Hackensack University Medical Center, Hackensack, New Jersey
Paul Sorace is a clinical exercise physiologist at Hackensack University Medical Center and an instructor for the American Academy of Personal Training (AAPT).
Thomas P. Mahady is the senior exercise physiologist for The Cardiac Prevention & Rehabilitation Program at Hackensack University Medical Center and an adjunct professor at William Paterson University in Wayne, New Jersey.
Nicole Brignola is a recent graduate from William Paterson University.
Peter Ronai, MS, CSCS*D, NSCACPT*D, ACSM RCEP
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OVERVIEW OF HYPERTENSION
Hypertension (HTN; blood pressure that is greater than the normal range) is defined as a chronic medical condition affecting more than 65 million individuals in the United States (5), with Americans spending $37 billion annually on office visits, medications, and laboratory tests related to the treatment of HTN alone (2). HTN predisposes persons to increased risk of coronary artery disease, which may increase the risk of heart attack, heart failure, stroke, and kidney disease (3). The relationship between blood pressure and cardiovascular disease risk is independent of other risk factors, but the risks continue to increase with the presence of additional risk factors such as diabetes and dyslipidemia (3). For example, the 10-year risk for coronary heart disease is greater in someone who has increased total cholesterol and increased systolic blood pressure as apposed to someone who has only increased systolic blood pressure (3).
Reductions in morbidity and mortality have been mainly attributed to the increased availability and use of various drugs and lifestyle treatments. Some of the common medications prescribed to treat HTN include:
• Diuretics decrease the rate of fluid reabsorption in the tubules of the kidneys and increase the rate of urine output, reducing the total amount of fluid in the body, thereby lowering blood pressure. Potassium levels will drop with diuretics increasing the risk of hypokalemia. Because potassium regulates blood flow through skeletal muscle tissue, the risk of rhabdomyolysis (breakdown of muscle fibers) is increased.
• Beta blockers bind to beta-adrenoceptors and thereby block the binding of norepinephrine and epinephrine (adrenaline) to these receptors. As a result, the heart beats more slowly and with less contractility, thereby reducing blood pressure. Beta blockers also help blood vessels relax and dilate to improve blood flow. Beta blockers reduce heart rate and cardiac output. Reductions in heart rate and cardiac output play a role in decreasing V̇O2max, thus potentially reducing exercise performance.
• Angiotensin-converting enzyme (ACE) inhibitors control blood pressure by inhibiting the formation of angiotensin II. Angiotensin II causes arteries to constrict and thereby increases blood pressure. (Although ACE inhibitors and beta blockers reduce systolic and diastolic pressure during exercise, the overall response to dynamic and static activities is not impaired with these drugs because catecholamine action to drive potassium back into the cell is not impaired.)
• ACE receptor blockers block the action of angiotensin II, which allows blood vessels to dilate and thereby reduce blood pressure.
• Calcium channel blockers lower blood pressure by preventing calcium from entering the cells of the heart and blood vessel walls. Calcium ions excite the contractile process of the heart and arterial muscles. Systolic and diastolic blood pressures are reduced during exercise because of the vasodilatory effects, which may result in light headedness and peripheral edema post-exercise. Because of the risk of orthostatic hypotension (decrease in blood pressure occurring when an individual arises from a seated or lying position; can cause light headedness or fainting), caution should be used when transitioning from seated or lying resistance training (RT) exercises.
Guidelines are based upon the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure released in 2003 for both patients and physicians in tracking and initiating antihypertensive treatments (see Table 1) (3).
Prehypertension is not considered a disease category, and the treatment plan is to encourage lifestyle modifications (e.g., physical activity, sodium restriction) to prevent cardiovascular disease or HTN from developing (3,8). However, drug therapy may be initiated in persons with prehypertension if other medical conditions are present (e.g., diabetes) and lifestyle modifications are unsuccessful at lowering blood pressure to 130/80 mm Hg or less (3). Antihypertensive medications are indicated for stage 1 and 2 HTN (3).
BENEFITS OF RT AND EFFECTS ON BLOOD PRESSURE
Substantial research indicates that regular cardiopulmonary exercise has a favorable effect on lowering overall blood pressure and should be the main emphasis of an exercise program designed to prevent and control HTN (1,8,9). Research has demonstrated that the effects of RT on resting blood pressure are equivocal (1). However, there is evidence to indicate that RT can lower resting blood pressure (1,4,6). A meta-analysis by Kelley and Kelley (6) indicated that engaging in regular RT resulted in approximately a 2% decrease in systolic pressure and a 4% reduction in diastolic pressure. This reduction by itself may seem insignificant but when it is combined with the additive effects of other healthy lifestyle habits (e.g., cardiopulmonary exercise, reduced sodium intake, weight loss if needed), it adds up to a more substantial decrease in resting blood pressure. In addition, a systolic blood pressure reduction of 3 mm Hg has been associated with reduced cardiac morbidity by 5-9%, stroke by 8-14%, and all-cause mortality by 4% (9). However, the majority of the outcomes in these 2 meta-analyses (4,6) were based on resting blood pressures below 140 mm Hg and/or 90 mm Hg. More research is needed regarding the effects of RT on blood pressure in persons with HTN.
