Exercise intensity: Its effect on the high-density lipoprotein profile

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Exercise Intensity: Its Effect on the High-Density Lipoprotein Profile Ten-i Spate-Douglas,

MHS, RN, Randall E. Keyser, PhD

ABSTRACT. Spate-Douglas T, Keyser R. Exercise intensity: its effect on the high-density lipoprotein profile. Arch Phys Med Rehabil 1999;80:691-5. Objective: To determine the effect of aerobic exercise intensity on the active subfraction of serum high-density lipoprotein (HDL) concentration. Design: A randomized control, before-and-after investigation that tested the hypothesis that high-intensity exercise training would result in improvements in serum concentrations of HDL subfraction 2 (HDL2) greater than those accompanying moderate-intensity training. Setting: Exercise tests were completed in a hospital stress testing laboratory, and cholesterol analyses were performed in a university research laboratory. Exercise training was performed in the community at a site determined by the subject. Subjects: Subjects were 25 healthy female employees of a teaching hospital. Intervention: Maximum treadmill tests and serum cholesterol profiles were assessedin 25 women before and after a 12-week aerobic walking regimen; 12 women in a highintensity exercise group (HIG) walked at a target heart rate of 80% and 13 women in a moderate-intensity exercise group (MIG) walked at a heart rate of 60% of their heart rate reserve for a distance of 2 miles three times weekly. Main Outcome Measures: The main dependent variable was HDL,; other measures of the HDL profile were total HDL and HDL+ Peak oxygen uptake (VO2) was also evaluated as a dependent variable to ensure a general aerobic adaptation resulted from the exercise regimen. Measures were analyzed as pretraining to posttraining change scores and absolute values using independent and dependent t tests as appropriate. Statistical significance was assigned at p < .05. Results: Total HDL was 32.3 Itr 8.5mg/dL before and 40.3 t 10.6mg/dL after training in the MIG and 31.6 2 6.2mg/dL before and 38.2 t 12.0mg/dL after training in the HIG. HDLz was 14.2 2 5.7mg/dL before and 18.5 -+ 6.9mgldL after training in MIG. HDLz was 13.0 t 6.2mg/dL before and 19.6 ? 8.9mgldL after training in the HIG. Total HDL and HDL2 increased significantly in both groups as a result of exercise training, and intragroup differences were not observed. HDL3 was not affected by exercise training. Training resulted in significant increases in peak VOZ in both MIG and HIG (29.0 + 5.0 to 31.9 ? 5.4mL/kg/min in the MIG and 30.7 + 5.2 From the School of Health Sciences, Grand Valley State University, Allendale, and Cardiovascular Physiology and Rehabilitation Section, Butterworth Hospital, Grand Rapids, MI (Ms. Spate-Douglas), and the Department of Physical Therapy, University of Maryland School of Medicine, Baltimore, MD (Dr. Keyser). Submitted for publication July 20, 1998. Accepted in revised form December 16, 1998. No commercial party having a direct financial interest in the results of the research supporting this article has or will confer a benefit upon the authors or upon any organization with which the authors are associated. Reprint requests to Terri Spate-Douglas, RN, MHS, Doctors Medical Center, Cardiac Rehabilitation Department, 1441 Florida Avenue, PO Box 3438, Madesto, CA 95355. 0 1999 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation 0003-9993/99/8006-5136$3.00/O

to 33.5 2 6.3mL/kg/min in the HIG). Intergroup differences in change scores for peak VOZ, HDL, and HDL2 were not observed. Conclusion: The results and analyses did not support the hypothesis that the HIG would acquire increases in HDLz profile beyond those observed for the MIG. Moderate-intensity training was sufficient to improve the HDL profile, and high-intensity training appeared to be of no further advantage as long as total training volume (total walking distance per week) was constant. 0 1999 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation

E

PIDEMIOLOGIC STUDIES have identified a strong inverse relationship between plasma high-density lipoprotein (HDL) and coronary atherosclerosis.1-4HDL has been underscored as the strongest predictor of both prevalence and severity of atherosclerosis5,6and is thought to be the primary carrier mechanism in reverse cholesterol transport. Serum concentrations higher than 60mg/dL appear to exert a protective effect against atherosclerosis.4 Information obtained from the Helsinki Heart Study7 suggest that therapies that increase HDL are associated with a decrease in the incidence of coronary artery disease. Angiographic analyses of this relationship have varied. Serum HDL exists in two forms, HDLz and HDLa; the former is thought by most to be the active and protective subfraction.5,8 Total serum HDL concentrations greater than 42mg/dL and HDLz levels higher than 25mg/dL have been associated with 3.32- and 4.0-fold decreasesin the risk of acute myocardial infarction.* Failure to differentiate among HDL and the HDLz and HDLs subfractions may explain some of the variation among angiographic findings leading to the inability to corraborate reports of reduced coronary artery disease associated with HDL-increasing therapies. Physical activity positively influences HDL2 levels9,10and is associated with decreasesin morbidity and mortality.‘i Physical activity thresholds for cardiorespiratory fitness’* have been identified. Specific training volume and intensity requirements for favorably changing HDLz levels are not known. The purpose of this study was to determine the effect of highversus moderate-intensity cardiorespiratory exercise training on serum HDLz concentrations. We arbitrarily selected a 12-week exercise training duration to coincide with other ongoing health promotion programs sponsored by the institution. SUBJECTS AND METHODS Subjects The subjects of the study were 25 female employees of a 529-bed teaching hospital and their acquaintances who answered in-house advertisements and volunteered to participate in the study. Inclusion criteria included absence of pertinent medical or health history indicative of cardiovascular, pulmonary, neurologic, metabolic, or musculoskeletal diseases that would limit exercise or training at the time of the study. In Arch

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addition to those recommended by the American College of Sports Medicine,12 exclusion criteria included lipid-altering medications, antihypertensive medications, medications known to limit the heart rate or blood pressure response to exercise, abnormal electrocardiogram or blood pressure, cigarette smoking or recent history of smoking cessation, and participation in a routine exercise program during the 6 months before the study. The subjects were randomly assigned to two groups: a moderateintensity exercise group (MIG) of 13 subjects and a highintensity exercise group (HIG) of 12 subjects. The descriptive characteristics of the subjects are summarized in table 1. Age and height were similar for both groups. Body weight was significantly higher in the MIG than in the HIG. The rationale for the study, procedures, risk of participation, confidentiality, and rights as a human subject were explained, and written consent to participate was obtained from each subject in accordance with the respective institutional human rights committees. Apparatus Heart rate and electrocardiogram were measured using a 1Zlead electrocardiograph with electrodes placed in the MasonLikar configuration.13 Tests were conducted on a motorized treadmill with speed and percent grade controlled by a microprocessor. The exercise intensity was automatically increased every 3 minutes according to the standard Bruce protocol.12 Oxygen uptake and other cardiorespiratory variables were measured using a metabolic cart. Blood pressure was auscultated at the brachial artery using a mercury sphygmomanometer and stethoscope. A 21-gauge needle and a 1OmL heparinized plastic test tube were used for each blood sample. Training information from the thrice-weekly home exercise sessionswas recorded by each subject in a personal exercise log with space for date; pulse rate before, during, and after exercise; distance walked; duration of session; and general comments. Procedure Subject evaluation. General information regarding a walking health program was distributed throughout the hospital. Women who were interested in the program were informed of the study and chose to participate either in the study or in the walking program only. Women who self-selected to be part of the study underwent an initial interview, had blood drawn for cholesterol measurement, and underwent a maximal exercise test no longer than 24 hours after the blood was drawn. During the initial interview, the informed consent procedure was completed and the health history was obtained. Participants were instructed to abstain from food, beverages (with the exception of water), and exercise for at least 12 hours before blood was drawn. After the 1Zhour fast and while observing universal precautions, a 21-gauge needle was inserted into the median cubital vein and 1OmL of blood was extracted and frozen immediately. Within 24 hours of the blood draw, subjects completed a maximal treadmill exercise test. Resting heart rate, electrocardiogram, and blood pressure were measured after a 5-minute Table

