International Journal of Cardiology 97 (2004) 115 – 122

www.elsevier.com/locate/ijcard

Effects of a weight reduction program with and without aerobic exercise in

the metabolic syndrome
Michael Christ a,*, Carsten Iannello a,b, Patricia G. Iannello b, Wolfram Grimm a
a
Klinik für Innere Medizin, Kardiologie, Philipps University Marburg, Baldingerstrasse, D-35033 Marburg, Germany
b
Praxis für Allgemeinmedizin, Limbach, Germany
Received 26 September 2003; received in revised form 25 December 2003; accepted 8 January 2004

Abstract

Background: In the setting of a rural, primary care practice, evidence for the efficacy of intentional weight loss with or without aerobic
exercise training (AET) in hypertensive patients with the metabolic syndrome remains controversial. Design of study, methods: We analysed
data of 52 hypertensives with the metabolic syndrome, who attended a weight management program with or without AET (diet/exercise
group, n = 18; diet group, n = 20) for 36 months. Patients with a similar risk profile, who declined antihypertensive therapy beyond ACE
inhibition, served as controls (n = 14). Results: Body mass index (BMI) was significantly reduced over time in the diet and diet/exercise
group (DBMI:
7.2 F 1.1 and
6.6 F 1.5 kg/m2) vs. the control group (DBMI: + 0.4 F 1.3 kg/m2; p < 0.001 at 36 m). While systolic and
diastolic blood pressures (BPs) did not change over time in controls (175 F 5/89 F 7 mm Hg), BPs were significantly reduced in the diet
group (151 F 8/75 F 10 mm Hg) and in the diet/exercise group (139 F 12/71 F 8 mm Hg; p < 0.001 vs. diet group). Metabolic abnormalities
were significantly improved over time in the diet group vs. controls, while AET did not add further benefits. However, heart rate recovery
after acute exercise was improved and body cell mass (BCM) was increased in the diet/exercise group vs. patients without AET ( p < 0.001
vs. others). Conclusions: Weight management significantly improves the lipid and nonlipid abnormalities of the metabolic syndrome, which
is associated with reduced blood pressure. Addition of AET does not add further benefits on metabolic parameters, but improves blood
pressure regulation. Effective lifestyle modifications are feasible even in the setting of a rural practice.
D 2004 Elsevier Ireland Ltd. All rights reserved.

Keywords: Metabolic syndrome; Hypertension; Weight reduction; Aerobic exercise training

1. Introduction patients [2]. Because increased blood pressure and the

Arterial hypertension is an important contributor to an
increased morbidity and mortality for cardiovascular dis-
eases [1]. Large prospective, randomized trials have clearly
demonstrated that overall mortality is significantly reduced
by diuretics, h-blockers, long-acting calcium antagonists or
drugs affecting the renin –angiotensin– aldosterone system
(RAAS) alone or in combination compared to placebo
treatment [1]. Although the merits of drug treatment are
not under question, antihypertensive drugs do not change
pathophysiologic processes involved in primary hyperten-
sion. Metabolic abnormalities such as overweight, glucose
control and lipoprotein dysregulation are common in those
* Corresponding author. Tel.: +49-6421-2866462; fax: +49-6421-286-
8954.
E-mail address: christ_michael@yahoo.de (M. Christ).
metabolic disorder are often associated with overweight,
and experimental studies suggest a causal role of overweight
in affected persons, the reduction of energy intake or an
increase of energy expenditure appears to be a causal
treatment regimen [3].
The metabolic syndrome or ‘‘deadly quartet’’ is a cluster
of metabolic abnormalities involving abdominal obesity,
hypertension, diabetes and dyslipidemia that greatly in-
crease the risk for cardiovascular disease [2,4,5]. There
are many definitions of the metabolic syndrome, which
are all in dispute. The diagnosis of this syndrome, which
is closely related to hyperinsulinemia and insulin resistance,
is suggested to be made when three or more of following
risk determinants are present: abdominal obesity, increased
triglycerides, reduced high-density lipoprotein (HDL) cho-
lesterol, increased blood pressure or a disorder of glucose
control [6]. The prevalence of patients with the metabolic
syndrome is high (f 22%) and increases with age as found

