Substrate oxidation during exercise: Type 2 diabetes is associated with a decrease in lipid oxidation and an earlier shift towards carbohydrate utilization

CHU de Montpellier, Service central de Physiologie Clinique, Unité d'Exploration Métabolique (CERAMM), Hôpital Lapeyronie, 34000 Montpellier, France.
Diabetes & Metabolism (Impact Factor: 3.27). 01/2007; 32(6):604-10. DOI: 10.1016/S1262-3636(07)70315-4
Source: PubMed
ABSTRACT
Exercise is a recommended treatment for type 2 diabetes but the actual pattern of metabolic adaptation to exercise in this disease is poorly known and not taken in account in the protocols used. Metabolic defects involved in the pathways of substrate oxidation were described in type 2 diabetes. We hypothesized that type 2 diabetes, regardless of age, gender, training status and weight, could influence by its own the balance of substrates at exercise.
30 sedentary type 2 diabetic subjects and 38 sedentary matched control subjects were recruited. We used exercise calorimetry to determine lipid and carbohydrate oxidation rates. We calculated two parameters quantifying the balance of substrates induced by increasing exercise intensity: the maximal lipid oxidation point (PLipoxMax) and the Crossover point (COP), intensity from which the part of carbohydrate utilization providing energy becomes predominant on lipid oxidation.
Lipid oxidation was lower in the diabetic group, independent of exercise intensity. PLipoxMax and COP were lower in the diabetic group [PLipoxMax=25.3+/-1.4% vs. 36.6+/-1.7% %Wmax (P<0.0001)] - COP =24.2+/-2.2% vs. 38.8+/-1.9% %Wmax (P<0.0001).
Type 2 diabetes is associated with a decrease in lipid oxidation at exercise and a shift towards a predominance of carbohydrate oxidation for exercise intensities lower than in control subjects. Taking into account these alterations could provide a basis for personalizing training intensity.

Full-text

Available from: Jean Frederic Brun
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Diabetes Metab 2006;32:604-610 • www.masson.fr/revues/dm
O RIGINAL ARTICLE
Substrate oxidation during exercise:
type 2 diabetes is associated
with a decrease in lipid oxidation
and an earlier shift towards carbohydrate
utilization
E Ghanassia, JF Brun, C Fedou, E Raynaud, J Mercier
S UMMARY
Objectives: Exercise is a recommended treatment for type 2 diabetes
but the actual pattern of metabolic adaptation to exercise in this di-
sease is poorly known and not taken in account in the protocols
used. Metabolic defects involved in the pathways of substrate oxida-
tion were described in type 2 diabetes. We hypothesized that type 2
diabetes, regardless of age, gender, training status and weight, could
influence by its own the balance of substrates at exercise.
Methods: 30 sedentary type 2 diabetic subjects and 38 sedentary
matched control subjects were recruited. We used exercise calorime-
try to determine lipid and carbohydrate oxidation rates. We calcu-
lated two parameters quantifying the balance of substrates induced
by increasing exercise intensity: the maximal lipid oxidation point
(PLipoxMax) and the Crossover point (COP), intensity from which
the part of carbohydrate utilization providing energy becomes pre-
dominant on lipid oxidation.
Results: Lipid oxidation was lower in the diabetic group, independent
of exercise intensity. PLipoxMax and COP were lower in the diabetic
group [PLipoxMax=25.3±1.4% vs. 36.6±1.7% %Wmax (P<0.0001)]
– COP =24.2±2.2% vs. 38.8±1.9% %Wmax (P<0.0001).
Conclusions: Type 2 diabetes is associated with a decrease in lipid
oxidation at exercise and a shift towards a predominance of carbohy-
drate oxidation for exercise intensities lower than in control subjects.
Taking into account these alterations could provide a basis for per-
sonalizing training intensity.
Key-words: Type 2 diabetes
· Training intensity · Substrate
oxidation
· Crossover point.
