Blood Lipid and Lipoprotein Adaptations to Exercise: A Quantitative Analysis

Blood Lipid and LipoproteinAdaptations to ExerciseA Quantitative Analysis

J. Larry Durstine,1 Peter W. Grandjean,2 Paul G. Davis,3 Michael A. Ferguson,1 Nathan L. Alderson1 and Katrina D. DuBose1

1 Department of Exercise Science, University of South Carolina, Columbia, South Carolina, USA2 Department of Health and Human Performance, Auburn University, Auburn, Alabama, USA3 Department of Exercise and Sport Science, University of North Carolina – Greensboro,

Greensboro, North Carolina, USA

Contents Abstract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10331. Cross-Sectional Findings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1034

1.1 Total Cholesterol (TC) and Low-Density Lipoprotein–Cholesterol (LDL-C) DifferencesBetween Active and Sedentary Groups . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1034

1.2 High-Density Lipoprotein–Cholesterol (HDL-C) and Triglyceride (TG) DifferencesBetween Active and Sedentary Groups . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1037

1.3 Dose-Response Relationships Between Physical Activity and Blood Lipids . . . . . . . . . . . 10371.4 Characterising an Exercise Threshold for Modifying Blood Lipids . . . . . . . . . . . . . . . . . 10391.5 Summary of Cross-Sectional Findings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1039

2. Exercise Training Interventions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10402.1 Changes in TC and LDL-C Levels . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1040

2.1.1 Characterising an Exercise Dose for Significant TC and LDL-C Changes . . . . . . . . . 10402.1.2 Factors Influencing TC and LDL-C Changes with Exercise Training . . . . . . . . . . . . . 10412.1.3 Summary of TC and LDL-C Changes with Exercise Training . . . . . . . . . . . . . . . . . 1042

2.2 Changes in HDL-C and TG Levels . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10422.2.1 Factors Influencing HDL-C and TG Changes with Exercise Training . . . . . . . . . . . . 10422.2.2 Quantification of HDL-C and TG Changes with Exercise Training . . . . . . . . . . . . . 10432.2.3 Characterising an Exercise Dose for Significant HDL-C Changes . . . . . . . . . . . . . 10442.2.4 Characterising an Exercise Dose for Significant TG Changes . . . . . . . . . . . . . . . . 10442.2.5 Summary of HDL-C and TG Changes with Exercise Training . . . . . . . . . . . . . . . . 1045

3. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1045

Abstract Dose-response relationships between exercise training volume and blood lipidchanges suggest that exercise can favourably alter blood lipids at low trainingvolumes, although the effects may not be observable until certain exercise thres-holds are met. The thresholds established from cross-sectional literature occur attraining volumes of 24 to 32km (15 to 20 miles) per week of brisk walking orjogging and elicit between 1200 to 2200 kcal/wk. This range of weekly energyexpenditure is associated with 2 to 3 mg/dl increases in high-density lipoprotein–cholestrol (HDL-C) and triglyceride (TG) reductions of 8 to 20 mg/dl. Evidence

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from cross-sectional studies indicates that greater changes in HDL-C levels canbe expected with additional increases in exercise training volume. HDL-C andTG changes are often observed after training regimens requiring energy expendituressimilar to those characterised from cross-sectional data. Training programmes thatelicit 1200 to 2200 kcal/wk in exercise are often effective at elevating HDL-C levelsfrom 2 to 8 mg/dl, and lowering TG levels by 5 to 38 mg/dl. Exercise trainingseldom alters total cholesterol (TC) and low-density lipoprotein–cholesterol (LDL-C). However, this range of weekly exercise energy expenditure is also associated withTC and LDL-C reductions when they are reported. The frequency and extent to whichmost of these lipid changes are reported are similar in both genders, with the exceptionof TG. Thus, for most individuals, the positive effects of regular exercise are exertedon blood lipids at low training volumes and accrue so that noticeable differencesfrequently occur with weekly energy expenditures of1200 to 2200 kcal/wk. It appearsthat weekly exercise caloric expenditures that meet or exceed the higher end of thisrange are more likely to produce the desired lipid changes. This amount of physicalactivity, performed at moderate intensities, is reasonable and attainable for mostindividuals and is within the American College of Sports Medicine’s currently rec-ommended range for healthy adults.

There is substantial, consistent and strong evi-dence that physical activity is a deterrent for de-veloping many forms of cardiovascular disease.[1]

Among its many benefits, habitual physical activityis thought to reduce cardiovascular disease risk, atleast in part, by its favourable influence on circulatingblood lipids and lipoproteins.[2,3] Cross-sectionalstudies support a significant incremental effect ofexercise on blood lipids and lipoproteins in bothmen and women. However, the varied exercise in-terventions, experimental designs and participantsample characteristics of longitudinal investigationshave hindered efforts to quantify the exercise doseneeded to change lipids and lipoprotein levels invarious subgroups of the general population. In ad-dition, some lipids and lipoproteins, such as high-density lipoprotein–cholesterol (HDL-C) and tri-glyceride (TG), are more amenable to exercise thanothers.[2,3] Thus, thresholds for an exercise effecton lipids and lipoproteins are hard to identify fromthe existing literature and at present, remain elu-sive. In this review, we will address the magnitudeand direction of lipid and lipoprotein responses toendurance exercise training and attempt to quantifythe amount of physical activity that may elicit sig-nificant changes in blood lipid and lipoprotein vari-ables.

1. Cross-Sectional Findings

1.1 Total Cholesterol (TC) and Low-DensityLipoprotein–Cholesterol (LDL-C) DifferencesBetween Active and Sedentary Groups

Reports from cross-sectional studies over thelast several decades provide compelling evidencefor the positive influence of physical activity andexercise on blood lipid and lipoprotein levels (tableI).[2,3] In general, blood lipid and lipoprotein pro-files of physically active groups reflect a reducedrisk for the development of cardiovascular diseasewhen compared with their inactive counterparts.[1,4]

Nonetheless, there is limited evidence to suggestthat those who are physically active exhibit lowerlevels of total cholesterol (TC) and low-densitylipoprotein–cholesterol (LDL-C) than those whoare less active.[5-10] In these studies, total and LDL-Cvalues were lower by 14 to 31 mg/dl (7 to 21%) inthe physically active groups, suggesting that regu-lar physical exertion has a dramatic influence onthese lipid variables. However, a well-recognisedproblem with observational studies is that, by de-sign, they do not account for confounding factors,such as group differences in bodyweight and bodyfat, caloric intake, nutrient composition of diets,

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Table I. Differences in the levels of lipoprotein lipids reported from selected cross-sectional studies. Data are presented as mean ± standard deviation, unless otherwise stated

Study (n) TC(mg/dl)

TC differences(mg/dl)

LDL-C(mg/dl)

LDL-C differences(mg/dl)

TG(mg/dl)

TG differences(mg/dl)

HDL-C(mg/dl)

HDL-C differences(mg/dl)

Enger et al.[16]

Skiers (220) 231 ± 42 a NR NR 64 ± 15 b 9.8 (21%)

Controls (269) 255 ± 48 53 ± 13

Martin et al.[6]

Elite runners (20) 175 ± 26b –14 (7%) 108 ± 25b –16 (13%) 74 ± 25b –18 (20%) 56 ± 12b 7 (14.2%)

Good runners (8) 185 ± 35 121 ± 30 73 ± 40b –19 (21%) 52 ± 11a

Non-runners (72) 189 ± 36 124 ± 36 92 ± 37 49 ± 10.5

Wood et al.[5]

Male runners (41) 200 ± 22b –12 (6%) 125 ± 21b –14 (10%) 70 ± 24b –76 (52%) 64 ± 13b 21 (49%)

Controls (747) 212 ± 38 139 ± 32 146 ± 105 56 ± 10

Female runners (43) 193 ± 33b –16 (8%) 113 ± 33b –11 (9%) 56 ± 19b –57 (54%) 75 ± 14b 17 (30%)

Controls (932) 209 ± 38 124 ± 34 123 ± 89 56 ± 10

Lehtonen and Viikari[17]

Lumberjacks (12) 224 ± 32a 149 ± 34a 53 ± 21a 74.5 ± 10.8b 19.7 (36%)

Electricians (15) 201 ± 47 146 ± 47 80 ± 36 54.8 ± 12

Lehtonen and Viikari[18]

Active men >25 km/wk (23) 191 ± 39a NR 52 ± 24b –29 (36%) 68.5 ± 14.9b 13.6 (25%)

Active men <25 km/wk (10) 174 ± 47a 58 ± 13a 56.3 ± 10.8a

Inactive men (15) 201 ± 47 81 ± 36 54.9 ± 12.1

Adner and Castelli[19]

Marathoners (50) 191 ± 31a 111 ± 25a 85 ± 75a 54.8 ± 14.1b

Controls (43) 121 ± 28 89 ± 50 45 ± 9.4 9.8 (21%)

Hartung et al.[7]

Marathoners (59) 187 ± 28c –25 (12%) 107 ± 27c –30 (22%) 77 ± 29c –77 (50%) 65 ± 14b 22 (51%)

Joggers (85) 204 ± 44b –8 (4%) 125 ± 38b –12 (9%) 106 ± 63b –48 (31%) 58 ± 18b 15 (35%)

Inactive men (74) 212 ± 40 137 ± 36 154 ± 80 43 ± 14

Rotkis et al.[20]

Runners (90) 210 ± 37a 156 ± 37a NR 54 ± 10b 20 (59%)

Non-runners (19) 182 ± 32 147 ± 32 34 ± 7

Hagan and Gettman[21]

Distance runners (53) 190 ± 29 139 ± 29a 63 ± 28b 50.9 ± 11b 4.4 (9.5%)

Sedentary men (53) 197 ± 33 150 ± 33 97 ± 46 46.5 ± 10.7

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Table I. Contd

Study (n) TC(mg/dl)

TC differences(mg/dl)

LDL-C(mg/dl)

LDL-C differences(mg/dl)

TG(mg/dl)

TG differences(mg/dl)

HDL-C(mg/dl)

HDL-C differences(mg/dl)

Thompson et al.[22]

Distance runners (20) 204 ± 29 NR 85 ± 17a 66 ± 12b 20 (43%)

Non-runners (14) 198 ± 28 105 ± 21 46 ± 10

Herbert et al.[23]

Runners (5) 194 (127-242)a,d –25 (12%) NR 69 (55-79)a 65 (50-88)b 24 (58%)

Inactive (5) 155 (115-197)d 92 (45-129) 41 (37-48)

Williams et al.[24]

Runners (12) 191 ± 37b –26 (12%) 116 ± 31b –31 (21%) 71 ± 35b –52 (42%) 64.9 ± 12.5b 15 (30%)

Controls (64) 217 ± 31 147 ± 28 123 ± 59 49.6 ± 8.7

Durstine et al.[25]

Elite runners (16) 179 ± 6a 95 ± 7a 71 ± 4a 69 ± 3b 14 (25%)

Good runners (14) 179 ± 10a 94 ± 8a 77 ± 4 a 69 ± 4b 14 (25%)

Recreational (14) 165 ± 8a 91 ± 9a 76 ± 9a 59 ± 4b 4 (7%)

Sedentary (14) 163 ± 6 92 ± 7 80 ± 6 55 ± 3

Frey et al.[26]

<35y-old trained (11) 200 ± 31a 130 ± 26a 113 ± 88a 55 ± 7a

Untrained (14) 212 ± 20a 142 ± 21 100 ± 37 54 ± 7

>50y-old trained (12) 225 ± 31a 158 ± 27a 153 ± 69a 58 ± 11b 12 (26%)

Untrained (14) 229 ± 36 152 ± 30 113 ± 43 46 ± 8

Thompson et al.[27]

Endurance athletes (10) 200 ± 45a 130 ± 38a 60 ± 18b –50 (45%) 58 ± 14b 17 (41%)

Sedentary (10) 201 ± 37 138 ± 33 110 ± 48 41 ± 10

Blessing et al.[28]

Distance runners (12) 163 ± 19a 90 ± 18a 147 ± 52b –65 (31%) 71 ± 10b 17 (31%)

Controls (8) 176 ± 23 103 ± 21 212 ± 48 54 ± 12

Stevenson et al.[29]

Premenopausal active (13) 142 ± 8a 73 ± 5a 70 ± 5a 55 ± 4a

Premenopausal inactive (12) 135 ± 6 67 ± 6 71 ± 7 54 ± 3

Postmenopausal active (14) 183 ± 7a 93 ± 6b 93 ± 9a 72 ± 4b

Postmenopausal inactive (18) 207 ± 9 124 ± 8 31 (25%) 131 ± 18 57 ± 4 15 (26%)

a Not significant.b Reported significant difference from controls: p < 0.05.c Reported significant difference from all other groups: p < 0.05.d The values in parentheses are the range.HDL-C = high-density lipoprotein–cholesterol; LDL-C = low-density lipoprotein–cholesterol; n = number of participants; NR = not reported; TC = total cholesterol; TG = triglyceride.

alcohol intake, smoking habits and other potential-ly lipid-altering lifestyle characteristics. When thesefactors are statistically controlled, the group dif-ferences in TC and LDL-C diminish and often areno longer significant.[8,11,12] Moreover, most cross-sectional studies indicate smaller, nonsignificantdifferences in TC and LDL-C levels between exer-cise-trained and inactive individuals.[3,13] In addi-tion, regression analyses of data from large-scaleepidemiological investigations have failed to con-sistently demonstrate a relationship between phys-ical activity, TC and LDL-C in normo- and hyper-lipidaemic groups.[14,15]

1.2 High-Density Lipoprotein–Cholesterol(HDL-C) and Triglyceride (TG) DifferencesBetween Active and Sedentary Groups

Observational data provide stronger evidence forlower TG and higher HDL-C levels in physicallyactive individuals.[2,3] TG levels are almost alwayslower in endurance athletes, aerobically trained,and physically active individuals when comparedwith sedentary controls.[2,3] Significant TG differ-ences between these groups range from 18 to 77mg/dl or 19 to 50% in over half of all cross-sectionalstudies reviewed.[5-10,12,18,21,24,27,28,30-33] Blood lev-els of HDL-C are 4 to 24 mg/dl higher in thosehaving physically demanding jobs and individualsengaged in endurance exercise compared with theirless active counterparts. [5-7,16-23,26-29,34] The rela-tive differences in HDL-C that exist between exer-cisers and their inactive peers range from 9 to 59%.