0167-5273/$ - see front matter D 2004 Elsevier Ireland Ltd. All rights reserved.
doi:10.1016/j.ijcard.2004.01.034
116 M. Christ et al. / International Journal of Cardiology 97 (2004) 115–122
in a nationally representative sample of a civilian, noninsti-
tutionalized US population [7]. Although genetic factors
have been discussed, this syndrome is mainly due to an
increase of energy intake often combined with a decrease of
energy expenditure. Experimental data support this assump-
tion. That is, in a rat model, high-fat diet initiates insulin
resistance and/or hyperinsulinemia, subsequently leading to
weight gain, increased blood pressure and other features of
the metabolic syndrome [8], while diet modification
reverses the metabolic disorder [9]. Because insulin resis-
tance, metabolic abnormalities and abdominal obesity are
closely related to increased blood pressure [2,3,10,11],
lifestyle modifications appear advisable. Indeed, several
reports indicate a substantial improvement of metabolic
dysregulation and arterial hypertension by exercise training
and/or diet modification programs [12 – 15].
Clinical studies on lifestyle modification are usually
conducted in large medical centers. Because it is question-
able whether those interventions can be achieved in the
setting of a general practice, we screened data from a
primary care practice in a rural area of Germany. The aim
of our study was to analyze whether a guided weight
reduction program with or without aerobic exercise training
improves blood pressure regulation and metabolic abnor-
malities in those patients. We hypothesized that a tightly
controlled weight reduction program significantly improves
blood pressure control and metabolic abnormalities indica-
tive for hyperinsulinemia, which may be further improved/
stabilized by physical activity.
2. Patients, study design and methods
2.1. Patients, study design
For this study, patients of a primary care practice
(f 1.400 patients at any year) in a rural area of the
northeastern part of Germany (specialty: primary care phy-
sician, patients: >95% in German public health insurance,
location: region of Mecklenburg – Vorpommern) were
recruited, who presented during 1993 –1998 with the first
diagnosis of unmedicated, uncomplicated hypertension [1]
and two additional symptoms of the metabolic syndrome: (I)
type 2 diabetes mellitus or impaired glucose tolerance or
increased fasting glucose; (II) abdominal obesity [body
mass index (BMI)>27 kg/m2 or waist – hip ratio >0.9];
(III) hypertriglyceridemia (>150 mg/dl); (IV) low HDL
cholesterol (< 40 mg/dl; [7]). All potential study subjects
were informed about the consequences of the metabolic
syndrome and possible treatment options. Interested patients
could decide for their preferred intervention at their own
discretion after their initial visit:
(1) restriction of caloric intake by a standardized diet and
attendance to a weight management program (diet
group; n = 20), or
(2) restriction of caloric intake as in (1) combined with
aerobic exercise training (diet/exercise group; n = 18).
Enrollment into the study started after informed consent
has been obtained in each patient, and the study protocol
conforms to the ethical guidelines of the 1975 Declaration
of Helsinki as reflected in a priori approval by the
institution’s human research committee. Patients with a
similar risk profile, who declined standardized lifestyle
modification and antihypertensive therapy beyond ACE
inhibition, served as controls (n = 14). Follow-up was
available for 36 months.
Clinical parameters, resting heart rate and blood pressure,
laboratory parameters, parameters of exercise stress testing
and bioelectrical impedance analysis (BIA) were available
for each patient selected at baseline and on regular intervals
as follows: 3 months (3 F 1 months), 6 months (6 F 1
months), 12 months (12 F 3 months), 24 months (24 F 3
months), and at 36 months (36 F 3 months).
2.2. Interventions
2.2.1. Restriction of caloric intake (diet group)
The weight reduction program was conducted according
to national and international recommendations with the aim
to achieve a deficit of at least 1000 kcal/day until a BMI of 25
kg/m2 and of at least 500 kcal/day until a BMI of 23 kg/m2
[16]. The primary goal of the intervention was a weight loss
of 0.5 –1.0 kg/week, achieved gradually by decreasing en-
ergy and fat intake. Patients were weekly trained for all
nutritional aspects for the first 4 weeks and subsequently
every 2 weeks. Caloric intake was restricted using a middle
European, balanced diet ( f 50% carbohydrates, f 30%
protein, 20 – 60 g fat/day supplemented by vitamins and
minerals [17]. A minimum volume intake of at least 2 l was
suggested using mineral water or tea as beverage. Intentional
weight loss was controlled by weight control at 2 –4-week
intervals, and by bioelectric impedance analysis at indicated
times. Caloric intake restriction was further supported by a
behavioural program, which consisted of group sessions in
2 – 4-week intervals [18]. Record keeping was a key compo-
nent of the intervention, and all meetings began with a review
of each member’s food diary and homework of the previous
week. Furthermore, group members worked on individual-
ized plans for maintaining the changes they had made.
2.3. Aerobic exercise training (diet/exercise group)
In addition to their weight management program, patients
in the diet/exercise group underwent a regular training
program, which was performed two times per week at a
level of 60– 80% of their initial heart rate reserve. The
exercise routine consisted of 15 min of warm up exercises,
40 min of endurance training (cycle ergometry, walking or
jogging; type of exercise was randomly changed every or
every other day), and 15 min of cool down exercise.
 M. Christ et al. / International Journal of Cardiology 97 (2004) 115–122 117