R ÉSUMÉ
Objectifs : L’activité physique est recommandée dans le traitement
du diabète de type 2 mais l’adaptation métabolique à l’exercice chez
le diabétique est encore mal connue et n’est pas prise en compte
dans les divers protocoles de réentraînement. Plusieurs anomalies
des voies d’oxydation de substrats ont été décrites dans le diabète de
type 2. Nous avons émis l’hypothèse que le diabète de type 2 est
associé à des modifications de l’utilisation des substrats à l’exercice,
indépendamment de l’âge, du sexe, du poids et du niveau d’activité
physique.
Méthodes : 30 sujets sédentaires ayant un diabète de type 2 et
38 sujets non diabétiques appariés ont été recrutés. Nous avons
mesuré les taux d’oxydation des lipides et des glucides à l’exercice
par calorimétrie indirecte. Nous avons également calculé deux para-
mètres quantifiant l’utilisation respective de ces substrats en fonction
de l’intensité croissante de l’effort : le point d’utilisation maximale
des lipides (PLipoxMax) et le point de croisement (COP), niveau
d’effort à partir duquel la contribution des glucides à la production
d’énergie devient prédominante sur la contribution des lipides.
Résultats : l’oxydation des lipides était diminuée chez les sujets dia-
bétiques à tous les paliers d’efforts. Le PLipoxMax et le COP étaient
diminués chez les sujets [PLipoxMax = 25,3 ± 1,4 % vs 36,6 ± 1.7 %
% Wmax (P < 0,0001)] – COP = 24,2 ± 2,2 % vs 38,8 ± 1,9 %
% Wmax (P < 0,0001).
Conclusions : Les sujets diabétiques sédentaires présentent une
diminution de l’oxydation des lipides à l’exercice et une utilisation
prédominante des glucides pour des niveaux d’exercice moindres
que les sujets non diabétiques sédentaires appariés pour le poids,
l’âge et le sexe. La prise en compte de ces spécificités pourrait four-
nir les bases théoriques nécessaires à l’individualisation de l’intensité
d’effort optimale.
Mots-clés : Diabète de type 2 · Intensité d’effort · Oxydation des
substrats · Point de croisement.
Ghanassia E, Brun JF, Fedou C, Raynaud E, Mercier J. Substrate
oxidation during exercise: type 2 diabetes is associated with a
decrease in lipid oxidation and an earlier shift towards carbohydrate
utilization
Diabetes Metab 2006;32:604-610
CHU de Montpellier, Service central de Physiologie Clinique,
Unité d’Exploration Métabolique (CERAMM), Hôpital Lapeyronie,
34000 Montpellier, France.
Oxydation des substrats lors de l’exercice :
le diabète de type 2 est associé à une diminution
de l’oxydation des lipides et à une utilisation
prédominante des glucides pour une moindre
intensité d’exercice
Address correspondence and reprint requests to:
E Ghanassia. Service central de Physiologie Clinique, CERAMM,
CHU de Montpellier, Hôpital Lapeyronie, 371, avenue Gaston Giraud,
34295 Montpellier Cedex 5, France.
eghanassia@aol.com
Received: March 28th, 2006; accepted: June 12th, 2006.
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xercise training has been recently demonstrated
to be a powerful treatment for the prevention
of type 2 diabetes (T2D) [1,2] and appears to be
also promising for correcting most metabolic defects such
as insulin resistance [3] and lipid disorders [4].
However, some degree of controversy remains about its
impact on glycaemic control [5] and may be related to dif-
ferences in protocols applied by various investigators. In
fact, these exercise protocols have generally been defined
according to theoretical concepts of exercise physiology,
while the actual pattern of metabolic adaptation to exercise
in patients suffering from T2D appears to be uncompletely
known.
Since specific metabolic defects in the pathways
involved in carbohydrate (CHO) and lipid oxidation have
been described in T2D, we hypothesized that, indepen-
dently of obesity, sedentarity and aging, T2D could influ-
ence substrate balance at exercise by its own.
