Developing a thorough understanding of coronary artery disease (CAD) can help fitness professionals fight one of the world’s deadliest diseases.

How deadly? For starters, CAD is the leading cause of death around the world, accounting for 13.2% of all deaths in 2012 (WHO 2014a). It kills almost 380,000 Americans every year (CDC 2014a). Exercise professionals can do something about these statistics by designing fitness programs that reduce CAD risk factors in clients while improving their quality of life.

CAD results from (and is detected by) progressive accumulation of fatty plaque substances, called atherosclerosis, on the inner walls of coronary arteries (NIH 2011). The plaque restricts oxygen-rich blood to the myocardium, or heart muscles.

Note that CAD and cardiovascular disease (CVD) are not the same thing. CAD is just one variety of CVD—a cluster of diseases that include abnormal heart rhythms, heart failure, heart valve disease, congenital heart disease, heart muscle disease, pericardial disease, aorta disease and blood vessel disease.

Understanding Coronary Artery Structure and Arteriosclerosis

The heart’s coronary arteries, and all blood vessels for that matter, have three distinct layers (Hendry, Farley & McLafferty 2012) (see Figure 1):

  • Tunica intima. The inner layer—the name means “inner coat” in Latin—is smooth, thin and elastic. The tunica intima is lined with endothelial cells that come in direct contact with the blood.
  • Tunica media. The middle layer consists of elastic tissue intertwined with smooth muscle layers that permit contraction and dilation (the enlarging or expanding diameter of a blood vessel).
  • Tunica adventitia. The tough outer layer, which is made up primarily of collagen fibers and connective tissue, provides a supportive role. The tunica adventitia anchors blood vessels to surrounding structures. This layer also keeps blood vessels from overexpanding in response to abnormally high blood pressure.

Fig 1

With aging, some of the larger arteries lose some of their elastic fibers and become stiffer. The inner layer becomes thicker and harder owing to a buildup of fat and calcium deposits behind it. This disease process is called arteriosclerosis (or hardening of the artery walls), which increases resistance to the flow of blood in an artery (because the artery loses some of the elasticity that allows it to expand); this often leads to a persistent elevation in blood pressure (Hendry, Farley & McLafferty 2012).

What Are the Endothelial Cells, and What Do They Do?

Endothelial cells make up the innermost lining of the tunica intima of blood vessels, maintaining a physiological equilibrium for inflammation, platelet aggregation (the sequence of events leading to the formation of a clot, or thrombosis) and blood vessel wall remodeling in response to injury (Schwartz et al. 2010). These specialized endothelial cells also regulate constriction of vessel blood flow, profoundly affecting the overall function of the cardiovascular system. Schwartz et al. (2010) explain that endothelial cell dysfunction (discussed in the next section) is an early sign of atherosclerosis.

Understanding CAD and the Pathophysiology of Atherosclerosis

CAD occurs when atherosclerotic plaque builds up in arteries over decades (see Figure 2). In the earliest stages of the disease, chronic inflammation happens in response to damage to the endothelial lining, such as injury from chemical intrusion (e.g., elevated blood glucose, abnormal LDL cholesterol levels and/or carcinogens from tobacco or the environment) or from physical forces (e.g., high blood pressure).

Louis and Zahradka (2010) explain that chronic inflammation leads to endothelial cell dysfunction, the first step in atherosclerotic plaque formation. This dysfunction causes endothelial cells to produce less nitric oxide, hindering their major role in maintaining and controlling vascular wall functions such as muscular tone, oxidative stress and inflammation. Endothelial dysfunction also makes the tunica intima more permeable, allowing molecules to enter into and embed behind this innermost layer. Phagocytic cells, which engulf cell debris, begin to adhere to the endothelial cells in an effort to clear out some of the debris, but gradually transform into larger macrophage cells, which start to engulf LDL cholesterol molecules under the tunica intima.

The LDL cholesterol molecules oxidize; that is, each molecule loses an electron. Yang, Mohamed and Zhou (2012) explain that oxidized LDL particles are toxic and can further damage the endothelial cells. The macrophages continue to enlarge, developing into foam cells (which are fat-filled macrophages). The foam cells progressively become fatty streaks and then thicker intermediate lesions, which eventually become atherosclerotic plaque (made of smooth muscle cells, cholesterol, fatty substances, cellular debris and fibrin).