Subjects were instructed in how to monitor their radial
pulses, and maintained their heart rates at or above their
target heart rates for at least 35 min. A trained exercise
physiologist supervised all exercise sessions, and performed
two to three random checks of heart rate. The aim of the
training unit was to conduct aerobic exercise without lactate
formation, which was controlled at regular intervals.
3. Methods
categorical variables or using one-way analysis of variance
(ANOVA) followed by Scheffe’s post hoc test for continu-
ous variables. Treatment effects over time were evaluated
using a repeated measure ANOVA followed by a paired
Student’s t-test and Bonferroni correction to detect before –
after differences within a group. A p-value < 0.05 was
considered to be significant. Statistical analysis was done
using StatView 5.0 for the Apple Macintosh (SAS Institute,
Cary, NC).

3.1. Anthropometry, laboratory parameters 4. Results

Body weight was measured in regular intervals without 4.1. Demographic parameters, body weight and blood
clothes and shoes during office visits, and blood pressure was pressure
determined with a sphygmomanometer in sitting position
after 5 min of rest. The average of three subsequent measure- At baseline, the BMI was significantly lower in control
ments was used for further calculation. Waist and hip ratio patients compared to patients on diet alone. All other
were assessed in standing position by a trained technician. parameters were not different among the examined groups
For determination of blood parameters, venous blood was (Table 1). During study time, weight loss was achieved by
drawn in fasting state into a serum tube or in a tube filled with caloric intake restriction in the diet (baseline: 84.7 F 4.4; 6
EDTA. Laboratory parameters [hemoglobin, hemoglobin months: 78.0 F 4.3; 12 months: 76.2 F 4.1; and 36 months:
A1c (HbA1c), blood glucose levels, creatinine, uric acid, total 75.8 F 4.1 kg; p < 0.001 vs. baseline) and in the diet/
cholesterol, high-density lipoprotein (HDL) cholesterol, tri- exercise group (baseline: 85.7 F 5.7; 6 months: 79.2 F 5.6;
glycerides] were determined in a certified laboratory using 12 months: 77.5 F 5.4; and 36 months: 72.7 F 4.9 kg;
standard methods, low-density lipoprotein (LDL) cholesterol p < 0.001 vs. baseline), while weight tended to increase in
was calculated using the formula of Friedewald. the control group (baseline: 83.0 F 5.8; 6 months: 84.9 F
5.7, p < 0.01; 12 months: 84.1 F 5.6, p < 0.01; and 36
3.2. Exercise stress testing months: 83.8 F 5.4 kg; p < 0.1 vs. baseline). Comparably,
BMI decreases in the diet and diet/exercise group over time,
Bicycle ergometry was conducted every 3 months (CAR- while there was a tendency to an increase in the control
DIBIKE 900, Ergo Fit GmbH, Pirmasens, Germany). After 4 group until the end of the observational period (Fig. 1).
min of rest, exercise was started at 50 W for 2 min and load Weight reduction was associated with a significant decrease
was increased in 25-W intervals to 100 W every 2 min. A
recovery period for 4 min followed. Blood pressure and heart
rate were noninvasively measured at the end of each step.
Table 1
Clinical characteristics of patients with arterial hypertension and the
3.3. Body composition analysis metabolic syndrome
Variable All patients Control Diet group Diet/exercise
Body composition was determined by the bioelectrical group group
impedance analysis (BIA) using the whole-body tetrapolar
Sample (n=) 52 14 20 18
contact electrode approach. A multifrequency impedance Age (years) 46.3 F 6.0 46.0 F 3.4 45.0 F 7.1 48.0 F 6.4
analyzer applying alternating electric currents of 100 AA at Sex (male/female) 12/40 2/12 3/17 7/11
