| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1 Department of Internal Medicine, Division of Geriatrics and Gerontology, and 3 Department of Obstetrics and Gynecology, Washington University School of Medicine, St. Louis, Missouri 63110; and 2 Department of Medicine, Division of Geriatric Medicine, University of Colorado Health Sciences Center, Denver, Colorado 80262
 |
ABSTRACT |
|---|
 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
The independent
and combined effects of exercise training and hormone replacement
therapy (HRT) on body composition, fat distribution, glucose tolerance,
and insulin action were studied in postmenopausal women, aged 68 ± 5 yr, assigned to control (n = 19), exercise (n = 18), HRT (n = 15), and
exercise + HRT (n = 16) groups. The exercise
consisted of 2 mo of flexibility exercises followed by 9 mo of
endurance exercise. HRT was conjugated estrogens 0.625 mg/day and
trimonthly medroxyprogesterone acetate 5 mg/day for 13 days. Total and
regional body composition were measured by dual-energy X-ray
absorptiometry. Serum glucose and insulin responses were measured
during a 2-h oral glucose tolerance test. There were significant main
effects of exercise on reductions in total and regional (trunk, arms,
legs) fat mass, increase in leg fat-free mass, and improvements in
glucose tolerance and insulin action. There were significant main
effects of HRT on the reduction of total fat mass (HRT, 
3.0 ± 4.0 kg; no HRT, 1.3 ± 2.6 kg), with a strong trend for
reductions in trunk and leg fat mass (both P = 0.07).
There was also a significant improvement in insulin action in response
to HRT. These results suggest that there are independent and additive
effects of exercise training and HRT on the reduction in fat mass and
improvement in insulin action in postmenopausal women; the effect of
HRT on insulin action may be mediated, in part, through changes in
central adiposity.
hormone replacement therapy; insulin resistance; abdominal obesity; estrogens
| |
INTRODUCTION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
THE MENOPAUSAL TRANSITION results in deleterious changes in body composition and body fat distribution (30, 38). Although increased fat mass, specifically abdominal obesity, is associated with an increased risk for glucose intolerance and insulin resistance (8), results from studies of the independent effects of menopause on glucose metabolism are equivocal (38).
Hormone replacement therapy (HRT) attenuates the menopause-related increase in body fatness and abdominal adiposity (11, 13, 17, 33, 38). HRT has also been found to have beneficial effects on insulin action and glucose tolerance (6, 7, 36), although this is not a uniform finding (2, 5, 10, 15). It is possible that beneficial effects of HRT on insulin resistance are mediated through its actions on abdominal fat depots. Therefore, one aim of this study was to determine whether beneficial effects of HRT on insulin action are associated with reductions in central adiposity.
It is well established that endurance exercise training can improve glucose tolerance and reduce insulin resistance and central adiposity in older adults (16, 21, 35). However, the combined effects of exercise and HRT on glucose tolerance and insulin action in older women are unknown. An additional aim of the present study was to investigate the independent and combined effects of endurance exercise training and HRT on body composition, fat distribution, glucose tolerance, and insulin action in healthy, postmenopausal women.
| |
METHODS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Subjects. The 68 women who completed the study were nonsmokers, aged 60-84 yr, had not used estrogen for at least 2 yr, and were sedentary. Participants were assigned to the following treatment groups: control (n = 19), exercise (n = 18), HRT (n = 15), and exercise + HRT (n = 16). Random assignment to treatment arms was not performed because the supervised exercise training sessions had to be coordinated with other exercise intervention studies being conducted within the division. To minimize the limitations imposed by nonrandom assignment, all participants met inclusion criteria for the study and were willing and able to participate in an exercise program and take HRT. Thirty-six of the participants (8 control, 10 exercise, 6 HRT, 12 exercise + HRT) also participated in a study of the effects of HRT on bone mineral density and body composition (17). All of the participants provided written, informed consent to participate in the study, which was approved by the Washington University Institutional Review Board.
Screening tests included a medical history, physical examination, chest X-ray, blood and urine chemistries, graded exercise test with monitoring of blood pressure and electrocardiogram, gynecological examinations, and a mammogram. Volunteers were excluded from participation if they had medical problems that contraindicated HRT or exercise.Diet evaluation. Participants completed 7-day food records at the beginning and end of the intervention. A registered dietician instructed the participants on the procedures for weighing and recording foods in household measures and conducted interviews after food records were completed to validate their accuracy. Subjects were instructed to maintain their usual eating habits during the period of study. Records were analyzed by using Nutritionist IV (N-Squared Computing, Salem, OR).
