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Nutrition, Metabolism & Cardiovascular Diseases (2014) 24, 792e798

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Time-course effects of aerobic interval training and detraining in

patients with metabolic syndrome
R. Mora-Rodriguez a,*, J.F. Ortega a, N. Hamouti a, V.E. Fernandez-Elias a,
J. Cañete Garcia-Prieto b, A. Guadalupe-Grau c, A. Saborido d, M. Martin-Garcia a,
V. Guio de Prada e, I. Ara a, V. Martinez-Vizcaino b
a
Exercise Physiology Laboratory and GENUD Group University of Castilla-La Mancha, Toledo, Spain
b
Social and Health Care Research Center, University of Castilla-La-Mancha, Cuenca, Spain
c
Xlab, Center for Healthy Aging, University of Copenhagen, Copenhagen, Denmark
d
Departamento de Bioquímica y Biología Molecular I, University Complutense, Madrid, Spain
e
Sports Medicine Center, Diputacion de Toledo, Spain

Received 8 September 2013; received in revised form 20 December 2013; accepted 7 January 2014
Available online 29 January 2014

KEYWORDS Abstract Background and aims: Exercise training can improve health of patients with metabolic
Aerobic exercise; syndrome (MetS). However, which MetS factors are most responsive to exercise training remains un-
Insulin resistance; clear. We studied the time-course of changes in MetS factors in response to training and detraining.
Obesity therapy; Methods and results: Forty eight MetS patients (52
8.8 yrs old; 33
4 BMI) underwent 4 months (3
Cardiovascular days/week) of supervised aerobic interval training (AIT) program. After 1 month of training, there
disease; were progressive increases in high density lipoprotein cholesterol (HDL-c) and reductions in waist
Fatty acid oxidation; circumference and blood pressure (12
3, 3.9
0.4, and 12
1%, respectively after 4 months;
Muscle mitochondria all P < 0.05). However, fasting plasma concentration of triglycerides and glucose were not reduced
by training. Insulin sensitivity (HOMA), cardiorespiratory fitness (VO2peak) and exercise maximal fat
oxidation (FOMAx) also progressively improved with training (17
5; 21
2 and 31
8%, respec-
tively, after 4 months; all P < 0.05). Vastus lateralis samples from seven subjects revealed that mito-
chondrial O2 flux was markedly increased with training (71
11%) due to increased mitochondrial
content. After 1 month of detraining, the training-induced improvements in waist circumference
and blood pressure were maintained. HDL-c and VO2peak returned to the values found after 1e2
months of training while HOMA and FOMAx returned to pre-training values.
Conclusions: The health related variables most responsive to aerobic interval training in MetS pa-
tients are waist circumference, blood pressure and the muscle and systemic adaptations to consume
oxygen and fat. However, the latter reverse with detraining while blood pressure and waist circum-
ference are persistent to one month of detraining.
ª 2014 Elsevier B.V. All rights reserved.

Introduction Exercise training studies on MetS patients revealed that

Individuals with metabolic syndrome (MetS) are at higher
risk of developing type 2 diabetes, cardiovascular disease
and hypertension than age-matched counterparts [1].
* Corresponding author. Sport Sciences Department, University of
Castilla-La Mancha, 45071 Toledo, Spain. Tel.: þ34 925268800; fax:
þ34 925268846.
E-mail address: ricardo.mora@uclm.es (R. Mora-Rodriguez).
exercise with [8,23] or without dietary energy restriction
[28,29] improves some components of MetS [7]. Resistance
training in MetS patients increases HDL cholesterol [12]
and lower mean arterial pressure [23]. However, resis-
tance training does not seem to improve insulin sensitivity
in MetS patients [19]. In contrast, aerobic training is more
effective at improving MetS components and as effective
as the combination of resistance and aerobic training
[3,28]. Within the different modes of aerobic training,