1 kHz, and of 800 AA at 5, 50, and 100 kHz (BIA 2000-M, Weight (kg) 84.6 F 5.3 83.0 F 5.8 84.7 F 4.4 85.7 F 5.7
Data Input GmbH, Frankfurt, Germany) was used in all BMI (kg/m2) 30.3 F 1.9 29.0 F 1.8 31.1 F 1.7# 30.5 F 1.7#
patients [19,20]. During measurements, the patients were in Waist – hip ratio 1.23 F 0.12 1.24 F 0.14 1.21 F 0.14 1.23 F 0.08
Heart rate 76.2 F 4.7 75.1 F 4.8 77.9 F 4.8 75.2 F 4.3
supine body position, while the arms were relaxed without (beats per min)
touching the body or the thighs. Total body water (TBW), BPsys (mm Hg) 172 F 8 174 F 9 171 F 8 173 F 7
fat-free mass (FFM) and body cell mass (BCM) were BPdia(mm Hg) 98 F 6 97 F 6 99 F 6 99 F 5
calculated from resistance, reactance and the phase angle Hemoglobin (g/dl) 15.2 F 0.9 15.1 F 0.8 15.2 F 0.9 15.2 F 1.0
at 1 and 50 kHz [19,20]. Creatinine (mg/dl) 1.1 F 0.2 1.0 F 0.1 1.1 F 0.2 1.0 F 0.1
Fasting glucose 113.0 F 19.3 121.1 F 17.1 111.4 F 20.4 108.5 F 18.6
(mg/dl)
3.4. Statistical analysis Uric acid (mg/dl) 6.6 F 1.7 6.8 F 1.5 6.7 F 1.5 6.4 F 2.0
HbA1c 6.8 F 0.7 6.8 F 0.7 6.8 F 0.6 6.7 F 0.8
Values are given as mean F standard deviation. Differ- Systolic blood pressure (BPsys); diastolic blood pressure (BPdia).
ences among treatment groups were assessed by v2 tests for #
p < 0.05 vs. control group for between-group differences.
118 M. Christ et al. / International Journal of Cardiology 97 (2004) 115–122
Fig. 1. Follow-up (36 months) of body mass index (BMI) in hypertensive
patients with the metabolic syndrome. Patients were either treated with a
standardized weight reduction diet (.), diet and exercise training (n) or
with an ACE inhibitor (controls, o). Between-group differences: #p < 0.001
and §p < 0.05 vs. diet and diet/exercise group; within-group differences:
*p < 0.001 vs. respective values at baseline.
Fig. 2. Follow-up (36 months) of systolic (A) and diastolic (B) office blood
pressure in hypertensive patients with the metabolic syndrome. Patients
.
were either treated with a standardized weight reduction diet ( ), diet and
exercise training (n) or with an ACE inhibitor (controls, o). Between-
group differences: #p < 0.001 vs. diet and diet/exercise group; and
y y
p < 0.001 vs. control and diet/exercise group; within-group differences:
*p < 0.001 and zp < 0.05 vs. respective values at baseline.
of systolic and diastolic blood pressures at rest in the diet
and diet/exercise group, while resting blood pressure was
not significantly changed in controls (control group, Fig. 2).
At 36 months, systolic and diastolic blood pressures were
significantly lower in the diet/exercise group compared to
the diet group, while blood pressure levels were not differ-
ent among latter groups at previous time points (Fig. 2).
Resting heart rate did not differ among the examined groups
during the whole treatment period (control: baseline:
75.1 F 4.8, 6 months: 75.5 F 4.2, 12 months: 76.4 F 4.3,
and 36 months: 76.3 F 5.3 bpm; diet: baseline: 77.9 F 4.8, 6
months: 74.9 F 4.4, 12 months: 76.7 F 5.1, 36 months:
74.9 F 4.5 bpm; diet/exercise group: baseline: 75.2 F 4.3,
6 months: 76.2 F 4.3, 12 months: 76.4 F 4.8, 36 months:
74.9 F 4.1 bpm).
Fig. 3. Follow-up (36 months) of HbA1c levels (A) and the waist – hip ratio
(B) in hypertensive patients with the metabolic syndrome. Patients were
.
either treated with a standardized weight reduction diet ( ), diet and
exercise training (n) or with an ACE inhibitor alone (controls, o).
Between-group differences: #p < 0.001 vs. diet and diet/exercise group; and
p < 0.01 vs. control group; within-group differences: *p < 0.001 and
z
p < 0.05 vs. respective values at baseline.
 M. Christ et al. / International Journal of Cardiology 97 (2004) 115–122 119