HRT. HRT consisted of continuous conjugated estrogens (0.625 mg/day) and medroxyprogesterone acetate (MPA; 5 mg/day), for 13 consecutive days every third month (Wyeth-Ayerst, Philadelphia, PA). Because we were primarily interested in the effects of estrogens, the intent of the hormone replacement regimen was to use the minimal effective progestin dose that provides protection against the development of endometrial hyperplasia. In this respect, trimonthly cycling of MPA has been shown to reduce the incidence of endometrial hyperplasia to <2% (12, 45). In the exercise + HRT group, HRT was initiated at the start of the exercise program.
Exercise program. The exercise intervention consisted of a 2-mo, low-intensity conditioning program that focused on range of motion and flexibility, followed by 9 mo of weight-bearing exercise training. Participants were required to attend a minimum of three exercise sessions per week. The initial flexibility training was designed to reduce the likelihood of injury in the subsequent, more vigorous endurance exercise program.
The 9-mo endurance exercise program, as previously described (17), consisted of walking (treadmills, indoor track), jogging (treadmills, indoor track), and stair climbing and descending. Exercise prescriptions were individualized and updated on a weekly basis. The initial goal was to walk 30 min at a moderate intensity corresponding to ~70% of maximal heart rate. Subsequently, the exercise prescription was increased via intensity and duration, depending on individual tolerance, with the ultimate goal being 45 min of exercise at 80-85% of maximal heart rate during the last 3 mo of the exercise program.Maximal aerobic power.
Maximal aerobic power (
O2 max) was
assessed as previously described (19) before and after the
treatment period in all subjects. Additional assessments were made in
exercising subjects at 3-mo intervals during the treatment period.
Body composition and anthropometric measures. Total and regional body composition (fat mass and fat-free mass) were determined by dual energy X-ray absorptiometry (DXA) using a Hologic QDR-1000/W instrument (version 5.64, enhanced whole body software, Hologic, Waltham, MA). The standard recommendations of the manufacturer were used to define the arm, leg, and trunk regions. Waist circumference was measured as the minimum circumference between the top of the iliac crest and the distal end of the rib cage along the midaxillary line. Waist area was calculated from waist circumference, with the assumption that the geometric shape of the cross-sectional waist area is a circle.
Oral glucose tolerance test. The 75-g oral glucose tolerance test (OGTT) was administered in the morning after a 12- to 14-h fast. To minimize potential deleterious effects of progestins on glucose tolerance, the postintervention OGTT was administered at least 3 wk after a MPA cycle. In exercising subjects, the postintervention OGTT was performed 14-19 h after an exercise session. Diet was monitored for 3 days before an OGTT to ensure an intake of at least 150 g/day of carbohydrates. Blood samples for the determination of glucose and insulin concentrations were obtained before and 30, 60, 90, and 120 min after ingestion of the glucose beverage. The total areas under the glucose and insulin curves (GluAUC and InsAUC, respectively) were calculated using the trapezoidal rule. The GluAUC × InsAUC product was calculated as an index of insulin action (24, 26). Plasma glucose concentrations were measured by the glucose oxidase method (Beckman Instruments, Fullerton, CA), and serum insulin concentrations were measured by a double-antibody radioimmunoassay (28).
Statistical analysis.
Differences among groups in baseline measurements were evaluated using
one-way ANOVA. The changes that occurred in response to exercise and/or
HRT were evaluated by two-way (exercise × HRT) ANOVA. Sequential
stepwise multiple-regression analyses were used to determine the
relationships among variables of interest. Statistical significance was
defined as an alpha level 
0.05. Data are reported as means ± SD
except in the figures, which reflect means ± SE.
| |
RESULTS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
There were no significant differences among the groups at baseline
in parameters of interest (Table 1).
Total energy intake averaged 1,679 ± 290, 1,738 ± 206, 1,724 ± 275, and 1,782 ± 343 kcal/day in the control,
exercise, HRT, and exercise + HRT groups, respectively, at the
beginning of the study (P = not significant). Macronutrient composition was similar among the groups, averaging 51-53% carbohydrate, 30-32% fat, and 16% protein. At the
end of the study, the reported energy intake was increased by 79 ± 271, 30 ± 227, 150 ± 299, and 52 ± 195 kcal/day in
the control, exercise, HRT, and exercise + HRT groups,
respectively (P = not significant for changes within
and between groups); macronutrient composition was unchanged.
|
Exercise training.
