- Email: [email protected]
Effect of a controlled exercise program on serum lipoprotein levels in women on oral contraceptives
Effect
of a Controlled Exercise Program on Serum Lipoprotein Levels in Women on Oral Contraceptives Terrance P. Wynne,
The effects of a lo-wk
individualized
eter interval training program group
of
13 sedentary
contraceptive
increase.
contraceptive group.
women
in a
on a specific
oral
1 mg norethiste-
lipoprotein
cholesterol
Six additional served
All subjects
were
bicycle ergom-
if. like men on physical training,
high-density
would
Bassett Frey, Lloyd L. Laubach,
were investigated
(50 pg mestranol,
rone) to determine their
Mary Anne
as
a
women
nonexercising
were between
nonsmokers.
Diet
levels
on the oral
and
control
18 and 30 yr and
alcohol
intake
were
stable throughout
the study period, and were moni-
tored throughout.
The interval training
three times per week, 30-min at 70% maximum rate
+
rate]).
0.7
Training
maximum
heart rate reserve
x [maximum
unchanged.
heart
produced
oxygen
Body
unlike
similar
was
per session.
(resting
heart
rate-resting
increases
uptake.
However,
program
exercise
heart
(p < 0.05)
in
weight
was
training
pro-
grams with males, there were no significant changes in
plasma
high-density
triglycerides. oral
In women
contraceptives.
may fail to elevate terol
levels,
marked
consistent high density
consistent
hormone-exercise effect
tein cholesterol
lipoprotein
cholesterol
receiving estrogen
with
effects
of exercise
exercise
programs
lipoprotein with
on high-density
tary controls.” In their study of 39 “mostly Altekruse and Wilmore sedentary men,” induced a significant increase in electrophoretitally measured alpha lipoproteins as a percent of total cholesterol through a IO wk, three-timesper-week program of walking, jogging, and running.” In their review of the effect of exercise on plasma C-HDL, Wood and Haskell” indicate that exercise training programs consistently increase C-HDL cholesterol levels in initially sedentary people. Lipson, et al.,” however. reported a decrease in C-HDL levels, which was more pronounced in female than male subjects, after a 6 wk treadmill training program. The present study was undertaken to determine whether a regular exercise program would effect changes in serum lipoprotein levels of women taking OC.
choles-
an interaction
and/or
or
progestin
and Charles J. Glueck
MATERIALS
of sex the
less
lipopro-
in women.
AND
METHODS
Subjects Nineteen
women participated
in the study. They ranged in
age from I9 to 30 yr and had been taking an OC with 50 pg
0
RAL CONTRACEPTIVES (OC) have been implicated in the incidence of coronary heart disease as well as all other cardiovascular diseases.‘.’ Estrogen-progestin oral contraceptive use is associated with elevated triglyceride levels3 Furthermore, since estrogen is directly related and progestins are inversely related to triglyceride levels and to high-density lipoprotein cholesterol (C-HDL),4 depending upon their estrogen/progesterone formulation, OC may be associated with lower levels of CHDL. Epidemiologic evidence indicates that CHDL is inversely correlated with coronary heart disease;5~8 thus, the serum C-HDL level may be one of the links between OC use and increased risk of heart disease. Any systematic program that elevates C-HDL levels might reduce the risk of heart disease in women taking OC. A regular, vigorous exercise program might be an approach to elevate CHDL levels in young women either taking or not taking OC. Male and female marathon runners have higher C-HDL levels than matched seden-
Metabolism,
Vol.
29,
No.
12
(December),
1980
mestranol,
I
mg norethisterone
were nonsmokers
and were
for a minimum found
disease by physical examination tered by a cardiologist.
and treadmill
Thirteen
IO-wk bicycle exercise training
of 2 mo. All
free of cardiovascular test adminis-
subjects participated
in a
program; the other six were
nontraining controls. All subjects had normal prestudy levels of plasma LDL.
total cholesterol.
None
were
diabetic:
triglyceride, and
none
diseases. They took no other medications.
C-HDL. had
and C-
any
chronic
I
summa-
Table
rizes the subjects’ age, height. weight, percent body fat, and Quetelet index (kg/cm2
x 1000).
From the 5epartment of‘ PhysioIog_v. Wright State University School of Medicine, Dayton, Ohio, and the Lipid Research Center and General Clinical Research Center. University of Cincinnati Medical Center, Cincinnati. Ohio. Received for publication April 17. 1980. Supported in part by grants from the American Heart Association, Miami Valley Chapter, Ortho Pharmaceutical. and a Biomedical Research Grant to Wright State Universily College of Science and Engineering from N.I. H. and II) GCRC grant RROOOG-I 9. Address reprint requests to M.A.B. Frey. Ph.D., Department of Physiology, Wright State University. School oJ‘ Medicine. P.O. Box 927. Dayton. Ohio 45401. 0 1980 by Grune & Stratton. inc. 0026-0495/80/291220012$01.00/0
1267
WYNNE
1268
Table 1. Age, Height, Weight,
Percentage
Body Fat, and Quetelet
ET AL.