The specific effects RT and exercise have on lowering blood pressure are uncertain, but it is likely that a number of different mechanisms are involved (e.g., neural and vascular) (1,10). These potential mechanisms include:
• Chronic exercise (decreased total peripheral resistance)
• Acute exercise (postexercise hypotension by sympathetic inhibition and altered vascular responsiveness)
• Reduced sympathetic nervous activity and circulating norepinephrine
• Improved endothelial function
• Vascular remodeling
• Genetic influences
RT has cardioprotective effects other than lowering resting blood pressure. Regular RT has been shown to reduce the blood pressure response to maximal exercise and improve heart rate recovery after cardiopulmonary exercise (7). RT prolongs the onset of peak cardiovascular responses, decreases the cardiovascular response to exertion, and improves recovery from maximal exertion (7). These effects are beneficial, since the rate of increase in blood pressure and heart rate can cause a cardiac event. Activities requiring physical exertion (e.g., yard work, activities that involve lifting or carrying) will become safer to perform, because hemodynamic responses may be less as a result of regular RT.
SAFETY ISSUES WITH RT IN INDIVIDUALS WITH HTN
The American Heart Association recommends that uncontrolled HTN (>180/110 mm Hg) be an absolute contraindication for RT (10). A client with such a resting blood pressure should seek medical evaluation to lower his or her blood pressure before starting RT. HTN of >160/>100 mm Hg is a relative contraindication for RT (10). This person should consult with a physician before initiating RT (10). High-intensity RT (80-100% 1-rep maximum) can invoke excessive elevations in blood pressure (10). As a result, RT at this intensity should be avoided in persons with HTN. However, there is evidence that RT results in a more favorable balance in myocardial oxygen supply and demand than aerobic exercise due to the lower heart rate and higher myocardial (diastolic) perfusion pressure (10). Moderate intensity RT (40-60% 1-rep maximum) appears to be safe for individuals with controlled HTN (10).
More research is needed in this area, particularly RT effects on blood pressure in individuals with HTN, with and without the influence of antihypertensive medications. A need also exists for studies that analyze data with an intention-to-treat approach, so the effectiveness of RT as a nonpharmacological intervention can be determined (6). This is particularly important for determining the role of RT in managing prehypertension.
RT is beneficial for persons with or at risk for HTN. Evidence indicates that RT can lower blood pressure and also reduce the cardiovascular response to physical activities. Increased muscular strength and endurance often enable persons to be more physically active, which can help control or prevent HTN.
It is important that exercise professionals understand HTN, its risks, medication effects, and RT benefits and effects on blood pressure. This will enable them to help their clients who have or are at risk for HTN, while minimizing the risks with participating in RT.
1. American College of Sports Medicine. Position stand: Exercise and hypertension. Med Sci Sports Exerc
36: 533-553, 2004.
2. American Heart Association. 2002 Heart and Stroke Statistical Update
. Dallas, TX: American Heart Association; 2001.
3. Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL, Jones DW, Materson BJ, Oparil S, Wright JT, and Roccella EJ, for the National Heart Lung and Blood Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure, National High Blood Pressure Education Program Coordinating Committee. Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure: the JNC 7 report. Hypertension
42: 1206-1252, 2003.
4. Cornelissen VA and Fagard RH. Effect of resistance training on resting blood pressure: a meta-analysis of randomized controlled trials. J Hypertens
23: 251-259, 2005.
5. Fields LE, Burt VL, Hughes J, Roccela EJ, and Sorlie P. The burden of adult hypertension in the United States 1999 to 2000: A rising tide. Hypertension
44: 1-7, 2004.
6. Kelley GA and Kelley KS. Progressive resistance exercise and resting blood pressure: A meta-analysis of randomized controlled trials. Hypertension
35: 838-843, 2000.
7. Vincent KR, Vincent HK, Braith RW, Bhatnagar V, and Lowenthal DT. Strength training and hemodynamic responses to exercise. Am J Geriatr Cardiol
12: 97-106, 2003.
8. Whaley MH, Brubaker PH, and Otto RM, eds. ACSM's Guidelines for Exercise Testing and Prescription
(7th ed). Baltimore, MD: Lippincott Williams, & Wilkins, 2005. pp. 43-44, 215.
9. Whelton SP, Chin A, Xin X, and He J. Effect of aerobic exercise on blood pressure: a meta-analysis of randomized, controlled trials. Ann Intern Med
136: 493-503, 2002.
10. Williams MA, Haskell WL, Ades PA, Amsterdam EA, Bittner V, Franklin BA, Gulanick M, Laing ST, and Stewart KJ; American Heart Association Council on Clinical Cardiology; American Heart Association Council on Nutrition, Physical Activity, and Metabolism. Resistance Exercise In Individuals With And Without Cardiovascular Disease: 2007 Update: A Scientific Statement from the American Heart Association Council on Clinical Cardiology and Council on Nutrition, Physical Activity, and Metabolism. Circulation
116: 572-584, 2007.
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