1.3 Dose-Response Relationships BetweenPhysical Activity and Blood Lipids

Several investigators have used cross-sectionaldesigns to quantify dose-response relationships be-tween the volume of exercise and changes in bloodlipid levels (table II).[8,10,12,32,33,35,36] Kokkinos etal.[10] compared the blood lipid levels of 2906middle-aged men who were partitioned into 6 groupsbased on their self-reported kilometres run per week.TG levels, HDL-C, and the TC : HDL-C ratio im-proved incrementally with training volume. HDL-Cincreased ~0.20 mg/dl/km (~0.31 mg/dl/mile) and

the relationships between kilometres run per weekand improvements in HDL-C, TG and theTC : HDL-C ratio were consistent across activity groups. Theseresults suggest that, although exercise may have aneffect on blood lipid levels at low exercise trainingvolumes, lipid and lipoprotein concentration dif-ferences between exercise and sedentary groups be-come significant in individuals running 11 to 23km(7 to 14 miles) per week (700 to 1500 kcal/wk).The differences between individuals running at thislevel and the sedentary group were ~3.5 mg/dl and–20 mg/dl for HDL-C and TG levels, respectively,and 0.59 for the TC : HDL-C ratio.

Using a similar cross-sectional design, Drygasand colleagues[35] found that significant HDL-C dif-ferences between male exercisers and those in thelowest activity category (~6 mg/dl) occurred with ex-ercise energy expenditures of 1500 to 3000 kcal/wk.Their results also indicated that further increasesin exercise volume can impart additional benefitson this lipid fraction, since the HDL-C differenceincreased by 3.5 mg/dl in those reporting exerciseenergy expenditures exceeding 3000 kcal/wk. In asubsequent study, these same investigators notedthat the threshold for significant HDL-C differencesbetween middle-aged male exercisers and seden-tary controls was 4 mg/dl and occurred at an exer-cise energy expenditure of 2000 kcal/wk.[36] Re-ports from the National Runner’s Health Study,which included 8283 men[33] and 1837 women[32]

showed patterns that were similar to those reportedby Kokkinos et al.[10] In men, HDL-C increased by0.135 mg/dl/km (0.218 mg/dl/mile), while TG andthe TC : HDL-C ratio decreased by 0.48 mg/dl and0.012 per kilometre, respectively.[32] Williams[32,33]

observed higher levels of HDL-C and lower TGlevels with each 16km (10-mile) increment in weeklyrunning distance in both men and women. How-ever, in men, differences in HDL-C (+1.5 mg/dl)and TG (–7 mg/dl) between the least active andnext exercise group were somewhat lower than thatreported by Kokkinos et al.[10] The relationship be-tween HDL-C and running distance in both pre- andpostmenopausal women were strikingly similar tothose observed in men; however, TG and the TC :HDL-C ratio were unchanged.[32] In women, each

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Table II. Cross-sectional evidence for a dose-response relationship between physical activity and blood lipids

Study Participants Stratification Evidence for exercise volume Evidence for exercise intensity

Lakka and Salonen[8] 2492 M Self-reported total, occupationaland leisure-time physicalactivitya

Those reporting >31 km/wk (>19 miles/wk)had 4% greater HDL-C, 9% lower TG and4% lower LDL-C than lowest activity groupa

Those reporting average leisure-time physicalactivity intensities >6 METs had 6.6% greaterHDL-C, 15.6% lower TG than those reportinglower intensitiesa

Kokkinos et al.[10] 2906 M Self-reported km run/wkand GXT

HDL-C increased (0.20 mg/dl/km/wk (0.308mg/dl/mile/wk), significantly greater HDL-C,lower LDL-C and TC : HDL-C were observedat 11 to 23 km/wk (7 to 14 miles/wk)

Williams[33] 8283 M Self-reported km run/wk HDL-C increased 0.135 mg/dl/km/wk(0.218 mg/dl/mile/wk), TG decreased by0.47 mg/dl/km/wk (0.766 mg/dl/mile/wk),TC : HDL-C decreased 0.01 per km/wk(0.19 per mile/wk), significantly greaterHDL-C was observed for each 16 km/wk(10 miles/wk) increment

Drygas et al.[35] 146 M Volume and intensity ofself-reported leisure-timephysical activity

Significantly greater HDL-C (6 mg/dl) was observedin those reporting 1500 to 3000 kcal/wk versus lowactivity group

>5 kcal/min was suggested as a possible physicalactivity threshold for reducing CVD risk

Drygas et al.[36] 224 M Volume and intensity ofself-reported leisure-timephysical activity

Significantly greater HDL-C (6 mg/dl) was observedin those reporting >2000 kcal/wk vs low activity group

Williams[12] 7059 M Self-reported km run/wkand 10km race times

HDL-C increased 0.096 mg/dl/km/wk (0.156mg/dl/mile/wk), TG increased 0.176 mg/dl/km/wk(0.284 mg/dl/mile/wk)b

HDL-C increased 0.68 mg/dl/km/h(1.1 mg/dl/mile/h), TG decreased 5.27 mg/dl/km/h(8.5 mg/dl/mile/h), LDL-C decreased 0.78mg/dl/km/h (1.25 mg/dl/mile/h)b

1837 F HDL-C increased 0.115 mg/dl/km/wk(0.185 mg/dl/mile/wk)b

TG increased 1.80 mg/dl/km/h (2.9 mg/dl/mile/h)b

Williams[32] 1837 F Self-reported km run/wk HDL-C increased 0.137 mg/dl/km/wk(0.214 mg/dl/mile/wk). No changes in TG andLDL-C across groups

a Lipid differences reported for leisure-time physical activity only.

b Relationship between lipid variable and weekly running distance or training velocity before adjusting for differences in body mass index.

CVD = cardiovascular disease; F = females; GXT = graded exercise testing; HDL-C = high-density lipoprotein–cholesterol; LDL-C = low-density lipoprotein–cholesterol; M = males;METs = metabolic equivalents (1 MET = 3.5 ml/kg/min); TC = total cholesterol; TG = triglyceride.

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16km (10-mile) increase in weekly running dis-tance was associated with a 2.1 mg/dl increase inHDL-C levels. These findings were supported in sep-arate investigations by Moore et al.[37] and Durstineet al.[25] Moore and colleagues[37] determined thatrunning distance was predictive of greater HDL-Clevels in inactive females, recreational joggers andlong-distance runners. In their study, the influenceof running distance on HDL-C remained significantafter adjusting for group differences in body fat. Dur-stine and co-workers,[25] demonstrated that HDL-Clevels were greater in female recreational runners andwere even higher in runners classified in the goodand elite groups versus age-matched sedentary con-trols. The time spent running each week was stronglyassociated with HDL-C levels, providing additionalevidence for a positive relationship between exercisevolume and favourable lipid and lipoprotein changes.

Interestingly, the studies by Williams,[12,32,33]

Kokkinos et al.,[9,10] and others[8,11,35] suggest thatalong with a training volume, the intensity of train-ing may be related to exercise-induced blood lipidand lipoprotein changes. Kokkinos et al.[9] found sig-nificantly better blood lipid and lipoprotein profilesin women who were able to achieve exercise inten-sities of 6 to 11 metabolic equivalents (1 MET =3.5 ml/kg/min) versus those exhibiting lower in-tensity levels (>6 METs). Williams[12] observed pre-dictive relationships between blood lipid and lipo-protein levels and increasing 10km run velocity,which was related to training intensity. However,results from these cross-sectional studies indicatedthat training volume, rather than training intensity,has the greatest influence on favourable blood lipidchanges. This is especially true for exercise-inducedchanges in HDL-C levels.[8,12]

1.4 Characterising an Exercise Threshold forModifying Blood Lipids

The statistical relationships between exercise andblood lipid and lipoprotein levels occur across ac-tivity levels in several of the cross-sectional studiesreviewed. These relationships demonstrate that theeffects of exercise on lipid and lipoprotein levelscan be initiated at low training volumes and willcontinue in a dose-response fashion with increas-

ing volume. With respect to gender and lipid andlipoprotein adaptations to exercise, men and womenmay respond similarly to exercise training, althoughthe sensitivity of the regression slopes for HDL-Cand TG imply that women may be more resistant toexercise-induced changes than men.[9,32,33] Arunningvolume of 11 to 23km (7 to 14 miles) has been pro-posed as a possible threshold for observing signif-icant HDL-C and TG concentration differences.[10,38]

However, this may be an underestimate of the re-quired exercise volume, since others have reportedthat significant HDL-C differences occur with en-ergy expenditures between 1500 and 3000 kcal/wk(~24 to 48 km/wk: ~15 to 30 miles/wk).[8,35] Morerecently, thresholds have been characterised with ca-loric expenditures of ≥2000 kcal/wk, which equatesto roughly 20 miles/wk of jogging or brisk walk-ing.[8,36] Although Williams[32,33] reported that sig-nificant differences in HDL-C and TG levels oc-cur in 16km (10-mile) increments in both men andwomen, the groups reporting the lowest amount ofphysical activity in these studies were already run-ning up to 16 km/wk (10 miles/wk). The next cat-egory of runners averaged between 16 to 32 km/wk(10 and 20 miles/wk). Therefore, a 24 to 32 km/wk(15 to 20 mile/wk), 1500 to 2200 kcal/wk thresholdfor significant HDL-C and TG changes comparesfavourably with the findings of Williams,[12,32,33] issupported by the current body of cross-sectional data,but is somewhat greater than what has been postu-lated as the threshold elsewhere.[38] At this point itshould be emphasised that walking and running arenot the only modes of physical activity in which fa-vourable lipid and lipoprotein changes occur. Manyinvestigators have reported similar relationships be-tween lipid levels and the volume of swimming, cy-cling and recreational sports participation.[8,35,36]

Thus, the volume of physical activity, in which a rel-atively large muscle mass is employed, relates to ca-loric expenditure and seems to be the stimulus foraltering blood lipids and lipoprotein levels.

1.5 Summary of Cross-Sectional Findings

Taken together, the cross-sectional data indi-cate that most sedentary individuals will experi-ence elevations of 3.5 to 6 mg/dl in HDL-C by

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increasing their exercise energy expenditure to 1500to 2200 kcal/wk. Further increases in HDL-C of 1.5to 3 mg/dl can be expected for each 16 km/wk (10miles/wk) increment in running volume, whichequates to ~1100 kcal/wk of exercise energy ex-penditure. Differences in TG range from 7 to 20mg/dl at an energy expenditure of 1500 to 2200kcal/wk and further reductions of 3 to 8 mg/dl mayoccur for each 16km (10-mile) increase in trainingvolume. There is little support in the cross-sectionalliterature for significant differences in TC andLDL-C between active and inactive groups, inde-pendent of bodyweight and body fat differences.[8]

Causality can not be established from cross-sectional data and results from these observationalstudies may embellish the association between ex-ercise and blood lipid levels. Indeed, the greatestdisparities in blood lipids, and most often HDL-C,are generally reported when physiological differ-ences and the volume of physical activity betweengroups are extreme. The differences in blood lipidsand lipoprotein levels are often diminished or are nolonger observed when controlling for group char-acteristics that influence lipid levels,[8,11,12] and whenmore heterogeneous groups are compared.[39-42] Fur-thermore, blood lipid and lipoprotein level changesassociated with exercise training are not as frequentlyobserved and are generally more modest than thegroup differences reported between exercisers andnon-exercisers.[2,3] Therefore, it is important to ex-amine longitudinal training studies in order to de-termine the efficacy of threshold recommendationsfrom cross-sectional evidence.