1: Subject

Demographics MIG

Age (vs) Height (cm) Pretraining weight Posttraining weight Data

are reported

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41 2 162 2 762 752

2 SD.

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HIG 8 8 19 19

38 rt 8 165 + 4 64 t 7

64 2 7

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rest in the supine position. After resting information was recorded, subjects walked on the treadmill as the Bruce protocol was initiated and advanced. Heart rate was measured continuously. Blood pressures and 12-lead electrocardiograms were recorded every 3 minutes and at peak exercise. The test endpoint was volitional exhaustion. After the test, subjects completed an active cool-down and sitting rest while remaining on the electrocardiographic monitoring equipment for at least 6 minutes and until heart rate and blood pressure approximated baseline. Exercise training. Using data obtained from the maximal exercise tests, target heart rates were calculated by the heart rate reserve method with training intensity set at 60% heart rate reserve for the MIG and 80% heart rate reserve for the HIG. The procedure for these calculations was as follows: Target for MIG = 0.6 (PeakHeart Rate - Resting Heart Rate) f Resting Heart Rate or Target for HIG = 0.8 (PeakHeart Rate - Resting Heart Rate) + Resting Heart Rate. After computation of the target heartrate, subjectswere instructedin palpation of the radial pulse. Radial pulse rate was used to monitor the exerciseintensity, and subjectsadjustedwalking pace to maintain the target heart rate. Subjectswere then instructedto participate in a home-based exerciseprogram by walking 2 miles three times per week at their individually prescribed target heart rate. A slow walking warm-up period of 5 minutes before training and a cool-down period of 5 minutes after training were also recommended to the participants.These periods were not included in the 2-mile training distance.Training logs were completed after each exercisesession.Pulserate was recorded in the training log before, during, and after each exercisesession.Logs were used to ensure compliance with the training recommendations.Minimum compliance was accepted as participation according to the exercise prescription in at least 80% or 29 of the 36 sessionsprescribed for the study. The importance of accurate monitoring of intensity, recording of information, and program adherencewas emphasized biweekly at meetingsof program participantsand studypersonnelto review the exerciselogs and subjectprogress.Subjectsfalling below the 80% adherencerequirement were dismissedfrom the study. Subject reevaluation. After completion of the exercise training phase, subjects again fasted and refrained from exercise in a manner similar to the initial evaluation. Blood was drawn for the posttraining cholesterol analysis. A posttraining maximal treadmill test was completed using the Bruce protocol. All data collection procedures were similar for the pretraining and posttraining evaluations to facilitate test-retest comparison. Subfractionation of HDL. Blood samples were immediately frozen at the time of acquisition in a 1OmL heparinized test tube. Samples remained frozen until all samples had been obtained. All samples were then analyzed using the same laboratory equipment on the same day. A modification of the procedures of Wamick and colleagues14-16was used to subfractionate HDL. The validity of this method as well as other dual-precipitation procedures is generally accepted.17-21The method required two precipitations with dextran sulfate solution containing different amounts of magnesium chloride. Total HDL was measured after serum low-density lipoprotein and very low-density lipoprotein were selectively precipitated by magnesium-dextran sulfate and removed by centrifugation. The supematant contained the cholesterol associatedwith the soluble

