese, and those with diabetes, renal disease, or a family history of hypertension. Wheelchair athletes with spinal cord injuries may also have hypertension because of loss of autonomic control of blood pressure.2
Hypertension often begins in early adulthood. It becomes more prevalent with increasing age, affecting 5 to 10 percent of adults 20 to 30 years of age and 20 to 25 percent of adults 30 to 60 years of age.3 Almost 80 percent of adolescents found to have a blood pressure above 142/92 mm Hg during a presportsparticipation physical examination eventually develop chronically elevated blood pressure.4
All athletes and physically active patients should be screened for hypertension. If the condition is diagnosed, appropriate treatment should be started to reduce the risk of morbidity and mortality associated with cardiovascular disease.5
Hypertension Classification and Secondary Hypertension
The sixth report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure emphasizes the progressive nature of hypertension and divides blood pressure into six classes (Table 1).5 Most athletes and physically active patients with hypertension fall into stage 1 or 2.
|Class||Systolic blood pressure (mm Hg)||Diastolic blood pressure (mm Hg)|
|High normal||130 to 139||85 to 89|
|Stage 1||140 to 159||90 to 99|
|Stage 2||160 to 179||100 to 109|
Secondary hypertension develops in fewer than 5 percent of athletes and physically active patients.6 It tends to occur in younger patients, adult patients with rapid onset of severe hypertension, and patients with hypertension that responds poorly to routine therapies. The most common cause of secondary hypertension is vascular or parenchymal renal disease.6
Hypertension can also occur secondary to estrogen in oral contraceptive pills, which are commonly taken by female athletes. This secondary hypertension generally develops soon after they start taking the pills. About 5 percent of all women who take oral contraceptive pills develop hypertension over a five-year period.7
In athletes and other physically active patients with hypertension, the history should focus on behaviors that may affect blood pressure, such as a high intake of sodium and saturated fats (e.g., in processed and “fast” foods) and the use of alcohol, drugs (specifically, stimulants taken before competitions, or cocaine), tobacco, or anabolic steroids (Table 2).5,7–9 Many over-the-counter medications, including non-steroidal anti-inflammatory drugs (NSAIDs), caffeine, diet pills, and decongestants, can also cause blood pressure to rise.
|High sodium intake|
|Excessive alcohol consumption (binge drinking)|
|Illicit drug use (e.g., cocaine)|
|Anabolic steroid use|
|Stimulant use (e.g., in supplements taken to enhance energy or control weight)|
|High stress levels|
|Race (blacks affected more often than whites by about a 2-to-1 ratio, and Asians affected the least)|
|Family history of hypertension or cardiac disease in men over 55 years of age and women over 65 years of age|
|Diabetes mellitus or glucose intolerance|
|Smoking or chewing tobacco|
Patients should also be questioned about the use of herbs and dietary supplements, with special attention given to substances purported to increase energy or control weight. These supplements often contain “natural” substances such as guanara, ma huang, and ephedra, which are stimulants.
Stress levels should be evaluated. Chronic environmental or social stress may result in higher levels of circulating catecholamines and chronic neurogenic activation of the sympathetic nervous system, which can contribute to hypertension.8
The clinical evaluation should include proper measurement of blood pressure7 and laboratory tests directed at excluding causes of secondary hypertension or identifying end-organ damage. Studies should include an electrocardiogram, a complete blood count, urinalysis, and measurements of sodium, potassium, blood urea nitrogen, creatinine, fasting glucose, and total, low-density lipoprotein (LDL), and high-density lipoprotein (HDL) cholesterol levels. Other studies and further evaluation may be performed if a secondary cause of hypertension is suspected.
Compared with the general population, athletes and other physically active patients are often more motivated to comply with nonpharmacologic interventions, because these measures have virtually no side effects. Although lifestyle modifications cannot eliminate the need for antihypertensive drug therapy in all patients, dietary and behavioral changes may reduce the amount of medication needed and, thus, the possibility of side effects. Dietary and lifestyle changes may include decreasing sodium intake, increasing potassium intake, losing weight, decreasing alcohol consumption, avoiding stimulant use, applying relaxation techniques, and performing aerobic exercise.
A reduction in sodium intake can lead to a decrease in blood pressure.5 In particular, patients should be advised to reduce their intake of processed foods such as luncheon meat and fast foods. Processed foods provide 75 percent of the sodium recommended for the typical American diet.9 These foods are particularly common in the diets of adolescent athletes. Blacks, older persons, and those with diabetes mellitus seem to be especially sensitive to the effects of dietary sodium.9
Potatoes and bananas, as well as many other fruits, contain significant amounts of potassium. These foods should be included in the diet of athletes and other physically active patients. High dietary potassium intake may provide some protection against high blood pressure or may improve blood pressure control.10 A high-potassium diet is especially important in endurance athletes, who may tend to be hypokalemic.5
Calcium or magnesium supplementation for the sole purpose of improving blood pressure control is not routinely recommended in physically active patients.5
Losing just 4.5 kg (10 lb) can reduce blood pressure in overweight patients who have hypertension.11 Loss of this much weight also seems to enhance the blood pressure–lowering effects of many medications.12 The weight reduction plan should include foods that are high in fiber and low in saturated fats.13
Excessive alcohol use can decrease the effectiveness of antihypertensive drug therapy. Adults should limit alcohol intake to the equivalent of two beers per day. Women and lighter weight persons should consume no more than the equivalent of one beer per day.5
Some athletes routinely use biofeedback, muscle relaxation techniques, meditation, yoga, and stress management techniques. These stress reduction tools may have value as adjunctive therapy in patients with hypertension.