2. Exercise Training Interventions

2.1 Changes in TC and LDL-C Levels

TC and LDL-C levels infrequently change withexercise training in either men or women.[2,3] Infact, lower TC and LDL-C levels result after exer-cise training in just over 25% of the publicationsreviewed (Appendix I). When exercise training hasbeen shown to alter TC levels, the reductions aresimilar in both men and women and range from 7to 27 mg/dl, or 4 to 20%. Likewise, lower LDL-Clevels ranging from 6 to 28 mg/dl (5 to 19%) have

been reported after exercise training in both genders.The adaptations reported with exercise training aresimilar to differences observed between exercisersand sedentary groups from the cross-sectional lit-erature. However, control groups were not includedin many of these training studies, and therefore, theeffects of exercise on TC and LDL-C levels may beoverstated.[43-51] Indeed, the extent to which exer-cise training lowers these lipid fractions is eithersomewhat lower (6 to 13 mg/dl or 4 to 7%)[52-56] orno longer significant[57-59] when the exercise effectis adjusted for the TC and LDL-C changes that oc-cur in control groups over the training period. Es-timates from a recent meta-analysis of randomisedcase-control studies suggest that exercise trainingmay only be expected to lower TC and LDL-C lev-els by ~4 mg/dl.[60]

2.1.1 Characterising an Exercise Dose forSignificant TC and LDL-C ChangesSignificant changes in TC and LDL-C levels are

generally not observed after exercise training witha few exceptions. Therefore, there is little evidenceto support a training threshold for lowering TC andLDL-C levels. When changes have been reported,they are often associated with exercise training pro-grammes in which participants expended more than1200 kcal/wk.[43,44,47,51,52,56,61-65] Endurance exer-cise programmes producing this level of caloric ex-penditure are most effective at lowering TC andLDL-C in previously untrained individuals, sincetrained individuals do not seem to respond, evenwith extreme increases in training volume.[58,66,67]

Some investigators have suggested that the differ-ent lipid responses to exercise in trained versus un-trained individuals may be caused by differencesin initial TC and LDL-C levels. They reason thatphysically inactive individuals who exhibit higherinitial TC or LDL-C levels may be expected to showgreater exercise-induced changes than those withlower baseline cholesterol levels.[68,69] However,baseline TC and LDL-C levels probably do not ex-ert a significant influence on cholesterol adapta-tions to exercise training, since similar reductionsin TC and LDL-C can occur in those with high[43,70]

or normal baseline cholesterol levels.[62,65] Further-more, in a recent meta-analysis of 31 randomised,

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controlled exercise training studies, Halbert and co-workers[60] did not find a significant relationshipbetween baseline lipid levels and the changes inlipids that occur with exercise training.

2.1.2 Factors Influencing TC and LDL-C Changeswith Exercise TrainingWhen non-obese men and women are directly

compared, there is limited evidence to suggest thatwomen may be more resistant to exercise-inducedchanges in TC and LDL-C than their male counter-parts.[44,45] This seems to be the case when weeklycaloric expenditure meets or exceeds 1200 kcal.However, Shephard et al.[61] have reported just theopposite, and Brownell et al.[71] observed no gen-der differences after low-volume exercise traininginterventions. Others have shown that TC and LDL-C do not change in pre- and postmenopausal womenfollowing aerobic exercise training;[72] however, theuse of hormone replacement therapy may enhancethe lipid and lipoprotein adaptations to exercise inpostmenopausal women.[54]

Some investigators have suggested that theexercise-induced changes in TC and LDL-C arecaused by bodyweight and body fat reductions.[13]

This may be true for subsets of the population inwhich large bodyweight or fat losses are reported,such as in obese women.[50,73-76] However, the pres-ent exercise literature does not provide definitiveevidence that bodyweight and fat loss are requisitefor changing TC or LDL-C. First, there are severalexercise training studies in which TC and LDL-Cwere significantly reduced in the absence of body-weight and/or body fat changes.[45-47,52,62,65,77] Sec-ond, TC and LDL-C are often unchanged after ex-ercise training programmes in which bodyweightand body fat are significantly lowered.[59,67,78-89]

Third, when TC and LDL-C changes are reportedafter exercise training, they are of similar magni-tude with and without losses in bodyweight or bodyfat (Appendix I). However, lower TC and LDL-Clevels are more frequently observed when substan-tial bodyweight loss occurs through a combinationof diet and exercise.[59,74-76,90-93] However, it is un-clear as to whether the reductions in TC and LDL-Cafter these interventions are caused by greater ca-loric deficits and bodyweight loss than what is gen-

erally reported after exercise alone, or if a decreasein dietary saturated fat and cholesterol intake aremore strongly associated with these lipid changes.A conclusive position on these issues can not bemade from the current literature, as Schwartz[86]

observed decreases in TC and LDL-C with diet-induced, but not exercise-induced bodyweight loss.Nieman et al.[75] reported similar reductions in TCand LDL-C levels with diet alone or in combina-tion with exercise. On the other hand, Wood et al.[59]

and Coon et al.[94] found small, comparable, butnonsignificant reductions in TC and LDL-C levelsafter bodyweight loss by diet or by exercise.

It is difficult to evaluate the effects of exerciseintensity on TC and LDL-C changes, since mosttraining studies were conducted with intensities>60% of maximum heart rate or maximal oxygenuptake (V

.O2max). As such, most of the reductions

in TC and LDL-C that have been reported withexercise occur at these training intensities or greater.Despres and colleagues,[64] however, observed sig-nificant reductions in TC and LDL-C with a low-intensity/high-volume training regimen. Others havecompared the effects of training intensities, rang-ing from 40 to 85% of V

.O2max and did not find an

intensity effect on TC and LDL-C.[79,95-98] Stein etal.[99] and Tomiyasu et al.[48] reported greater re-ductions in TC and LDL-C levels with high- versusmoderate-intensity training; however, a failure tocontrol for the exercise volume in both of thesestudies makes their findings hard to interpret.

Resistance training does not seem to alter bloodlipid and lipoprotein levels.[100-104] Some investi-gators have reported lower TC and/or LDL-C levelsafter several weeks of resistance training.[55,105,106]

However, the sample sizes in these studies weresmall and, other than the results from Hurley etal.,[106] these findings have been generally limitedto females.[55,105] Resistance exercise, in general,may be less effective than endurance activities formodifying TC and LDL-C levels, since relativelyfewer calories are expended with resistance versusaerobic activity. In fact, the work of Blumenthal etal.[101] and Smutok et al.[100] have shown that lipidsand lipoproteins changes should not be expected

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after low-volume exercise interventions of eitherresistance or aerobic activities.

2.1.3 Summary of TC and LDL-C Changes with Exercise TrainingIn summary, a careful evaluation of the literature

indicates that exercise training, more often than not,results in unaltered TC and LDL-C levels. In someinstances, regular exercise can produce smallchanges in TC and LDL-C of 4 to 7% in both menand women. Reductions in these lipid fractions oc-cur with greater frequency in previously sedentaryindividuals and when exercise caloric expenditureexceeds 1200 kcal/wk. At present, baseline levelsof TC and LDL-C, changes in bodyweight and bodyfat, and exercise intensity do not seem to be deter-minants for exercise-induced changes in TC andLDL-C levels.

2.2 Changes in HDL-C and TG Levels

Based on the frequency of reported changes inHDL-C and TG levels following exercise training,these lipid variables are more responsive to regularexercise than TC and LDL-C. Significantly greaterHDL-C and lower TG levels have been reportedafter exercise training in over half of the manu-scripts reviewed (Appendix I).[2,3] Therefore, reg-ular aerobic exercise is often cited as consistentlyimproving these lipid and lipoprotein levels. HDL-Cand TG changes, however, are not always observedafter exercise training interventions. Suggestedreasons for the disparate findings include differ-ences in exercise training regimens, baseline char-acteristics between study cohorts, and the extent towhich bodyweight or body fat changes with exer-cise training. Other factors, such as the influenceof alcohol, tobacco, lipid altering medications andthe level of dietary intervention or control, mayaffect HDL-C and TG adaptations to exercise train-ing.[3,13,68,107]

2.2.1 Factors Influencing HDL-C and TG Changes with Exercise TrainingIn a 1983 meta-analysis of longitudinal studies,

Tran et al.[69] reported that the changes in HDL-Clevels with exercise training were inversely relatedto baseline HDL-C levels. These findings suggested

that individuals with the lowest HDL-C levels wouldexhibit the greatest increases in HDL-C with exer-cise training. However, this notion does not seemto hold true in light of more recent findings. Forexample, Raz et al. [53] reported that aerobic exer-cise training was ineffective in modifying HDL-Clevels in young men with low initial HDL-C val-ues. Williams and colleagues[108] found that exer-cise training increased HDL-C to a lesser extent inmen with low versus normal baseline HDL-C lev-els. Others have demonstrated that HDL-C adaptsmost favourably to exercise training in men withnormal initial HDL-C values (>38 mg/dl) and isresistant to change in men with baseline HDL-Cvalues lower than 37 mg/dl.[81,109,110] To our knowl-edge, analogous studies have not been conductedwith women. However, elevations in HDL-C havebeen observed in women with moderate baselineHDL-C levels[82,111,112] and in those with high pre-existing HDL-C levels after large increases in ex-ercise training volume. [66,67] Therefore, it appearsthat exercise training may be most effective at elevat-ing HDL-C in those with normal or higher HDL-Clevels before undergoing an exercise programme.Present literature does not support the contentionthat baseline TG values influence TG adaptationsto exercise training in either gender.[60]

Inverse relationships have been established be-tween body mass index (BMI), percentage bodyfat, regional body fat measured at baseline and theextent to which HDL-C and TG levels change withexercise training.[86,94,110] Observations from thesestudies suggest that exercise-induced changes inHDL-C and TG are smaller in individuals with agreater BMI, body fat or with more central fat dis-tribution. These physical characteristics may beindicative of underlying metabolism that impedestraining-induced changes in these blood lipids. Forexample, unique metabolic characteristics relatedto HDL-C and TG metabolism have been observedin adipocytes of different fat depots and suggest amechanistic link between body fat, regional fat dis-tribution and HDL-C and TG adaptations to exer-cise training.[113-115]

Contrary to a commonly held notion, a reduc-tion in bodyweight or body fat is not requisite for

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exercise to produce significant changes in HDL-Cand TG. In men, favourable changes in these lipidsoccur with equal frequency when bodyweight andbody fat are reduced[53,59,62-64,81,83,86,89,90,116,117] ornot altered with exercise.[48,52,99,109,118-125] In women,TG and HDL-C changes occur most often in theabsence of bodyweight and fat loss.[66,67,87,95,111,126]

Interestingly, when bodyweight loss is induced byeither dietary intervention, alone or in combinationwith exercise, HDL-C can increase,[76,108,127] how-ever, a majority of studies indicate that HDL-C willdecrease[74,75,91] or not change.[92,128] In fact, someinvestigators have suggested that exercise mayprevent a decrease in HDL-C when combined withdietary means of bodyweight or body fat reduc-tion.[75,91] Nevertheless, these studies provide evi-dence that bodyweight loss and body fat reductionare not necessary for exercise to have a beneficialeffect on HDL-C and TG levels, as changes in thesephysical characteristics do not seem to influencethe magnitude or direction of change in these lipidand lipoprotein fractions.