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concentration of magnesium chloride-dextran solution to precipitate HDLs. The final supernatant was analyzed for HDLs, and the difference in the total HDL and HDLs was recorded as a close approximation of HDL2. Statistics and Research Design This study used longitudinal, prospective, and postselection randomization methods and a two-group, repeated-effects design to study the effect of training intensity on changes in the plasma HDL profile. It was hypothesized that exercising at an intensity of 80% heart rate reserve would increase serum HDLz more than exercising at an intensity of 60% heart rate reserve. Independent t tests were used to test this hypothesis; the independent variable classes were the MIG and HIG. Dependent variables included total HDL and HDLs, as well as HDL2. Other dependent variables assessedby independent t tests were peak VOz, heart rate, and test duration. These variables were used to determine the presence of a cardiorespiratory training adaptation. Variables were assessedas the actual values corresponding to the variables before and after training as well as the associated change scores. Dependent t tests were used to assess the intragroup pretraining versus posttraining differences. Onetailed probability of type I error 55% was required for significance (p 5 .05). All data are reported as means i SD. RESULTS Resting heart rate was similar for the MIG (pretraining, 80 5 9; posttraining, 75 5 10) and the HIG (pretraining, 78 I 11; posttraining, 77 2 8) before and after training. Heart rate (table 2) increased during exercise (p < .Ol), and a significant difference in the heart rate response was not observed between the MIG and HIG. Training heart rate was approximately 140beats/min for the MIG and 160beats/min for the HIG. As a result of training (table 3), exercise test duration and peak VOz were increased (p < .005) for both the MIG and the HIG. Improvement in exercise capacity was similar for both groups. Total cholesterol decreased significantly (p i .025) in the HIG but not in the MIG as a result of training (table 3). Total HDL before training was within ranges associated with increased risk for atherosclerosis in both the MIG and the HIG. Pretraining and posttraining total HDL, HDLz, and HDLs concentrations were similar for the MIG and the HIG (table 3). Similar increases in total HDL (p < .02) and HDLz (p < .03) were observed for both groups (table 4). When expressed as a percentage of the pretraining concentrations, total HDL increased by 25% for the MIG and 21% for the HIG. Percent increase in HDLz was 50% for the HIG and 31% for the MIG. HDLa was not significantly altered by exercise training. When analyzed as a percentage of total HDL, the proportion of HDL2 Table

2: Exercise

Responses

Before

and After

Training

MIG Peak heart Before After Test duration Before After Peak oxygen

HIG

rate (beats/min) 180 5 14 179 t 14

178 -c 11 182 t 12

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Table

3: HDL Profile

Before

and After

Training

MIG Total cholesterol Before

188 i

After Total HDL (mg/dL) Before

HIG

36

193 2 34 181 + 40*

187 + 34

After HDL2 (mg/dL) Before After HDLB (mg/dL) Before After

32.3

_t 8.5

40.3

I

31.6 38.2

10.6*

i i

6.2 12.0”

14.2 i- 5.7 18.5 2 6.9*

13.0 + 6.2 19.6 + 8.9”

18.2 ir 5.4 21.7 i- 6.7

17.8 + 5.6

Data are reported as mean t SD. * Significantly different from before

training

18.6 t

5.6

concentration,

p 5.05.

relative to total HDL increased with training from 41.1% t 3.4% to 51.3% t 4.7% in the HIG (p < .005) but not in the MIG (44.0% f 3.6% before training and 45.9% -t 4.2% after training). Before training, %HDL2/HDL was similar for the HIG and the MIG. After training, %HDL2/HDL was significantly higher for the HIG (p < .O1). DISCUSSION Both the high- and moderate-intensity exercise training regimens resulted in aerobic adaptations and elicited similar improvements in HDL profile. Improvements in both total HDL and HDLz were observed. Statistically significant and clinically relevant improvements in peak VOz, HDL, and HDLz indicated that the statistical power of the sample was sufficient to identify important, exercise training-mediated differences in pretraining and posttraining measures. The data did not support the hypothesis that high-intensity training would increase serum [HDLlJ more than moderate-intensity training. It was concluded that high-intensity training offered no generalizable benefit over moderate-intensity training in improving plasma concentrations of HDL and HDL2. HDL is inversely related to atherosclerosis.1-3,7Serum HDL concentrations lower than 35mg/dL are thought to be associated with increased risk for atherosclerosis,4*22and concentrations of 60mg/dL or higher have been cited as a negative risk factor.4 Each lOmg/dL increase in HDL results in a 50% reduction in the risk of atherosclerosis,23and every lmL/dL increment in HDL appears to be associated with a 3.2% to 3.9% decrease in the incidence of coronary heart disease.2,24Even small increases in HDL levels may result in a large reduction in the risk of atherosclerosis. HDL levels were increased after training by approximately 8mg/dL in the MIG and 7mg/dL in the HIG, representing 35% and 40% reductions in the risk of atherosclerosisz3 Thus, even moderate training resulted in dramatic improvement in the risk of diseases such as coronary heart disease, peripheral arterial disease, and stroke. Total plasma HDL can be profiled by the proportions of its Table

4: Training-Induced

Changes

in the

HDL Profile

(min)

uptake

7.98

+ 1.68

8.53

? 2

9.22

t

9.75

+ 2.32”

I.951

(mUkg/min) 29.0 31.9

Before After Data are reported as mean * Significantly higher than

t SD. before

training,

2 5.0 i: 5.4”

p 5 .05.