The exercise groups performed a similar amount of exercise. Subjects in
the exercise group attended 3.5 ± 0.7 sessions/wk and exercised
45 ± 6 min/day at a heart rate of 126 ± 15 beats/min, corresponding to 78 ± 7% of maximal heart rate. Similarly,
subjects in the exercise + HRT group attended 3.5 ± 0.7 sessions/wk and exercised 46 ± 6 min/day at a heart rate of
132 ± 10 beats/min, corresponding to 80 ± 5% of maximal
heart rate. During the final 3 mo of the exercise training program,
subjects in the exercise group were exercising 3.3 ± 1.0 days/wk,
48 ± 7 min/day, at 81 ± 7% of maximal heart rate, and
subjects in the exercise + HRT group were exercising 3.2 ± 0.7 days/wk, 51 ± 10 min/day, at 82 ± 6% of maximal heart
rate. The exercise and exercise + HRT groups had similar
improvements in O2 max of 19.5 ± 15.0 and 15.6 ± 17.1%, respectively (both P < 0.01). There were no significant changes in
O2 max in the control (2.2 ± 7.3%) or HRT (3.7 ± 11.1%) groups.
Total and regional adiposity (Table
2, Figs.
1 and
2).
The only measure for which there was a significant exercise × HRT
interaction was the change in arm fat mass, which decreased significantly only in response to exercise + HRT (different from all other groups, P < 0.05). Changes in arm fat mass
in the control, exercise, HRT, and exercise + HRT groups were
0.1 ± 0.4, 0.1 ± 0.4, 0.1 ± 0.6, and 0.6 ± 0.5 kg, respectively. There were significant main effects of exercise
for the reductions in waist area and total, trunk, and leg fat mass
(all P < 0.001). There was a significant main effect
of HRT for the reduction in total fat mass (P < 0.05),
with strong trends for reductions in trunk and leg fat mass (both
P = 0.07).
|
|
|
9 ± 14%) than the relative reductions in
arm (2 ± 16%; P < 0.001) or leg fat mass
(4 ± 9%; P < 0.001), indicating a
disproportionate loss of central body fat in response to exercise
and/or HRT.
Total and regional fat-free mass (Table 2, Figs. 1 and 2). There were no exercise × HRT interactive effects on any of the measures of fat-free mass, nor were there any significant main effects of HRT. There were significant main effects of exercise for increases in total (P < 0.05) and leg fat-free mass (P < 0.001). There was a strong trend for trunk fat-free mass to be increased, in response both to exercise (P = 0.08) and HRT (P = 0.09).
OGTT glucose and insulin responses (Table 2 and Fig.
3).
There was a significant main effect of exercise, but not HRT, to reduce
GluAUC. In contrast, there were significant main effects of
exercise (P < 0.001) and HRT (P < 0.01) on reducing both the InsAUC and the
GluAUC × InsAUC product.
|
Associations of changes in body composition, fat distribution, and
O2 max with changes in glucose
tolerance and insulin action.
Sequential stepwise multiple-regression analyses were used to determine
the independent effects of changes in total fat mass, trunk
fat mass, waist area, fat-free mass, and
O2 max on changes in
GluAUC, InsAUC, and the GluAUC × InsAUC product (Table 3).
Waist area was selected to adjust for the nonsignificant differences in
baseline waist girth among the groups (i.e., for a given change in
waist circumference, the change in waist area is dependent on the
initial circumference). Additionally, because visceral fat is typically
measured as an area, it was theorized that waist area is a more
relevant measure than waist circumference, particularly in terms of
expressing change. Trunk fat mass was included in the model because DXA
may be a more sensitive measure of changes in central adiposity than
simple anthropometric measurements (38).
|
O2 max
were not significant. The change in waist area accounted for 29% of
the variance in the change in InsAUC and increased to 35%
when the change in trunk fat mass was included in the model. Similarly,
the change in waist area accounted for 31% of the variance in the
change in GluAUC × InsAUC product and
increased to 38% when the change in trunk fat mass was added to the model.
Effects of exercise and HRT, adjusted for change in waist area, on glucose tolerance and insulin action. To determine whether the effects of exercise and HRT on the glucose and insulin responses to the OGTT were mediated primarily through changes in waist area, we repeated the two-way ANOVA and included change in waist area as a covariate. Preliminary analyses were conducted to verify that the interactions between the covariate and independent variables were not significant, which is an underlying assumption for analysis of covariance. Only the interaction of the change in waist area and the effect of HRT on GluAUC was significant.