0939-4753/$ - see front matter ª 2014 Elsevier B.V. All rights reserved.
http://dx.doi.org/10.1016/j.numecd.2014.01.011
 Author's personal copy
Time-course effects in patients with metabolic syndrome
aerobic interval training (AIT) is more efficacious than
continuous moderate-intensity training to reverse MetS
[29] although this finding is not without discussion [14].
Low level of aerobic fitness has revealed as an inde-
pendent and strong predictor of mortality compared to
classical risk factors [5]. Aerobic fitness level is low in in-
dividuals with MetS [9] and it is possible that their low
aerobic capacity underlies the metabolic and cardiovas-
cular abnormalities that compose their syndrome. Further,
exercise training reverses some of the MetS components in
direct association with improved maximal aerobic capacity
(i.e., VO2max) in the elderly [13]. The adaptations that lead
to increased VO2max with training involve, improved
cardiovascular function, oxygen carrying capacity of the
blood and mitochondria biogenesis. With exercise training,
MetS patients improve diastolic function [4] and oxygen
carrying capacity of blood [26] to a similar magnitude than
in healthy subjects. However, to our knowledge nobody
has reported weather exercise training results in improved
mitochondrial respiration in MetS patients.
In this study our aim was to determine the time-course
progression towards healthy values of the different com-
ponents of MetS with aerobic interval training (AIT). The
identification of metabolic syndrome factors that do not
readily respond to exercise could help to design in-
terventions combining exercise, diet and medication for
these less modifiable factors. We also studied which of the
exercise modifiable factors relapse towards pre-training
values after 1 month of detraining. This information may
help to prescribe training-break duration to avoid losing
important health benefits obtained from exercise training
in these patients.
Methods
Study population
This study was conducted between January 2012 and
September 2012 in accordance with a protocol approved
by the local Hospital’s Ethics Committee. Forty eight obese
subjects (22 men and 26 women) between 31 and 68 years
old (mean 52.0
8.8 yr old) completed the study. Partic-
ipants were enrolled based on fulfilling 3 MetS criteria as
per harmonized definition [1] using population Europid
waist circumference cutpoints. Subjects were instructed to
continue with their current medication prescriptions dur-
ing the study. Exclusion criteria included cardiovascular or
renal disease, peripheral vascular disease and any disease
associated with exercise intolerance. Body weight stability
in the last six months was also a requirement. All subjects
provided written, witnessed, informed consent.
Exercise training and dietary records
Subjects underwent supervised aerobic interval training
(AIT) with a frequency of 3 times per week during 4
months. Training consisted on pedaling for 10-min as
warm up at 70% HRmax followed by 4 x 4-min intervals at
90% of HRmax interspersed with 3-min active recovery at
793
70% HRmax and a 5-min cool-down period for a total of
43 min. Exercise intensity was increased as training ad-
aptations developed to maintain the target heart rate
(Accurex coded, Polar, Finland). Participants were required
to attend at least 85% of all the exercise sessions. Subjects
were instructed to maintain their dietary patterns during
the duration of the study. A three day dietary log was
collected monthly and analyzed for caloric intake and
macronutrient composition.
Clinical investigation
Before training, monthly during the 4 months of training
and after 1 month of detraining we tested all subjects for
body composition, anthropometry (weight and waist
circumference), resting blood pressure, blood metabolites,
exercise maximal fat oxidation (FOMAx) and peak oxygen
consumption (VO2peak) using a graded exercise test. Blood
was drawn in the morning after a 10 h overnight fast. All
tests were scheduled at least 72 h after the last exercise
training session to avoid measuring the acute effects of the
last exercise bout rather than the chronic effects of the
exercise training program. In addition, percent body fat,
trunk body fat and fat-free mass were determined by dual
energy X-ray absorptiometry (DXA Hologic Serie Discovery
Wi QDR, Bedford, USA). Supine resting blood pressure was
recorded using a hand-held aneroid sphygmomanometer
(Gamma GST, Heine, Germany) as the average of 4
measurements.
Cardio-respiratory and metabolic fitness
Peak aerobic capacity (VO2peak) was assessed on an
electronically-braked cycle ergometer (Ergoselect 200,
Ergoline, Germany) during a graded exercise testing using
indirect calorimetry, (Quark b2, Cosmed, Italy) with 12 lead
ECG monitoring (Quark T12, Cosmed, Italy). The highest
heart rate value obtained during the test was considered
HRPEAK. Maximal fat oxidation (FOMAx) was assessed in a
fasted state using a graded exercise test with 3 min stages
until respiratory exchange ratio exceeded 1.0. The last
minute of each stage was averaged to calculate non-
protein respiratory quotient and fat oxidation rate [10].
Blood analyses
Plasma glucose was analyzed using the glucose oxidase-
peroxidase method with intra-inter assay coefficient of
variation (iCV) of 0.9e1.2%. Glycated hemoglobin (HbA1c),
apolipoprotein B (Apo B) and high sensitive protein C
reactive (hsPCR) using immune-turbidimetry tests (iCV;
0.7e2.1%). HDL-c using accelerator selective detergent
method (iCV; 1.7e2.9%). Blood triglycerides (TG) with
glycerol-3-phosphate oxidize method (iCV; 0.8e1.7%).
Total serum cholesterol (T Chol) by an enzymatic method
with a single aqueous reagent (iCV; 1.1e1.4%). Low-density
lipoprotein-cholesterol (LDL-c) was calculated as proposed
by Friedewald [11]. All the above analyses were run in an
automated Mindray BS 400 Chemistry Analyzer (Mindray
 Author's personal copy