Atherosclerotic plaque significantly hinders blood flow. The plaque is surrounded by a fibrous cap that is weak and prone to rupturing. For example, a surge in blood pressure may crack a portion of the plaque. The body then sends a team of platelets to form a blood clot to stop the bleeding. This blood clot is called a thrombus. If a piece of plaque or thrombus breaks off from the tunica intima, it is known as an embolus (or thromboembolus), which will move into the bloodstream and potentially occlude smaller blood vessels downstream.

Exercise Is a Powerful Way to Combat CAD

According to Alves (2014), physical activity’s ability to reduce cardiovascular risk is as meaningful as the risk reduction from drug therapies such as cholesterol-lowering statins. Alves cites research documenting that regular exercise helps prevent CAD risk factors such as type 2 diabetes, hypertension and metabolic syndrome. In addition, Alves says, aerobic and resistance exercise can decrease blood pressure (when elevated), improve body composition, lower chronic inflammation and improve lipid profiles in overweight and obese people.

Evidence is mounting that on a molecular level, regular physical activity increases endothelial cell function (Lenk et al. 2011). Alves (2014) explains that exercise appears to mobilize specialized endothelial progenitor cells (EPCs), releasing them from bone marrow into sites of endothelial damage in response to structured physical activity. EPCs promote the regeneration and repair of a damaged endothelium.

What Are the Safe and Effective Cardiovascular Recommendations for CAD Clients?

ACSM’s Guidelines for Exercise Testing and Prescription (2014) states that exercise is safe and effective for people with CVD. These are the ACSM guidelines for developing and implementing exercise programs for a CAD client:

Medical considerations. Appropriate monitoring and exercise supervision plus communication with the client’s doctor may enhance clinical progress. Personal trainers should regularly check preexercise heart rate, blood pressure, body weight (weekly), symptoms of clinical status (lightheadedness, irregular pulse, chest discomfort, etc.), medication changes and adherence to medications. Clients may not be aware of atypical variations in their daily lives.

Duration and intensity. Exercise should be performed at least on 3 days per week and preferably on most days of the week. A 5- to 10-minute light-intensity warm-up should precede exercise sessions. Aerobic frequency depends on the client’s baseline fitness, health goals and exercise capacity. Intensity can range from 40% to 80% of the client’s heart rate reserve. Exercise heart rate should be 10 or more beats per minute below the intensity that evokes any abnormal signs or symptoms. If rating of perceived exertion is used to monitor intensity, this would be an 11 (light) to 16 (hard) on the 6–20 RPE scale.

If a client has had medical testing for exercise, the intensity is often based on a heart rate from the medical assessment. If the exercise program begins relatively soon after a cardiac-related event, the trainer may want to start the client with just 5–10 minutes of aerobic exercise.

Progression. Individualized and gradual progression should depend on the client’s fitness level, goals, motivation and other physiological limitations. The stated ACSM (2014) goal for cardiovascular conditioning is that sessions should eventually last 20–60 minutes. The new American Heart Association (AHA 2015) heart health guidelines encourage 40 minutes of moderate to vigorous exercise three to four times a week.

Equipment. To promote whole-body fitness, the ACSM guidelines encourage using a variety of exercise equipment that involves the upper and lower extremities; for example, rowers, elliptical trainers, stair climbers, recumbent steppers, upright and recumbent cycle ergometers and treadmills. Brisk walking is a very tolerable exercise and leads to fewer orthopedic problems than jogging or running.

Table 1

Can CAD Clients Do High-Intensity Interval Training?

Pattyn et al. (2014) conducted a systematic review and meta-analysis of current research and found that high-intensity interval training is not only possible for CAD clients but, with respect to some physiological factors, is actually more effective than traditional moderate continuous cardiovascular training (MCT). The authors reviewed nine studies comparing HIIT and MCT with a total of 206 participants. In what may be pioneering findings, results indicated that HIIT elicits larger benefits for peak VO2 (maximal aerobic capacity) than MCT does in CAD patients.

In addition, cardiac output and stroke volume increase more after 12 weeks of HIIT than after 12 weeks of MCT. However, if weight loss is a priority, it should be noted that body weight tends to decrease more after MCT than after HIIT, according to Pattyn and colleagues (2014). This is because the capability to increase total exercise volume and duration in MCT makes it an effective strategy for enhancing weight (and fat) loss.

A word of caution about HIIT for CVD clients, from the 2014 ACSM guidelines: After highlighting and substantiating some of the impressive findings discussed above, ACSM has submitted that HIIT shows potential for people with CVD, but until further data are available regarding safety and efficacy, it cannot be universally recommended. Moreover, further research is required to determine optimal HIIT protocols for CAD clients.

