The association between high serum cholesterol levels and the incidence and severity of coronary heart disease (CHD) is so pronounced in epidemiological studies that the National Heart, Lung, and Blood Institute recognizes this association as causal (Expert Panel, 1993) . Recent overviews have indicated that a 1% reduction in a person's total serum cholesterol level yields a 2 to 3% reduction in the risk of coronary heart disease (Manson et al., 1992) . Aerobic fitness and exercise programs such as walking, jogging, and aerobics have been encouraged as a means to reduce total cholesterol, low-density lipoprotein cholesterol (LDL-C), and triglycerides while elevating the "good" high-density lipoprotein cholesterol (HDL-C). Several long-term, or longitudinal, studies have been conducted with healthy individuals to measure the effect of increased physical activity on serum lipoprotein concentrations. The results of these studies have been mixed. This paper will attempt to clarify the association between physical activity and blood lipoproteins.

What are lipoproteins?
Cholesterol is a fat-like substance used to help build cell membranes, make some hormones, synthesize vitamin D, and form bile secretions that aid in digestion. Since fat can't mix with water, which is the main ingredient of blood, cholesterol's most important job is to help carry fat through your blood vessels. Before cholesterol can enter the bloodstream it is coated with a protein. These cholesterol-protein packages are referred to as lipoproteins.

Lipoproteins are transport vehicles in the circulation plasma that are composed of various lipids such as cholesterol, phospholipids, triglycerides and proteins known as apoproteins. The major classes of lipoproteins are chylomicrons, very low-density lipoprotein cholesterol (VLDL-C), LDL-C, and HDL-C. Chylomicrons are the largest lipoproteins, consisting of approximately 85% triglycerides. Triglycerides are the main type of lipids found in adipose tissue and in the diet. Once the triglycerides are removed from the chylomicron at receptor sites in the body, the chylomicron remnant is returned to the liver for further metabolism. The principal lipid of VLDL-C is also triglycerides (60 - 70%).

LDL-C is the primary transport carrier of cholesterol in the circulation. About 50-60% of cholesterol is delivered to the cells by LDL-C. Evidence suggests that LDL-C may directly contribute to the cellular alterations of the inner walls of arteries which may ultimately lead to the development of atherosclerotic plaque (Scann, 1978) . Thus, LDL-C is proposed to be more highly associated with CHD than total cholesterol (Manson et al., 1992) .

On the other hand, HDL-C has an inverse relationship with coronary heart disease, offering a protecting mechanism against the development of CHD (Kannel, Castelli, & Gordon, 1971) . HDL-C is considered to be the most powerful lipid parameter for predicting CHD in people of all ages (Gordon et al., 1977) . The primary function of HDL-C is to transport cholesterol from the tissues and blood to the liver for excretion from the body or synthesis into bile acids. HDL-C also prevents the uptake of LDL-C at receptor sites in the body and participates in the metabolism of other lipoproteins.

HDL-C is predominantly composed of phospholipids and is separated into several subclasses, based on size and particle density. The major subclasses are referred to as HDL2 and HDL3. It is known that females have a higher content of HDL2 than males, which helps to protect women from developing CHD (Wood & Haskell, 1979) .

The Role of Physical Activity on Lipid and Lipoprotein Levels
There is a variety of environmental and personal factors that may influence a person's cholesterol composition such as age, gender, level of body fat, dietary intake of fat, cholesterol and carbohydrates, alcohol consumption, cigarette smoking, medication, menopausal status, and exercise. Because of complex interactions among these variables, it is difficult to assess how each of these factors independently affects cholesterol levels and composition.

