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Lifestyle Management of Dyslipidemia

Sorace, Paul M.S., CSCS; LaFontaine, Thomas Ph.D., FACSM, CSCS, NSCA-CPT; Thomas, Tom R. Ph.D.

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ACSM's Health & Fitness Journal: July 2006 - Volume 10 - Issue 4 - p 18-25
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Dyslipidemia

Abnormal blood lipids, known as dyslipidemia, are an increasing health problem in the United States and the world. Approximately 107 million American adults have borderline or high total cholesterol (1) (see Table 1 for cholesterol guidelines). Dyslipidemia is one of the major risk factors for heart disease (1-4). Excess cholesterol builds up in the walls of the arteries. Over time, this buildup contributes to atherosclerosis, a disease process in which arteries become narrowed and blood flow is impaired. If the blood supply to a portion of the heart is completely cut off by a blockage, the result is a heart attack.

Table 1
Table 1:
Cholesterol Guidelines Based on the National Cholesterol Education Program Adult Treatment Panel

There are a number of different forms of dyslipidemia. Hypercholesterolemia indicates elevated blood cholesterol levels (2). Hypertriglyceridemia implies elevated triglycerides (TGs). Hyperlipidemia indicates elevated cholesterol and TGs. Hyperlipoproteinemia is defined as elevated lipoproteins (2). Hypoalphalipoprotein syndrome denotes low high-density lipoprotein (HDL) cholesterol (2). Postprandial lipemia (PPL), discussed in greater detail later, is characterized by a postprandial rise in TG-rich lipoproteins after eating.

One of the first steps in atherogenesis is the infiltration and entrapment of low-density lipoproteins (LDLs) in the blood vessel wall. This leads to a series of events (e.g., oxidation of LDLs, monocyte migration, macrophage uptake of modified LDLs, foam cells, fatty streaks, etc.) that result in the development of fibrous plaques within the walls of the intima.

Dyslipidemia is caused by genetic and environmental factors that lead to problems with enzyme deficiencies, apolipoproteins, or lipoprotein particles. There are a number of factors that contribute to dyslipidemia (see Table 2 for a partial listing).

Table 2
Table 2:
Causative Factors for Dyslipidemia

Dyslipidemia also is a characteristic of the recently defined metabolic syndrome. The metabolic syndrome consists of a group of coronary heart disease (CHD) risk factors which includes glucose intolerance (fasting plasma glucose of 100-125 mg/dL), atherogenic dyslipidemia (TGs ≥150mg/dL and HDL cholesterol <40 mg/dL in men and <50 mg/dL in women), increased blood pressure (≥130/85 mm Hg), abdominal obesity (waist circumference of 102 cm or greater in men and 88 cm or greater in women), a prothrombotic state, and a proinflammatory state (5). A prothrombotic state is a condition that predisposes to venous or arterial thrombosis. A proinflammatory state is the presence of low-grade generalized inflammation within the body that increases cardiac risk.

Lipoproteins are the carriers of lipids (primarily cholesterol and TGs) in the blood. Because fat and water do not mix, the body combines protein plus lipid so that the lipid substance can be transported in plasma. There are several lipoproteins in the body, with different functions (see Table 3). Some contribute to cardiovascular disease (e.g., LDLs) and some help prevent it (e.g., HDLs). In summary, dyslipidemia refers to an abnormality of lipoproteins, covering a variety of disorders relating to abnormal levels of total cholesterol, LDL cholesterol, HDL cholesterol, and/or TGs.

Table 3
Table 3:
Cholesterol/Lipoprotein Classes
Figure
Figure

Postprandial Lipemia

Postprandial lipemia (PPL) refers to the rise in TG-rich lipoproteins (e.g., very low density lipoproteins [VLDLs]) after a meal. It is a dynamic condition in which humans spend the majority of their time (7). PPL reflects a combined measure of an individual's capacity to metabolize TGs. Elevated/prolonged PPL, defined as a delayed clearance of TGs after a high-fat meal, is a significant risk factor for the development of atherosclerosis (7, 8). The exchange of core lipids between postprandial lipoproteins and LDLs/HDLs increases during prolonged PPL in susceptible persons, resulting in elevated TGs; the production of small, dense LDL particles; and reduced HDLs (7). Smaller, denser LDLs are more atherogenic than the larger, less dense LDLs. Other atherogenic factors including clotting factors, platelet reactivity, and monocyte and cytokine expression, all of which contribute to endothelial dysfunction, may increase during PPL (7).