Also, as a special message to personal trainers who work with CAD clients in cold, snowy regions: Shoveling wet snow can become a very physically demanding, intermittent lifestyle activity with heavy-exertion shoveling spurts alternating with recovery, similar to structured HIIT training. However, shoveling wet snow may undesirably elevate heart rate and blood pressure, placing undue stress on the cardiovascular system.

Can CAD Clients Do Resistance Training?

Resistance training can improve muscle strength, endurance, hypertrophy, bone density, metabolism and functional independence in CAD patients (Wise & Patrick 2011). Wise and Patrick add that regular resistance training improves exercise capacity, mood and quality of life. These resistance training recommendations come from the ASCM guidelines (2014):

  • Equipment. Choose from free weights, wall pulleys, elastic bands, cuff and hand weights, and/or machines.
  • Technique. Use slow, controlled movements; maintain regular breathing and do not hold the breath; avoid too much straining; avoid excessive gripping of weights.
  • Intensity. Maintain light to somewhat hard exercise intensity, according to subjective assessment; this equates to an RPE of 11–14 on the 6–20 scale; use a 10- to 15-repetition zone of training.
  • Frequency. Schedule two to three sessions per week.
  • Number of exercises. Select eight to 10 exercises covering the major muscle groups of the body (chest, shoulders, abdominals, arms, back, hips, thighs, lower legs).
  • Number of exercises in a session. Use a one-set-per-exercise design to train all muscle groups in a single session.
  • Types of exercise. Include more multi-joint exercises that involve more muscle mass.
  • Progression. Increase slowly in 2- to 5-pound increments for upper body and 5- to 10-pound increments for lower body, with progressions to be considered weekly.Table 2Table 2
  • Number of sets. Begin with single-set training and progress to multiple-set regimens based on the client’s goals and ability to tolerate the additional exercise volume.
  • Cautionary signs for early termination of workout. Watch for dizziness, lightheadedness, unusual shortness of breath, chest or shoulder pain/discomfort, which are all signs for the client to stop and seek medical assistance.

Final Thoughts

After a review and synthesis of the data, it is clear that well-structured cardiovascular exercise and resistance training programs are powerful therapeutic strategies for combating CAD. From regular participation in exercise, CAD clients may develop more confidence and self-esteem, work with greater vigor and, most importantly, enjoy life to its fullest. Fitness professionals have the research and tools to improve quality of life for CAD clients by designing individualized, safe and effective exercise programs.

Major Risk Factors for Coronary Artery Disease

These are some of the factors that can increase the risk of developing atherosclerosis and coronary artery disease:

Blood cholesterol levels. The body creates cholesterol to form cell membranes and hormones. Although cholesterol is a known risk factor for CAD, not all cholesterols are atherogenic. It has been shown that the oxidized form of LDL (the particle missing an electron) is more responsible for the genesis and progression of atherosclerosis than the unmodified LDL (Yang, Mohamed & Zhou 2012). Low levels of HDL cholesterol are also a risk factor for CAD (see Table 1).

Hypertension. The constant forces of elevated blood pressure against the innermost layer of heart blood vessels can be a key factor in the development of atherosclerosis and CAD. One high reading does not necessarily mean a person hashigh blood pressure. However, if readings continue to remain at systolic 140 (or higher) or diastolic 90 (or higher) over days of repeated measurements, a treatment to address high blood pressure will be recommended (see Table 2). Children can also develop high blood pressure, particularly if they are overweight or obese (NIH 2014).

Smoking. Tobacco use and sustained exposure to second-hand smoke elevate the risk of CAD (NIH 2014) because smoking damages the endothelial lining of blood vessels, increasing the risk of fatty plaque buildup. Nicotine from tobacco also causes the heart rate to accelerate, leading to hypertension with chronic tobacco use.

Prediabetes and diabetes. Diabetes is a chronic metabolic disease characterized by elevated levels of glucose either because the body cannot produce enough insulin or because its cells cannot use insulin to take in glucose. Prediabetes means the body cannot use insulin effectively; blood sugar levels are above normal but lower than typically seen in people with diabetes. People with prediabetes who fail to manage their blood glucose levels are likely to get type 2 diabetes within 10 years (NIH 2014). Prediabetes and diabetes are associated with obesity, lack of physical inactivity and poor dietary choices.