After we adjusted for the change in waist area, the main effect of exercise on the change in GluAUC was no longer significant (P = 0.08). However, there remained significant main effects of exercise and HRT on both the changes in InsAUC (exercise, P < 0.01; HRT, P < 0.01) and the changes in GluAUC × InsAUC (exercise, P < 0.01; HRT, P < 0.01). These relationships are depicted graphically for the InsAUC in Fig. 4. Figure 4 shows that, for a given change in waist area, the change in InsAUC in HRT users is different from that in nonusers (left) and different in exercisers vs. nonexercisers (right).
|
| |
DISCUSSION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
The major new findings of this study included 1) a significant reduction in total fat mass in response to HRT; 2) significant improvements in InsAUC and the GluAUC × InsAUC product in response to HRT; and 3) independent and additive effects of exercise and HRT on the reduction of fat mass and improvements in InsAUC and the GluAUC × InsAUC product.
Effects of exercise and HRT on fat mass.
The exercise training program resulted in significant reductions in
total and regional fat mass. The reduction in total fat mass of 3.8
kg was larger than that reported in several other studies of older
women (21, 22, 29). This presumably reflected the
relatively long duration and high intensity of the exercise program, as
there were no apparent reductions in energy intake. However, this must
be interpreted cautiously due to the inaccuracy of the method used to
assess energy intake and the fact that energy intake was assessed only
at the beginning and end of the study.
Effects of exercise and HRT on fat-free mass. The increases in fat-free mass that occurred in the exercise groups may seem incongruent with the concept that endurance exercise training does not typically induce muscle hypertrophy. In that regard, it was not possible to determine whether the increase in fat-free mass specifically reflected an increase in muscle mass. However, stair climbing, which involves lifting the body weight, was an integral part of the exercise program and may have induced an increase in muscle mass. The finding that leg, but not arm, fat-free mass was increased in response to an exercise program that involved primarily lower extremity musculature supports this contention.
Estrogen receptors are present in skeletal muscle (32, 34) and may mediate the anabolic effects of estrogen supplementation on muscle that occur in some species (42). The question of whether estrogen has anabolic effects on skeletal muscle in humans remains controversial. There is evidence from cross-sectional (1) and prospective (40) studies that menopause is associated with an accelerated loss of lean tissue other than bone mineral. In our previous studies, long-term HRT (18 mo) resulted in an increase in fat-free mass in older women (17), but HRT did not significantly augment the increases in fat-free mass or muscle strength that occurred in response to exercise training (4, 17). In the present study, there were no significant effects of HRT on total or regional fat-free mass. As in our laboratory's previous studies (4, 17), the increase in fat-free mass that occurred in response to exercise was not augmented by HRT. Because estrogens promote fluid retention by upregulating osmotic secretion of arginine vasopressin and increasing renal sodium resorption (37), it seems likely that small increases in fat-free mass in response to HRT reflect an expansion of the water fraction of the fat-free mass.Effects of exercise and HRT on glucose tolerance and insulin action. Abdominal obesity is a strong determinant of insulin resistance and glucose intolerance (8, 18). Both glucose tolerance and insulin action can be favorably affected by exercise, but the effect is short lived, lasting only about 48 h after an exercise bout (14). More persistent improvements in glucose tolerance and insulin action in response to exercise training occur as a result of reductions in fat mass, particularly in central depots (9, 23). The results of the present study confirm the beneficial effects of exercise on the glucose and insulin responses to OGTT and on the product of the glucose and insulin areas, which is an index of insulin action (26). The findings further corroborate the importance of reducing abdominal obesity, as the reduction in waist area explained 18% of the improvement in glucose tolerance and reductions in waist area and trunk fat mass explained 35 and 38% of the respective improvements in insulin area and insulin action.