794 R. Mora-Rodriguez et al.

Medical Instrumentation, USA). Insulin concentration was

measured in duplicate using chemiluminescent micro
particle immunoassay (iCV; 2.0e2.8%) in an automated
immunoassay analyzer (Architect ci4100, Abbott Labora-
tories, USA). Insulin sensitivity was calculated using the
homeostasis model assessment (HOMA; [20]).

Mitochondrial respiration

Muscle biopsies were obtained in seven subjects (5 men

and 2 women) before training and 4 days after the last
training session. Biopsies from the vastus lateralis were
obtained under local anesthesia (2% lidocaine without
epinephrine; Braun, Germany) and rapidly cleaned of
blood, fat and connective tissue. Then a 20e40 mg piece
was immersed in BIOPS solution for mitochondrial respi-
ration analysis [16]. The remaining of the biopsy sample
was immediately frozen in liquid nitrogen and stored at
80  C for latter fluorometric analysis of citrate synthase Figure 1 Schematic diagram of study phases and participants.
activity [21]. Mitochondria respiration was assessed in
saponin-permeabilized muscle fibers using a high-
resolution respirometer (Oxygraph, Hansatech In-
struments Ltd, Norfolk, England). Malate (M), octa- Factors comprising metabolic syndrome
noylcarnitine (O), glutamate (G), succinate (S), NADH, ADP
were progressively added to the medium to measure the Evolution of the MetS factors with exercise is depicted in
different mitochondria respiration states. Intactness of the Table 1. After 4 months of training patients had a reduction
outer mitochondrial membrane was tested by quantifying in waist circumference of 3.9
0.4% a 12
3% increase in
respiration after addition of cytochrome c (10 mM). HDL-c, a 12
1% reduction in SBP and DBP (all P < 0.05).
However, plasma glucose and triglycerides concentrations
were not significantly reduced after 4 months of training. Z
Statistical analyses
scores revealed that at pre-training, patients were
3.2
0.4 standard deviations above the mean of a healthy
We calculated a Z score to assess the continuous rather than
value for their respective gender. After four months of
dichotomous evolution on the MetS risk factors. Z score was
training, subjects were only 1.9
0.4 standard deviations
calculated in each MetS criteria using the monthly standard
away from normal values (Table 1; P < 0.05). Most of these
deviations. Blood and muscle biochemistry data, body
changes were already significant after 1e2 months of
composition, anthropometry and exercise data, were
training.
analyzed during training and detraining using one-way
ANOVA with repeated measures. Tukey’s post-hoc analysis
was performed when a significant F value was obtained. Additional physiological parameters
Data are presented as the mean
s.e. except for descriptive
data which are presented as mean
s.d. Statistical signifi- Subjects progressively reduced their body weight by
cance level was set at P < 0.05. 1.8
0.4 kg, fat mass by 1.1
0.3 kg and trunk body fat by
0.9
0.2 kg after 4 months of training (Table 2; all
Results P < 0.05). HbA1c showed a progressive reduction with
exercise training reaching the lower values after 4 months
Subjects and diet of training (4
1% reduction; Table 2; P < 0.05). Insulin
and HOMA suggested improved insulin sensitivity
Participants were all Caucasians and their responses to although the improvements were not progressive with
training did not vary between genders (46% males and 54% training duration (Table 2). Fasting glucose and blood pa-
females). Thus data were analyzed as a group without rameters of lipid metabolism (Apo B, T Chol and LDL-c)
gender distinctions. Two subjects dropped out after base- were not reduced from pre-training values at any time
line testing, however, they did not differ from the others during the 4 months of training. hsPCR was reduced below
with regards to age, fitness or blood chemistry (Fig. 1). No pre-training values after 1 month of training and further
significant diet alterations were detected during the 4 after 3 and 4 months of training (Table 2; P < 0.05).
month exercise intervention period or during detraining.
Subjects ingested an average of 1880
85 kcals $ day1 Exercise parameters
with a distribution of 41
1.2%, 38
1.1% and 21
1.0% for
carbohydrate, fat and protein. Saturated fat ingestion was FOMAx during exercise increased above pre-training values
maintained as 40% of total fat ingested. after 3 months of training and increased further with 4
 Author's personal copy