Several investigators have demonstrated that ex-ercise can alter HDL-C and TG levels to the sameextent in men and women.[49,97,129] However, fa-vourable changes in HDL-C and TG levels are re-ported less frequently in women (Appendix I).[130]

Reasons for less consistent findings in women arenot completely clear. Some physiologic and meta-bolic factors that can influence lipid metabolism,such as smaller muscle and greater fat mass, differ-ent fat distribution, menstrual cycle fluctuations,the use of oral contraceptives in premenopausalwomen, menopausal status, and the use of hormonereplacement therapy in postmenopausal women arethought to contribute to a greater variance in the lipidadaptations to exercise training in females.[54,72,131]

2.2.2 Quantification of HDL-C and TG Changeswith Exercise TrainingWhen HDL-C levels are significantly elevated

after exercise training, the increases are similar inboth men and women and generally range from 2 to8 mg/dl, or 4 to 22%. However, increases of 15 to 19mg/dl have been reported in both genders.[66,120,122]

Likewise, significant reductions in TG levels, rang-ing from 5 to 38 mg/dl or 4 to 37%, have been

reported for males after exercise training, but lessfrequently in females. In their recent meta-analysis,Halbert and co-workers[60] suggested that the ef-fects of exercise training on HDL-C and TG favouredthe more conservative ends of these ranges. Theseinvestigators estimated that exercise training in-creased HDL-C levels by 2 mg/dl and reduced TGvalues by 9 mg/dl. Although these estimates aremodest, they may represent a reduction in cardio-vascular disease risk of 2 to 4%.[132,133]

In both men and women, extreme increases inrunning volume have been effective at elevatingHDL-C by 6 to 17 mg/dl (10 to 29%).[48,66,67,119,134]

In men but not women, TG levels were also re-duced by 30 to 38 mg/dl, or 30 to 37%.[48,119] Alongwith greater exercise training volumes, the abso-lute and relative lipid changes are greater in thesestudies when compared with the rest of the train-ing literature, suggesting that there may be a dose-response effect of exercise on HDL-C and TG lev-els. However, most individuals would not adopt theexercise volumes or intensities utilised in these stud-ies as part of a permanent lifestyle practice. More-over, recommending training regimens similar tothe ones described in these investigations wouldnot be prudent for the general population, as theycan lead to an increased rate of injury and dropout.[135] Investigators who have addressed the dose-response issue with training volumes more likelyto be accepted by the general public have not founda relationship between increasing exercise frequency,volumes or intensities and changes in HDL-C orTG levels.[48,111,136] In addition, a preponderanceof training interventions that encompassed only afew weeks are of limited value because the fre-quency and intensity were not at a level that wouldproduce significant lipid changes. These issues allcontribute to the difficulty in quantifying an exer-cise training threshold for modifying HDL-C andTG levels. Thus, training threshold stimuli for al-tering these lipids and lipoproteins can be approx-imated, but not definitively established from theexercise training literature.

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2.2.3 Characterising an Exercise Dose for Significant HDL-C ChangesIn men, significantly higher HDL-C levels are

observed consistently with moderate exercise train-ing programmes requiring ≥1200 kcal/wk. Althoughexceptions exist,[58,96,129,137,138] this energy expen-diture threshold was met in 21 out of the 25 studiesshowing significant increases in HDL-C levels (Ap-pendix I). Elevations in HDL-C are seldom reportedwith weekly training volumes eliciting less than1200 kcal.[46,99,116,139] Thus, a training volume of1200 kcal/wk or greater may be necessary to raiseHDL-C levels in men. Interestingly, a review of theexercise training literature indicated that the thresh-old for significant changes in HDL-C may be sim-ilar in both men and women. Changes in HDL-Care consistently shown in females when the weeklyexercise caloric expenditure meets or exceeds 1200kcal.[45,49,97,111,129] Training volumes that elicit 1000to 1200 kcal/wk in energy expenditure have alsobeen shown to elevate HDL-C levels in sedentaryand moderately fit women.[54,85,87,95,112,126] Yet, moreoften than not, weekly exercise energy expenditure inthe 1000 to 1200 kcal/wk range is not enough to ele-vate HDL-C levels in females.[51,72,73,101,136,138,140-145]

As with men, training volumes that require less than1000 kcal/wk are not enough to favourably improveHDL-C values.[55,71,78,80,104,146-149]

Currently, there is no evidence from the exer-cise training literature to support an exercise inten-sity threshold for producing HDL-C level changes.In many instances where exercise intensity was re-ported to influence HDL-C in males, investigatorsfailed to control for energy expenditure.[48,99,118]

As such, it can be argued that energy expenditureor training volume, rather than intensity, affectedthe results. When energy expenditure or trainingvolume is controlled, exercise intensity was notshown to influence HDL-C changes in men orwomen.[79,95,97,98,111]

2.2.4 Characterising an Exercise Dose for Significant TG ChangesIn an early training study, Holloszy and col-

leagues[150] determined that TG reductions attrib-uted to exercise training, are in fact an acute re-sponse to the last exercise session. Subsequent

research examining the effect of one exercise ses-sion on lipid metabolism has corroborated this ob-servation.[3] Therefore, the frequency and extent towhich TG level changes are reported after exercisetraining may be a function of when the final bloodsample was obtained relative to the last exercisesession, rather than a cumulative effect of the train-ing regimen. If exercise training imparts an effect onTGs, independent of the changes that occur from thelast exercise session, then the exercise volume thres-hold necessary for a TG level change may be sim-ilar to that necessary for HDL-C. For example, aweekly energy expenditure of ≥1200 kcal generallyproduces lower post-training TG levels in seden-tary and moderately fit men,[48,62,63,90,119,123-125,151]

with few exceptions.[44,58,83,120] Significant re-uctions in TG levels have occurred with weeklyexercise energy expenditures of 1000 to 1200kcal; [46,52,53,59,81,116,117,121,152] yet, this energy expen-diture does not consistently lower TG levels, as othershave reported no change in TG levels at similartraining volumes.[64,65,79,84,86,94,97,109,129,153,154] Othershave demonstrated that TG changes in men shouldnot be expected when exercise energy expenditureis lower than 1000 kcal/wk.[43,47,89,98-100,137,139,155]

An exercise threshold for lowering TG levels inwomen is not evident from the present training lit-erature. Many barriers contribute to the difficulty intrying to quantify a threshold stimulus. First, lowerTG levels are reported less frequently in women ver-sus men after exercise training.[56,73,85,87,117,126,149]

Second, when TG reductions occur, they are ob-served with training volumes eliciting 1000 to 3000kcal/wk and intensities ranging from 50 to 80% ofcardiovascular capacity.[73,85,117,126] These traininginterventions are similar in frequencies, volumesand intensities to those producing no change. Third,TGs are not altered when training volumes and in-tensities are increased to extreme levels,[66] indicat-ing that a dose-response relationship between ex-ercise training and TG changes may not exist forwomen. However, it should be emphasised that alack of evidence for a dose-response relationshipbetween exercise and TGs does not mean that ex-ercise has no effect on blood TG levels in women.Woods and Graham[149] have shown that measur-

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able fluctuations in TG levels occur throughout themenstrual cycle, indicating that the menstrual phasein which blood samples were obtained may maskthe effects of exercise in premenopausal women.In addition, Binder’s group[54] determined that ex-ercise can attenuate the elevations in TG that mayaccompany hormone replacement therapy in post-menopausal women. Therefore, exercise can ben-eficially influence TG levels in women, whether ornot significant changes are observed with training.

2.2.5 Summary of HDL-C and TG Changes with Exercise TrainingIn summary, regular aerobic exercise can increase

HDL-C and TG levels in men and women. The effectof exercise on HDL-C is similar in both males andfemales; however, TG changes are more common-ly reported in males. The training effect is strongestin non-obese individuals with normal or elevatedHDL-C before the exercise intervention. In con-trast, baseline TG levels do not seem to impact TGresponses to exercise. In addition, changes in body-weight or body fat do not appear to be necessaryfor favourable exercise adaptations in these lipids.Regular exercise can raise HDL-C levels by 2 to 8mg/dl and lower TGs from 5 to 38 mg/dl in menand women. The training volumes that elicit energyexpenditures ≥1200 kcal/wk are most frequentlyassociated with elevations in HDL-C levels in bothgenders and reduced TG levels in men. At present,a threshold for lowering TGs in women can not beestablished from the exercise training literature.

3. Conclusion

Comparisons between sedentary and physicallyactive groups have been used to establish a positiveinfluence of physical activity on blood lipids. Physi-cally active individuals typically exhibit greaterHDL-C and lower TG levels versus their less ac-tive counterparts. In some instances, lower TC andLDL-C levels may also be observed in physicallyactive groups; however, this is not a consistent find-ing. Dose-response relationships between the amountof exercise and favourable blood lipid changes sug-gest that exercise can exert a positive influence onblood lipids at low training volumes, although the

effects may not be observable until certain exercisethresholds are met. The thresholds established fromcross-sectional literature appear to be similar in menand women and occur at training volumes of 24 to32 km/wk (15 to 20 miles/wk) of brisk walking orjogging and elicit between 1200 to 2200 kcal/wk.This range of weekly energy expenditure is asso-ciated with 2 to 3 mg/dl increases in HDL-C andTG reductions of 8 to 20 mg/dl.

Cross-sectional evidence also suggests that theselipid fractions are enhanced further with additionalincreases in exercise training volume. There is lim-ited support in the cross-sectional or interventionliterature for favourable changes in TC and LDL-Cwith exercise training. However, favourable changesin HDL-C and TGs are often observed after train-ing regimens requiring energy expenditures sim-ilar to those characterised from cross-sectional data.Training programmes that elicit 1200 to 2200 kcal/wkin exercise are often effective at elevating HDL-Clevels from 2 to 8 mg/dl and lowering TGs by 5 to38 mg/dl. This weekly exercise energy expenditureis also associated with TC and LDL-C reductions,when they are reported. The frequency and extentto which most of these lipid changes are reportedare similar in both genders, with the exception ofTG levels. Thus, for most individuals, the positiveeffects of regular exercise are exerted on blood lipidsat low training volumes and accrue so that notice-able differences frequently occur with weekly en-ergy expenditures of 1200 to 2200 kcal/wk. It ap-pears that weekly exercise caloric expenditures thatmeet or exceed the higher end of this range aremore likely to produce the desired lipid changes.This training volume threshold is slightly greaterthan what has been suggested previously for favoura-bly altering blood lipids. However, this amount ofphysical activity, performed at moderate intensi-ties, is reasonable and attainable for most individ-uals and is within the American College of SportsMedicine’s currently recommended range for healthyadults.

Acknowledgements

The authors have no conflicts of interest.

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Appendix I. Blood lipid and lipoprotein changes from 100 selected exercise-training studies in men and womena

Study characteristics ∆ lipid and lipoprotein variables ∆ physiological characteristics

author purpose n exerciseintervention

TC(mg/dl)

LDL-C(mg/dl)

TG(mg/dl)

HDL-C(mg/dl)

bodyweight(% ∆)

% fat ∆ V.O2max

(%∆)

Aellen et al.,1993[118]

Effects ofintensity usingAT

Age 20-30y; 33 M:16 intensity > AT,17 intensity < AT,12 C

Cycle ergometry;9 weeks; f = 4/wk;I ≥and < AT; D = 30min

NS: bothgroups

NS: bothgroups

NR <AT: ±2 (4%),>AT: NS,C: NS

NS: bothgroups

NS: bothgroups

NR

Allison et al.,1981[153]

Effects ofduration

Age 17-26y; 25 M,23 F: 22 C;30-min group; 45-min group

Fitness class,jogging; 8 wk; f =3/wk; I = 85% HRmax;D = 30 and 45 min

NS: allgroups

NS: allgroups

NS: allgroups

M 30-min:–7 (–12%),M 45-min:–6 (–10%),F 30-min: –5(–8%), F 45-min: –4 (–7%),C: NS

NS: allgroups

NS: allgroups

±5-10% in Mand F, both30- and 45-min groups

Altekruse andWilmore, 1973[43]

Effects ofexercise training

Age 17-59y; 39 M Walk/jog/run;10 weeks; f = 3/wk;I = mod-high; D = 5to 15 km/wk (2.7-9miles/wk)

–24 (–11%) NR NS ±19 (±50%):α lipoprotein %

–1% NR NR

Andersen et al.,1999[74]

Effects of diet +exercise anddiet + lifestyle

Age 21-60y;obese; 38 F:19 DE, 19 DL

Step aerobics; 16wkand 1y follow-up;f = 3/wk; I = 7-11METs; D = 15-45 min(450-500kcal/session)

16wk;DE: –22(–11%),DL: –23(–9%). 1yfollow-up (vsbaseline):DE: –5 (–2%),DL: –7 (–3%)

16wk;DE: –12(–11%),DL: –15(–6%). 1yfollow-up (vsbaseline):DE: NS,DL: NS

16wk;DE: –24(–18%),DL: –18(–15%). 1yfollow-up (vsbaseline):DE: NS,DL: NS

16wk;DE: –5 (–9%),DL:–5 (–10%).1y follow-up(vs baseline):DE: ±4 (8%),DL: ±2 (5%)

16wk;DE: –10%,DL: –9%. 1y(vs baseline):DE: –8%,DL: –8%

16wk;DE: –14%,DL: –19%. 1y(vs baseline):DE: NR,DL: NR

16wk;DE: ±19%,DL: ±16%.1y (vsbaseline):DE: ±16%,DL: ±24%

Baker et al.,1986[62]

Effects ofexercise training

Age >50y; 34 M:20 Ex (walk/run),14 C

Walk/run: 20wk;f = 3/wk; I = 65-85%HRR; D = 48 min

Ex: –9 (–4%),C: ±6 (3%)

Ex: –10(–5%),C: ±9 (6%)