In obese patients, we have developed a specific protocol
of exercise calorimetry, designed to target training at a level
at which the ability to oxidize lipids reaches a maximum
[6]. Such a targeted training protocol has been shown to
improve the ability to oxidize lipids and to reduce fat mass
in both adult [7] and adolescent subjects [8], resulting in
metabolic improvements including an increase in insulin
sensitivity which is expected to improve glycaemic control
in subjects with T2D. However, in T2D, optimizing CHO
oxidation could be another way of normalizing glycaemia.
So, before extending the protocol we successfully used
in obese subjects to T2D, it was necessary to investigate
the effect of diabetes by its own on the respective percent-
age of lipids and CHO oxidized at various exercise inten-
sities. This study was thus undertaken in order to describe
the specific pattern of balance of substrates at exercise in
T2D, which would represent a basis to propose targeted
exercise.
Using exercise calorimetry we aimed at investigating
substrate utilization at various exercise intensities in a
group of sedentary diabetic subjects and at comparing them
with a group of sedentary control subjects matched for age,
sex and BMI.
Subjects, materials and methods
Subjects
We recruited 30 subjects with non insulin-requiring
T2D and 38 subjects with non impaired glucose tolerance
who came to our unit for a metabolic check-up. They were
aged 40 to 65, sedentary (<2 hours of physical activity per
week, including the everyday life) and overweight
(BMI>25 kg/m
2
).
Subjects with coronary heart disease, retinopathy, lung or
muscular disease and those suffering from a disability pre-
venting them from performing exercise testing (peripheral
vascular disease, arthropathy) were excluded. Subjects with
no data available concerning these criteria were also
excluded. T2D was diagnosed using the criteria of the
American Diabetes Association [9] and all control subjects
had an oral glucose tolerance test (OGTT) performed dur-
ing the previous year or between inclusion and the day of
the test. Diabetic subjects treated with insulin or glitazones
were also excluded.
All patients received detailed printed and oral informa-
tion and gave their informed consent. The protocol was
approved by the local ethics committee according to French
legislation (law of March 5, 2002, N° 2002-1138 describing
the rights of patients and the quality of the French health
care system, and modifying the “Huriet-Sérusclat” law
(N° 88-1138) which regulates biomedical research proto-
cols.).
Anthropometric measurements
The day of the test, we measured weight (W), size (S),
waist and hip circumferences (WC, HC). Waist to Hip
Ratio (WHR) and BMI (W/S
2
in kg/m
2
) were calculated.
Body composition was assessed with a multifrequency
bioelectrical impedancemeter (Dietosystem Human IM
Scan) that uses low intensity (100-800 µA) at the following
frequencies : 1, 5, 10, 50 and 100 kHz. Analysis was per-
formed with the software Master 1.0.
Biochemical analysis
In addition to the tests asked by their physician, all sub-
jects were screened for fasting glycaemia. Plasma glucose
was determined with a Vitros Product Chemistry Analyzer
(Johnson & Johnson, Clinical Diagnostics, Rochester, USA)
with routine well-standardized procedures.
Exercise testing
All subjects were asked to come and perform the testing
in the morning after an overnight fast (at least 12 hours).
As generally used to individualize the increment of
exercise intensity during cardiopulmonary exercise testing,
the theoretical maximal aerobic power (Wmax), corre-
sponding to the power reached when theoretical VO
2
max
is reached, was calculated from Wassermann’s equations
modified for overweight subjects [10].
The test consisted on five six minute steady-state work-
loads at 20, 30, 40, 50, and 60% of Wmax. Consequently,
they underwent a test with the same relative incremental
workload and were compared at the same percentage of
their Wmax.
The subjects performed the test on an electromagneti-
cally braked cycle ergometer (Ergoline Bosch 500). Heart
rate and electrocardiographic parameters were monitored
continuously throughout the test by standard 12-lead
E
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procedures. Metabolic and ventilatory responses were
assessed using a digital computer based breath to breath
exercise analyzing system (CPX Medical Graphics, Minne-
apolis, Minnesota, USA). Thus we could measure VO
2
,
VCO
2
(in ml/min) and calculate the non-protein respira-
tory quotient (RER=VCO
2
/ VO
2
).