30.7

t

33.5

-t 6.3*

5.2

MIG

HIG

7.9 t 9.9, 4.4 2 6.3*

Total HDL (mg/dL) HDLZ (mg/dL) HDLB (mg/dL)

6.6 i

3.6 -t 7.7

Data are reported as mean -C SD. Change minus pretraining plasma HDL. * Significant change, p 5 .05.

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6.5 i 8.3* 0.8 i 4.5 score

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subfractions HDL2 and HDLs. HDLz concentration is a strong predictor of the presence and severity of coronary atherosclerosis.7,8Exercise training-mediated antiatherogenic properties of the HDL profile appear to be specific to the HDLz subfraction.5s6,gJ0Although neither group increased [HDLz] to levels high enough to minimize atherosclerotic risk, the significant posttraining increase in [HDLz] underscored the effectiveness of aerobic training in improving the risk for atherosclerosis. Prolonged training duration beyond 3 months and increased total caloric expenditure per session are likely to have resulted in further improvements in the HDL profile. Well-accepted guidelines for the quantity of exercise, or training volume, necessaryto develop and maintain cardiorespiratory fitness have been established.22A variety of methods are available for monitoring intensity, many of which are based on the linear relationship of heart rate and V02.12 The heart rate reserve method closely corresponds to similar percentages of maximal V02.12 Previous studies have demonstrated that moderate training intensities are adequate to elicit improvements in HDL.2s-28 Findings of the current study were in agreement, indicating that moderate intensity activity is sufficient to increase total plasma HDL and HDLz concentrations. Inaccuracy in intensity monitoring would effect this conclusion, particularly if subjects in the HIG reported exercising at higher intensities than they actually attained during the sessions.It is doubtful if those in the MIG exercised consistently at intensities higher than those of the study protocol. Twice-weekly reinforcement and keeping of training logs were methods implemented to control reporting inaccuracy as a source of error. Even if inaccurately high training heart rates were recorded in the exercise logs, the results still indicated that moderate-intensity exercise is sufficient for improving the risk for atherosclerosis. The short-term exercise response has been studied with respect to immediate and long-term recovery changes in total HDL. Stationary cycling for 30 minutes at 60% of the age-predicted maximal heart rate has been found to increase total HDL.2g Hughes and associates30reported that at a constant intensity, exercise sessions of 45 minutes produced longerlasting total HDL increases than sessions of 30 minutes, illustrating the effect of exercise duration and training volume on HDL profile changes. Crouse and coworkers31 observed increased total HDL 24 hours after single bouts of cycling but found no difference in this increase between high and moderate intensity trials as long as caloric expenditure was held constant. HaskelP reviewed the literature and suggested that the threshold for effecting plasma lipoprotein changes may be a weekly training volume of approximately 1,OOOkcal.Collectively, these studies underscore the necessity of holding the training volume constant when evaluating the effects of differing training regimens on the HDL profile. At a given weekly frequency, training volume can be controlled by increasing duration inversely with reduction of intensity to hold constant the number of calories expended throughout the activity. Training distance can also be held constant because the number of kilocalories required to cover a distance is constant within a range of velocities when walking on a treadmill or relatively flat terrain. The current study did not assessthe short-term HDL profile response to exercise. Factors other than exercise that positively affect HDL include cigarette smoking cessation and weight reduction to ideal body weight.33 It is possible that increased body weight contributed to the baseline levels of HDL that were lower than desired to improve risk of atherosclerosis in the MIG. Body weight did not change in either group, however, so weight reduction was not a determinant of observed improvement in the respective HDL Arch