Ex: –21(–24%),C: NS

Ex: ±6(±17%),C: –3 (–8%)

Ex: –2%,C: NS

Ex: –2%,C: NS

Ex:±17%,C: NS

Barr et al.,1991[58]

Effects ofprogressiveendurancetraining

Age 18-22y; 24 Mswimmers: 13 HV,11 NV

Swimming; 25wkseason; f = daily;I = moderate;D = HV: increasedfrom 22 to 44 km/wk;NV: 22 km/wk (6wk)

–11(–6%) NSat wk 20: bothgroups; –7(–4%) NS atwk 25: bothgroups

–15 (–15%)at wk 20:both groups;–6 (–6%) NSat wk 25:both groups

NS NS NS –10% (sum ofskinfolds):both groups

NR

Bassett-Freyet al., 1982[78]

Effects ofexercise training

Age 19-29y; 18 F:12 IT, 6 CT

Cycle ergometry;10wk; f = 3/wk;I = 70% HRR;D = 30 min

NS: bothgroups

NS: bothgroups

NS: bothgroups

NS: bothgroups

NS: bothgroups

–2%: bothgroups

±16%: bothgroups

Binder et al.,1996[54]

Effects ofexercise +hormonereplacementtherapy

Age 60-72y; 71 Fpostmenopausal:23 Ex, 16 ExH, 15H, 17 C

Walk/jog/stair climb;11mo; f = 3-5/wk;I = 60-70% V

.O2max;

D = 30+ min

Ex: –13 (–6%),ExH: –13(–6%), H: NS,C: NS

Ex: –9 (7%),ExH: –25(–20%),H: –24(–17%),C: NS

Ex: NS,ExH: NS,H: ±45 (42%),C: NS

Ex: NS,ExH: ±9(17%),H: ±9 (17%),C: NS

Ex: –2%,ExH: –3%,H: NS,C: NS

Ex: –8%,ExH: –6%,H: NS,C: NS

Ex: ±18%,ExH: ±22%,H: NS,C: NS

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Blumenthalet al., 1991[126]

Effects ofactivityintervention

Age >60y;M and F: 33 AE,34 Y, 34 C

Cycle ergometry;14mo; f = 3/wk;I = 50-60% HRR;D = 60 min

AE: NS,Y: NS,C: NS

AE: NS,Y: NS,C: NS

AE: –30 (20%),Y: –17 (12%),C: ±20 (±14%)

AE: ±4 (7.5%),Y: NS,C: NS

AE: NS,Y: NS,C: NS

NR AE: ±18%,Y: ±6%,C: ±7%

Blumenthalet al., 1988[95]

Effects ofintensity

Age 28-66y,M, post-MI: 23 at65-75% V

.O2max,

23 at <45% V.O2max

Walk/jog for 12wk;f = 3/wk; I = mod vslow; D = 30 vs 45 min

NS: bothgroups

NS: bothgroups

NS: bothgroups

Mod: ±5(±18%), low:±6 (±22%)

NS: bothgroups

NR ±11-14% forboth

Blumenthalet al., 1991[101]

Effects ofaerobic andresistanceexercise

Age 45-57y; 46 F:22 RE, 24 AE

Circuit training orwalk/jog; 12wk;f = 3/wk; I = 70%HRR (AE);D = 35 min

NS: bothgroups

NS: bothgroups

NS: bothgroups

NS: bothgroups

≤1%: bothgroups

NR AE: ±18%,RE: NS

Boyden et al.,1993[55]

Effects ofresistanceexercise

Age 28-39y; 88 F:46 RE, 42 C

Resistance exercise;5mo; f = 3/wk;I = 70% 1RM;D = 3 sets, 8 reps,12 exercises

RE: –13 (–7%),C: –3 (–2%),NS

RE: –14(–12%),C: –3 (–3%)NS

NS: bothgroups

NS: bothgroups

NS: bothgroups

–1% NS: bothgroups

Brownell et al.,1982[71]

Compareexerciseresponsesbetweengenders

Age 20-60y; 24 M,37 F

Various aerobic +resistance activities;10wk; f = 3/wk;I = 70% HRmax;D = 15-20 min

M: NS,F: NS

M: –8.5(–6%),F: –5.3 (–5%)

M: NS,F: NS

M: NS,F: NS

M: –1%,F: –1.5%

NR ±8-10% in Mand F

Buono et al.,1988[50]

Effects ofhypocaloric dietand exercise

Age 20-26y;10 obese F

Walking + diet; 42d;f = daily; I = low(HR:>132beats/min); D = 5 h/d

–31 (–15%) NR –25 (–24%) NS –8% –5% ±19%

Cauley et al.,1987[140]

Effects ofexercise onHDL-C

Age 50-62y;204 F: 100 Ex,104 C

Walking; 2y;f ≥ 3/wk;I = low-mod;D = 5 km/session(3 miles/session)

NS: bothgroups

NS: bothgroups

NS: bothgroups

NS: bothgroups

NS: bothgroups

NR NR

Coon et al.,1989[94]

Effect ofexercisetraining vs diet

Age 46-73y; 20obese M: 10 Ex,10 Dt

Walk/jog/cycle;9-12mo; f = 3/wk;I = 50 –85% HRR;D = 40 min

Ex: –11 NS,Dt: –8 NS

Ex: –9 NS,Dt: –6 NS

Ex: –11 NS,Dt: –26 (–25%)

Ex: NS,Dt: ±4 (±12%)

Ex: NS,Dt: –12%

Ex: NS,Dt: –6%

Ex: ±32%,Dt: NS

Crouse et al.,1997[79]

Effect oftraining intensity

Age 37-57y; 26 Mwith highcholesterol: 12 HI,12 MI

Cycle ergometry;24wk; f = 3/wk;I = HI: 80% V

.O2max,

MI: 50% V.O2max;

D = 350 kcal /session

–16 (–6%):both groups;significant at16wk, NS at24wk

NS: bothgroups

NS: bothgroups

NS: bothgroups;HDL2-C(±82%)HDL3-C(–13%)

–2%: bothgroups

NS HI: +51%,MI: +25%

Despres et al.,1988[63]

Effects ofheredity andexercise training

12 adult M: 6pairs ofmonozygotic twins

Cycle ergometry;22d; f = V

.O2max;

D = 1000 kcal, 22000total kcal deficit

–18 (–11%);NS

–18 (–16%);NS

–32 (32%) ±4.4 (16%) –3% –2.4% ±10%

Despres et al.,1990[64]

Effects ofexercise training

Age 22-28y; 5 M Cycle ergometry;100d; f = 6/wk;I = low; D = 2 × 53min sessions toexpend 1000 kcal/d

–8 (–4%) –6 (–5%) NS ±5 (±12%) –9% –38%: fatmass

NR

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Appendix I. Contd

Study characteristics ∆ lipid and lipoprotein variables ∆ physiological characteristics

author purpose n exerciseintervention

TC(mg/dl)

LDL-C(mg/dl)

TG(mg/dl)

HDL-C(mg/dl)

bodyweight(% ∆)

% fat ∆ V.O2max

(%∆)

Despres et al.,1991[51]

Effects ofexercise training

Age 33-50y;13 obese F

Walk/jog/swim/cycle/aerobic dance;14mo; f = 4-5/wk;I = 55% V

.O2max;

D = 90 min

–15 (–7%) –15 (–10%) NS NS; HDL2-C:±3, HDL3-C: –3

–4% –3.3% ±15%

Duncan et al.,1991[111]

Exercise dose-response forlipid changes inwomen

Age 20-40y; 59 F:16 AW, 12 BW,18 St, 13 C

Walking; 24wk;f = 5/wk; I = varied;D = 4.8 km/d

AW: NS,BW: NS,St: NS,C: NS

AW: NS,BW: –10(8%),St: NS,C: NS

AW: NS,BW: NS,St: NS,C: –13 (18%)

AW: ±3 (±6%),BW: ±2 (±4%),St: ±3 (±6%),C: NS

AW: NS,BW: NS,St: NS,C: NS

AW: NS,BW: NS,St: –1.7%,C: NS

AW: ±16%,BW: ±9%,St: ±4%,C: NS

Dressendorferet al., 1982[119]

Effects of a 20droad race

Age 23-60y; 12 Mrunners

Running: 20d;f = 10 successivedays; 70h rest;8 successive days;I = high; D = 28 km/d

NS NR –30 (–30%) ±7.5 (22%) NS NS NR

el-Sayed,1996[155]

Effects ofexercisetraining intensity

18 M, 9 HI, 9 LI Cycle ergometry;12wk; f = 3/wk;I = HI: 80% V

.O2max;

L: 30% V.O2max;

D = 20 min

NS: bothgroups

NR NS: bothgroups

NS: bothgroups

NS: bothgroups

NS: bothgroups

HI: ±15%,LI: NS

Farrell andBarboriak,1980[141]

Effects ofexercise training

Age 20-27y; 7 M,9 F

Walking; 8wk;f = 3-4/wk; I = 70%V.O2max; D = 30 min

NS: M and F NR NS: M and F NS: M and F NS: M and F –1%: M and F ±9%:M and F

Filipovsky et al.,1991[70]

Effects ofexercisetraining inhypertensives

Age 26-76y; 77hypertensives:60 M, 17 F

Walking/callisthenics/cycle ergometry;5wk; f = 2-3/wk;I = 70% HRmax:D = 7-10km walk, 30min callisthenics +30 min cycle

–43 (–19%) –32 (–21%) –64 (–35%) –5 (–14%) –1.6: BMI(kg/m2)

NR NR

Franklin et al.,1979[80]

Effects of bodyfat on lipidresponse toexercise

Age 29-40y; 36 F:23 obese, 13 N

Walk; 12wk;f = 4/wk; I = 75%V.O2max; D = 15-25

min

Obese: NS,N: NS

NR Obese: NS,N: NS

NR Obese: –3%,N: NS

Obese: –5%,N: –3%

Obese:±16%,N: ±12%

Fonong et al.,1996[137]

Effects ofexercisetraining in oldermen andwomen

Age 60-75y; 23 M,14 F

Cycle ergometry;8wk; f = 3/wk;I = 60-75% V

.O2peak;

D = 200-300 kcal/session

NS NR NS NS NS NS ±15%

Gaesser andRich, 1984[96]

Effect oftraining intensity

Age 20-30y; 16 M:7 HI, 9 MI

Cycle ergometry;18wk; f = 3/wk;I = HI: 80-85%V.O2max, MI: 45%

V.O2max; D = HI: 25

min, MI: 50 min

HI: NS,MI: NS

HI: NS,MI: NS

HI: NS,MI: NS

HI: NS,MI: NS

HI: NS,MI: NS

HI: NS,MI: NS

HI: ±19%,MI: ±15%

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Goldberg et al.,1984[105]

Effects ofresistancetraining

Age 24-36y; 6 M,8 F

Resistance training;16wk; f = 3/wk;I = 3-8 reps, 3 sets,2 min rest;D = 8 exercises

M: NS,F: –21 (–11%)

M: –23(–16%)F: –20(–19%)

M: NS,F: –20 (–28%)

M: NS,F: NS

M: NS,F: NS

M: –20%,skinfoldthickness,F: –15%,skinfoldthickness

NR

Goodyear et al.,1986[66]

Effects ofprogressiveendurancetraining

Age 20-25y; 10 F:5 runners, 5 C

Running; 8wk;f, I and D =individualised tomeet volume:incremental increasefrom 60-100 km/wk(37-62 miles/wk)

NS: bothgroups

NS: bothgroups

NS: bothgroups

±17 (±29%) NS: bothgroups

NS: bothgroups

±5%

Grandjeanet al., 1996[57]

Effects ofexercise training

Age 30-45y; 37 F:20 Ex, 17 C

Walk/jog/cycle; 24wk;f = 3/wk; I = 60-70%V.O2max; D = 20-60

min (1200 kcal/wk)

Ex: –20(–10%),C: –20 (–10%)

Ex: –25(–21%)C: –17(–14%)

Ex: NS,C: NS

Ex: ±6 (±11%)NS,C: NS

Ex: NS,C: NS

Ex: NS,C: NS

Ex: +15%,C: NS

Grandjeanet al., 1998[72]

Effects ofmenopausalstatus onexercisechanges inlipids

Age 36-68y; F:21 PRE, 16 POM

Walk/jog; 12wk;f = 4/wk; I = 50-70%V.O2max; D = 200-300

kcal

PRE: NS,POM: NS

PRE: NS,POM: NS

PRE: NS,POM: NS

–3 (5.5%) incombinedgroups

PRE: NS,POM: NS

PRE: NS,POM: NS

±16% incombinedgroups

Hardman et al.,1989[112]

Effects ofexercise training

Age 37-53y; 44 F:28 Ex, 16 C

Brisk walking; 1y;f = varied; I = 60%predicted V

.O2max;