Time-course effects in patients with metabolic syndrome 795

Table 1 Evolution of metabolic syndrome factors and compound Z score with training and detraining.

Pre-training 1 month 2 months 3 months 4 months Post 1 month

a a,b a,b a,b
Waist circumference (cm) 105.4
1.3 104.1
1.3 102.8
1.2 102.2
1.2 101.4
1.2 101.4
1.3a
HDL-c (mmol/l) 1.27
0.02 1.32
0.05 1.37
0.02a 1.34
0.02a 1.42
0.05a,b,c,d 1.34
0.05a,b
Glucose (mmol/l) 6.27
0.22 6.16
0.17 6.27
0.17 6.05
0.17d 5.99
0.16d 6.11
0.17
Triglycerides (mmol/l) 1.53
0.10 1.49
0.11 1.82
0.15 1.47
0.09 1.41
0.11 1.53
0.11
SBP (mmHg) 139
2 127
2a 124
2a 123
2a,c 121
2a,c 123
2a,c
DBP (mmHg) 89
1 80
1a 79
1a 79
1a 78
1a 79
1a
MetS Z score 3.2
0.4 2.1
0.4a 3.0
0.4b 2.2
0.4a,b 1.9
0.4a,b,d 1.9
0.4a
Subjects with 3 MetS factors 0% 23% 24% 25% 29% 17%
Values are the mean
s.e. for 48 MetS subjects.
a
Significantly different from pre-training.
b
Significantly different from the previous month.
c
Significantly different than 1 month.
d
Significantly different than 2 months (all P < 0.05).