baseline) and in the diet/exercise group (total cholesterol:

baseline: 289 F 27, 36 months: 176 F 31 mg/dl, p < 0.001
vs. baseline; LDL cholesterol: baseline: 178 F 28, 36
months: 133 F 23 mg/dl, p < 0.001 vs. baseline) compared
to the control group (total cholesterol: baseline: 273 F 31, 36
months: 275 F 22 mg/dl, n.s.; LDL cholesterol: baseline:
180 F 29, 36 months: 170 F 21 mg/dl, n.s.). In addition,
there was a significant reduction of uric acid over the
treatment period in the diet (baseline: 6.7 F 1.5, 6 months:
4.3 F 0.8, 12 months: 4.2 F 0.8, and 36 months: 4.1 F 0.6
mg/dl; p <0.001 vs. baseline) and in the diet/exercise group
(baseline: 6.4 F 2.0, 6 months: 5.8 F 1.4, 12 months:
4.3 F 1.0, and 36 months: 4.2 F 0.7 mg/dl; p < 0.001 vs.
baseline) compared to control patients (baseline: 6.8 F 1.5, 6
months: 6.7 F 1.0, 12 months: 6.8 F 1.5, and 36 months:
6.8 F 0.9 mg/dl, n.s.).

4.3. Exercise stress testing

Heart rate, systolic blood pressure and rate –pressure

product were significantly increased during exercise stress
testing (ergometry, 100 W) compared to respective resting
values ( p < 0.0001). Up to the end of the observational
period, maximum heart rate, systolic blood pressure and
rate pressure product during bicycle ergometry at 100 W
were not significantly different among the three groups
(Table 2). However, the heart rate recovery (difference of
maximum heart rate at 100 W and heart rate 4 min after
maximum exercise) was significantly larger in the diet/
exercise group after 12 months compared to the other
groups, while no differences were detectable between the
control and the diet groups (Table 2).