Index of Subjects in the Exercise and Control Groups. Pre-
and Posttraining M&SIl
Variable
Pretraining.
Posttraining*
Difference
Paired t
Exercise group (n = 13) Age (~1 Height (cm)
23.2
f 3.37
167.2
i 6.15
-
Weight (kg)
66.0
+ 8.26
65.8
k 8.31
-0.2
0.69
Bodv fat (%)
28.3
+ 4.1
26.3
+ 4.3
-2.0
4.19t
2.37
f 0.357
2.36
-t 0.378
-0.01
0.43
-0.5
0.00
Quetdet index ([kg/cm’]
x 1000)
Control group (n = 6) Age (vr) Height (cm)
24.2
f 3.19
165.6
f 3.70
Weight (kg)
60.4
+ 7.45
59.9
t 6.17
Body Fat (%I
27.8
+ 1.4
26.7
+ 1.9
1.1
2.18
+ 0.185
2.18
+ 0.157
0
1.85
Quetelet index ([kg/cm’]
x 1000)
-0.10
*Values are Mean + SD. tp < 0.05 paired t test pretraining vs. posttraining.
Procedures The program consisted of: (A) a pretraining
period during
which venous blood samples were drawn after a 12-hr fast and lipid and lipoprotein levels were quantitated Research
Center
in Cincinnati,
Ohio,
methods;”
maximum
performed
on a bicycle ergometer;”
mated
from
at the Lipid
by standard
oxygen uptake tests (i’,,
skinfolds;”
LRC
max)
were
and body fat was esti-
(B) an interim
period
of 10 wk
in the training program described below and all subjects maintained daily diet diaries on which they recorded all foods and beverages consumed except water; (C) a posttraining period during which blood values, ir, max, and body fat were redetermined. Exercise consisted of a supervised bicycle ergometer interval training program with 5-min work bouts, averaging 70% maximum heart rate reserve (resting heart rate during
which exercise subjects participated
Table 2. Maximum
Oxygen Uptake (\i,
+ 0.7 x [maximum heart rate-resting heart rate]), separated by 2-min rest periods. Heart rate was monitored immediately after each work bout. Subjects exercised 30 min per session, three sessions per week, for IO wk. Workloads were increased regularly to maintain target heart rates. Pretraining and posttraining data for all variables were analyzed by paired t test for both the controls and the training subjects. Controls and training subjects were compared by analysis of covariance, using “pretraining” values as the covariant. Differences are considered significant if p < 0.05.
RESULTS
Participation in the training program was 100%; that is, each subject in the training group completed the program, attending 30 training
max), Resting Heart Rate and Maximum Heart Rate of Subjects in the exercise and Control Groups Pre- and Posttraining
Difference
Paired t
4.72
J.OOt
M&W
Variable
Pretraining*
Posttraining*
Exercise group (n = 13) \ig maximum (ml/kg
.
min)
29.22
+ 4.85
33.94
-t 4.55
Resting heart rate (bpm)
76 * 10
68 + 6.7
190 & 8.75
191 i 5.47
-8.0
4.94t
Maximum heart rate (born1
1.0
--0.14
1.o
-0.76
Control group (n = 6) \ioz maximum (ml/kg
.
min)
25.04
f 1.79
26.04
-t 3.61
Resting heart rate (bpm)
JO * 6.6
67 * 11
-3.0
188 + 14
186 + 8.7
-2.0
0.53
Maximum heart rate (bpm) *Values are mean f SD. tp i 0.05 paired t test pretraining vs. posttraining.
-0.07
EXERCISE AND LIPOPROTEINS IN WOMEN
Table 3. Total Plasma CholesteroL
1269
Triglyceride,
High- and Low-Density
Lipoprotein
Cholesterol
(C-HDL and C-LDL) of
Subjects in the Exercise and Control Groups, Pre- and Posttraining MIXII Pretraming*
Posttraining*
Odference
Paired
(mg/dl)
lmg/dl)
(mgldl)
t
Total cholesterol
188 k 26
183 + 24
~
Tnglyceride
139 k 59
118t50
-21
Vanable
Exercise group (n = 13) 5
0.96 2.11
1
1.10
-
1
0.33
167 + 30
-
5
0.74
97 2 28
-4
55 t 18
52 t 14
-
3
1.36
97 ? 24
96 + 19
-
1
0.27
C-HDL
56k
12
57 t 14
C-LDL
104 i
19
103 * 20
Total cholesterol
172 t 37
Triglyceride
101 + 51
C-HDL C-LDL
Control group (n = 6) 0.32
*Values are mean + SD.