The literature on the independent effects of estrogen on glucose tolerance and insulin resistance is equivocal and difficult to interpret due to numerous differences in treatment duration, small sample sizes, variation in methods of measuring insulin resistance, and different hormone replacement regimens (e.g., dose and type of estrogen; dose, type, and cycling of progestins; oral vs. transdermal). However, our results are consistent with those of several studies that found that oral glucose tolerance was unchanged in response to oral estrogens but that the insulin response to glucose was significantly reduced, indicating enhanced insulin action (6, 25, 27, 36). For example, the multicenter Menopause Study (25) of 525 women found that glucose tolerance was unchanged in response to unopposed estrogen but deteriorated in the groups treated with continuous (2.5 or 5.0 mg/day) or cyclic (5 or 10 mg/day for the last 14 days of 28-day cycles) MPA. Insulin areas, on the other hand, were significantly reduced, by up to 40%, in all of the treatment groups except the low-dose, continuous MPA group. Moreover, the decreases in insulin area became progressively larger with increasing duration of treatment (i.e., from 3 to 6 to 13 cycles). If estrogen does indeed play a role in the regulation of visceral fat metabolism, it would be plausible to hypothesize that the progressive reduction in hyperinsulinemia occurred as a result of a slow, steady decline in visceral adiposity. Regardless of the mechanism of action, if estrogen replacement reduces hyperinsulinemia, it would be logical to assume that this would be accompanied by decreased insulin resistance. Yet among several recent studies (2, 5, 7, 10, 15) that used the hyperinsulinemic-euglycemic clamp procedure, which is the most rigorous method of assessing insulin resistance, most found that insulin action was not significantly increased in response to HRT (2, 5, 10, 15). However, the latter studies involved only 6-12 wk of HRT. If a reduction in visceral adiposity is the driving mechanism for improvement in insulin action in response to HRT, the periods of treatment were probably not of sufficient duration to achieve significant changes. Interestingly, in the study that found enhanced insulin action in response to estrogen replacement, the period of therapy was 24 wk and improvements occurred only in women who were initially hyperinsulinemic (7). In that study, insulin-stimulated glucose disposal increased by ~50%, and there was a 30% reduction in the insulin response to an oral glucose challenge, despite no change in the integrated glucose response. The improvement in insulin action did not appear to be related to a reduction in the waist-to-hip circumference ratio, but the latter measure is not a sensitive index of change in abdominal adiposity (43). In the present study, there remained significant main effects of HRT on the reductions in the insulin area and the glucose × insulin area product even after adjusting for reductions in waist area. Clearly, further studies are necessary to confirm the effects of long-term HRT on insulin action and elucidate the mechanisms of action. As expected, exercise training resulted in significant reductions in total and regional fat mass, increases in total and leg fat-free mass, and improvements in glucose tolerance and insulin action. The major new findings of this study were that HRT and exercise training had independent and additive effects on the reduction of total fat mass, the attenuation of the insulin response to an OGTT, and the improvement in insulin action in older, postmenopausal women. The effects of HRT on insulin action were mediated, in part, by changes in central adiposity, as reductions in waist area and trunk fat mass explained almost 40% of the improvement in these outcomes. However, the effects of HRT on the OGTT insulin response and the glucose × insulin area product remained significant after adjusting for changes in waist area; the mechanism for this action of HRT is unknown.| |
ACKNOWLEDGEMENTS |
|---|
We are grateful for the expert technical assistance and support provided by the staffs of the Division of Geriatrics and Gerontology, the General Clinical Research Center (RR-00036), and the Diabetes Research and Training Center (DK-20579).
| |
FOOTNOTES |
|---|
This research was supported by National Institute of Arthritis and Musculoskeletal and Skin Diseases Grant AR-40705 and by the Washington University Claude Pepper Older Americans Independence Center (AG-13629).
Address for reprint requests and other correspondence: W. M. Kohrt, Division of Geriatric Medicine, Univ. of Colorado Health Sciences Center, 4200 East Ninth Ave., Box B-179, Denver, CO 80262 (E-mail: Wendy.Kohrt{at}uchsc.edu).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 11 September 2000; accepted in final form 27 December 2000.
| |
REFERENCES |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
1.
Aloia, JF,
McGowan DM,
Vaswani AN,
Ross P,
and
Cohn SH.
Relationship of menopause to skeletal and muscle mass.
Am J Clin Nutr
53:
1378-1383,
1991
2.
Andersson, B,
Mattsson LA,
Hahn L,
Marin P,
Lapidus L,
Holm G,
Bengtsson BA,
and
Bjorntorp P.
Estrogen replacement therapy decreases hyperandrogenicity and improves glucose homeostasis and plasma lipids in postmenopausal women with noninsulin-dependent diabetes mellitus.
J Clin Endocrinol Metab
82:
638-643,
1997
3.
Bjorntorp, P.
The regulation of adipose tissue distribution in humans.
Int J Obes
20:
291-302,
1997.
4.
Brown, M,
Birge SJ, Jr,
and
Kohrt WM.
Hormone replacement therapy does not augment gains in muscle strength or fat-free mass in response to weight-bearing exercise.
J Gerontol Biol Sci Med Sci
52A:
B166-B170,
1997.
5.
Brussaard, HE,
Gevers Leuven JA,
Frolich M,
Kluft C,
and
Krans HM.
Short-term oestrogen replacement therapy improves insulin resistance, lipids and fibrinolysis in postmenopausal women with NIDDM.
Diabetologia
40:
843-849,
1997[ISI][Medline].
6.
Crook, D,
Godsland IF,
Hull J,
and
Stevenson JC.