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profiles. This study maintained a constant training volume by having subjects in the HIG and the MIG walk similar distances. Both training regimens resulted in similar improvements in the HDL profile. The finding that intensities of 60% and 80% heart rate reserve had similar effects on the HDL profile was most likely caused by the similar training volumes over the 12-week training duration. CONCLUSION This study tested the hypothesis that plasma HDLz concentrations would be increased to a greater extent using high than moderate exercise intensity in women. The hypothesis was not supported by the data. It appeared that the proportion of the gain in total HDL afforded by HDL2 increasesmay have been greater with high than with moderate intensity, but this suggestion must be interpreted with caution because gain scoresin actual plasma HDL2 concentrations were statistically similar. This study differed from previous training studies of exercise intensity and HDL profile in that the total volume of training was held constant. Women in both the HIG and the MIG had low baseline levels of total HDL and HDL2 that placed them at increased risk for atherosclerosis. This risk was reduced by 35% to 40%i6 as a result of training. The current study indicated that moderateintensity exercise is sufficient for reducing an individual’s risk of atherosclerosis. Furthermore, the results of this study suggest that when training volume is held constant, there is no advantage to high rather than more moderate exercise intensities when the goal of the exercise program is to increase the antiatherogenic aspectsof reverse cholesterol transport. References 1. Rhoads GG, Gullbrandsen CL, Kagan A. Serum lipoproteins and coronary heart disease in a population study of Hawaiian-Japanese men. N Engl .I Med 1976;294:293-8. 2. Gordon T, Castelli WP, Hjortland MC, Kannel WB, Dawber TR. High density lipoprotein as a protective factor against coronary heart disease: the Framingham Heart Study. Am J Med 1977;62: 707-14. 3. Gordon DJ, Knoke J, Probstfield JL, Superko R, Tyroler HA. High-density lipoprotein cholesterol and coronary heart disease in hypercholesterolemic men: the Lipid Research Clinics Coronary Prevention Trial. Circulation 1986~74: 1217-25. 4. National Cholesterol Education Program. Summary of the NCEP Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel). JAMA 1993:269:3015-23. 5. Drexel H, Amann FW, Rentsch K, Neuenschwander C, Leuthy A, Khan S, et al. Relation of high density lipoprotein subfractions to the presence and extent of coronary artery disease. Am J Cardiol 1992;70:436-40. 6. Romm PA, Green CE, Reagan K, Rackley CE. Relation of serum lipoprotein cholesterol levels to presence and severity of angiographic coronary artery disease. Am J Cardiol 1991;67:479-83. I. Manninen V, Huttunen JK, Heinonen OP, Tenkanen L, Frick H. Relation between lipid and lipoprotein values and the incidence of coronary heart disease in the Helsinki Heart Study. Am J Cardiol 1989;63:H42-7. 8. Salonen JT, Salonen R, Seppanen K, Rauramaa R, Tuomilehto J. HDL, HDL2, and HDL3subfractions and the risk of acute mvocardial infarction. Circulation 1991:4: 129-39. 9. H&tung GH, Reeves RS, Foryet JP, Pa&h W, Gotto AM. Effect of alcohol intake and exercise on plasma high-density lipoprotein cholesterol subfractions and apolipoprotein A-l in women. Am J Cardiol1986;58:148-51. 10. Robinson D, Ferns GA, Bevan EA, Stocks J, Williams PT, Galton DJ. High density lipoprotein subfractions and coronary risk factors in normal men. Arteriosclerosis 1987;7:341-6. 11. Fletcher GF, Blair SN, Blumenthal J, Casperson C, Chaitman B, Epstein S, et al. Statement on exercise: benefits and recommendations for physical activity for all Americans: a statement for health

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professionals by the Committee on Exercise and Cardiac Rehabilitation of the Council on Clinical Cardiology, American Heart Association. Circulation 1992;86:340-4. 12. American College of Sports Medicine. Guidelines for exercise testing and prescription. 4th ed. Philadelphia: Lea & Febiger; 1991. 13.