Overweight and obesity. CAD risk factors such as high blood cholesterol, high blood pressure, diabetes and high triglyceride levels are all correlated with overweight and obesity, which is why these conditions are considered CAD risk factors. See Table 3 for body mass index classifications for under-weight, overweight and obesity in adults.

Genetics. Family history of heart disease can predispose a person to CAD. People are at higher risk if either their mother or a sister was diagnosed with CAD before age 65, or if their father or a brother was diagnosed with CAD before age 55. However, just because CAD runs in a family, it is not certain that others in the family will get it. Much depends on lifestyle and whether an individual has other CAD risk factors. Also, some medicines that treat another risk factor (e.g., high blood pressure) may lessen the genetic influences and slow the progression of CAD (NIH 2014).

Stress. Anxiety and stress can play a role in CAD development. These psychological conditions may trigger arteries to tighten, constricting blood flow and leading to hypertension (NIH 2014).

Triglyceride levels. Some research indicates that high levels of triglycerides (or blood fats) may be a risk factor for CAD, especially in women (NIH 2014).

Age. CAD risk increases with age. Most people have some plaque buildup in their heart arteries by the time they’re in their 70s (NIH 2014). In women, the risk increases faster after age 55; in men, it increases more quickly after age 45.

Gender. Some CAD risk factors cause different problems depending on gender. For instance, diabetes raises the risk of CAD more in women than in men (NIH 2014). Also, preeclampsia is a risk factor for CAD. Affecting approximately 5%-8% of all pregnancies, preeclampsia is a progressive disorder distinguished by high blood pressure and the presence of protein in the urine (Preeclampsia Foundation 2010). Before age 55, women have a lower risk of CAD than men of the same age because estrogen appears to provide a protection against the development of CAD (NIH 2014). After 55, CAD risk is similar for women and men.

Unhealthy diet. Dietary choices will directly affect CAD (NIH 2014). The key is to limit foods that are high in trans fats (deep-fried and processed foods), cholesterol (some meats, dairy products, eggs, commercially baked goods) and saturated fats (deep-fried, dairy products, processed foods), as they have been shown to raise LDL cholesterol levels in the blood (NIH 2014). It is also important to monitor salt intake, as high-salt foods can elevate blood pressure (NIH 2014). Added sugars from desserts, nondiet sodas, canned fruits packed in syrup, and fruit drinks may bump up calorie intake and thus be a precursor to overweight and obesity (raising the risk for CAD). Last, alcohol consumption should be limited (no more than one drink per day for women and two for men), as too much alcohol raises blood pressure and adds extra undesirable calories to the diet.

Physical inactivity. According to the NIH (2014), inactive people are nearly twice as likely to develop CAD as those who are active. Physical inactivity is highly associated with other CAD risk factors such as high blood pressure, high LDL cholesterol, prediabetes, diabetes, overweight and obesity (NIH 2014).

A Brief Historical Review of CAD

3000 bc. Coronary artery disease is described in ancient Egyptian writings on mortuary transcriptions, tombsand papyri (MacKinnon 1987). Research using computer tomography (an imaging process with X-ray equipment), conducted by Allam et al. (2011), has now confirmed the presence of atherosclerotic lesions in the arteries of ancient Egyptian mummies.

17th-19th centuries. In the 17th century, William Harvey identifies the “third circulation” of the body—coronary circulation through the heart (MacKinnon 1987). In 1809, Allan Burns proposes the myocardial theory of angina pectoris(a term for chest pain), describing a type of lesion formation in the vessels of the heart (MacKinnon 1987). In 1880, Carl Weigert explains a myocardial infarction (damaged heart) and associates it with a disease of the coronary arteries (MacKinnon 1987).

20th century. In 1912, James Bryan Herrick uses electrocardiography (a new technology at that time) to show how CAD impedes the heart’s electrical rhythm (MacKinnon 1987).

21st century CAD is rare in people under the age of 45. Poulose & Raju (2014) explain that deaths resulting in heart disease, cancer, diabetes, stroke and hypertension patients increase with age, becoming especially more common in those who are 65 years and older. However, atherosclerosis buildup (the antecedent to CAD) may begin in early life, thus signifying the need for prevention during childhood (McGill, McMahan & Gidding 2008).

Four Heart Disease Facts
  1. Every 34 seconds, someone in the United States has a heart attack.
  2. Each minute, someone dies from a heart disease-related event in the United States.
  3. CAD costs the U.S. $108.9 billion each year in healthcare services, medications and lost productivity.
  4. High blood pressure, high LDL cholesterol and smoking are key risk factors for CAD, and 49% of Americans have at least one of them.
  5. Source: CDC 2014b.