Hormone replacement therapy with dydrogesterone and 17
-oestadial: effects on serum lipoproteins and glucose tolerance during 24 mo follow up.
Br J Obstet Gynaecol
104:
298-304,
1997[ISI][Medline].
7.
Cucinelli, F,
Paparella P,
Soranna L,
Barini A,
Cinque B,
Mancuso S,
and
Lanzone A.
Differential effect of transdermal estrogen plus progestagen replacement therapy on insulin metabolism in postmenopausal women: relation to their insulinemic secretion.
Eur J Endocrinol
140:
215-223,
1999[Abstract].
8.
Deprés, JP.
The insulin resistance-dyslipidemic syndrome of visceral obesity: effect on patients' risk.
Obes Res
6:
8S-17S,
1998[Medline].
9.
Deprés, JP,
Pouliot MC,
Moorjani S,
Nadeau A,
Tremblay A,
Lupien PJ,
Theriault G,
and
Bouchard C.
Loss of abdominal fat and metabolic response to exercise training in obese women.
Am J Physiol Endocrinol Metab
261:
E159-E167,
1991
10.
Duncan, AC,
Lyall H,
Roberts RN,
Petrie JR,
Perera MJ,
Monaghan S,
Hart DM,
Connell JM,
and
Lumsden MA.
The effect of estradiol and a combined estradiol/progestagen preparation on insulin sensitivity in healthy postmenopausal women.
J Clin Endocrinol Metab
84:
2402-2407,
1999
11.
Espeland, MA,
Stefanick ML,
Kritz-Silverstein D,
Fineberg SE,
Waclawiw MA,
James MK,
and
Greenfield M.
Effect of postmenopausal hormone therapy on body weight and waist and hip girths.
J Clin Endocrinol Metab
82:
1549-1556,
1997
12.
Ettinger, B,
Selby J,
Citron JT,
Vangessel A,
Ettinger VM,
and
Hendrickson MR.
Cyclic hormone replacement therapy using quarterly progestin.
Obstet Gynecol
83:
693-700,
1994[ISI][Medline].
13.
Gambacciani, M,
Ciaponi M,
Cappagli B,
Piaggesi L,
De Simone L,
Orlandi R,
and
Genazzani AR.
Body weight, body fat distribution, and hormonal replacement therapy in early postmenopausal women.
J Clin Endocrinol Metab
82:
414-417,
1997
14.
Holloszy, JO,
and
Hansen PA.
Regulation of glucose transport into skeletal muscle.
In: Reviews of Physiology, Biochemistry and Pharmacology, edited by Blaustein MP,
Grunicke H,
Habermann E,
Pette D,
Schultz G,
and Schweiger M.. Berlin: Springer-Verlag, 1996, p. 99-193.
15.
Kimmerle, R,
Heinemann L,
Heise T,
Bender R,
Weyer C,
Hirschberger S,
and
Berger M.
Influence of continuous combined estradiol-norethisterone acetate preparations on insulin sensitivity in postmenopausal nondiabetic women.
Menopause
6:
36-42,
1999[ISI][Medline].
16.
Kirwan, JP,
Kohrt WM,
Wojta DM,
Bourey RE,
and
Holloszy JO.
Endurance exercise training reduces glucose-stimulated insulin levels in 60- to 70-yr-old men and women.
J Gerontol
48:
M84-M90,
1993[ISI][Medline].
17.
Kohrt, WM,
Ehsani AA,
and
Birge SJ.
HRT preserves increases in bone mineral density and reductions in body fat after a supervised exercise program.
J Appl Physiol
84:
1506-1512,
1998
18.
Kohrt, WM,
Kirwan JP,
Staten MA,
Bourey RE,
King DS,
and
Holloszy JO.
Insulin resistance in aging is related to abdominal obesity.
Diabetes
42:
273-281,
1993[Abstract].
19.
Kohrt, WM,
Malley MT,
Coggan AR,
Spina RJ,
Ogawa T,
Ehsani AA,
Bourey RE,
Martin WH, III,
and
Holloszy JO.
Effects of gender, age, and fitness level on the response of O2 max to training in 60-71 yr olds.
J Appl Physiol
71:
2004-2011,
1991
20.
Kohrt, WM,
Malley MT,
Dalsky GP,
and
Holloszy JO.
Body composition of healthy sedentary and trained, young and older men and women.
Med Sci Sports Exerc
24:
832-837,
1992[ISI][Medline].
21.
Kohrt, WM,
Obert KA,
and
Holloszy JO.
Exercise training improves fat distribution patterns in 60- to 70-yr-old men and women.