Although total cholesterol levels are lower in persons with high aerobic fitness compared to low aerobic fitness, it has not been conclusively demonstrated that exercise training lowers total cholesterol. Measurements made before and after exercise training have produced variable results with no clear consensus as to whether or not moderate or vigorous exercise can lower total cholesterol. In studies where total cholesterol has been significantly reduced, it appears that the activities were more dynamic and vigorous in nature, such as running programs. In contrast to the variable effects of exercise on total cholesterol, endurance exercise consistently lowers triglycerides (Martin, Haskell, & Wood, 1977) . A physically active lifestyle may help to prevent the age-related rise in triglycerides normally observed in men. It also appears that endurance exercise lowers triglyceride levels more so in individuals having elevated initial baseline levels. Lower triglyceride concentrations in the blood have been attributed to increases in skeletal muscle and adipose tissue lipoprotein lipase activity resulting from aerobic training. Lipoprotein lipase is the key enzyme for the breakdown of triglyceride-rich lipoproteins. On a long-term basis, the decrease of body fat that often accompanies endurance training may be a contributing factor for this lowering effect of triglycerides due to exercise.

Like total cholesterol, the impact of habitual aerobic exercise on LDL-C appears to be quite variable. However, the majority of studies comparing endurance athletes to sedentary controls or the general population reported that athletes have lower LDL-C levels, with leaner athletes frequently having the lowest values. Although it appears that endurance training may decrease LDL-C, there is little information about the biochemical mechanism producing this change.

Endurance-trained athletes have much higher HDL-C values compared to sedentary populations (Haskell, 1984) . Although it is not yet definitive, moderate and high intensity aerobic exercise training appears to be associated with elevated HDL-C values. The primary reason for the elevation in HDL-C is an increase in lipoprotein lipase activity in response to exercise. Lipoprotein lipase accelerates the breakdown of triglycerides, resulting in a transfer of cholesterol and other substances to the HDL-C. It is interesting to note that healthy patients whose physical activity was restricted to bed rest for three to six weeks because of some type of traumatic fracture, showed a significant decrease in HDL-C levels (Nikkila, Kuusi, & Myllynen, 1980) .

In addition to aerobic training, there are a few studies suggesting that resistance training may also improve lipid and lipoprotein profiles (Goldberg & Elliot, 1985) . Decreases in total cholesterol and LDL-C have been reported for both men and women, with women also showing a significant decrease in triglycerides, from resistance training (Goldberg et al., 1984). However, the alteration of personal lifestyle habits in conjunction with a decrease in body fat and increase in fat-free mass may contribute to these favorable changes.

Women, Lipoproteins and Exercise
From puberty until menopause, women generally have lower total cholesterol and LDL-C values than men. After menopause, these values equal or exceed those of men, however (Heiss et al., 1980) . Women also tend to have higher HDL-C (mainly HDL2) and lower triglyceride concentrations than men. This may be partially explained by the relatively higher lipoprotein lipase activity in women (Haskell, 1984) . Also, estrogen seems to have a major role in lowering the risk of CHD for premenopausal women (Manson et al., 1992). However, female sex hormones, found in oral contraceptives or used in hormone replacement therapies have variable effects on lipoprotein profiles. Additionally, women who consume alcohol in moderation tend to have higher HDL-C levels than nondrinkers; while women who smoke have much lower levels than nonsmokers (Taylor & Ward, 1993) .

Cross-sectional studies confirm that active women have higher HDL-C levels than their sedentary counterparts. Apparently, the duration and frequency of aerobic exercise may be more important in altering HDL-C than the intensity of the exercise. However, because of the confounding effects of diet, body composition, exogenous hormone use, contraceptive use, alcohol consumption, and age, the specific exercise recommendations for increasing HDL-C have yet to be determined (Taylor & Ward, 1993) .

Although resistance training has become more popular with women the last several years, the effects of this type of training on blood lipid levels needs more research. Nevertheless, one recently published and well-designed study indicated that five months of sustained resistance training significantly decreased total cholesterol and LDL-C in women (Boyden et al., 1993) .
Conclusion
Prevailing evidence supports the concept that physical activity can help slow the progression of CHD. The independent effect of exercise type (aerobic vs resistance training) on total cholesterol, HDL-C, LDL-C, and triglyceride levels is not fully confirmed. A major exercise effect on blood cholesterol levels appears to be an increase in HDL-C as a result of aerobic training. This change is very important because HDL-C is the most critical determinant of CHD. As health and fitness practitioners, designing exercise programs that alter the individual's blood lipid and lipoproteins in a positive way is an important component to be included in your program objectives. Unfortunately, the missing part of the puzzle is just how much exercise is needed to raise HDL-C. Until specific recommendations based on further research are developed, we recommend following ACSM guidelines for frequency, intensity and duration of exercise because these are the most current and scientifically-documented recommendations. In addition to regular physical activity, you can help your clients develop a low-cholesterol living style by advising them about wise food choices, effective weight control measures, and other health-risk factors.