D = varied to meet16-18 km/wk (10-11miles/wk)

NS: bothgroups

NR NR Ex: ±12(±27%),C: NS

NR NR NR

Higuchi et al.,1984[120]

Effects ofexercise training

Age 28-31y; 5 M Running; 4 wk;f = 5/wk; I = 80%V.O2max; D = 50 min

NS NR NS ±19 (35%) NS NS NS

Hill et al.,1989[45]

Effects ofexercise training

Age 25-45y; 8 M,9 F

Walk/jog; 10wk;f = 3-4/wk; I = 70%HRmax; D = 20-60min (1500-2000kcal/wk)

M: –25 (–13%),F: NS

NR NR M: NS,F: ±3 (±6%)

M: NS,F: NS

M: NS,F: NS

M: ±18%,F: ±13%

Hinkleman andNieman,1993[142]

Effects ofexercise training

Age 25-45y; 36 F:18 Ex, 18 C

Walk/jog; 15wk;f = 5/wk; I = 60%V.O2max; D = 45 min

NS NS NS Ex: –1.5 (–3%),C: ±7 (±15%)

Ex: NS,C: ±2%

Ex: NS,C: NS

Ex: NS,C: NS

Holloszy et al.,1964[150]

Effects ofexercisetraining andacute response

Age 35-55y; M: 27Ex (15supervised, 12unsupervised), 8 C

Walk/running +callisthenics; 24wk;f = 3-4/wk; I = mod-high; D = 3-6.5 km(2-4 miles)

Ex: NS,C: NS

NR Ex:–83 (–40%):determined tobe an acuteresponse,C: NS

NR NS NR ±106%,treadmill testtime

Houmard et al.,1994[81]

Effects ofexercise training

Age 45-50y; 13 M StairMaster; 14wk;f = 3/wk; I = 70-85%V.O2max; D = 30-45

min

NS NS:increasedcholesterolandphospholipidcompositionof LDL

–35 (–20%) ±2.7 (8.5%) –2% –2% ±21%

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Appendix I. Contd

Study characteristics ∆ lipid and lipoprotein variables ∆ physiological characteristics

author purpose n exerciseintervention

TC(mg/dl)

LDL-C(mg/dl)

TG(mg/dl)

HDL-C(mg/dl)

bodyweight(% ∆)

% fat ∆ V.O2max

(%∆)

Hurley et al.,1988[106]

Effects ofresistancetraining

Age 40-55; 21 M:11 Ex, 10 C

Resistance training;16wk; f = 3-4/wk;I = 8-20 reps, 1 set15 sec rest betweenexercises;D = 14 exercises

Ex: NS, C: NS Ex: –7 (–5%),C: NS

Ex: NS,C: NS

Ex: ±5 (13%),C: NS

Ex: NS,C: NS

Ex: NS,C: NS

Ex: NS,C: NS

Huttunen et al.,1979[116]

Effects ofexercise training

Age 40-45y;100 M: 50 Ex,50 C

Walk/jog/ski/cycle;16wk; f = 3-4/wk;I = 40-66% V

.O2max;

D = 30 min

Ex: –30(–12%),C: –15 (–6%)

Ex: –23(–12%),C: –10 (–5%)

Ex: –25(–18%),C: ±15 (±12%)

Ex: ±6 (16%),C: NS

Ex: –1%,C: <1%

NR Ex: ±9%,C: NS

Keins et al.,1980[52]

Effects ofexercise training

Age 35-45y; 40 M:24 Ex, 13 C

Run/swim/gymnasticgames; 12wk;f = 3/wk; I = 80%V.O2max; D = 45 min

Ex: –10 (–4%),C: NS

NR Ex: –29(–21%),C: NS

Ex: ±3 (±8%),C: NS

Ex: NS,C: NS

Ex: NS,C: NS

Ex: ±11%,C: NS

King et al.,1995[97]

Effects ofexercisetrainingintensities andformats in oldermen andwomen

Age 50-65y;149 M, 120 F: 69HG, 74 HH, 64 LH

Walk/jog/cycleergometry; 2y;f = 3-5 /wk; I = HGand HH: 73-88%;LH: 60-73% HRmax;D = 30-40 min

HG: NR,HH: NR,LH: NR

HG: NS,HH: NS,LH: NS

HG: NS,HH: NS,LH: NS

HG: NS,HH: ±2(±4.5%),LH: ±4 (±8.5%)

HG: NS, BMI,HH: NS, BMI,LH: NS, BMI

HG: NR,HH: NR,LH: NR

HG: ±4%,HH: ±9%,LH: ±8%

Kokkinos et al.,1988[103]

Effects ofresistancetraining

Age 19-22y; 37 M:15 L rep, 14 H rep,8 C

Resistance training;10wk; f = 3/wk;I = variableresistance 60-80 secbetween sets;D = sets adjusted tomeet equal volume

L rep: NS,H rep: NS,C: NS

L rep: NS,H rep: NS,C: NS

L rep: NS,H rep: NS,C: NS

L rep: NS,H rep: NS,C: NS

L rep: NS,H rep: NS,C: NS

L rep: NS,H rep: NS,C: NS

L rep: NS,H rep: NS,C: NS

Kokkinos et al.,1991[102]

Effects ofresistancetraining

Age 35-60y; 24 M:16 Ex, 8 C

Resistance training;20wk; f= 3/wk;I = 12-15 reps withadjusted resistance,90 sec rest, 2 sets;D = 11 exercises

NS: bothgroups

NS: bothgroups

NS: bothgroups

NS: bothgroups

NS: bothgroups

NS: bothgroups

NS: bothgroups

Lamarche et al.,1992[73]

Effects of fatloss withexercisetraining inobese women

Age 30-40y;31 obese F:20 FL, 11 FG

Walk/jog; 24wk;f = 4-5/wk; I = 55%V.O2max; D = 90 min

FL: –16 (8%),FG: NS

FL: –15(11%),FG: NS

FL: –30(18%),FG: NS

FL: NS,(HDL2-C: ±2),(HDL3-C: –2),FG: NS,(HDL2-C: NS),(HDL3-C: –5)

FL: –2%,FG: ±2.5%

FL: –2%,FG:±1.7%

FL: ±13%,FG: ±10%

Lapman et al.,1985[152]

Effects ofresistancetraining

Age 34-58y;10 hyper-triglyceridaemicM

Jogging; 9wk;f = 3/wk; I = 85%HRmax; D = 30-40 min

NS NS –77 (–38%) NS NS NR ±26%

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Leon et al.,1979[83]

Effects ofexercise training

Age 19-31y;6 obese M

Brisk walking; 16wk;f = 5/wk; I = >7METs; D = 15-90min, 1100kcal/session

NS NS NS ± 5 (±16%) –6% –4.9% NR

Lewis et al.,1976[82]

Effects ofphysical activity

Age 30-52y;22 obese F

Walk/jog; 17wk;f = 2/wk; I = 80%HRmax; D = 5km (2.5miles) + 1h ofcallisthenics

NS NS NS ±4.7 (±9%) –5% –5% ±33%, GXTduration

Lopez et al.,1974[46]

Effects ofexercise andphysical fitness

Age 22y;13 medicalstudents

Jog/cycle/callisthenics;7wk; f = 4/wk;I = 7 METs; D = 30min

–7 (–4%) –28 (–17%) –27 (–24%) ± 46 (±16%):α lipoprotein

NS NR NR

Manning et al.,1991[104]

Effects ofresistancetraining

Age 30-40y;16 obese F

Resistance training;12wk; f = 3/wk;I = 60-70% 1RM;D = 3 sets, 6-8 reps

NS NS NS NS NS NR NR

Marti et al.,1990[139]

Effects ofexercise training

Age 27-50y; 61 M:39 Ex, 22 C

Jogging; 16wk;f = 2-6/wk; I = 85%of AT; D = varied tomeet 120 min/wk

Ex: NS,C: NS

Ex: NS,C: NS

Ex: NS,C: NS

Ex: ±3 (±6%),C: NS

NS: bothgroups

NS: bothgroups

Ex: ±6%,estimatefrom runtest, C: ±4%,estimatefrom run test

Milesis et al.,1976[84]

Effects ofexerciseduration

Age 20-35y;59 M inmates:14 in 15-mingroup, 17 in30-min group,12 in 45-mingroup, 16 C

Jogging; 12wk;f = 3/wk; I = 80-95%HRmax; D = 15, 30 or45 min

NS NR NS NR 15-min: NS,30-min: –2%,45-min: –1%,C: NS

15-min: –1%,30-min: –1%,45-min: –1%,C: NS

15-min: ±9%,30-min:±16%,45-min:±17%,C: NS

Moll et al.,1979[77]

Effects ofexercise training

Age 22-26y;14 F

Jogging; 6wk;f = 5/wk; I = 70%HRmax; D = 30-45 min

–10 (–6%) NR NR NS NS NR ±17%, maxtreadmillwork rate

Nieman et al.,1990[75]

Effects of dietand exercise

Age 35-40y;21 obese F:11 DE, 10 Dt

Walking; 5wk; f =5/wk; I = 60% HRR;D = 30-40 min

DE: –34(–17%),D: –24 (–12%)

DE: –17(–14%),D: –17(–14%)

DE: –42(–36%),D: –31 (–27%)

DE: NS,D: –6 (–11%)

DE: –7%,D: –7%

DE: –4%,D: –4%

DE: ±18%,D: –2%

Nieman et al.,1993[143]

Effects ofphysical activity

Age 67-85y; 32 F:14 WK, 16 CL

Walking/callisthenics;12wk; f = 5/wk;I = 60% HRR (WK);D = 30-40 min

NS: bothgroups

NS: bothgroups

NS: bothgroups

NS: bothgroups

NS: bothgroups

NS: bothgroups

WK: ±13%,CL: NS

Nye et al.,1981[47]

Effects ofexercise training

Age 30-45y; 16 M Callisthenics tomusic; 10wk;f = 2/wk; I = NR;D = 30-45 min

–12 (–5%) –8 (–5%) NS NS NS NR NS

Peltonen et al.,1981[65]

Effects ofexercise training

Age 26-53y; 27 M:20 Ex, 7 C

Jog /cross-countryski/swim; 15wk;f = 3/wk; I = mod-high (HR: 140-160bpm); D = 30-60 min

Ex: –9 (–4%),C: NS

Ex: –11(–6%),C: NS

Ex: NS,C: NS

Ex: ±3 (±6%),C: NS

Ex: NS, C: NS NR Ex: ±14,work rate at150 bpm,C: NS

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Appendix I. Contd

Study characteristics ∆ lipid and lipoprotein variables ∆ physiological characteristics

author purpose n exerciseintervention

TC(mg/dl)

LDL-C(mg/dl)

TG(mg/dl)

HDL-C(mg/dl)

bodyweight(% ∆)

% fat ∆ V.O2max

(%∆)

Pollock et al.,1969[121]

Effects ofexercisefrequency

Age 30-47y; 18 M:5 in 2/wk group, 6in 4/wk group, 7 C

Walk/jog/run/interval;16wk; f = 2 or 4/wk;I = low-mod;D = 30 min

2/wk group:–22 (–11%),4/wk group:–10 (–5%),C: ±8 (±5%)

NR 2/wk group:–13 (–16%),4/wk group:–13 (–14%),C: NS

NR 2/wk group:NS,4/wk group:–1%,C: NS

2/wk group:NS,4/wk group:–3%,C: NS

2/wk group:±10%, 3.2km (2-mile)run time,4/wk group:±12%,3.2km runtime

Ponjee et al.,1995[44]

Effects ofmarathontraining

Age 27-49y;sedentary 20 M,14 F

Jogging/running;9mo; f = 3-6/wk;I = variable;D = variable;increasing volumeand intensity in amarathon trainingprogramme

M: –27 (12%),F: NS

M: –19(–12%),F: NS

M: NS,F: NS

M: NS,F: NS

M: –3%,F: NS

M: –5%,F: –3%

NR

Raz et al.,1988[53]

Effects ofexercisetraining in menwith low HDL-C

Age 24-26y; 55 M;28 Ex, 27 C

Jogging/circuittraining; 9wk;f = 2/wk; I = 75-85%V.O2max;

D = 45 min

Ex: NS,C: NS

Ex: –6 (–6%),C: NS

Ex: –14(–14%),C: NS

Ex: NS,C: ±3 (±10%)

Ex: –<1%,C: ± <1%

Ex: NS,C: NS

Ex: ±14%,C: NS

Ready et al.,1995[56]

Effects ofexercise training

Age 57-67y; 40postmenopausalF: 24 Ex, 16 C

Walking; 24wk;f = 5/wk; I = 54%HRR;D = 55 min

Ex:–12 (–5%),C: NS

Ex: NS,C: NS

Ex:–11 (–7%),C: ±15 (±10%)