J Gerontol
47:
M99-M105,
1992[ISI][Medline].
22.
Kohrt, WM,
Snead DB,
Slatopolsky E,
and
Birge SJ, Jr.
Additive effects of weight-bearing exercise and estrogen on bone mineral density in older women.
J Bone Miner Res
10:
1303-1311,
1995[ISI][Medline].
23.
Lamarche, B,
Deprés JP,
Pouliot MC,
Moorjani S,
Lupien PJ,
Theriault G,
Tremblay A,
Nadeau A,
and
Bouchard C.
Is body fat loss a determinant factor in the improvement of carbohydrate and lipid metabolism following aerobic exercise training in obese women?
Metabolism
41:
1249-1256,
1992[ISI][Medline].
24.
Levine, R,
and
Haft D.
Carbohydrate homeostasis.
N Engl J Med
283:
237-246,
1970.
25.
Lobo, RA,
Pickar JH,
Wild RA,
Walsh B,
and
Hirvonen E.
Metabolic impact of adding medroxyprogesterone acetate to conjugated estrogen therapy in postmenopausal women. The Menopausal Study Group.
Obstet Gynecol
84:
987-995,
1994
26.
Matsuda, M,
and
DeFronzo RA.
Insulin sensitivity indices obtained from oral gluocse tolerance testing.
Diabetes Care
22:
1462-1470,
1999
27.
Mendoza, S,
Velazquez E,
Osona A,
Hamer T,
and
Glueck CJ.
Postmenopausal cyclic estrogen-progestin therapy lowers lipoprotein(a).
J Lab Clin Med
123:
837-841,
1994[ISI][Medline].
28.
Morgan, DR,
and
Lazarow A.
Immunoassay of insulin: two antibody system.
Diabetes
12:
115-126,
1963[ISI].
29.
Nelson, ME,
Fisher EC,
Dilmanian FA,
Dallal GE,
and
Evans WJ.
A 1-yr walking program and increased dietary calcium in postmenopausal women: effects on bone.
Am J Clin Nutr
53:
1304-1311,
1991
30.
Poehlman, ET,
Toth MJ,
and
Gardner AW.
Changes in energy balance and body composition at menopause: a controlled longitudinal study.
Ann Intern Med
123:
673-675,
1995
31.
Ross, R,
Dagnone D,
Jones PJH,
Smith H,
Paddags A,
Hudson R,
and
Janssen I.
Reduction in obesity and related comorbid conditions after diet-induced weight loss or exercise-induced weight loss in men.
Ann Intern Med
133:
92-103,
2000
32.
Saartok, T.
Steroid receptors in two types of rabbit skeletal muscle.
Int J Sports Med
5:
130-136,
1984[ISI][Medline].
33.
Samaras, K,
Hayward CS,
Sullivan D,
Kelly RP,
and
Campbell LV.
Effects of postmenopausal hormone replacement therapy on central abdominal fat, glycemic control, lipid metabolism, and vascular factors in type 2 diabetes: a prospective study.
Diabetes Care
22:
1401-1407,
1999
34.
Sauerwein, H,
and
Meyer HH.
Androgen and estrogen receptors in bovine skeletal muscle: relation to steroid-induced allometric muscle growth.
J Anim Sci
67:
206-212,
1989.
35.
Seals, DR,
Hagberg JM,
Allen WK,
Hurley BF,
Dalsky GP,
Ehsani AA,
and
Holloszy JO.
Glucose tolerance in young and older athletes and sedentary men.
J Appl Physiol
56:
1521-1525,
1984
36.
Spencer, CP,
Godsland IF,
Cooper AJ,
Ross D,
Whitehead MI,
and
Stevenson JC.
Effects of oral and transdermal 17-estradiol with cyclical oral norethindrone acetate on insulin sensitivity, secretion, and elimination in postmenopausal women.
Metabolism
49:
742-747,
2000[ISI][Medline].
37.
Stachenfeld, NS,
DiPietro L,
Palter SF,
and
Nadel ER.
Estrogen influences osmotic secretion of AVP and body water balance in postmenopausal women.
Am J Physiol Regulatory Integrative Comp Physiol
274:
R187-R195,
1998
38.
Tchernof, A,
and
Poehlman ET.
Effects of the menopause transition on body fatness and body fat distribution.
Obes Res
6:
246-254,
1998[ISI][Medline].
39.
Tchernof, A,
Poehlman ET,
and
Deprés JP.
Body fat distribution, the menopause transition, and hormone replacement therapy.
Diabetes Metab
26:
12-20,
2000[ISI][Medline].
40.