Testing for PPL involves a 12-hour fast and initial blood collection. Subjects then ingest a high-fat beverage, and blood samples are collected every 2 hours for 8 hours. Triglyceride concentrations are measured by colorimetry (quantitative chemical analysis by color), and values are plotted over time. PPL is assessed using total area under the curve (AUC). A large value for TG area AUC indicates that the TGs were maintained in the blood longer than expected.

Exercise Effects on Lipid Metabolism

The lowering of TGs is the most consistent effect exercise has on lipoproteins. HDLs often are increased with sustained aerobic exercise that results in an expenditure of >1,200 calories/week, but this effect is less consistent and may be genetically predetermined (9). The greater the exercise volume (and caloric expenditure), the more likely an exerciser will achieve a significant increase in HDL cholesterol. Lower TGs are typically observed with both acute exercise and sustained aerobic exercise training (3). TGs are used as energy by skeletal muscles during endurance exercise. The enzyme lipoprotein lipase (LPL) splits TGs from VLDLs, making them available for uptake by skeletal muscles. Chronic exercise training also increases hepatic HDL production and the conversion of HDL3 to HDL2 in the blood, both of which protect against heart disease (3).

Figure
Figure

The evidence for exercise alone reducing LDLs and total cholesterol is less conclusive. It appears that weight loss/fat loss is required for significant reductions in LDLs and total cholesterol (3, 10). Regular aerobic exercise does, however, produce favorable changes in LDL subfractions, which will reduce the risk of CHD. For example, aerobic exercise has been shown to convert smaller LDLs to larger LDLs, reducing cardiac risk (3, 11).

Exercise training also favorably alters lipid enzyme activity, resulting in improved lipid profiles. Table 4 lists and defines the major enzymes involved in lipid metabolism. LPL and lecithin-cholesterol acyltransferase are increased with aerobic exercise, whereas hepatic lipase is usually decreased (3). The effects of exercise training on cholesterol ester transport protein are inconclusive at this time (3). Genetic deficiencies can alter the exercise response for some individuals. For example, LPL activity will not be increased in those who have a LPL deficiency (2). It was recently demonstrated in 35 pairs of monozygotic twins (active twins ran a mean of 63 km/week vs. a mean of 7 km/week in the inactive twins) that low HDL cholesterol may be largely determined by genetic factors and is less effectively treated with vigorous exercise (12).

Figure
Figure
Table 4
Table 4:
Lipid Enzymes

Lifestyle Effects on Dyslipidemia

National Cholesterol Education Program III recommends nutritional intervention, increased exercise/physical activity, and weight loss for many individuals with dyslipidemia (5). There is substantial evidence to support the profound beneficial effects of lifestyle changes on dyslipidemia (3, 4, 10, 11). Although there are a number of medications (e.g., statins) that are effective for treating dyslipidemia, lifestyle changes alone can often normalize lipid profiles. Lipid lowering typically results in modest plaque regression and stabilization, reducing the risk of a cardiac event (3).

Regular aerobic exercise is an essential lifestyle component for improving/controlling blood lipids. The total amount of physical activity seems to be more important than the intensity to induce beneficial effects on lipoproteins (10, 11). Significant daily and weekly energy expenditures are recommended to produce notable changes in individuals with dyslipidemia (3, 4, 10). Cross-sectional studies have shown that lipids continue to improve across weekly running distances from <10 to >40 miles in a direct dose-response relationship (13).

The effect of exercise on PPL also is significant. Individuals who regularly perform aerobic exercise typically display low levels of PPL (14). Vigorous aerobic exercise has been shown to reduce PPL in men with elevated TGs, even when performed 12 hours before a high-fat meal (15). In a recent study, intermittent exercise in young, normolipidemic men and women was shown to improve PPL significantly more than continuous exercise (16). The breakdown of blood TGs (and some TG-rich lipoproteins) is increased during exercise and continues well into the recovery phase. Exercise that stimulates fat use as a substrate during and after the activity helps clear TG from the blood. In addition, exercise stimulates the enzyme LPL and this enzyme may remain active for several hours. Thus, moderate intensity exercise attenuates PPL (17, 18). It is important to note that the favorable effects (e.g., TG lowering) of endurance exercise on PPL seem to be a result of acute metabolic changes as opposed to chronic exercise effects (14, 15). This encourages daily or near daily aerobic exercise to treat elevated PPL. Possible mechanisms for the exercise-induced TG reductions include increased muscle LPL activity and reduced hepatic TG secretion (14, 17).

