Hypertension (HTN) is the medical term for high blood pressure (Table). It affects 60 million adults in the United States or approximately 25% of the population (1). Worldwide, more than 1 billion people have HTN, with 7.1 million deaths directly related to elevated blood pressure (2). Elevated blood pressure leads to heart failure, kidney disease, and stroke. Recent studies have shown that cardiovascular disease risk doubles for each 20/10 mmHg measure of blood pressure more than 115/75 mmHg (3).
Before a diagnosis of HTN is assigned to a person, the pressure must be elevated on at least two separate occasions, measured with the person seated and after rest (1). Untreated HTN can lead to serious health complications. To prevent these adverse effects, it is imperative to lower the blood pressure to near normal levels once the diagnosis is made. Some providers delay starting treatment of athletic patients, which does not make sense because regular aerobic exercise can lower blood pressure by 5 to 15 mmHg. An athlete with pressures that remain elevated requires treatment as soon as possible, just like all patients diagnosed with HTN.
There are various classes of antihypertensive medications. All medicines have side effects or unwanted outcomes associated with usage. However, some medications must be used cautiously in athletes because of the side effects. Many people will respond well to one class of medication but not to another. Current treatment guidelines recommend adding a second agent, rather than maximizing a dose of a single agent (4,5). People usually have fewer side effects at lower doses, so adding a second agent may result in fewer problems than increasing doses of a single agent to maximal levels.
First-line agents for the nonathletic population are diuretics (4). Diuretics lower blood pressure in two ways. They increase the excretion of water and salts from the kidneys as the main mechanism. Most diuretics also have an immediate effect of widening blood vessels in the skeletal system. There are different types of diuretics that act at different areas of the kidneys. The most commonly used diuretics are thiazide diuretics, but they can result in loss of potassium and sodium salts. Low potassium can be very dangerous, so thiazide diuretics often are prescribed with potassium supplements, or potassium-sparing diuretics are used.
For most people, diuretics do not pose a hazard, but for competitive athletes, they may be problematic. Side effects are associated with the increased excretion of water and salts that can contribute to dehydration. Even mild dehydration can negatively affect athletic performance. Fatigue, weakness, and dizziness are common with diuretics. Athletes also can experience increased muscle cramps and heat stress. Because diuretics increase water excretion, they can alter testing for performance-enhancing drugs, making them banned by the International Olympic Committee (IOC) and the National Collegiate Athletic Association (NCAA).
β-Adrenergic blockers, or β-blockers, work at the level of the sympathetic nervous system. The full effect of this class of medication is not well understood. There are β receptors in the heart, blood vessels, airway tubules, pancreas, kidneys, and liver. The sympathetic, or adrenergic, system is responsible for the involuntary responses to stress in our lives: the basic fight or flight instinct. The sympathetic nerves result in increased heart rate and blood pressure. β-Blockers counteract these effects by lowering the heart rate and force of pumping of the heart.
β-Blockers are contraindicated for use in athletes and are actually banned by some sporting organizations. β-Blockers lower the maximal achievable heart rate and the V˙O2max. Because of the reduction in cardiac output, athletes experience early fatigue and decreased exercise tolerance. These effects are more prominent with highly trained athletes. β-Blockers slightly alter glucose metabolism and can lead to hypoglycemia-low blood glucose-with prolonged exercise. Because of their effect of lowering the heart rate and giving a calming sensation to the athlete, β-blockers are banned by the NCAA and IOC for shooting competitions and by the IOC for diving, fencing, gymnastics, ski jumping, luge, bobsled, and equestrian events.
β-Blockers worsen asthma and may mask symptoms of low blood glucose. Therefore, they are not commonly used in people with asthma or diabetes. They can cause fatigue, dizziness, sleep disturbance and nightmares, and various skin disorders. Some people experience cold hands and feet because of decreased blood flow to the limbs. β-Blockers are best used for people who have had a myocardial infarction because they lower the work of the heart. They also are a good agent to use for people who have exercise-induced high blood pressure.