Toth, MJ,
and
Poehlman ET.
Effects of exercise on daily energy expenditure.
Nutr Rev
54:
S140-8,
1996[ISI][Medline].
41.
Toth, MJ,
Tchernof A,
Sites CK,
and
Poehlman ET.
Effect of menopausal status on body composition and abdominal fat distribution.
Int J Obes Relat Metab Disord
24:
226-231,
2000[ISI][Medline].
42.
Trenkle, A.
The anabolic effect of estrogens on nitrogen metabolism of growing and finishing cattle and sheep.
In: Anabolic Agents in Animal Production, edited by Lu FC,
and Rendel J.. Stuttgart, Germany: Thieme, 1976, p. 79-88.
43.
Van der Kooy, K,
Leenen R,
Seidell JC,
Deurenberg P,
Droop A,
and
Bakker CJ.
Waist-hip ratio is a poor predictor of changes in visceral fat.
Am J Clin Nutr
57:
327-333,
1993
44.
Van Pelt, RE,
Davy KP,
Stevenson ET,
Wilson TM,
Jones PP,
DeSouza CA,
and
Seals DR.
Smaller differences in total and regional adiposity with age in women who regularly perform endurance exercise.
Am J Physiol Endocrinol Metab
275:
E626-E634,
1998
45.
Williams, DB,
Voigt BJ,
Fu YS,
Schoenfeld MJ,
and
Judd HL.
Assessment of less than monthly progestin therapy in postmenopausal women given estrogen replacement.
Obstet Gynecol
84:
787-793,
1994
This article has been cited by other articles:
|
|
 |
|
  M. J. Toth, B. C. Cooper, R. E. Pratley, A. Mari, D. E. Matthews, and P. R. Casson Effect of ovarian suppression with gonadotropin-releasing hormone agonist on glucose disposal and insulin secretion Am J Physiol Endocrinol Metab, June 1, 2008; 294(6): E1035 - E1045. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. E. Wierman and W. M. Kohrt Review Article: Vascular and Metabolic Effects of Sex Steroids: New Insights Into Clinical Trials Reproductive Sciences, May 1, 2007; 14(4): 300 - 314. [Abstract] [PDF]
|
|
|
|
 |
|
 V. B. O'Leary, C. M. Marchetti, R. K. Krishnan, B. P. Stetzer, F. Gonzalez, and J. P. Kirwan Exercise-induced reversal of insulin resistance in obese elderly is associated with reduced visceral fat J Appl Physiol, May 1, 2006; 100(5): 1584 - 1589. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D.-J. Kim and E. Barrett-Connor Association of serum proinsulin with hormone replacement therapy in nondiabetic older women: the rancho bernardo study. Diabetes Care, March 1, 2006; 29(3): 618 - 624. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. E. Van Pelt, C. M. Jankowski, W. S. Gozansky, R. S. Schwartz, and W. M. Kohrt Lower-Body Adiposity and Metabolic Protection in Postmenopausal Women J. Clin. Endocrinol. Metab., August 1, 2005; 90(8): 4573 - 4578. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. S. Fairey, K. S. Courneya, C. J. Field, G. J. Bell, L. W. Jones, and J. R. Mackey Effects of Exercise Training on Fasting Insulin, Insulin Resistance, Insulin-like Growth Factors, and Insulin-like Growth Factor Binding Proteins in Postmenopausal Breast Cancer Survivors: A Randomized Controlled Trial Cancer Epidemiol. Biomarkers Prev., August 1, 2003; 12(8): 721 - 727. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. E. Van Pelt, W. S. Gozansky, R. S. Schwartz, and W. M. Kohrt Intravenous estrogens increase insulin clearance and action in postmenopausal women Am J Physiol Endocrinol Metab, August 1, 2003; 285(2): E311 - E317. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Figueroa, S. B. Going, L. A. Milliken, R. M. Blew, S. Sharp, P. J. Teixeira, and T. G. Lohman Effects of Exercise Training and Hormone Replacement Therapy on Lean and Fat Mass in Postmenopausal Women J. Gerontol. A Biol. Sci. Med. Sci., March 1, 2003; 58(3): M266 - 270. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. E. Van Pelt, E. M. Evans, K. B. Schechtman, A. A. Ehsani, and W. M. Kohrt Contributions of total and regional fat mass to risk for cardiovascular disease in older women Am J Physiol Endocrinol Metab, May 1, 2002; 282(5): E1023 - E1028. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
significant main effect of HRT
(P < 0.05).
significant interaction of exercise and HRT (exercise + HRT
different from all other groups) (P < 0.05).