There only have been a couple of studies on resistance training and PPL, and the results were inconsistent (19, 20). Thus, there are no specific guidelines to recommend at the present time.

Weight loss is another lifestyle factor that significantly improves dyslipidemia. Obesity typically elevates VLDL and LDL fractions, increases TG levels, lowers HDL cholesterol, increases blood pressure, and promotes insulin resistance. Weight loss typically lowers LDLs, TGs, and total cholesterol (2, 3). HDLs may increase, decrease, or remain the same (2, 3). If weight loss is combined with aerobic exercise, HDLs are more likely to be sustained or increase following training. Weight loss also lowers blood pressure, improves glycemic control, and reduces inflammation linked to metabolic and cardiac diseases (3, 5, 21, 22).

Exercise training can improve lipid profiles either directly (without weight loss) by increased lipid enzymatic activity or indirectly (reduced body weight) (2). When weight loss occurs in conjunction with exercise, LDL and total cholesterol are usually lowered (2, 3). Weight loss also has beneficial effects on lowering PPL, as obesity increases PPL. When weight loss is indicated, a loss of 5% to 10% body weight from baseline is a starting goal (4). This amount of weight loss can significantly improve blood lipids. However, even when there is minimal or no weight loss, an improved lipid profile can still be achieved with adequate exercise (11).

Exercise/Physical Activity Guidelines

It is prudent that the fitness professional check with the individual's physician if he or she is taking lipid-lowering medications or other medications for any coexisting diseases (e.g., obesity, hypertension, type 2 diabetes) that may require medical clearance. Statins, for example, can cause muscle damage (myopathy) and this should be considered (4). Table 5 summarizes general exercise guidelines for dyslipidemia. The emphasis should be on aerobic exercise and total weekly caloric expenditure. A good initial goal is to perform aerobic exercise three to five times per week for 20 to 60 minutes, expending ≥1,200 calories/week. Ideally, aerobic exercise for dyslipidemia should gradually progress, as tolerated, to five to seven times per week for 40 to 60 minutes, creating an energy expenditure of >2,000 calories/week (4). A gradual increase in aerobic exercise intensity should also occur. Exercise programs with higher volumes and intensities have been shown to be most effective for increasing HDL cholesterol (11). These guidelines may also need adjusting based on coexisting diseases, current fitness level, and time constraints that may be present. The aerobic training may need to be performed intermittently throughout the day. It is important to remember that lifestyle physical activity (e.g., climbing stairs, lunchtime walks, housework) contributes to the total weekly energy expenditure. Also, for a well-rounded exercise program, resistance and flexibility training should be incorporated (see Table 5 for guidelines).

Table 5
Table 5:
Summary Exercise Programming

Nutritional Guidelines

Dietary modification is a powerful nonpharmacological strategy for improving blood lipids. Diets that are high in saturated and trans-fat and cholesterol increase TGs, LDL, and total blood cholesterol. Polyunsaturated fats (e.g., corn oil) seem to have a neutral effect on blood cholesterol, whereas monounsaturated fats (e.g., olive oil) seem to sustain HDLs and lower LDLs and TGs. Reducing saturated and trans-fats and cholesterol intake will usually improve blood lipids. Even though there is variability in individual responses to dietary changes, reducing total calories consumed, particularly saturated fat calories, which results in weight loss, typically lowers total and LDL cholesterol. HDL cholesterol is sometimes lowered as well, but when dieting is coupled with exercise, HDL cholesterol can be maintained (2, 3, 23, 24).