sessions. Table 1 reveals no significant changes in any body size parameters due to the training program, except percent body fat. Significant (p < 0.001) differences were evoked in the training group for ifoZ max, both relative (ml/kg.min) and absolute (1.92 t 0.33 l/min to 2.21 + 0.27 l/min), and in resting heart rate, as shown in Table 2. Examination by analysis of covariance revealed significant (p < 0.05) differences between exercise and control groups for change in \;ro, max over the training period. There were no significant pre- to posttraining changes in lipid and lipoprotein levels, in either the exercise group or the nonexercised control group (Table 3). In the exercise group, plasma triglycerides decreased approximately 15%; total cholesterol, however, was practically unchanged, as were the C-HDL and C-LDL fractions. By analysis of covariance there were no significant differences between the exercise and control groups for changes in lipoprotein variables over the training period. There was a weak positive correlation between the change (A) in vo* max over the training period and A triglyceride (r = 0.42, p > 0.10). Frequency of alcohol intake ranged from a low of 1.2 times per subject per week in week 4 to a high of 2.1 times per week during week 1, and average wine intake varied from 0 to 1 .l glass per week per subject, based on 10 subjects. (Excluded from this analysis is 1 subject who drank no alcohol and 2 subjects for whom records are incomplete. Their intakes for the weeks that are reported, however, fall within these ranges.) With the exception of week 4 in which no wine was consumed, there were no
significant differences in total alcohol consumption or wine consumption throughout the training period, as tested by analysis of variance. From inspection of the diet histories, it appears that food habits for each individual were qualitatively consistent week by week. The control subjects showed no significant changes from preto posttest in any of the above mentioned parameters. DISCUSSION
In this study, we have investigated whether, by regular exercise, women on OC might alter their lipid and lipoprotein levels, at stable body weight, while improving exercise tolerance and decreasing percent body fat. Thirteen women, nonsmokers, on a single specific OC participated in a vigorous, controlled physical training program that notably increased the physical fitness level of every participant. Although their serum lipoprotein levels were not significantly changed, there was a trend toward decreased triglycerides; however, there was no increase in C-HDL. This outcome was surprising to us, since there is a preponderance of evidence that exercise training will increase C-HDL levels in a variety of populations.” Long-distance runners-male and female-who regularly ran more than 15 miles a week had C-HDL levels greater than matched groups of nonexercising controls (runners: male = 64 + 13 mg/dl, female = 75 + I4 mg/dl; controls: male = 43 _+ 10 mg/di, female = 56 + 14 mg/dl).’ This was a crosssectional study, however, and therefore, like all such studies, has the disadvantage that the
1270
groups are self-selected. In addition, runners differed from controls in that the runners were significantly leaner as determined by ratio of actual to ideal weight, the runners were all nonsmokers, and the runners had a greater frequency of drinking alcoholic beverages and, in particular, drank more wine. Evidence also exists, moreover, that longitudinal training programs can change C-HDL levels in initially sedentary individuals. A IO-wk training program less rigorous than ours was effective in increasing the percent of total cholesterol as alpha lipoprotein in sedentary men (from 36.9% & 11.7% to 55.5% + 1 l.O%.” Subjects meeting merely a 60% participation criterion were included in the data for those men.” The report, however, does not provide a record of the smoking and alcohol consumption habits of the participants.” Participants were asked to continue a set dietary pattern throughout the 10 wk program, but this was not monitored.” Concurrent changes in smoking, alcohol, and diet patterns often accompany exeicise programs and may account in part for the changes in C-HDL. Furthermore, the lipid analyses involved the separation of alpha lipoprotein by electrophoresis” rather than the more precise determination of C-HDL that is presently used by the Lipid Research Clinicsi Lopez-S et al.16 report a significantly increased C-HDL (alpha lipoprotein) (286 mg/ 100 ml to 332 mg/ 100 ml) in 22 young males after only a 7-wk exercise program. Although the report states “dietary intake” was individually adjusted as to maintain caloric balance with no change of the composition of the diet, there is no report of smoking or alcohol intake. Fewer studies report responses to an exercise program in female subjects. In a study of 22 obese middle-aged women who participated in a 17-wk program of “jog-walking and calisthenics” and diet control, Lewis et al.,” reported the lipoprotein fractions were not significantly changed (C-HDL, 50 * 11 to 54 -t 14, C-LDL, 139 + 28 to 134 + 27 mg/dl). The ratio C-HDL to C-LDL, however, significantly changed from 0.38 k 0.14 to 0.43 k 0.16. This study was specifically aimed, however, at dietary change as well as exercise.
MNNE
ET AL.