Calculation of substrate utilization,
COP and PLipoxmax
Lipid oxidation (Lipox) and carbohydrate utilization
(Glucox) rates were calculated by indirect calorimetry from
gas exchange measurements according to the non-protein
respiratory quotient technique and using Peronnet and
Massicote’s equations [11]:
– Glucox (mg/min)=4,585xVCO
2
– 3,2255xVO
2
– Lipox (mg/min)=1,6946xVO
2
– 1,7012xVCO
2
VO
2
and VCO
2
were determined as the mean of meas-
urements during the fifth and sixth minutes of each step,
where CO
2
production from bicarbonates to compensate
for lactate acidosis becomes negligible [12].
This technique provided carbohydrate and lipid oxida-
tion rates at different exercise intensities. These values were
then converted in Kcal/min.
Additionally, after smoothing the curves, we calculated
the two parameters quantifying the balance between carbo-
hydrates and lipids induced by increasing exercise intensity:
the maximal lipid oxidation point (PLipoxmax) and the
Crossover Point (COP).
The PLipoxMax is the exercise intensity at which lipid
oxidation reaches its maximal level before decreasing while
carbohydrate utilization further increases. It is calculated as
previously reported after smoothing of the curve plotting
lipid oxidation as a function of power [6].
The crossover point (COP) is the exercise intensity at
which the part of carbohydrate utilization used to provide
energy becomes predominant over lipid oxidation. Beyond
this point, the subject is referred to as “glucodependent”. It
was calculated as the exercise intensity where 70% of the
substrates used to provide energy are carbohydrates and
30% are lipids, according to Brooks [13].
The PLipoxmax and the COP were expressed either in
absolute power values (Watts) or in percentage of the theo-
retical Wmax.
Validity and reproducibility of this test were assessed in
a previous publication. Coefficients of variation (CV) were
calculated for RER, PLipoxMax and COP at four different
intensities. CV of RER were between 2.8 and 4.75%. CV of
PLipoxMax and COP was respectively 11.41%Wmax and
11.63%Wmax. VO
2
, CO
2
, RER, CHO and lipid oxidation
rates were also compared during the incremental test and
during steady-state workloads of the same intensity per-
formed isolately and at random order. These parameters
were not significantly different [6].
Statistical analysis
Results are given as mean ± standard error of the mean
(SEM). Normality each parameter’s distribution was
assessed using the Shapiro-Wilk test.
If normality was established, we used the Student’s t test
for unmatched series. If normality was not established, we
used the non-parametric Mann-Whitney’s U test. Signifi-
cance was set at P<0.05.
All calculations were performed with the software
Xlstat-pro 7.5 (Addinsoft Software, Paris, France).
Results
Subjects characteristics
Anthropometric measurements are given in table I.
There were no significant differences for age, BMI, fat-free
mass, percentage of fat mass and Wmax (expressed in
Watts or adjusted to fat-free mass and expressed in W/Kg
of fat-free mass). WHR tended to be higher in the diabetic
group but the difference was not significant. Sex ratio was
Table I
Characteristics of subjects (Values expressed as mean±SEM; BMI=Body mass Index; WHR=Waist/Hip circumferences Ratio;
Wmax=Theoretical maximal aerobic power).
Diabetic subjects Control subjects
All (n=30) Men (n=18) Women (n=12) All (n=38) Men (n=23) Women (n=15)
Age (years) 54±1.6 56.2±1.9 51.8±354±1.5 53.4±1.5 54.9±2.2
BMI (kg/m
2
) 30.4±0.6 30.8±0.8 29.8±0.7 30.6±0.6 30.4±0.8 30.9±0.9
WHR 0.97±0.01 1±0.02 0.92±0.02 0.93±0.02 0.97±0.01 0.87±0.02
Fat mass (% of weight) 34.5±1.1 31±1.2 39.7±1.1 33.3±1.3 28.7±1.2 40.4±1.6
Fat-free mass (kg) 55.4±2.1 63.8±1.6 44±1.1 58.3±1.8 65.9±1.2 46.6±1.3
Wmax (W) 149±8.1 174.7±7.5 106.2±3.8 151.2±6.3 177.1±5.6 111.5±2.6
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identical in both groups and no differences in any parame-
ters were reported when gender was taken into account.