months of training (31
8%; Table 2; P < 0.05). VO2peak
increased progressively throughout the 4 months of
training reaching a 21
2% improvement. This increase
was accompanied by enhanced maximal pedaling work-
load (WMAx; 39
3%, Table 2; P < 0.05) and peak heart
rate (HRPEAK; 4
2%, Table 2; P < 0.05).
Mitochondrial respiration
O2 flux in vastus lateralis per mg of wet tissue increased
after 4 months of AIT in state 3 respiration representing
electron input from complex I and fatty acid b-oxidation
(i.e., MO3, Fig. 2; P < 0.05). The substrate control ratio
remained elevated for complexes I and II and maximal
coupled state 3 flux rate was also elevated (i.e., GMOS,
Fig. 3; P < 0.05). The addition of cytochrome c did not
result in significant increases in O2 flux, ensuring the
intactness of the outer mitochondrial membrane. Citrate
synthase activity increased 61% after 4 months of training
from 12.0
4.3 to 19.3
5.0 mmol/g wet weight/min
(P < 0.05). When O2 flux data was normalized by citrate
synthase activity training effects disappeared suggesting
that the training induced increase in oxygen flux was
attributable to an increase muscle mitochondrial content
(Fig. 2b).
Relapse after one month of detraining
After one month of detraining subjects maintained their
average reduction in body weight (1.7
0.4 kg), waist
circumference (4.1
0.4 cm) and trunk fat losses
(0.8
0.2 kg). One month of detraining returned blood
pressure to the 3 month level (Table 2; Fig. 3a). However,
HDL-c returned to the levels observed after 2e3 months of
training. Resting insulin and HOMA returned towards pre-
training values (Table 2 and Fig. 3b). The following exercise

Table 2 Change in anthropometric, blood and exercise variables after 4 months of training and 1 month of detraining.

Pre-training 1 month 2 months 3 months 4 months Post 1 month

Body composition
Weight (kg) 86.9
1.9 86.1
1.9a 85.9
1.8a 85.4
1.8a,b 85.1
1.8a,b 85.1
1.8a
BMI (kg/m2) 32.8
0.6 32.5
0.6a 32.5
0.6a 32.3
0.6a,b 32.1
0.6a,b 32.1
0.6a
Body fat (%) 38.7
1.0 e 38.9
1.0 e 38.2
1.1a,d 38.4
1.1a,d
Trunk body fat (kg) 19.0
0.6 e 18.9
0.6 e 18.1
0.6a,d 18.2
0.6a,d
Leg fat-free mass (kg) 8.6
0.3 8.5
0.3 8.5
0.3 8.4
0.3a
Blood variables
Insulin (pmol/l) 71.1
4.9 63.8
4.2a 62.7
4.1 61.2
4.0a 63.9
4.5 71.1
6.3b
HbA1c (%) 6.11
0.11 6.00
0.10a 5.90
0.08a 5.87
0.10a,c 5.86
0.09a,b 5.73
0.07a,b,c
HOMA 3.41
0.31 2.90
0.24a 2.90
0.22 2.70
0.21a 2.91
0.27 3.28
0.40b
Apo B (g/l) 1.19
0.06 1.06
0.03 1.12
0.04 1.09
0.04 1.18
0.06 1.17
0.04
T Cholesterol (mmol/l) 5.12
0.08 5.04
0.08 4.99
0.08 5.09
0.10 5.07
0.08 4.94
0.07a
LDL-c (mmol/l) 3.13
0.08 3.02
0.07 2.79
0.07a 3.10
0.10 2.99
0.08 2.87
0.05a
hs CRP (nmol/l) 65.7
0.9 45.7
0.7a 36.2
0.5a 31.4
0.5a,c 33.3
0.5a,c 24.8
0.3a,c,d
Exercise parameters
FOMAx (g/min) 0.25
0.01 0.25
0.01 0.27
0.01b 0.29
0.01a,c 0.33
0.02a,b,c,d 0.25
0.01b
VO2peak (ml$kg1$min1) 21.5
0.7 23.4
0.8a 24.4
0.7a,b 25.7
0.8a,b,c 26.1
0.9a,c,d 23.7
0.9a,b
WMAx (watts) 138
6 156
6a 169
6a,b 181
7a,b,c 188
7a,b,c,d 178
7a,b,c,d
HRMAx (bpm) 150
3 154
3a 155
3a 156
3a 156
3a 155
3a
Values are mean
s.e. for 48 MetS subjects.
a
Significantly different from pre-training.
b
Significantly different from the previous month.
c
Significantly different than 1 month.
d
Significantly different than 2 months (all, P < 0.05).
 Author's personal copy