High-carbohydrate diets can increase TG levels and decrease HDL cholesterol, but again, this effect is negated with aerobic exercise (2, 3, 23, 24). Dietary fiber, particularly soluble fiber, helps to lower blood cholesterol levels. Omega-3 fatty acids lower blood TG levels (3). Plant sterols also have been shown to favorably alter lipid profiles, particularly when combined with aerobic exercise (25). Moderate alcohol consumption (no more than one drink per day in women and lighter persons and no more than two drinks per day in most men) (4) may raise HDL cholesterol levels. It may also increase TGs, but its effect on LDL cholesterol appears to be minimal.

Table 6 summarizes the key components of a diet to help lower blood lipids. The emphasis should be on restricting fat, particularly saturated fats, and cholesterol intake while increasing intake of soluble fiber and other foods such as soy, almonds, walnuts, plant sterols and stanols, cold water fish (e.g., salmon), etc., which have been shown to have a beneficial effect on blood lipids. Here are some nutrition tips that favorably help impact blood lipids:

  • Eat fish two to three times per week. The fish should be baked, not fried.
  • Use healthy oils for cooking, such as olive oil and walnut oil.
  • Eat whole grain products. Avoid or limit starchy white pasta and bread.
  • Add or increase oats and oatmeal intake.
  • Increase consumption of green vegetables. Broccoli, spinach, lettuce, and green beans are all examples of healthy carbohydrate, low-calorie green vegetables.
  • Eat whole fruits and berries.
  • Avoid/reduce rich, fattening desserts.
  • The amount of each type of fiber varies in different plant foods. To receive the greatest health benefit, eat a wide variety of high-fiber foods.
Table 6
Table 6:
Healthy Dietary Guidelines for Improving Blood Lipids

Case Study

In December of 2003, a 75-year-old man was referred for lifestyle management to lose body weight and manage cardiovascular risk factors. On medical history and physical fitness, he was found to have had a recent surgical repair of a left quadriceps muscle rupture and had gained 45 lbs over six to eight months of recovery and rehabilitation. He had a history of dyslipidemia and overweight but was not diabetic nor hypertensive. He was a nonsmoker, and his mother and father died of cardiovascular disease at age 78 and 84, respectively. He has been an avid golfer since retirement in 1995, walking nine holes, three days/week. He also has been very active in his daily life but had not been following a regular exercise program. His dyslipidemia was being treated only with Altaprev, 20 mg/day, started in April of 2001. He had had no advice in regard to weight loss, exercise, or other therapeutic lifestyle changes. He was enrolled in the INTERXVENTUSA Cardiovascular Risk Reduction Program (www.interventusa.com). After one year, he had lost 43 lbs (from 244 to 201 lbs). He was eating a low-fat, high-fiber diet (22% fat calories and 45 g of fiber per day by seven day food recall) and exercising 260 minutes/week on average (walking 200 minutes and Airdyne bicycle ergometer 60 minutes). Lipid changes with indicated therapy from 04/01 through 01/05 are summarized below:

Table
Table

Summary

Dyslipidemia is a condition that promotes the genesis and progression of atherosclerosis. Dyslipidemia and PPL can often be prevented or treated with lifestyle management of exercise/physical activity, proper nutrition, and weight loss (if needed). Having a sound knowledge of lipid disorders, their associated risks, guidelines for treatment, and understanding how lifestyle management can prevent/improve dyslipidemia will better enable the fitness professional to coach individuals to live healthier lives.

Condensed Version and Bottom Line

A large body of evidence suggests that dyslipidemia is directly related to the progression of coronary artery disease. Lifestyle changes, which include increased exercise/physical activity, dietary modifications, and weight loss (if needed) have profound effects on improving dyslipidemia and other lipid disorders such as PPL. This will result in a lower rate of coronary artery disease.

Recommended Readings

Durstine, J. Larry, Ph.D. ACSM Action Plan for High Cholesterol. Human Kinetics, 2006.
    ACSM Fitness Book. 3rd ed. Human Kinetics, 2003.
      Cooper, Kenneth H., M.D., MPH. Controlling Cholesterol the Natural Way: Eat Your Way to Better Health With New Breakthrough Food Discoveries. Bantam, 1999.
        http://www.americanheart.org
          http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3_rpt.htm
            http://www.nutrition.gov/
              http://www.shapeup.org

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                  Keywords:

                  Cholesterol; Dyslipidemia; Postprandial Lipemia; Exercise; Physical Fitness

                  © 2006 American College of Sports Medicine