Of further interest is the recent report of decreased levels of C-HDL after a treadmill training program involving six women whose OC status is unreported.” For the group of 11 subjects that also included 5 males, the decrease in C-HDL was not significant, although there was a significant fall in total cholesterol.‘2 These results are reported in abstract, however, and the details of the “constant composition diet,” smoking, and alcohol consumption are not available. Another investigation provides additional evidence that longitudinal exercise training programs may be ineffective in changing serum C-HDL levels of women.‘* In the present study, we have avoided many of the methodological pitfalls warned of by Wood and Haskell.” Duration of training was long enough to evoke physiologic changes, but not so long that there were subject dropouts. Lipid and lipoprotein analyses were performed in a continuously standardized laboratory,‘3 the Cincinnati Lipid Research Center, with high level precision, accuracy, and absence of longitudinal drift in values. Furthermore, we have controlled for the possible confounding variables of sex, age, OC formulation, and smoking, while monitoring diet and alcohol intake. The subjects were all women, all between 19 and 30 yr, all taking the same OC, all nonsmokers who maintained their same individual diet and alcohol consumption patterns throughout the period of the study. Within this framework of reference, we can only speculate about the lack of significant change in C-HDL levels during the exercise training program. It may be that alterations of covariables associated with initiation of exercise programs are themselves responsible for changes seen in C-HDL. Hence, weight loss, cessation of smoking, and increased alcohol intake, all of which may elevate C-HDL and many of which occur in chronic exercise programs, may account for the C-HDL increments in studies where they occur. Whether duration of exercise is a determinant is also not known. It may be that 10 wk is just too short a time period for exercise training to effect changes in C-HDL in OC users who have relatively normal levels to begin with. It has been suggested that aerobic, as contrasted to anaerobic, exercise increased C-HDL levels in male subjects and that differing results from
EXERCISE AND LIPOPROTEINS
IN WOMEN
1271
various studies might, in part, be accounted for by the relative amounts of aerobic and anaerobic exercise.lg In this study, there were no significant changes in weight, alcohol intake, or smoking (all nonsmokers initially), and no significant change in C-HDL. The exercise levels were judged to be aerobic. The lack of change of C-HDL under the circumstances of this study is
consistent with the preliminary evidence that exercise appears to have more consistent and marked effect in men than in women.‘G’2.‘6m’8 ACKNOWLEDGMENT The authors express their appreciation to B. Doerr, S. McNeely. L. Wynne, and J. Hespeth for their participation in this project, to the physicians and nursing staff of the Cox Heart Institute. to A. Mercer for statistical analysis, and to H. Ira Fritz for providing diet history forms.
REFERENCES 1. Royal College of General Practioners’ Oral Contraception Study. Mortality among oral-contraceptive users. Lancet 2~7277733, 1977 2. Beral V: Cardiovascular-disease mortality trends and oral-contraceptive use in young women. Lancet 2:10477 1051. 1976 3. Wynn V, Mills CL, Doar JWH. et al: Fasting serum triglyceride, cholesterol, and lipoprotein levels during oralcontraceptive therapy. Lancet 2:756-760, 1969 4. Bradley DD, Wingerd J, Petitti DB, et al: Serum high-density-lipoprotein cholesterol in women using oral contraceptives, estrogens and progestins. N Engl-J Med 299: 17-20, 1978 5. Berg K. Bdrresen A-L. Dahlen G: Serum-high-densitylipoprotein and atherosclerotic heart disease. Lancet 1:499501, 1976 6. Castelli WP, Doyle JT, Gordon T. et al: HDL cholesterol and other lipids in coronary heart disease: The cooperative lipoprotein phenotyping study. Circulation 55:767-772, 1977 7. Gordon T, Castelli WP, Hjortland MC, et al: High density lipoprotein as a protective factor against coronary heart disease: The Framingham study. Am J Med 62:707714,1977 8. Miller NE, Thelle DS, Fdrde OH et al: The Tromsd Heart-Study: High-density lipoprotein and coronary heart disease: A prospective case-control study. L,ancet I :965-967, 1977 9. Wood PD, Haskell WL, Stern MP, et al: Plasma lipoprotein distributions in male and female runners. Ann NY Acad Sci 301:748-763. 1977
IO. Altekruse EB, Wilmore JH: Changes in blood chemistries following a controlled exercise program. J Occup Med 15:110-I 13, 1973 I I Wood PD. Haskell WL: The effect of exercise on plasma high density lipoproteins. Lipids 14:417-427, I979 12. Lipson LC, Bonow RO, Schaefer E, et al: Effects of exerciseon human plasma lipoproteins (abstr). Am J Cardiol 43:409, 1979 13. Lipid Research Clinics Program. Manual of laboratory methods: Lipid and lipoprotein analysis. Department of Health, Education. and Welfare publication No. 75-628, 1974 14. Astrand P-O, Rodahl K: Textbook of Work Physiology (ed 2). New York, McGraw-Hill. 1976 15. Durnin JVGA, Womersley J: Body fat assessed from total body density and its estimation from skinfold thickness: Measurement on 481 men and women aged I6 to 72 years. Br J Nutr 32~77-97, 1974 16. Lopez-S A. Vial R, Balart L, et al: Effect of exercise and physical fitness on serum lipids and lipoproteins. Atherosclerosis 20: l-9. 1974 17. Lewis S. Haskell WL. Wood PD, et al: Effects of physical activity on weight reduction in obese middle-aged women. Am J Clin Nutr 29: I5 l-1 56, I976 18. Brilla LR: Effects of a I O-week physical conditioning program on plasma high- and low-density lipoprotein cholesterol concentrations in young women. University Park, Penn. The Pennsylvania State University, 1978 (unpublished thesis) 19. Lehtonen A, Viikari J: Serum lipids in soccer and ice-hockey players. Metabolism 29:36-39. 1980
of a Controlled Exercise Program on Serum Lipoprotein Levels in Women on Oral Contraceptives Terrance P. Wynne,
The effects of a lo-wk
individualized
eter interval training program group
of
13 sedentary
contraceptive
increase.
contraceptive group.
women
in a
on a specific
oral
1 mg norethiste-
lipoprotein
cholesterol
Six additional served
All subjects
were
bicycle ergom-
if. like men on physical training,
high-density
would
Bassett Frey, Lloyd L. Laubach,
were investigated
(50 pg mestranol,
rone) to determine their
Mary Anne
as
a
women
nonexercising
were between
nonsmokers.