Fig. 4. Follow-up (36 months) of HDL cholesterol (A) and triglyceride Table 2
levels (B) in hypertensive patients with the metabolic syndrome. Patients Exercise stress testing in patients with arterial hypertension and the
.
were either treated with a standardized weight reduction diet ( ), diet and metabolic syndrome
exercise training (n) or with an ACE inhibitor alone (controls, o). Variable Control group Diet group Diet/exercise group
Between-group differences: #p < 0.001 vs. diet and diet/exercise group; and
y Systolic blood pressure (100 W)
p < 0.05 vs. control group; within-group differences: *p < 0.001 and
z Baseline 192.5 F 7.5 193.5 F 10.1 196.1 F 7.8
p < 0.01 vs. respective values at baseline.
6 months 195.4 F 10.1 186.3 F 10.5 192.2 F 11.9
12 months 187.9 F 11.6 180.5 F 10.5 188.9 F 11.7
36 months 188.9 F 10.2 181.8 F 9.4 181.9 F 6.9
4.2. Parameters of metabolism
Rate – pressure product (100 W)
Weight reduction was accompanied by a significant Baseline 28,916 F 1857 29,773 F 1625 29,474 F 1702
improvement of parameters reflecting the metabolic syn- 6 months 30,707 F 1864 28,453 F 2407 29,560 F 2364
12 months 28,693 F 1843 27,519 F 1764 29,064 F 1967
drome. We found a time-dependent, significant reduction of 36 months 28,451 F 1651 28,234 F 2080 28,607 F 1049
HbA1c levels, the waist – hip ratio, and a significant in-
crease of HDL cholesterol and a significant decrease of Heart rate recovery (4 min after exercise; Dbpm)
triglyceride levels in the diet and diet/exercise groups Baseline
44.1 F 15.4
44.4 F 12.8
42.8 F 9.5
compared to the control group (Figs. 3A, B and 4A, B). 6 months
49.6 F 11.5
45.9 F 12.4
49.7 F 7.8z
12 months
43.0 F 8.4
41.8 F 13.9
55.7 F 10.2y,*
Starting at 3 months of treatment, total and LDL choles- 36 months
41.4 F 14.5
46.3 F 12.3
62.7 F 9.9*,#
terol levels were significantly reduced in the diet (total
* p < 0.001 vs. respective values at baseline for within-group differences.
cholesterol: baseline: 289 F 26, 36 months: 175 F 29 mg/ #
p < 0.001 vs. control and diet group for between-group differences.
dl, p < 0.001 vs. baseline; LDL cholesterol: baseline: y
p < 0.05 vs. control and diet group for between-group differences.
z
185 F 24.9, 36 months: 128 F 17 mg/dl, p < 0.001 vs. p < 0.01 vs. respective values at baseline for within-group differences.
120 M. Christ et al. / International Journal of Cardiology 97 (2004) 115–122