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Chaitman B, Hanson JS. Comparative sensitivity and specificity of exercise electrocardiographic lead systems. Am J Cardiol 1981;47: 1335-49. Warnick GR, Benderson JM, Abers JJ. Dextran sulfate-MG2+ precipitation procedure for quantification of high densitylipoprotein cholesterol. Clin Chem 1982;28:1379-88. Warnick GR, Nguven T, Albers AA. Comparison of inproved precipitation methods for quantification of high-density lipoprotein cholesterol. Clin Chem 1985:31:217-22. Warnick GR, Mayfield C, Benderson J, Chen JS, Albers JJ. HDL cholesterol quantification by phosphotungstate-Mg2-t and by dextran sulfate-Mn2+-polyethylene glycol precipitation both with enzymic cholesterol assay compared with the lipid research method. Am J Clin Path01 1982;78:718-23. Verdery RB, Benham DF, Baldwin HL, Goldberg AP, Nichols AV Measurement of normative HDL subfraction cholesterol levels by Gaussian summation of gradient gels. J Lipid Res 1989;30: 1085-95. Dias VC, Parsons HG, Boyd ND, Keane P. Dual-precipitation method evaluated for determination of high-density lipoprotein (HDL), HDL2, and HDW cholesterol concentrations, Clin Chem 1988;34:2322-7. Cloey TA, Bachorik PS. Use of a dual-precipitation procedure for measuring high-density lipoprotein 3 (HDLS) in normolidemic serum. Clin Chem 1989;35:1390-7. Patsch W, Brown SA, Morrisett JD, Gotto AM Jr, Patsch JR. A dual-precipitation method evaluated for measurement of cholesterol in high-density lipoprotein subfractions HDL2 and HDL3 in huma plasma. Clin Chem 1989;35:265-70. Gidez LI, Miler GJ, Burstein M, Slagle S, Eder HA. Separation and quantitation of subclasses of human plasma high density lipoproteins by a simple precipitation procedure. J Lipid Res 1982;23:1206-23. American Heart Association. Nurses’ cholesterol education hand-

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book: guidelines for education and counseling of the individual with hyercholesterolemia. Dallas (TX): American Heart Association; 1980. 23. American Heart Association and National Heart, Lung, and Blood Institute. A summary from the evidence relating dietary fats, serum cholesterol, and coronary heart disease. Circulation 1990;8 1: 172133. 24.

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Jacobs DR. High density lipoprotein cholesterol and coronary heart disease, cardiovascular disease and all cause mortality [abstract]. Circulation 1985;72 Suppl III:III-85. Motoyama M, Sunami Y, Kinoshita F, Irie T, Saski J, Arakawa K, et al. The effects of long term low intensity aerobic training and detraining on serum lipid and lipoprotein concentrations in elderly men and women. Eur JAppl Physiol 1995;70:126-31. Stein RA, Michelli DW, Galntz MD, Sardy H, Cohen A, Goldberg N, et al. Effects of different exercise training intensities on lipoprotein cholesterol fractions in healthy middle aged men. Am Heart J 1990;119:277-83. Fernandez-Pardo J, Rubies-Prat J, Pedro-Botet J, Terrer C, Lopez MD, Sent M, et al. High-density lipoprotein subfractions and physical activity: changes after moderate and heavy resistance traininp. Rev Soan Facial 1991:47:181-6. Guess; GA, Rich R. Effects of high- and low-intensity exercise training on aerobic capacity and blood lipids. Med Sci Sports Exert 1984;16:269-74. Hubinger LM, Mackinnon LT. The acute effect of 30 min of moderate intensity exercise on high density lipoprotein cholesterol in untrained middle-aged men. Eur J Ann1 Phvsiol 1992:65:555-60. Hughes RA, Thor&d WG, Eyford T,LHood T. The acute effects of exercise duration on serum lipoprotein metabolism. J Sports Med Phys Fitness 1990;30:37-44. Crouse SF, O’Brien BC, Rohack JJ, Lowe RC, Tolson H, Reed JL. Changes in serum lipids and lipoproteins after exercise in men with high cholesterol: influence of intensity. J Appl Physiol 1995;79:279-86. Haskell WL. Exercise induced changes in plasma lipids and lipoproteins. Prev Med 1984;13:23-36. Kwiterovich PO Jr. The antiatherogenic role of high-density lipoprotein cholesterol. Am J Cardiol 1998;82:13-21Q.

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