Ex: NS,C: NS

Ex:–2%,C: NS

Ex: NS,C: NS

Ex:±8%,C: NS

Ready et al.,1996[136]

Effect ofexercise volume

Age 55-67y; 76postmenopausalF: 19 in 3/wkgroup, 17 in 5/wkgroup, 20 C

Walking; 24wk;f = 3 or 5/wk; I =60% V

.O2peak;

D = 60 min

NS: allgroups

NS: allgroups

NS: allgroups

NS: allgroups

3/wk group:–<1%,5/wk group:NS,C: NS

3/wk group:–1%,5/wk group:–1%,C: NS

3/wk group:±9%,5/wk group:±12%,C: NS

Rotkis et al.,1984[67]

Effects ofincreasingrunning volume

Age 24-37y;19 run-trained F

Running; 15mo;f = 5-6/wk;I = variable;D = variable to meetrun volume [runningvolume increasedfrom 24-102 km/wk(15-63 miles/wk)]

NS NR NR ±10 (±16%) NS –3.6% NR

Santiago et al.,1987[144]

Effects ofexercisetraining intensity

Age 20-40y; 25 F:9 WK, 8 J, 8 C

Walking/jogging;20wk;f = 3-4/wk;I = WK: 70-74%V.O2max; J: 85-90%

V.O2max;

D = 5 km/session(3 miles/session)

NS: allgroups

NS: allgroups

NS: allgroups

NS: allgroups

NS: allgroups

NS: allgroups

WK: ±21%,J: ±31%,C: NS

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Santiago et al.,1995[145]

Effects ofexercise training

Age 22-40y; 27 F:16 WK, 11 C

Walking; 40wk;f = 4/wk;I = 72% HRmax;D = 5 km/session(3 miles/session)

NS: bothgroups

NS: bothgroups

NS: bothgroups

NS: bothgroups

NS: bothgroups

NS: bothgroups

WK: ±22%,C: –2%

Savage et al.,1986[98]

Effects ofexercisetraining intensity

Age 6-10y,34-40y;HI: 12 boys and12 men;LI: 8 boys and 8men;C: 10 boys and10 men

Walk/jog/run; 10wk;f = 3/wk;I = HI: 75% V

.O2max;

LI: 40% V.O2max;

D = 2.4-5.8km/session

NS: allgroups

NS: allgroups

NS: allgroups

NS: allgroups

NS: allgroups

NS: allgroups

HI: ±3%,LI: NS,C: NS

Schwartz,1987[86]

Independenteffects ofdietary vsexercisebodyweight loss

Age 20-38y; 26 M:12 Ex, 14 Dt

Walk/jog; 12wk;f = 3-5/wk;I = 70-85% HRR;D = 40 min

Ex: NS,Dt: –29 (–16%)

Ex: NS,Dt: –33(–22%):VLDL-C +LDL-C

Ex: NS,Dt: –54 (–35%)

Ex: ±3 (±8%),Dt: ±4 (±12%)

Ex: –3%,Dt: –13%

Ex: –11% fatmass,Dt: –30% fatmass

Ex: ±19%,Dt: NS

Schwartz et al.,1992[90]

Effects ofexercise training

Age 28-68y; 27 M:12 young, 15 older

Walk/jog/cycle;24wk;f = 5/wk;I = 50-85% HRR;D = 45 min

Young: NS,older: NS

Young: NS,older: NS

Young: NS,older: –23(–20%)

Young: ±6(±13%),older: ±6(±14%)

Young: NS,older: –3%

Young: NS,older: –1.7%

Young:±18%,older: ±22%

Seip et al.,1993[49]

Effects ofexercise training

Age 60-72y; 57sedentary older Mand F: 28 M, 29 F

Walk/jog/cycle;9-12mo; f = 3-5/wk;I = 65-85% HRmax;D = 45-60 min;1200-1800 kcal/wk

–8 (–4%) –6 (–5%) –26 (–20%) ±3 (±5%) –3-3.5% –2-3% ±18-22%

Shephard et al.,1979[61]

Effects of anindustrialfitnessprogramme

Age 24-53y; 98 M,158 F: 101 HA, 57LA, 37 C

Jog/rhythmcallisthenics;24wk; f = 3/wk;I = 60-70% V

.O2max;

D = 30 min

HA M: NS,HA F: –15(–7%)LA M: –9(–4%),LA F: NS,C M: NS,C F: –4 (–2%)

HA M: NS,HA F: –16(–14%),LA M: –10(–8%),LA F: NS,C M: NS,C F: –13(–10%)

HA M: NS,HA F: NS,LA M: NS,LA F: NS,C M: NS,C F: NS

HA M: NS,HA F: NS,LA M: NS,LA F: NS,C M: –5(–8%),C F: –7 (–10%)

NR HA M:–1%,HA F:–2%,LA M: NS,LA F: –2%,C M: NS,C F: NS

HA M:+9%,HA F:+5%,LA M: +5%,LA F: NS,C M: NS,C F: +3%

Smutok et al.,1993[100]

Effects ofstrength vsaerobic training

Age 40-60y; 44 M:14 ST, 13 AT, 10 C

Walk/jog/resistance;20wk; f = 3/wk;I = AT: 50-85% HRR;ST: 12-15 reps,2 sets, 90 sec rest;D = AT: 30 min;ST: 11 exercises

NS:all groups

NS: allgroups

NS:all groups

NS:all groups

NS:all groups

AT: –1.6%,ST: NS,C: NS

AT: ±17%,ST: NS,C: NS

Sopko et al.,1983[127]

Effects of dietand exercise inoverweight,hypercholesterolaemic men

Age 43-60y: 23 M:10 DE, 13 Dt

Walking; 12wk;f = 3/wk; I =moderate;D = 60 min (400-500kcal /session)

DE: –10(–4%) NS,Dt: –6 (–3%)NS

DE: NS,Dt: NS

DE: NS,Dt: NS

DE: ±5(±11%),Dt: NS

DE: –4%,Dt: NS

DE:–17%sum ofskinfolds, Dt:NS

NR

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Appendix I. Contd

Study characteristics ∆ lipid and lipoprotein variables ∆ physiological characteristics

author purpose n exerciseintervention

TC(mg/dl)

LDL-C(mg/dl)

TG(mg/dl)

HDL-C(mg/dl)

bodyweight(% ∆)

% fat ∆ V.O2max

(%∆)

Stefanick et al.,1998[128]

Effects ofNCEP step 2diet andexercise in menand women

Age 30-64y;190 M, 177 F:47 M Ex, 43 F Ex,49 M Dt, 46 F Dt,48 M DE, 43 F DE,46 M C, 45 F C

Walking; 1y;f = 3/wk; I = low-mod; D = varied tomeet goal of 16km/wk (10 miles/wk)

Ex M: NS,Ex F: NS,Dt M: NS,Dt F: NS,DE M: –21(–9%),DE F: –18(–7%),C M: NS,C F: NS

Ex M: NS,Ex F: NS,Dt M: NS,Dt F: NS, DEM: –20(–13%),DE F: –15(–9%),C M: NS,C F: NS

Ex M: NS,Ex F: NS,Dt M: NS,Dt F: NS,DE M: NS,DE F: NS,C M: NS,C F: NS

Ex M: NS,Ex F: NS,Dt M: NS,Dt F: NS,DE M: NS,DE F: NS,C M: NS,C F: NS

Ex M: NS,Ex F: NS,Dt M: –3%,Dt F: –4%,DE M: –5%,DE F: –4%,C M: NS,C F: NS

NR Ex M: ±5%,Ex F: ±9%,Dt M: NS,Dt F: NS,DE M: ±7%,DE F: ±9%,C M: NS,C F: NS

Stein et al.,1990[99]

Effects ofexerciseintensity

Age 36-52y; 49 M:13 at 65%HRmax,,14 at 75%HRmax, 12 at 85%HRmax,10 C

Cycle ergometry;12wk; f = 3/wk;I = 65, 75, 85%HRmax; D = 30 mininterval training

65%: NS,75%: NS,85%: NS,C: NS

65%: NS,75%: –17(–10%),85%: NS,C: NS

65%: NS,75%: NS,85%: NS,C: NS

65%: NS,75%: ±7(±19%),85%: ±6(±13%),C: NS

NS: allgroups

NS: allgroups

65%: ±11%,75%: ±18%,85%: ±43%,C: NS

Stubbe et al.,1983[154]

Effects ofexercise training

Age 32-53y; 18 M:12 HI, 6 MI

Cycle ergometry;HI: 6wk; MI: 12wk;f = 3-5/wk; I = HI:85% HRmax; MI: 70%HRmax; D = 50 min

NR HI: NS,MI: –27(–17%)

NS: bothgroups

HI: NS,MI: NS

NS: bothgroups

NS: bothgroups

HI: ±19%,MI: ±18%

Sunami et al.,1999[129]

Effects of low-intensityexercise training

Age 60-77y; 20 M,20 F: 10 M Ex, 10F Ex, 10 M C, 10F C

Cycle ergometry;20wk; f = 2-4/wk;I = 50% estimatedV.O2max; D = 60 min

NS: bothgroups

NS: bothgroups

NS: bothgroups

Ex: ±5(±10%),C: NS

NS: bothgroups

NS: bothgroups

Ex: ±7%,C: NS

Suter and Marti,1992[146]

Effects of self-monitoredexercise

Age 25-55y; 33 F:17 Ex, 16 C

Walk/jog; 16wk;f = 2-6/wk;I = moderate;D = variable to meet2h or 11 km/wk(7 miles/wk)

NS: bothgroups

NS: bothgroups

NS: bothgroups

NS: bothgroups

NS: bothgroups

NS: bothgroups

NR

Sutherlandet al., 1983[122]

Effects ofcholesterollevels onexercisetrainingresponse

Age 16-50y; 18 M:8 HC, 10 NC

Running/circuittraining; 16wk;f = 2-3/wk;I = mod-high;D = 60 min

HC: ±55(±14%),NC: ±20(±10%)

HC: ±66(±22%),NC: ±16(±11%)

HC: NS,NC: NS

HC: NS,NC: NS

HC: NS,NC: ±3%

HC: NS,NC: NS

HC: NS,NC: NS

Sutherlandet al., 1984[134]

Effects ofmarathontraining

Age 18-47y; 12 M Running; 18wk; f =variable; I = variable;D = self-monitoredmarathon training(increased 33 km/wk)

NS NR NS ±15 (±26%) NS NR NR

Svendsen et al.,1994[156]

Effects ofexercise afterdiet intervention

Age 49-58y; 118postmenopausalF: 51 Dt, 49 DE,21 C

Walking; 24wk;f = 3/wk; I = 70%V.O2max; D = 60-90

min; includedresistance training

NS: allgroups

NS: allgroups

Dt: –25(–25%),DE: –27(27%),C: ±18 (±15%)

Dt: ±6 (±9%),DE: ±8(±12%),C: NS

Dt: –13%,DE: –13%,C: NS

Dt: –23% fatmass,DE:–23% fatmass,C: NS

Dt: NS,DE: NS,C: –13%

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Szmedra et al.,1998[147]

Effects ofexercise training

Age 20-22y;7 obese F

Walk-jog/cycle/row;6wk; f = 3/wk;I = 70% V

.O2max;

D = 30 min

NS NS NS NS –2% –4% ±30%

Thomas et al.,1984[138]

Effects ofinterval andcontinuoustraining

Age 18-32y; 24 M,35 F: 6.5km(4-mile) run 9 M,13 F; 3.2km(2-mile) run: 9 M,12 F; IT: 10 M, 11F; 16 C

Walk/jog; 12wk;f = 3/wk; I = 6.5km(4-mile), 3.2km(2-mile): 75%HRmax; IT: 90%HRmax; D = 6.5km:500 kcal ; 3.2km:250 kcal ; IT: 500kcal

NS: allgroups

NR NS: allgroups

NS: allgroups

NS: allgroups

6.5km: –8%,3.2km: –8%,IT: 10%,C: NS

6.5km: ±4%,3.2km: ±7%,IT: ±12%,C: NS

Thomas et al.,1985[157]

Effects ofinterval andcontinuoustraining

Age 18-25y; 36 Mcollege students:11 in 8km (5-mile)run, 8 in 4-mininterval, 9 in 2-mininterval, 8 C

Running; 11wk;f = 3/wk; I = 5-min:70-85% HRmax;4-min, 2-min:90-100% HRmax;D = 500-550kcal/session

NS: allgroups

NR NR NS: allgroups

NS: allgroups

NR 5-min: NS,4-min:±18%,2-min: NS,C: NS

Tomiyasu et al.,1996[48]