Every subject completed the entire exercise protocol.
Fasting glycaemia was 8.44±0.37 mmol/l in the diabetic
subjects group and 5.18±0.07 mmol/l in the control subjects
group.
Ventilatory parameters
Results are given in table II.
VO
2
was not significantly different between the two
groups, at rest or during any workload step, even after
adjustment to fat-free mass.
RER was not significantly different between the two
groups at rest but was significantly higher in the diabetic
group, at every workload step (P<0.05).
Parameters of substrate utilization
Lipid oxidation rate (Lipox) at rest was not signifi-
cantly different between the two groups. In contrast, dur-
ing exercise, whatever the exercise intensity, Lipox was
significantly lower in the diabetic group (figure 1A). The
difference remained significant even when expressed in
ml
-1
.min
-1
.kg
fat-free mass
-1
(figure 1B).
The COP was significantly lower in the diabetic group:
24.2±2.2% vs. 38.8±1.9% %Wmax (P<0.0001). The PLipox-
Max was also significantly lower in the diabetic group:
25.3±1.4% vs. 36.6±1.7% %Wmax (P<0.0001). These differ-
ences remained significant even when gender was taken
into account (figures 2 and 3).
Fasting glycaemia was positively correlated with COP
(r=0.54, P<0.05) and PLipoxMax (r=0.5, P<0.05).
Discussion
This study aimed at determining the parameters of sub-
strate utilization at various exercise intensities in a group of
sedentary subjects with T2D and at comparing them with a
group of sedentary subjects without impaired glucose tolerance
matched for age, sex and weight. Our results demonstrate that
subjects with T2D exhibit a decrease in lipid oxidation and
a predominance of carbohydrate utilization occurring at lower
intensities when compared to control subjects.
Table II
Comparisons of VO
2
and R between diabetic subjects and control subjects at rest and during each workload step (Values expressed in
mean ±SEM; *P<0.05; **P<0.01 – Mann-Whitney’s test).
VO
2
(ml/min) VO
2
(ml/min/kg fat-free mass) RER
Diabetic subjects Control subjects Diabetic subjects Control subjects Diabetic subjects Control subjects
Rest 341.3±5.6 321.8±17.5 6.2±0.2 5.8±0.3 0.83±0.01 0.83±0.01
20%Wmax 843.6±43.7 832.1±29.2 15.2±0.6 14.3±0.3 0.9±0.01** 0.85±0.01
30%Wmax 1021.7±59.2 979.5±34.2 18.3±0.7 17.1±0.4 0.94±0.02** 0.9±0.008
40%Wmax 1143.9±78.5 1205.5±49.3 21.1±1 20.4±0.6 0.95±0.01* 0.92±0.007
50%Wmax 1390.5±90.5 1388±54.5 25.2±1.1 23.3±0.7 0.99±0.02** 0.94±0.004
60%Wmax 1601±110.5 1574±72 29.2±2.6 26.6±0.7 1±0.02** 0.95±0.006
Figure 1
A: Lipid oxidation rates at rest and during exercise in diabetics and con-
trols (Values expressed in mean ±SEM; * P<0.05; ** P<0.005 – Stu-
dent’s t test). B: Lipid oxidation rates at rest and during exercise in
diabetic and control (Values expressed in mean ±SEM; * P<0.05; **
P<0.005 – Mann-Whitney’s test).
A
B
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Weight and training status interfere with the balance of
substrate oxidation [6]. Our two groups were matched for
age, BMI and training status. Thus, these parameters can-
not explain our results. The exercise testing we used has
already been described and its validity and reproducibility
are assessed in a previous study [6].