Table 3 Epidemiological studies have clearly demonstrated that

Body composition of hypertensive patients with metabolic syndrome
blood pressure is positively correlated with the BMI and the
Variable Control group Diet group Diet/exercise group percentage body fat [21,22]. Indeed, diet-induced weight
Total body water (kg) loss has been shown to significantly lower blood pressure
Baseline 41.8 F 2.0 46.6 F 2.1§ 42.8 F 2.0 [12,14,23– 25]. Our data obtained in a rural primary care
6 months 42.8 F 1.3 43.5 F 1.9 41.7 F 2.2
practice comparably indicate that adherence of patients to a
12 months 41.9 F 1.3 42.8 F 1.7 42.8 F 2.2
36 months 42.5 F 1.3 42.5 F 1.9 43.1 F 1.6 weight management program induces a significant abdom-
inal weight loss within 6 months and a parallel decrease of
Body fat mass (kg) blood pressure levels. Those beneficial effects further con-
Baseline 22.5 F 2.2 23.4 F 1.7 22.8 F 2.4 tinued and were maintained up to the end of observation
6 months 23.5 F 2.1y 22.5 F 1.3z 21.5 F 2.0z
period at the 36 months with a decline in systolic and
12 months 23.1 F 2.3# 17.2 F 2.4* 17.9 F 1.3*
36 months 23.5 F 2.2# 13.8 F 2.8* 18.6 F 1.5* diastolic blood pressure (14.6 and 21.2 mm Hg, respective-
ly). A comparable absolute reduction of blood pressure
Body cell mass (kg) levels has been reported previously [12,14,23 – 25]. The
Baseline 23.8 F 3.1 24.1 F 1.5 24.0 F 1.3 mechanisms involved in weight loss-induced reductions of
6 months 24.5 F 2.4 23.8 F 1.4 26.9 F 1.1z,yy
blood pressure are not well characterized. An increased
12 months 23.8 F 2.0 24.3 F 1.2 27.3 F 1.1*,yy
36 months 24.4 F 2.0 25.1 F 1.0 28.1 F 1.6*,yy lipolytic rate in visceral adipocytes of upper-body obesity
may activate the sympathetic nervous system and the
* p < 0.001 vs. respective values at baseline (within-group differences).
#
p < 0.001 vs. diet and diet/exercise group. hypothalamus– pituitary adrenal axis, subsequently leading
§
vs. control and diet/exercise group. to increased blood pressure [3]. Thus, reduction of abdom-
y
p < 0.05 vs. diet and diet/exercise group. inal obesity may appease the activation of those neurohu-
yy
p < 0.001 vs. control and diet group (between-group differences). moral systems [3].
z
p < 0.05 vs. respective values at baseline (within-group differences).
In contrast to large, randomised studies conducted in
health care centers, treatment of patients in ‘‘real life’’ often
4.4. Intervention induced changes of body composition differs. We found a persistently high body weight and systolic
blood pressure in patients on ACE inhibitors alone, which
TBW as determined by BIA was significantly higher in even tended to increase after 36 months of treatment. Al-
the diet group compared to the control and the diet/exercise though, compliance was not measured in our study, we
group at baseline (Table 3). No before – after changes of speculate that patients in the ‘‘control’’ group were neither
TBW within the groups were observed during the whole compliant to weight reduction strategies nor to ACE inhibitor
study period (Table 3), indicating that weight reduction was therapy.
not achieved by water restriction of the patients. Body fat Abdominal obesity is an independent risk factor for
mass (BFM) was significantly decreased in the diet and diet/ coronary artery disease and noninsulin-dependent diabetes
exercise group compared to the control group during the mellitus [26,27], and restriction of caloric intake improves
study period (Table 3). BCM was similar among the groups metabolic abnormalities [25,28,29]. Indeed, standardized
at baseline. BCM was significantly increased in the diet/ weight management significantly reduced abdominal obesi-
exercise group during 36 months of treatment compared to ty in our cohort, which was associated with beneficial
the control and diet groups, while no differences were changes of lipid and nonlipid abnormalities including re-
detectable among the latter (Table 3). duction of HbA1c levels indicative for improved glucose
control. However, the mechanisms are not quite clear.
Experimental data suggest that restriction of caloric intake
5. Discussion reverses insulin resistance and hyperinsulinemia [9]. Fur-
thermore, regulators of lipid metabolism such as LDL
The results of this study are as follows. (1) An impressive receptor or lipase activity are modulated by diet modifica-
weight loss due to body fat mass reduction can be achieved tion [30,31], while oxidative and sympathoadrenergic stress
in patients adhering to a weight management program for at are reduced [3,11]. While the intentional weight loss sig-
least up to 36 months, which was associated with a nificantly improved metabolic parameters of the study
significant decrease of resting blood pressure. (2) Weight subjects, regular aerobic exercise training did not add
reduction is accompanied by a significant improvement of further benefits. These findings are consistent with data
glucose control, lipid and nonlipid abnormalities of the showing no enduring effect of exercise training on metab-
metabolic syndrome. (3) Interestingly, body weight and olism, despite beneficial effects on glucose control associ-
parameters of the metabolic syndrome are not different from ated with acute exercise [12,32,33]. Possibly, the amount of
the diet group, when regular aerobic exercise training was aerobic exercise training as currently recommended by