Angiotensin-converting enzyme (ACE) inhibitors block production of a blood pressure-regulating hormone, angiotensin II. Angiotensin II causes constriction, or narrowing, of the arteries that results in elevated blood pressure. Angiotensin-converting enzyme inhibitors allow blood vessels to relax by reducing circulating angiotensin II. This leads to lower blood pressure and improved cardiac output. Angiotensin-converting enzyme inhibitors also protect the kidneys and are indicated for use in people with diabetes and renal insufficiency (decreased kidney function). Angiotensin-converting enzyme inhibitors are frequently used in athletes.
Side effects of the ACE inhibitors are slightly different than those of other agents. The most common effect leading to cessation of treatment is a dry hacking cough. The cough completely resolves when treatment with the agent stops and may develop at any time or with an increase in dosage. Potentially fatal side effects are angioedema and exercise-induced anaphylaxis. Both result in rapid onset of swelling of the lips, mouth, throat, and airway that can interfere with breathing. People taking ACE inhibitors also can develop angioedema of the intestines. More common side effects include fatigue, dizziness, and elevated potassium. As a class, ACE inhibitors also cause muscle aching. Because of the risk for elevated potassium and decreased renal function, people on this class of medicine must have their salts and kidneys checked with blood tests at the onset of treatment and then twice yearly. Reproductive-age women who are not on birth control should never take ACE inhibitors; they are known to cause birth defects.
For people who develop a cough with ACE inhibitors but otherwise respond well to this class of medicines, health-care providers may try the angiotensin II receptor blockers (ARBs). These medicines block the effect of angiotensin II on blood vessels and the heart. Angiotensin II receptor blockers do not produce a cough; otherwise they work similarly to the ACE inhibitors. Although the incidence is lower with ARBs, anyone who develops angioedema with ACE inhibitors should not be tried on ARBs. Angiotensin II receptor blockers also are associated with rare incidents of rhabdomyolysis or breakdown of muscle tissue.
Calcium channel blockers (CCBs) are another type of antihypertensive medications that reduce the flow of calcium across cell membranes in the smooth muscles of artery walls and heart cells. Because muscles, even smooth muscles of arteries, require calcium to contract, the CCBs cause the arteries to relax and therefore dilate, reducing the blood pressure. Calcium channel blockers are well tolerated by athletes and are not banned.
There are two types of CCBs: dihydropyridines (amlodipine, felodipine, and nifedipine) and nondihydropyridines (verapamil and diltiazem). Side effects and treatment effects vary by the class of CCB. The dihydropyridines cause swelling, headaches, dizziness, and flushing. They also cause overgrowth of the gums and elevated heart rate in some people. The nondihydropyridines also can cause edema, headaches, and dizziness. They also carry risk of heart failure, heart block, palpitations, and severe bradycardia. Verapamil causes constipation, and diltiazem causes nausea.
There are a few other agents used to treat high blood pressure, but the above medications are the most commonly prescribed.
As mentioned previously, the first-line agent for HTN is low-dose thiazide diuretics. Besides being banned by all athletic oversight agencies, the side effects of diuretics are not well tolerated by athletes. The side effects of the ACE inhibitors and ARBs are better tolerated by athletes and are recommended as second-line agents (4,5). Calcium channel blockers also can be used to treat HTN in athletes. None of these medications are banned or monitored by athletic organizations. Young women must be on a reliable source of birth control before starting ACE inhibitors or ARBs.
The response rate to treatment of HTN is 40% to 60% treated with a single agent. Addition of a second agent usually controls the blood pressure in up to 85% of people (4). Adding a second agent to control blood pressure at lower doses of medications results in fewer side effects. Although many people do not want to take medicines, it is very important to start and maintain treatment of people who cannot lower their blood pressure with nonpharmacological interventions. People respond differently to pharmaceutical interventions, so it is very important for clients to follow up with their health-care provider until appropriate treatment levels have been reached. Because blood pressure changes with time, it is important to recheck blood pressure one to two times per year in the clinic once the treatment is stable.
In summary, it is important for all athletes to have blood pressure checked by a health professional at least once a year. Over 60 million Americans have HTN, but less than two thirds are being treated. One third of Americans with HTN do not even know that they have HTN. Additionally daunting is the fact that only one third of those people being treated are at treatment goals. With the number of available medications for the treatment of HTN, even competitive athletes can reach treatment goals without hindering their athletic performance.