    CAD Risk Factors
    • high blood pressure
    • high LDL cholesterol (the bad cholesterol)
    • low HDL cholesterol (the good cholesterol)
    • smoking
    • diabetes
    • overweight/obesity
    • poor diet
    • physical inactivity
    • excessive alcohol consumption

    Source: CDC 2014a.


ACSM (American College of Sports Medicine). 2012. ACSM’s Guidelines for Exercise Testing and Prescription (9th edition). Baltimore: Wolters Kluwer/Lippincott Williams & Wilkins.
AHA (American Heart Association). 2014. Understanding blood pressure readings. Accessed Jan. 4, 2015.
AHA. 2015. New diet, exercise guideline for heart health. Accessed Jan. 5, 2015.
Allam, A.H., et al. 2011. Atherosclerosis in ancient Egyptian mummies: The Horus Study. Journal of the American College of Cardiology, 4 (4), 315-27.
Alves, A.J. 2014. Physical activity and coronary artery disease: Looking beyond risk factors. Archives of Exercise in Health and Disease, 4 (2), 251-53.
CDC (Centers for Disease Control). 2014a. Heart disease facts: America’s heart disease burden. Accessed Jan. 3, 2015.
CDC. 2014b. Heart disease fact sheet. Accessed Jan. 6, 2015.
Hendry, C., Farley, A., & McLafferty, E. 2012. Blood vessels, circulation and blood pressure. Nursing Standard, 27 (11), 35-40.
Lenk, K., et al. 2011. Role of endothelial progenitor cells in the beneficial effects of physical exercise on atherosclerosis and coronary artery disease. Journal of Applied Physiology, 111 (1), 321-28.
Luis, S., & Zahradka, P. 2010. Vascular smooth muscle cell motility: From migration to invasion. Experimental & Clinical Cardiology, 15 (4), e75-e85.
MacKinnon, A. 1987. The origin of the modern epidemic of coronary artery disease in England. Journal of the Royal College of General Practitioners, 37 (297), 174-76.
McGill, H.C., McMahan, C.A., & Gidding, S.S. 2008. Preventing heart disease in the 21st century: Implications of the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Study. Circulation, 117 (9), 1216-27.
NIH (National Heart, Lung, and Blood Institute). 2011. How does smoking affect the heart and blood vessels? Accessed Jan. 4, 2015.”
NIH. 2012. How is high blood cholesterol diagnosed? Accessed Jan. 4, 2015.
NIH. 2014. Coronary heart disease risk factors. Accessed Jan. 5, 2015.
Lenk, K., et al. 2011. Role of endothelial progenitor cells in the beneficial effects of physical exercise on atherosclerosis and coronary artery disease. Journal of Applied Physiology, 111 (1), 321-28.
Pattyn, N., et al. 2014. Aerobic interval training vs. moderate continuous training in coronary artery disease patients: A systematic review and meta-analysis. Sports Medicine, 44 (5), 687-700.
Poulose, N., & Raju, R. 2014. Aging and injury: Alterations in cellular energetics and organ function. Aging and Disease, 5 (2), 101-108.
Preeclampsia Foundation. 2010. About preeclampsia. Accessed Jan. 5, 2015.
Schwartz, B.G., et al. 2010. The endothelial cell in heath and disease: Its function, dysfunction, measurement and therapy. International Journal of Impotence Research, 22 (2), 77-90.
Stary, H.C., et al. 1995. A definition of advanced types of atherosclerotic lesions and a histological classification of atherosclerosis. Circulation, 92, 1355-74.
WHO (World Health Organization). 2014a. The top 10 causes of death. Accessed Jan. 3, 2015.
WHO. 2014b. BMI classification. Accessed Jan. 5, 2015.
Wise, F.M., & Patrick, J.M. 2011. Resistance exercise in cardiac rehabilitation. Clinical Rehabilitation, 25, 1059-65.
Yang, H., Mohamed, A.S.S., & Zhou, S-H. 2012. Oxidized low density lipoprotein, stem cells, and atherosclerosis. Lipids in Health and Disease, 11 (85), 1-9.

Kevin N. Do

Leave a Comment

When you buy something using the retail links in our content, we may earn a small commission. IDEA Health and Fitness Association does not accept money for editorial reviews. Read more about our Terms & Conditions and our Privacy Policy.