added. However, resting blood pressure is further decreased international societies and applied in our study is not
and heart rate recovery after exercise was improved in the sufficient to offer significant benefits on metabolic param-
diet/exercise group compared to the diet group alone. eters by exercise-mediated mechanisms alone compared to
 M. Christ et al. / International Journal of Cardiology 97 (2004) 115–122
the impressive effects of moderate weight loss. Moreover,
benefits of exercise training on insulin sensitivity and
metabolism may be short-lived and/or relate to exercise-
induced weight loss [33 – 35]. Thus, the reduction of ab-
dominal obesity appears to be the primary goal in the
treatment of overweight patients with the metabolic syn-
drome to beneficially modulate lipid and nonlipid risk
factors.
The before –after measures of TBW content did not differ
within the groups during the observational period. Thus, the
reduction of the BMI in the diet and diet/exercise group was
not due to water restriction. In contrast, the BFM was
significantly reduced in both groups supporting that a
long-lasting reduction of the body fat has been achieved
as similarly shown by the reduction of BMI and the waist –
hip ratio. Of note, BCM did not differ among the control
and the diet group, while BCM was significantly increased
up to 36 months in the exercise group compared to the other
groups suggesting that exercise training increases the mus-
cle mass. Although measurement of BCM by BIA is
certainly not the gold standard for BCM determination, it
correlates well with the BCM determined by total body
potassium counting [19] and, thus, may provide an accept-
able estimate of BCM. Additional benefits of exercise
training is further supported by the trend to lower blood
pressure values at rest and the improvement of heart rate
recovery after exercise stress testing in the exercise group
indicating improved physical endurance. This may be asso-
ciated with improved outcome in patients at increased
coronary risk [36]. Thus, aerobic exercise training adds
further benefits on cardiovascular parameters independent
of metabolic control, which may further improve cardiovas-
cular prognosis.
There are several limitations inherent with the study
design. We conducted a prospective, per protocol analysis
of data obtained during the routine management of patients
by a primary care physician. Second, all patients could
decide for their preferred intervention at their own discretion
after their initial visit, which has unintentionally led to the
situation that more male patients attended the diet/exercise
group compared to the other two groups. Thus, the assign-
ment to the treatment groups might be strongly biased, e.g.,
by extremes of motivation, and the amount of beneficial
effects of lifestyle modifications may be overestimated.
Because we were unable to control for this bias in the
statistical analysis and most study patients were female, the
apparent beneficial effects by diet with or without aerobic
exercise in our patient groups cannot be generalized to the
overall population of patients with the metabolic syndrome.
However, our data are comparable to results of prospective
studies conducted in large medical health care centers
[12,25,33]. This indicates that beneficial effects of lifestyle
modifications on blood pressure control and metabolic
abnormalities in sedentary, overweight patients with the
metabolic syndrome are achievable even in the setting of
a general practitioner in a rural area.
121
Our data and previous studies clearly show that inten-
tional weight loss induces beneficial changes of metabolic
parameters and blood pressure regulation associated with an
increased cardiovascular risk in patients with the metabolic
syndrome [2,5]. However, those long-lasting effects may
only be achieved by continuous motivation of the patients
by trained experts [18], while simple physician counseling
appears to be ineffective [37]. Weight loss should be the
preferred treatment in overweight, middle-aged patients as
suggested previously [25], but aerobic exercise training may
add further benefits on the cardiovascular system. Various
pharmacological attempts are currently made to influence
key enzymes/regulators of metabolism to favorable change
the metabolic syndrome [38]. Because those attempts are
costly, do not change the initiators of this metabolic disor-
der, and will further strain the exploding budget of the
health care systems, we suggest to place more emphasis on
the education and motivation of affected patients, and of the
general population.
In conclusion, weight reduction improves the metabolic
abnormalities and beneficially modulates increased blood
pressure control in patients with the metabolic syndrome.
Significant weight reduction is feasible even in the setting of
a doctor’s practice in a rural area. Addition of regular
aerobic exercise training obviously does not modulate
metabolic abnormalities, while blood pressure regulation
and physical endurance are beneficially changed. Thus,
lifestyle modifications appear to be the preferred treatment
strategies to improve increased blood pressure and metabolic
abnormalities of patients with the deadly quartet [4].
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