Diet
levels
on the oral
and
control
18 and 30 yr and
alcohol
intake
were
stable throughout
the study period, and were moni-
tored throughout.
The interval training
three times per week, 30-min at 70% maximum rate
+
rate]).
0.7
Training
maximum
heart rate reserve
x [maximum
unchanged.
heart
produced
oxygen
Body
unlike
similar
was
per session.
(resting
heart
rate-resting
increases
uptake.
However,
program
exercise
heart
(p < 0.05)
in
weight
was
training
pro-
grams with males, there were no significant changes in
plasma
high-density
triglycerides. oral
In women
contraceptives.
may fail to elevate terol
levels,
marked
consistent high density
consistent
hormone-exercise effect
tein cholesterol
lipoprotein
cholesterol
receiving estrogen
with
effects
of exercise
exercise
programs
lipoprotein with
on high-density
tary controls.” In their study of 39 “mostly Altekruse and Wilmore sedentary men,” induced a significant increase in electrophoretitally measured alpha lipoproteins as a percent of total cholesterol through a IO wk, three-timesper-week program of walking, jogging, and running.” In their review of the effect of exercise on plasma C-HDL, Wood and Haskell” indicate that exercise training programs consistently increase C-HDL cholesterol levels in initially sedentary people. Lipson, et al.,” however. reported a decrease in C-HDL levels, which was more pronounced in female than male subjects, after a 6 wk treadmill training program. The present study was undertaken to determine whether a regular exercise program would effect changes in serum lipoprotein levels of women taking OC.
choles-
an interaction
and/or
or
progestin
and Charles J. Glueck
MATERIALS
of sex the
less
lipopro-
in women.
AND
METHODS
Subjects Nineteen
women participated
in the study. They ranged in
age from I9 to 30 yr and had been taking an OC with 50 pg
0
RAL CONTRACEPTIVES (OC) have been implicated in the incidence of coronary heart disease as well as all other cardiovascular diseases.‘.’ Estrogen-progestin oral contraceptive use is associated with elevated triglyceride levels3 Furthermore, since estrogen is directly related and progestins are inversely related to triglyceride levels and to high-density lipoprotein cholesterol (C-HDL),4 depending upon their estrogen/progesterone formulation, OC may be associated with lower levels of CHDL. Epidemiologic evidence indicates that CHDL is inversely correlated with coronary heart disease;5~8 thus, the serum C-HDL level may be one of the links between OC use and increased risk of heart disease. Any systematic program that elevates C-HDL levels might reduce the risk of heart disease in women taking OC. A regular, vigorous exercise program might be an approach to elevate CHDL levels in young women either taking or not taking OC. Male and female marathon runners have higher C-HDL levels than matched seden-
Metabolism,
Vol.
29,
No.
12
(December),
1980
mestranol,
I
mg norethisterone
were nonsmokers
and were
for a minimum found
disease by physical examination tered by a cardiologist.
and treadmill
Thirteen
IO-wk bicycle exercise training
of 2 mo. All
free of cardiovascular test adminis-
subjects participated
in a
program; the other six were
nontraining controls. All subjects had normal prestudy levels of plasma LDL.
total cholesterol.
None
were
diabetic:
triglyceride, and
none
diseases. They took no other medications.
C-HDL. had
and C-
any
chronic
I
summa-
Table
rizes the subjects’ age, height. weight, percent body fat, and Quetelet index (kg/cm2
x 1000).
From the 5epartment of‘ PhysioIog_v. Wright State University School of Medicine, Dayton, Ohio, and the Lipid Research Center and General Clinical Research Center. University of Cincinnati Medical Center, Cincinnati. Ohio. Received for publication April 17. 1980. Supported in part by grants from the American Heart Association, Miami Valley Chapter, Ortho Pharmaceutical. and a Biomedical Research Grant to Wright State Universily College of Science and Engineering from N.I. H. and II) GCRC grant RROOOG-I 9. Address reprint requests to M.A.B. Frey. Ph.D., Department of Physiology, Wright State University. School oJ‘ Medicine. P.O. Box 927. Dayton. Ohio 45401. 0 1980 by Grune & Stratton. inc. 0026-0495/80/291220012$01.00/0
1267
WYNNE
1268
Table 1. Age, Height, Weight,
Percentage
Body Fat, and Quetelet
ET AL.