SIDE BARS FOR ARTICLE
Blood Lipid and Lipoprotein Norms

National Cholesterol Education Program, JAMA 269 (23): 3015-3023, 1993.

ACSM Guidelines
Frequency of training 3-5 days per week

Intensity of training 60-90% of maximum heart rate or
50-85% of maximum oxygen uptake or
50-85% of heart rate reserve

Duration of activity 20-60 minutes of continuous aerobic activity

Mode of activity Any activity that uses large muscle groups, can be maintained continuously, and is rhythmical and aerobic in nature

Resistance training Strength training of a moderate intensity, sufficient to develop and maintain fat-free weight should be an integral part of an adult fitness program.
One set of 8-12 repetitions of eight to ten exercises that condition the major muscle groups at least 2 days per week

ACSM. (1990). The recommended quantity and quality of exercise for developing and maintaining cardiorespiratory and muscular fitness in healthy adults. Medicine Science and Sports in Exericse, 22, 265-274.

References
Boyden, T. W., Pamenter, R. W., & Going, S. B. et al. (1993). Resistance exercise training is associated with decreases in serum low-density lipoprotein cholesterol levels in premenopausal women. Archives of Internal Medicine, 153, 97-100.
Expert Panel. (1993). Summary of the second report of the national cholesterol education program (NCEP) expert panel on detection, evaluation, and treatment of high blood cholesterol in adults. Journal of the American Medical Association, 269, 3015-3023.
Goldberg, L., & Elliot, D. L. (1985). The effect of physical activity on lipid and lipoprotein levels. Medical Clinics of North America, 69(1), 41-55.
Goldberg, L., Elliot, D. L., Schutz, R. W., Kloster, F. E. (1984). Changes in lipid and lipoprotein levels after weight training. Journal of the American Medical Association, 252, 504-507.
Gordon, T., Castelli, W. P., Hjortland, M. J., Kannel, W. B., & Dawbaer, T. R. (1977). High density lipoprotein as a protective factor against CHD. The Framingham study. American Journal of Medicine, 62, 707-714.
Haskell, W. L. (1984). The influence of exercise on the concentrations of triglyceride and cholesterol in human plasma. Exercise and Sport Sciences Reviews, 12, 205-244.
Heiss, G., Tamir, I., & Davis, C. E. et al. (1980). Lipoprotein-cholesterol distributions on selected North American populations. The Lipid Research Clinic Program Prevalence Study. Circulation, 61, 302-315.
Kannel, W. B., Castelli, W. B., & Gordon, T. (1971). Serum cholesterol, lipoproteins and the risk of coronary heart disease. Annals of Internal Medicine, 74, 1-12.
Manson, J. E., Tosterson, H., Ridker, P. M., Satterfield, S., Hebert, P., G.T., O., Buring, J. E., & Hennekens, C. H. (1992). The primary prevention of myocardial infarction. The New England Journal of Medicine, 326, 1406-1416.
Martin, R. P., Haskell, W. L., & Wood, P. D. (1977). Blood chemistry and lipid profiles of elite distance runners. Annals of New York Academy of Science, 301, 346-360.
Nikkila, F. A., Kuusi, T., & Myllynen, P. (1980). High-density lipoprotein and apolipoprotein A-I during physical inactivity. Athersclerosis, 37, 457-462.
Scann, A. M. (1978). Plasma lipoproteins and coronary heart disease. Annals of Clinical and Laboratory Science, 8, 79-88.
Taylor, P. A., & Ward, A. (1993). Women, high-density lipoprotein cholesterol, and exercise. Archives of Internal Medicine, 153, 1178-1184.
Wood, P. O., & Haskell, W. L. (1979). The effect of exercise on plasma high density lipoprotein. Lipids, 14, 417-427.