Effect of short-term exercisetraining

Age 19-30y; 20 M:13 HI, 7 MI

Running; 3wk;f = daily; I = HI: 19km/h (12 miles/h);MI: 10 km/h(6 miles/h); D = HI:6.5km (4 miles);MI: 3.2km (2 miles)

HI: –16 (–9%),MI: –12 (–6%)NS

NR HI: –38(–37%),MI: –33(–28%) NS

HI: ±6 (±10%),MI: ±6 (±10%)

NS: bothgroups

NR NR

Thompsonet al., 1988[123]

Effects ofexercise training

Age 20-40y; 8 M:6 Ex, 2 C

Cycle ergometry;48wk; f = 4-5/wk;I = 80% HRmax;D = 60 min

NS: bothgroups

NS: bothgroups

–19 (–16%) ±5 (±14%) NS: bothgroups

NS: bothgroups

±27%

Thompsonet al., 1997[124]

Effects ofexercise training

Age 30-50y; 17 M Walk/jog/cycle; 1y;f = 4/wk; I = 60-80%HRmax; D = 50 min

NS NS –11 (–8%) ±4 (±9%) NS NS ±27%

Vermeulen,1990[92]

Effects of‘modified fastdiet’ andexercise

Age 42-65y; 46obesepostmenopausalF: 26 DE(exercise + 400-kcal/d diet), 20 Cat baseline

Swim/gymnastics;4wk; f = daily;I = low-moderate;D = 20-min swim,30-min gymnastics

DE: –59(–22%),C: NS

NR DE: –50(–26%),C: NS

NS: bothgroups

DE: –8kg,C: NS

NR NR

Van Der Eemsand Ismail,1985[87]

Effects ofexercise training

Age 27-59y; 20 F:10 PRE, 10 POM

Jog/callisthenics;8mo; f = 3/wk;I = 60-70% HRmax;D = 45 min

NS: bothgroups

NS: bothgroups

PRE: –23(–27%)significant forcombinedgroups,POM: –14(–16%)significant forcombinedgroups

PRE: ±4(±4%) NS forcombinedgroups,POM: –2(–3%) NS forcombinedgroups

NS PRE: –3%,POM: NS

NS: bothgroups

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Appendix I. Contd

Study characteristics ∆ lipid and lipoprotein variables ∆ physiological characteristics

author purpose n exerciseintervention

TC(mg/dl)

LDL-C(mg/dl)

TG(mg/dl)

HDL-C(mg/dl)

bodyweight(% ∆)

% fat ∆ V.O2max

(%∆)

Warner et al.,1989[93]

Effects ofdietary fish oiland exercise

Age 27-63y; 22 M,12 F: 7 FE, 7 FO,10 CN, 10 C

Walk/jog; 12wk;f = 3/wk;I = 70-85% HRmax;D = 45-50 min

FE: –23(–10%),FO: –29(–13%),CN: NS,C: NS

FE: –11(–8%),FO: NS,CN: NS,C: NS

FE: –90(–39%),FO: –158(–61%),CN: NS,C: NS

FE: NS,F: NS,CN: NS,C: NS

NR FE: –3%,FO: NS,CN: NS,C: NS

FE: ±22%,FO: NS,CN: NS,C: NS

Weltman et al.,1980[91]

Effects ofcaloricrestriction andexercise

Age 58-47y; 50 M:23 DE, 11 Dt, 11Ex, 5 C

Walking; 10wk;f = 4/wk;I = 5.6 km/h (3.5miles/h) walkingspeed;D = 15 –45 min/d[4.2 km/d(2.6 miles/d)]

≥16 (–8%) alltreatments vsC

≥14 (–9%) inDE and Exvs C

NR DE: NS,Ex: NS,Dt: ≥8 (–16%),C: NS

DE: –7%,Ex: –1%,Dt: –7%,C: NS

DE: –4%,Ex: –1%,Dt: –3%,C: NS

NR

Weintraub et al.,1989[125]

Effects ofexercise training

Age 22-33y; 6 M Jogging; 7wk;f = 4/wk;I = 80% estimatedHRmax;D = 30 min; 25km/wk (15 miles/wk)

NS NS –11 (–14%) NS NS NR ±43%

Whitehurst andMenendez,1991[85]

Effects ofexercise training

Age 61-81y; 34postmenopausalF: 20 Ex; 14 C

Walking; 8wk;f = 3/wk; I = 70-80%HRmax;D = 25-40 min

NS: bothgroups

NS: bothgroups

Ex: –5 (–4%),C: NS

Ex: ±4 (±7%),C: NS

Ex: –2%,C: NS

Ex: –1%,C: NS

Ex: ±5%,improved1.6km(1-mile)time,C: NS

Williford et al.,1988[148]

Effects ofaerobic dancetraining

Age 18-30y;18 college F:10 Ex, 8 C

Aerobic dance class;10wk; f = 3/wk;I = 60-90% HRR;D = 30 min

NS: bothgroups

NS: bothgroups

NS: bothgroups

NS: bothgroups

NS: bothgroups

NS: bothgroups

Ex: ±12%,C: NS

Williams et al.,1994[108]

Effects ofHDL-C levelsand weight lossby diet andexercise

Age 30-59y;130 M: 34 LHDL-C,,

63 MHDL-C,36 HHDL-C;

Ex: 13 LHDL-C,21 MHDL-C,12 HHDL-C;Dt: 8 LHDL-C,20 MHDL-C,14 HHDL-C;C: 13 LHDL-C,21 MHDL-C, 8 HHDL-C

Jogging/running;1y; f = 3-4/wk;I = 60-85% HRmax;D = 25-40 min

NR NR NR Ex LHDL-C: NS,Ex MHDL-C:±4.9 changevs C,Ex HHDL-C: ±7change vs C,Dt LHDL-C: ±6change vs C,Dt MHDL-C: ±5change vs C,Dt HHDL-C: ±5change vs C

Ex LHDL-C:–1.1 ∆BMI,Ex MHDL-C:–1.2 ∆BMI, ExHHDL-C:–1.5 ∆BMI,Dt LHDL-C:–2 ∆BMI,Dt MHDL-C:–2.4 ∆BMI,Dt HHDL-C:–2.3 ∆BMI,C LHDL-C: NS,C MHDL-C: NS,C HHDL-C: NS

Ex LHDL-C:–2%,Ex MHDL-C:–2%,Ex HHDL-C:–1%,Dt LHDL-C:–3%,Dt MHDL-C:–2%,Dt HHDL-C:–2%,C LHDL-C: NS,C MHDL-C: NS,C HHDL-C: NS

NR

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Wirth et al.,1985[88]

Effects ofexercisetraining inhypertriglyceridaemia

Age 35-51y; 21 M:10 Ex, 11 C

Jog/recreationalgames; 4mo;f = 3/wk;I = moderate-high;D = 60 min

Ex: –13 (–5%)NS,C: –5(–2%) NS

NS: bothgroups

NR NS: bothgroups

NS: bothgroups

Ex: –2%,C: NS

Ex: ±28%max aerobicpower,C: NS maxaerobicpower

Woods andGraham,1986[149]

Effects ofmenstrual cycleon exercisechanges

Age 20-25y; 8 F;no effect ofmenstrual phaseon TC and HDL,TG > at mensesonset

Cycle ergometry;56-77d; f = 3/wk;I = 60% HRR;D = 30 min

NS NR –19 (–22%)measured atonset ofmenses after3mo of training

NS NS NS ±6%

Wood et al.,1983[89]

Effects ofexercise training

Age 30-55y; 81 M:48 Ex, 33 C

Jogging/running; 1y;f = 3-5/wk; I = 70-85% HRmax;D = 25 min

NS: bothgroups

NS: bothgroups

NS: bothgroups

NS, HDL-C ±4in M running≥12.8 km/wk(8 miles/wk)

Ex: –2%, C:NS

Ex: –2%, C:NS

Ex: ±21%,C: NS

Wood et al.,1988[59]

Effects ofbodyweightloss by diet andexercise

Age 30-59y;131 overweight M:47 Ex, 42 Dt, 42 C

Briskwalking/jogging; 1y;f = 3-5/wk; I = 60-80%HRmax; D = 25-50min + increased non-exercise physicalactivity

Ex: –9 (–4%)NS, Dt: –14(–6%) NS,C: –9 (–4%)NS

Ex: –10(–7%),Dt: –12(–8%) NS,C: –8 (–5%)NS

Ex: –14(–11%),Dt:–24(–17%),C: NS

Ex: ±4(±10%),Dt: ±5 (±11%),C: NS

Ex: –4%,Dt: –8%,C: NS

Ex: –16% fatmass,Dt: –23% fatmass,C: NS

Ex: ±12%,Dt: NS,C: –7%

Wood et al.,1991[76]

Effects ofNCEP step 1diet andexercise training

Age 25-49y;231 overweight Mand F. DE: 39 M,42 F; Dt: 40 M, 31F; C: 40 M, 39 F

Briskwalking/jogging; 1y;f = 3/wk; I = 60-80%HRmax; D = 25-45 min

DE M: NS,DE F: –11(–6%),Dt M: NS,Dt F:–15 (–8%),C F: NS,C M: NS

DE M: NS,DE F: –11(–9%),Dt M: NS,Dt F: –11(–9%),C M: NS,C F: NS

DE M: –41(33%),DE F: NS,Dt M: NS,Dt F: NS,C M: NS,C F: NS

DE M: ±5(±13%),DE F: NS,Dt M: NS,Dt F: NS,C M: NS,C F: NS

DE M: –9%,DE F: –7%,Dt M: –5%,Dt F: –5%,C M: NS,C F: NS

DE M: –28%,DE F:–20%,Dt M: –16%,Dt F: –15%,C M: NS,C F: NS

DE M: ±25%,DE F: ±24%,Dt M: NS,Dt F: NS,C M: NS,C F: NS

Wynne et al.,1980[117]

Effects exercisetraining

Age 19-30y; 19 Fcontrolled oralcontraceptive use:13 Ex, 6 C

Cycle ergometry;10wk; f = 3/wk;I = 70% HRR;D = 30 min

Ex: –5 (–3%)NS,C: –5(–3%) NS

NS: bothgroups

Ex: –21(–15%) NS,C: NS

NS: bothgroups

Ex: NS,C: NS

Ex: –2%,C: NS

Ex: ±16%,C: NS

Zmuda et al.,1998[109]

Effects ofHDL-C levelson exercisetrainingresponse

Age 26-49y; 17 M:7 LHDL-C, 10 NHDL-C

Walk/jog/cycle; 1y;f = 4/wk; I = 60-80%HRmax; D = 50 min

NS: bothgroups

NS: bothgroups

NS: bothgroups

LHDL-C: NS,NHDL-C: ±5(±12%)

NS: bothgroups

NS: bothgroups

LHDL-C:±21%,NHDL-C: ±32%

a These 100 exercise-training studies were selected because they are the studies most often cited.AE = aerobic exercise group; AT = aerobic threshold; AW = walkers; BMI = body mass index; BW = brisk walkers; C = controls; CL = callisthenics; CN = corn oil; CT = continuoustraining; D = duration; DE = diet and exercise; DL = diet and lifestyle; Dt = diet; Ex = exercisers; ExH = exercise and hormone replacement therapy group; F = females; f = frequency;FE = fish oil and exercise; FG = fat gain; FL = fat loss; FO = fish oil; GXT = graded exercise testing; H = high; HA = high adherence; HC = high cholesterol; HDL-C = high-densitylipoprotein–cholesterol; HG = high intensity group; HH = high intensity at home; HHDL-C = high HDL-C; HI = high intensity; H Rep = high repetitions; HRmax = maximal heart rate; HRR= heart rate reserve; HV = high volume; I = intensity; IT = interval training; J = joggers; L = low; LA = low adherence; LC = low cholesterol; LDL = low-density lipoprotein; LDL-C =low-density lipoprotein–cholesterol; LH = low intensity at home; LHDL-C = low HDL-C; L Rep = low repetitions; M = males; METs = metabolic equivalents (1 MET = 3.5 ml/kg/min);MHDL-C = moderate HDL-C; MI = moderate intensity; N = normal bodyweight; n = number of participants; NC = no change; NCEP = National Cholesterol Education Program; NHDL-C

= normal HDL-C; NR = not reported; NS = not significant; NV = normal volume; POM = postmenopausal; PRE = premenopausal; RE = resistance exercise group; RM = repetitionmaximum; ST = strength training; St = strollers; TC = total cholesterol; TG = triglyceride; VLDL-C + LDL-C = very low-density lipoprotein-cholesterol + low-density lipoprotein-cholesterol;V.O2max = maximal oxygen uptake; V

.O2peak = peak oxygen uptake; WK = walkers; Y = yoga group.

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Correspondence and offprints: Professor J. Larry Durstine,Department of Exercise Science, University of South Caro-lina, 1300 Wheat Street, Columbia, SC 29208, USA.

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