Index of Subjects in the Exercise and Control Groups. Pre-
and Posttraining M&SIl
Variable
Pretraining.
Posttraining*
Difference
Paired t
Exercise group (n = 13) Age (~1 Height (cm)
23.2
f 3.37
167.2
i 6.15
-
Weight (kg)
66.0
+ 8.26
65.8
k 8.31
-0.2
0.69
Bodv fat (%)
28.3
+ 4.1
26.3
+ 4.3
-2.0
4.19t
2.37
f 0.357
2.36
-t 0.378
-0.01
0.43
-0.5
0.00
Quetdet index ([kg/cm’]
x 1000)
Control group (n = 6) Age (vr) Height (cm)
24.2
f 3.19
165.6
f 3.70
Weight (kg)
60.4
+ 7.45
59.9
t 6.17
Body Fat (%I
27.8
+ 1.4
26.7
+ 1.9
1.1
2.18
+ 0.185
2.18
+ 0.157
0
1.85
Quetelet index ([kg/cm’]
x 1000)
-0.10
*Values are Mean + SD. tp < 0.05 paired t test pretraining vs. posttraining.
Procedures The program consisted of: (A) a pretraining
period during
which venous blood samples were drawn after a 12-hr fast and lipid and lipoprotein levels were quantitated Research
Center
in Cincinnati,
Ohio,
methods;”
maximum
performed
on a bicycle ergometer;”
mated
from
at the Lipid
by standard
oxygen uptake tests (i’,,
skinfolds;”
LRC
max)
were
and body fat was esti-
(B) an interim
period
of 10 wk
in the training program described below and all subjects maintained daily diet diaries on which they recorded all foods and beverages consumed except water; (C) a posttraining period during which blood values, ir, max, and body fat were redetermined. Exercise consisted of a supervised bicycle ergometer interval training program with 5-min work bouts, averaging 70% maximum heart rate reserve (resting heart rate during
which exercise subjects participated
Table 2. Maximum
Oxygen Uptake (\i,
+ 0.7 x [maximum heart rate-resting heart rate]), separated by 2-min rest periods. Heart rate was monitored immediately after each work bout. Subjects exercised 30 min per session, three sessions per week, for IO wk. Workloads were increased regularly to maintain target heart rates. Pretraining and posttraining data for all variables were analyzed by paired t test for both the controls and the training subjects. Controls and training subjects were compared by analysis of covariance, using “pretraining” values as the covariant. Differences are considered significant if p < 0.05.
RESULTS
Participation in the training program was 100%; that is, each subject in the training group completed the program, attending 30 training
max), Resting Heart Rate and Maximum Heart Rate of Subjects in the exercise and Control Groups Pre- and Posttraining
Difference
Paired t
4.72
J.OOt
M&W
Variable
Pretraining*
Posttraining*
Exercise group (n = 13) \ig maximum (ml/kg
.
min)
29.22
+ 4.85
33.94
-t 4.55
Resting heart rate (bpm)
76 * 10
68 + 6.7
190 & 8.75
191 i 5.47
-8.0
4.94t
Maximum heart rate (born1
1.0
--0.14
1.o
-0.76
Control group (n = 6) \ioz maximum (ml/kg
.
min)
25.04
f 1.79
26.04
-t 3.61
Resting heart rate (bpm)
JO * 6.6
67 * 11
-3.0
188 + 14
186 + 8.7
-2.0
0.53
Maximum heart rate (bpm) *Values are mean f SD. tp i 0.05 paired t test pretraining vs. posttraining.
-0.07
EXERCISE AND LIPOPROTEINS IN WOMEN
Table 3. Total Plasma CholesteroL
1269
Triglyceride,
High- and Low-Density
Lipoprotein
Cholesterol
(C-HDL and C-LDL) of
Subjects in the Exercise and Control Groups, Pre- and Posttraining MIXII Pretraming*
Posttraining*
Odference
Paired
(mg/dl)
lmg/dl)
(mgldl)
t
Total cholesterol
188 k 26
183 + 24
~
Tnglyceride
139 k 59
118t50
-21
Vanable
Exercise group (n = 13) 5
0.96 2.11
1
1.10
-
1
0.33
167 + 30
-
5
0.74
97 2 28
-4
55 t 18
52 t 14
-
3
1.36
97 ? 24
96 + 19
-
1
0.27
C-HDL
56k
12
57 t 14
C-LDL
104 i
19
103 * 20
Total cholesterol
172 t 37
Triglyceride
101 + 51
C-HDL C-LDL
Control group (n = 6) 0.32
*Values are mean + SD.