Regular aerobic exercise adequate to achieve moderate fitness can lower blood pressure, enhance weight loss, and reduce mortality.14 The effects of exercise on hypertension are even more dramatic in patients with hypertension secondary to renal dysfunction.
|The recommended mode, frequency, duration, and intensity of exercise are generally the same as those for persons without hypertension.|
|Blood pressure should be controlled before resumption of participation in vigorous sports, because both dynamic and isometric exercise can cause remarkable increases in blood pressure.|
|Recommendations on exercise restrictions|
|High-normal blood pressure||No restrictions|
|Controlled mild to moderate hypertension (<140/90 mm Hg)||No restrictions on dynamic exercise; possible limit on isometric training or sports in some patients|
|Uncontrolled hypertension (>140/90 mm Hg)||Limited to low-intensity dynamic exercise; avoid isometric sports.|
|Controlled hypertension with end-organ damage||Limited to low-intensity dynamic exercise; avoid isometric sports.|
|Severe hypertension with no end-organ involvement||Limited to low-intensity dynamic exercise, with participation only if blood pressure is under adequate control.|
|Secondary hypertension of renal origin||Limited to low-intensity dynamic exercise; avoid “collision” sports that could lead to kidney damage.|
Athletes and other physically active patients need to monitor medication effects, because some antihypertensive drugs may have an adverse influence on exercise tolerance. Other drugs, including NSAIDs, may decrease the action of antihypertensive medications, including diuretics, beta blockers, and angiotensin-converting enzyme (ACE) inhibitors.16 Physicians and patients also need to be aware that the U.S. Olympic Committee (USOC) and the National Collegiate Athletic Association (NCAA) have banned the use of some antihypertensive medications.16–18 The effects of anti-hypertensive drug classes are summarized in Table 4.5,6,16–21
|Drug class||Heart rate||Stroke volume||Cardiac output||Vascular resistance||Plasma volume||Effects on training||Side effects||Patients in whom drug class is recommended||Patients in whom drug class should be avoided||Banned status|
|Thiazide diuretics*||No effect||Decrease||Decrease||Decrease||Significant decrease||No effect or decrease in endurance||Hypovolemia, orthostatic hypotension, and urinary loss of potassium and magnesium, which can lead to muscle cramps, arrhythmias, and rhabdomyolysis in patients exercising intensely or competing in warm weather||Elderly patients, black patients, patients with CHF||Endurance athletes, collegiate athletes||Use banned by USOC and NCAA|
|ACE inhibitors†||Slight increase||Increase||Increase||Decrease||No effect||No effect||Dry, nonproductive cough (angiotensin I blockers)||Patients with diabetes mellitus, renal insufficiency, CHF, asthma, or hyperlipidemia||Female patients who are not using contraception||None|
|Alpha blockers||No effect||No effect||No effect||Decrease||No effect||No effect||First-dose hypotensive effect with alpha1 blockers, especially in elderly patients||Patients with hyperlipidemia or BPH||May want to avoid in men older than 55 years||None|
|Centrally acting agents may cause drowsiness, dry mouth, and impotence; rebound hypertension can occur with abrupt discontinuation of clonidine (Catapres).|
|Beta blockers||Significant decrease||No effect||Significant decrease||Increase||No effect||Significant decrease||Increase in perceived exertion levels, impairment of cardiac output and maximum oxygen uptake, earlier fatigue and lactate threshold, possible exacerbation of exercise-induced bronchospasm or asthma||Patients with coronary artery disease||Patients with asthma, endurance athletes, collegiate athletes||Use banned in precision sports (i.e., shooting, archery, diving, ice skating)|
|Calcium channel blockers||Decrease, increase, or no effect||No effect or decrease||No effect or decrease||Decrease||No effect or increase||No effect||Nondihydropyridines (e.g., verapamil [Calan], diltiazem [Cardizem]) can cause heart rate suppression and minor impairment of maximum heart rate, decreased left ventricular contractility, and constipation.||Patients with asthma, black patients||None||None|
|Dihyrdopyridines (e.g., amlodipine [Norvasc], nifedipine [Procardia]) can cause reflex tachycardia, fluid retention, and vascular headaches.|
Both thiazide and loop diuretics decrease plasma volume, cardiac output, and vascular resistance.20 The thiazide diuretics have less pronounced effects.