Lipid oxidation rates were significantly lower at any
exercise intensity in the diabetic group and the difference
remained significant even after adjustment for fat-free
mass. The PLipoxMax was also lower in the diabetic group.
Consequently, maximal capacity of lipid oxidation is
decreased in subjects with T2D. Our results contrast with
those of previous studies [14,15] which did not conclude to a
significant difference in lipid oxidation rates between dia-
betic and control subjects. However, the number of subjects
was likely too small for a significant difference to appear.
Moreover, those protocols were realized at one or two exer-
cise intensities and subjects were not always matched for
weight. As a matter of fact, the effects of exercise intensity
on substrate utilization could not be studied.
The COP was significantly lower in subjects with T2D.
Consequently, these subjects become glucodependent for
exercise intensities lower than matched control subjects
with normal glucose tolerance.
We conclude that T2D is associated with an alteration
of substrate utilization during exercise with a decrease in
lipid oxidation and an earlier shift towards a predominance
of CHO oxidation for exercise intensities lower than sub-
jects without impaired glucose tolerance. These results can-
not be explained by either sex, age, weight or training
status. Thus, we assume that metabolic defects specific to
T2D can be responsible for these alterations.
Considering published data about substrate metabolism
during exercise, it is noticeable that they often show dis-
cordant results. Two facts are likely to explain this: first,
protocols designed for these studies use different frequen-
cies, durations, intensities, exercise types and subjects are
not always matched for their sex, age or training status.
Next, phenomena well established in the resting state are
sometimes extrapolated to the exercising state.
Two mechanisms resulting from exercise seems to initi-
ate metabolic adaptations: muscular contraction and cate-
cholamines production [16]. They cause a decrease in
insulin secretion and a variable increase in glucagon pro-
duction through neural afferences and α-adrenergic action.
Then, energy substrate availability is increased with an
increase in EGP and glucose uptake the synchronization of
which leads to a remarkable maintain in glycaemia whereas
decreased insulin-induced lipolysis provides a flux of non-
esterified fatty acids. Inside muscle, substrate interactions,
certainly different from what is described at rest such as
Randle’s glucose / fatty acid cycle or Winders’ “Reverse
Randle’s cycle”, modulate the proportion of CHO and lip-
ids getting to mitochondria [17,18].
Defects in insulin secretion and hyperglycaemia, specific
to T2D, are likely to interfere with all those mechanisms.
Defect in insulin secretion is a major characteristic of
T2D. Its effects on substrate utilization during exercise in
T2D remain poorly known. Muscular glucose uptake is
decreased in subjects with type 1 diabetes despite norma-
lized blood glucose and insulin levels [19]. However, in con-
trast with type 1 diabetes, insulinopenia is not absolute in
T2D. Insulin secretion slowly deteriorates at various speeds
depending of many factors such as the exposition of beta
cells to glucotoxicity or lipotoxicity [20]. Further studies
should be designed to quantify insulin secretion and kine-
tics during exercise and to determine their influence on
substrate utilization.
Muscular substrate utilization is also influenced by the
availability of these substrates. As shown in normal sub-
jects, an increase in glucose availability causes a relative
increase in glucose oxidation compared with lipid oxidation
Figure 2
Comparison of the crossover point expressed in %Wmax chez in diabetic
and control subjects (Values expressed in mean ±SEM; * P<0.05;
** P<0.0001 – Student’s t test).
Figure 3
Comparison of the maximal lipid oxidation point expressed in %Wmax
chez in diabetic and control subjects (Values expressed in mean ±SEM;
* P<0.05; ** P<0.0001 – Student’s t test).
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[21]. Similarly, an increase in lipid availability causes an
increase in muscular fatty acid oxidation [22]. Hyperglycae-
mia and lipid disorders are frequently associated in T2D
and are both likely to interfere with substrate utilization
with regard to their blood levels. According to our results,
fasting glycaemia before exercise is positively correlated to
COP and PLipoxMax in subjects with T2D.