sessions. Table 1 reveals no significant changes in any body size parameters due to the training program, except percent body fat. Significant (p < 0.001) differences were evoked in the training group for ifoZ max, both relative (ml/kg.min) and absolute (1.92 t 0.33 l/min to 2.21 + 0.27 l/min), and in resting heart rate, as shown in Table 2. Examination by analysis of covariance revealed significant (p < 0.05) differences between exercise and control groups for change in \;ro, max over the training period. There were no significant pre- to posttraining changes in lipid and lipoprotein levels, in either the exercise group or the nonexercised control group (Table 3). In the exercise group, plasma triglycerides decreased approximately 15%; total cholesterol, however, was practically unchanged, as were the C-HDL and C-LDL fractions. By analysis of covariance there were no significant differences between the exercise and control groups for changes in lipoprotein variables over the training period. There was a weak positive correlation between the change (A) in vo* max over the training period and A triglyceride (r = 0.42, p > 0.10). Frequency of alcohol intake ranged from a low of 1.2 times per subject per week in week 4 to a high of 2.1 times per week during week 1, and average wine intake varied from 0 to 1 .l glass per week per subject, based on 10 subjects. (Excluded from this analysis is 1 subject who drank no alcohol and 2 subjects for whom records are incomplete. Their intakes for the weeks that are reported, however, fall within these ranges.) With the exception of week 4 in which no wine was consumed, there were no
significant differences in total alcohol consumption or wine consumption throughout the training period, as tested by analysis of variance. From inspection of the diet histories, it appears that food habits for each individual were qualitatively consistent week by week. The control subjects showed no significant changes from preto posttest in any of the above mentioned parameters. DISCUSSION
In this study, we have investigated whether, by regular exercise, women on OC might alter their lipid and lipoprotein levels, at stable body weight, while improving exercise tolerance and decreasing percent body fat. Thirteen women, nonsmokers, on a single specific OC participated in a vigorous, controlled physical training program that notably increased the physical fitness level of every participant. Although their serum lipoprotein levels were not significantly changed, there was a trend toward decreased triglycerides; however, there was no increase in C-HDL. This outcome was surprising to us, since there is a preponderance of evidence that exercise training will increase C-HDL levels in a variety of populations.” Long-distance runners-male and female-who regularly ran more than 15 miles a week had C-HDL levels greater than matched groups of nonexercising controls (runners: male = 64 + 13 mg/dl, female = 75 + I4 mg/dl; controls: male = 43 _+ 10 mg/di, female = 56 + 14 mg/dl).’ This was a crosssectional study, however, and therefore, like all such studies, has the disadvantage that the
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groups are self-selected. In addition, runners differed from controls in that the runners were significantly leaner as determined by ratio of actual to ideal weight, the runners were all nonsmokers, and the runners had a greater frequency of drinking alcoholic beverages and, in particular, drank more wine. Evidence also exists, moreover, that longitudinal training programs can change C-HDL levels in initially sedentary individuals. A IO-wk training program less rigorous than ours was effective in increasing the percent of total cholesterol as alpha lipoprotein in sedentary men (from 36.9% & 11.7% to 55.5% + 1 l.O%.” Subjects meeting merely a 60% participation criterion were included in the data for those men.” The report, however, does not provide a record of the smoking and alcohol consumption habits of the participants.” Participants were asked to continue a set dietary pattern throughout the 10 wk program, but this was not monitored.” Concurrent changes in smoking, alcohol, and diet patterns often accompany exeicise programs and may account in part for the changes in C-HDL. Furthermore, the lipid analyses involved the separation of alpha lipoprotein by electrophoresis” rather than the more precise determination of C-HDL that is presently used by the Lipid Research Clinicsi Lopez-S et al.16 report a significantly increased C-HDL (alpha lipoprotein) (286 mg/ 100 ml to 332 mg/ 100 ml) in 22 young males after only a 7-wk exercise program. Although the report states “dietary intake” was individually adjusted as to maintain caloric balance with no change of the composition of the diet, there is no report of smoking or alcohol intake. Fewer studies report responses to an exercise program in female subjects. In a study of 22 obese middle-aged women who participated in a 17-wk program of “jog-walking and calisthenics” and diet control, Lewis et al.,” reported the lipoprotein fractions were not significantly changed (C-HDL, 50 * 11 to 54 -t 14, C-LDL, 139 + 28 to 134 + 27 mg/dl). The ratio C-HDL to C-LDL, however, significantly changed from 0.38 k 0.14 to 0.43 k 0.16. This study was specifically aimed, however, at dietary change as well as exercise.
MNNE
ET AL.