796 R. Mora-Rodriguez et al.

medication or their self-reported caloric intake, although

body weight was reduced by 2.1
0.4%. Of note, after 4
months of the AIT program, we did not observe a plateau
response in the factors that training improved (Fig. 3). This
suggests that an AIT program prolonged beyond 4 months
could reverse to normal clinical values three important
MetS components in most patients.
The most salient and consistent benefit of AIT was the
reduction in blood pressure that reached 12% (Table 1,
Fig. 3a) which to our knowledge, is unmatched in the
training literature in MetS patients [29]. A recent review
analyzing the effects of high-intensity interval training
suggests that 3 months of AIT are required for lowering
blood pressure with effects only visible in people not
taking antihypertensive medication [15]. In contrast, 67%
of our sample were under antihypertensive medication
and a large portion of the blood pressure reduction took
place after only 1 month of AIT (Fig. 3a; P < 0.05). Thus,

Figure 2 Effects of 4 months of training on (a), mitochondrial respi-

ration in vastus lateralis (O2 flux per mg wet weight tissue) when
adding different substrates and (b) mitochondrial respiration when
normalized for mitochondrial content (CS activity). Data are
mean
s.e. for 7 volunteers. * Significantly higher than Pre-training
(P < 0.05).

parameters were also sensitive to training discontinuation,

WMAx returning to the 3 months value, VO2peak to the 2
month value and FOMAx to pre-training values (Table 2 and
Fig. 3b).