Thiazide diuretics are useful as second-line therapy in salt-sensitive athletes and physically active patients with hypertension.5 These agents should be given in a low dosage and, in some patients, combined with a potassium-sparing agent. Thiazide diuretics are inexpensive and a good choice in patients who exercise only casually, in physically active elderly patients, and in black patients. Possible side effects include hypovolemia, orthostatic hypotension, and urinary loss of potassium and magnesium. These side effects can lead to muscle cramps, arrhythmias, and rhabdomyolysis in patients who are exercising intensely or competing in warm weather.
The side effects associated with thiazide diuretics are magnified with the more potent loop diuretics. Consequently, loop diuretics are inappropriate for use in the treatment of hypertension in athletes and other physically active patients. These agents have also been shown to cause short-term increases in plasma cholesterol, glucose, and uric acid levels.21
ACE inhibitors have been shown to have beneficial effects in patients with heart failure, systolic dysfunction or nephropathy. They reverse ventricular hypertrophy and microalbuminuria, with preservation of renal function. In exercise, ACE inhibitors have no major effects on energy metabolism and cause no impairment of maximum oxygen uptake. In general, these drugs have no deleterious effects on training or competition.20
The major side effect of ACE inhibitors is a dry, nonproductive cough. Because there have been anecdotal reports of postural hypotension after intense exercise in patients taking ACE inhibitors, an adequate cool-down period is recommended.
ACE inhibitors are excellent for treating mild to moderate hypertension. They are often the first-line agents for the treatment of high blood pressure in physically active patients, especially those with diabetes.5 Their effectiveness may be improved by adding a thiazide in a low dosage, with the drugs taken separately or in combination.
The potassium-sparing effect of ACE inhibitors may be increased when these agents are taken concomitantly with NSAIDs.19 Use of ACE inhibitors is contraindicated in pregnancy. Therefore, patients of childbearing age should use some form of contraception if they are taking an ACE inhibitor.
Angiotensin-II receptor blockers produce similar effects as ACE inhibitors. However, because of their action at the receptor level, they do not cause a dry cough. Currently, insufficient data are available to document whether angiotensin-II receptor blockers have cardiac and renal protective effects. Therefore, these agents are generally recommended only for patients who cannot tolerate ACE inhibitors.5
The alpha1-receptor antagonists competitively block postsynaptic alpha1 arteriolar smooth muscle receptors. They decrease systemic vascular resistance, with no reflex increase in heart rate or cardiac output. A first-dose hypotensive effect can occur, especially in the elderly.
Alpha blockers cause no major changes in energy metabolism during exercise, and maximum oxygen uptake is preserved. Therefore, these agents have no major effects on training or sports performance.20 Alpha blockers have been used in athletes with diabetes mellitus who have hypertension and hypercholesterolemia, because they do not exacerbate these conditions.7
The doxazosin arm of the ongoing Antihypertensives and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT)29 was discontinued because of an increased incidence of congestive heart failure, compared with use of a diuretic. The ALLHAT findings should be taken into consideration, especially in athletes older than 55 years.
Centrally acting alpha agonists have no major effects on training or sports performance.19 Because of their side effects, however, these agents are rarely used. These effects may include mild to moderate drowsiness, dry mouth, and impotence. Rebound hypertension can occur with the abrupt discontinuation of orally administered clonidine (Catapres).7
Noncardioselective beta blockers significantly decrease contractility of the heart and decrease heart rate. Systemic vascular resistance is increased, especially in the muscle and skin. Because these drugs inhibit lipolysis and glycogenolysis, hypoglycemia may occur after intense exercise. In addition, athletes who take beta blockers perceive greater exertion during exercise, which may affect adherence to the prescribed medication regimen.20 An increased total cholesterol level and a decreased HDL cholesterol level may also be noted.7
Although cardioselective beta blockers have fewer side effects than noncardioselective agents, they also impair cardiac output and maximum oxygen uptake, particularly in athletes. Cardioselective beta blockers should not be used in athletes and other physically active patients unless there is an underlying condition (e.g., coronary artery disease) that requires their use.20
When combined alpha-beta blockers are used, the beta effects are greater than the alpha effects. There is a decrease in the systemic vascular resistance, but less impairment of muscle blood flow and maximum oxygen uptake. If beta blockade is necessary, a combined alpha-beta blocker may be the best choice.21
Calcium Channel Blockers
These drugs inhibit calcium slow-channel conduction, thereby reducing the calcium concentration in vascular smooth muscle cells, which results in decreased systemic vascular resistance with generalized vasodilation.19 Calcium channel blockers are effective in reversing ventricular hypertrophy.
Dihydropyridines such as amlodipine (Norvasc) and nifedipine (Procardia) can cause reflex tachycardia, fluid retention (pedal edema), and vascular headaches. Nondihydropyridines such as verapamil (Calan) and diltiazem (Cardizem) can cause heart rate suppression, minor impairment of maximal heart rate, decreased left ventricular contractility, and constipation.5
Calcium channel blockers have no major effects on energy metabolism during exercise, and maximum oxygen uptake is generally preserved.20 There is a potential for competitive “steal” of muscle blood flow (because of vasodilatation) and earlier onset of the lactate threshold.30 However, calcium channel blockers, especially the dihydropyridines, are generally well tolerated and effective in physically active patients. They are often used as first-line agents in black athletes.5