Of further interest is the recent report of decreased levels of C-HDL after a treadmill training program involving six women whose OC status is unreported.” For the group of 11 subjects that also included 5 males, the decrease in C-HDL was not significant, although there was a significant fall in total cholesterol.‘2 These results are reported in abstract, however, and the details of the “constant composition diet,” smoking, and alcohol consumption are not available. Another investigation provides additional evidence that longitudinal exercise training programs may be ineffective in changing serum C-HDL levels of women.‘* In the present study, we have avoided many of the methodological pitfalls warned of by Wood and Haskell.” Duration of training was long enough to evoke physiologic changes, but not so long that there were subject dropouts. Lipid and lipoprotein analyses were performed in a continuously standardized laboratory,‘3 the Cincinnati Lipid Research Center, with high level precision, accuracy, and absence of longitudinal drift in values. Furthermore, we have controlled for the possible confounding variables of sex, age, OC formulation, and smoking, while monitoring diet and alcohol intake. The subjects were all women, all between 19 and 30 yr, all taking the same OC, all nonsmokers who maintained their same individual diet and alcohol consumption patterns throughout the period of the study. Within this framework of reference, we can only speculate about the lack of significant change in C-HDL levels during the exercise training program. It may be that alterations of covariables associated with initiation of exercise programs are themselves responsible for changes seen in C-HDL. Hence, weight loss, cessation of smoking, and increased alcohol intake, all of which may elevate C-HDL and many of which occur in chronic exercise programs, may account for the C-HDL increments in studies where they occur. Whether duration of exercise is a determinant is also not known. It may be that 10 wk is just too short a time period for exercise training to effect changes in C-HDL in OC users who have relatively normal levels to begin with. It has been suggested that aerobic, as contrasted to anaerobic, exercise increased C-HDL levels in male subjects and that differing results from
EXERCISE AND LIPOPROTEINS
IN WOMEN
1271
various studies might, in part, be accounted for by the relative amounts of aerobic and anaerobic exercise.lg In this study, there were no significant changes in weight, alcohol intake, or smoking (all nonsmokers initially), and no significant change in C-HDL. The exercise levels were judged to be aerobic. The lack of change of C-HDL under the circumstances of this study is
consistent with the preliminary evidence that exercise appears to have more consistent and marked effect in men than in women.‘G’2.‘6m’8 ACKNOWLEDGMENT The authors express their appreciation to B. Doerr, S. McNeely. L. Wynne, and J. Hespeth for their participation in this project, to the physicians and nursing staff of the Cox Heart Institute. to A. Mercer for statistical analysis, and to H. Ira Fritz for providing diet history forms.
REFERENCES 1. Royal College of General Practioners’ Oral Contraception Study. Mortality among oral-contraceptive users. Lancet 2~7277733, 1977 2. Beral V: Cardiovascular-disease mortality trends and oral-contraceptive use in young women. Lancet 2:10477 1051. 1976 3. Wynn V, Mills CL, Doar JWH. et al: Fasting serum triglyceride, cholesterol, and lipoprotein levels during oralcontraceptive therapy. Lancet 2:756-760, 1969 4. Bradley DD, Wingerd J, Petitti DB, et al: Serum high-density-lipoprotein cholesterol in women using oral contraceptives, estrogens and progestins. N Engl-J Med 299: 17-20, 1978 5. Berg K. Bdrresen A-L. Dahlen G: Serum-high-densitylipoprotein and atherosclerotic heart disease. Lancet 1:499501, 1976 6. Castelli WP, Doyle JT, Gordon T. et al: HDL cholesterol and other lipids in coronary heart disease: The cooperative lipoprotein phenotyping study. Circulation 55:767-772, 1977 7. Gordon T, Castelli WP, Hjortland MC, et al: High density lipoprotein as a protective factor against coronary heart disease: The Framingham study. Am J Med 62:707714,1977 8. Miller NE, Thelle DS, Fdrde OH et al: The Tromsd Heart-Study: High-density lipoprotein and coronary heart disease: A prospective case-control study. L,ancet I :965-967, 1977 9. Wood PD, Haskell WL, Stern MP, et al: Plasma lipoprotein distributions in male and female runners. Ann NY Acad Sci 301:748-763. 1977
IO. Altekruse EB, Wilmore JH: Changes in blood chemistries following a controlled exercise program. J Occup Med 15:110-I 13, 1973 I I Wood PD. Haskell WL: The effect of exercise on plasma high density lipoproteins. Lipids 14:417-427, I979 12. Lipson LC, Bonow RO, Schaefer E, et al: Effects of exerciseon human plasma lipoproteins (abstr). Am J Cardiol 43:409, 1979 13. Lipid Research Clinics Program. Manual of laboratory methods: Lipid and lipoprotein analysis. Department of Health, Education. and Welfare publication No. 75-628, 1974 14. Astrand P-O, Rodahl K: Textbook of Work Physiology (ed 2). New York, McGraw-Hill. 1976 15. Durnin JVGA, Womersley J: Body fat assessed from total body density and its estimation from skinfold thickness: Measurement on 481 men and women aged I6 to 72 years. Br J Nutr 32~77-97, 1974 16. Lopez-S A. Vial R, Balart L, et al: Effect of exercise and physical fitness on serum lipids and lipoproteins. Atherosclerosis 20: l-9. 1974 17. Lewis S. Haskell WL. Wood PD, et al: Effects of physical activity on weight reduction in obese middle-aged women. Am J Clin Nutr 29: I5 l-1 56, I976 18. Brilla LR: Effects of a I O-week physical conditioning program on plasma high- and low-density lipoprotein cholesterol concentrations in young women. University Park, Penn. The Pennsylvania State University, 1978 (unpublished thesis) 19. Lehtonen A, Viikari J: Serum lipids in soccer and ice-hockey players. Metabolism 29:36-39. 1980