Discussion

We monthly followed the evolution of the risk factors that

compose the metabolic syndrome (MetS) with aerobic
interval training (AIT) and its relapse with subsequent
detraining. We observed a doseeresponse relationship
between exercise training duration and improvements in
waist circumference (surrogate of abdominal obesity),
blood pressure (systolic and diastolic) and HDL-c. As a
consequence of these improvements 29% of our subjects
reduced the number of MetS factors below three (Table 1).
Thus, our data suggest that in previously sedentary MetS
Figure 3 Percent change from pre-training on (a) variables persistent
patients 4 months of an AIT program could reverse MetS in after 1 month of detraining and (b) variables that relapse with
roughly one third of this population. Of note, this outcome detraining. Data are mean
s.e. for 48 MetS subjects. * Significantly
is obtained when patients do not alter their regular different from Pre-training (P < 0.05).
 Author's personal copy
Time-course effects in patients with metabolic syndrome
our data suggest that the hypertension associated with the
MetS can be rapidly and substantially improved with AIT.
This improvement in conjunction with the increased HDL-
c lowers the cardiovascular disease mortality risk in MetS
patients that follow this AIT program.
Another of the variables most markedly improved with
AIT was cardio respiratory fitness with a 21
2% increase in
VO2peak. It has been proposed that the type of training that
result in larger increase in VO2max is the one associated
with the removal of more MetS factors [9]. Furthermore, in
a prospective study in 1226 men and women it was found
that one standard deviation increase in VO2max raised the
likelihood to resolve MetS 1.8 times [13]. We observed in
our subjects that a 1.3 SD improvement in their MetS Z
score was associated with a 1.4 SD raise in VO2peak.
Moreover, the improvements in cardio respiratory fitness
were accompanied by a 31
8% increased capacity to
oxidize fat during exercise (FOmax; Fig. 3b). Our data sup-
port that with AIT MetS patients experience the habitual
cardiovascular adaptations that improve VO2peak and the
metabolic adaptations that increase the reliance on fat as
energy substrate during exercise.
In a subset of our subjects (only seven) we studied
mitochondrial function in vivo within hours of vastus lat-
eralis muscle collection. The reason to perform this mea-
surement is that it has been suggested that mitochondrial
dysfunction may be a central cause of insulin resistance in
MetS patients as it is in T2DM patients [25]. However, our
MetS subjects greatly increased vastus lateralis oxygen flux
after 4 months of training (Fig. 2a). Those increases were
mostly due to increased mitochondrial density since when
normalize by CS activity (surrogate of mitochondrial pro-
liferation) the differences disappeared (Fig. 2b). Obese and
type 2 diabetic subjects [18] have reduced mitochondrial
density in comparison to lean controls but not O2 flux
when normalized per mitochondria unit [17]. Rather than
mitochondrial dysfunction, these sedentary populations
(e.g., our metabolic syndrome patients) seem to have un-
derdeveloped muscle mitochondrial mass that however
proliferates normally upon stimulation with AIT.
Our AIT program did not lower blood glucose below
100 mg $ dL1 (Table 1). However, HbA1c, an index of the
average plasma glucose concentration over prolonged pe-
riods of time significantly improved after AIT (Table 2). Some
studies propose the inclusion of HbA1c as an additional
factor in the definition of MetS [24]. HbA1c reduction with
the progression of training suggests that training decreased
the amount and/or magnitude of daily blood hyperglycemic
peaks. We could not detect a reduction in carbohydrate
ingestion in subject’s dietary records that could account for
the lower presence of glucose in blood. Thus, the reduced
glucose presence in hemoglobin suggests improved glucose
clearance from blood. In addition, the improvement in
HOMA (Fig. 3b) suggests that peripheral tissue insulin
sensitivity was improved by our AIT program. We observed
a significant reduction in hsPCR with exercise training along
with the early improvement in HOMA (Table 2). Our data
may support the theory of an inflammatory origin to the
carbohydrate metabolism disarrangements in MetS [30].
797
Our 4 months of AIT did not lower subject’s blood TG,
Apo B, LDL-c or total cholesterol. However, AIT increased
the capacity to oxidize fat during exercise and lowered
body fat by 0.9 kg in the trunk (Table 2). In addition, HDL-c
increased with exercise training in a progressive fashion
(Table 1) which has been shown to reduce coronary heart
diseases risk [6]. Some investigators have found tri-
glycerides resiliency to be reduced after 12e16 weeks of
AIT [15,29], while others find a lowering effect when a
Mediterranean hypocaloric diet is combined with exercise
training [8]. We have recently reported in overweight
subjects that exercise does not lower plasma triglycerides
when the diet is high in saturated fat [22]. Our training
program was neither accompanied by a reduction in di-
etary energy intake nor by restrictions in saturated fat
intake. It is possible that the combination of an exercise
training program with dieting be required to significantly
reduce blood TG and LDL-c in MetS patients.
While the improvements in body composition and
blood pressure resisted the effects of 1 month of detrain-
ing, HOMA, HDL-c, VO2peak and FOMAx returned to the
1e2 month training values (Fig. 3b). After 6 months of a
demanding training program in overweight individuals, 15
days of detraining does not completely revert the im-
provements in insulin sensitivity and HDL-c [2,27]. Either
due to our longer detraining period (1 month) or to our
shorter training program (4 months) we could not observe
remaining effects of training on insulin sensitivity. How-
ever, our data coincides on the persistent elevation of
2e3 mg$dL1 in HDL-c despite detraining. In the cited
studies as well as in the present study, subjects did not
regain body mass or body fat during detraining. It seems
that if body fat is not restored after short-term detraining
(15e30 days) some of the keys training adaptations are
preserved (i.e., blood pressure).
In conclusion, four months of aerobic interval training
progressively reduces body weight, trunk fat, blood pres-
sure and increases HDL-c which in combination greatly
lowers cardiovascular disease risk. MetS does not seem to
impede the exercise related muscle and systemic adapta-
tions to improve oxygen and fat consumption. However,
blood glucose and triglycerides did not improve and
combinations of exercise training with diet and medica-
tion should be sought. Lastly, the detraining data suggest
the importance of not regaining abdominal fat to preserve
the reductions in blood pressure.
Acknowledgments
The authors report no conflicts of interest. This work was
funded by a grant from the Spanish Ministerio of Economia
y Competitividad (grant number DEP2011-28615).
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