Many abnormalities are described in the skeletal muscle
of subjects with insulin resistance [23]. However, effects of
insulin resistance on substrate utilization during exercise
have been poorly studied. Previous works are very few,
with too small a number of subjects and were not designed
to delineate the effects of obesity, T2D and insulin resis-
tance by their own on substrate utilization. Once more,
they used only one exercise intensity and cannot establish a
pattern of substrate utilization at various exercise intensi-
ties.
Recent guidelines recommend, in T2D, endurance
training, at least 3 times a week, during 45 minutes (inclu-
ding a 5 minutes warm-up) at exercise intensities between
50 and 70% of Wmax [24,25]. These values, used by most
studies referred to in these guidelines, appear to have been
arbitrarily set. There seems to be no clear scientific evi-
dence of a specific efficiency of training at these intensities
rather than others in T2D.
Since the UKPDS, we know that an optimal glycaemic
control with an HbA
1c
<7% is crucial for preventing
microangiopathic and neuropathic complications and
greatly contributes to decrease cardiovascular events in
T2D [26]. If physical activity is used as a specific therapy, it
is mandatory to individualize an exercise intensity aiming
at an optimal glycaemic control and the already proven
benefits on cardiovascular events, other metabolic defects
and general well-being.
Overweight status can contribute to impaired glucose
tolerance and cardiovascular events in T2D. The use of
parameters allowing the individualization of an exercise
intensity at which lipid oxidation is maximal (such as the
PLipoxMax) or at which there is a compromise between
carbohydrate and lipid oxidation (such as the COP) seems
logical. According to a recent study from our group, a
2-months training at the PLipoxMax of subjects with the
metabolic syndrome results in a decrease in BMI, waist cir-
cumference and improves insulin sensibility, lipid oxidation
with an increase in PLipoxmax and COP [7].
Moreover, efficiency of physical activity on T2D is
dependent on the subject’s long-term adherence to training.
Many factors, specific to the patient or his environment can
explain the lack of adherence. The use of PLipoxmax or
COP as training intensity has two advantages likely to
improve adherence. First, the feeling of the activity as
strenuous or painful can result in training discontinuation.
On the other hand, the intensities proposed by the guide-
lines are particularly high for such subjects cumulating fac-
tors of unconditionning as sedentarity or muscular
abnormalities associated to insulin resistance. As far as
the PLipoxMax and the COP are at lower ranges of values,
the initial intensity of training would make it much easier
to perform. Next, individualizing the training, whatever
the way of choosing intensity, has proven effective for
improving long-term adherence, whatever the behaviour
asked to be changed [27].
However, improving insulin sensitivity and lipid oxida-
tion is obviously not the only way of improving glycaemic
control and the use of the COP or the PLipoxMax to set
training intensity must prove its efficiency compared to the
guidelines. A randomized controlled prospective study
assessing the short-term and long-term effects of an indi-
vidualized training using the COP, the PLipoxMax or per-
haps another workload individually determined and
compared to a training using the guidelines’ intensities is
necessary. Such a study should also assess the effects on
long-term adherence to individualized training compared
to training based on general theoretical guidelines.
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    • "Several studies have reported that fat oxidation decreases in patients with metabolic diseases [19,23] and that fat oxidation decreases more with exercise intensity in T2DM patients than in the control groups. Previous studies have also suggested that the range of Fatmax occurs from the 33% to 65% VO2 max exercise intensity recommended for Fatmax [1,24]. A review and meta-analyses on the use of calorimetry during exercise reported that the exercise intensity corresponding to Fatmax is approximately 55% to 75% of VO2 max intensity in the healthy group [13,25] . "
    [Show abstract] [Hide abstract] ABSTRACT: The purpose of this study was to determine the appropriate exercise intensity associated with maximum fat oxidation, improvement of body composition, and metabolic status in Korean women with type 2 diabetes mellitus (T2DM). The study included a T2DM group (12 women) and a control group (12 women). The groups were matched in age and body mass index. The subjects performed a graded exercise test on a cycle ergometer to measure their maximal fat oxidation (Fatmax). We also measured their body composition, metabolic profiles, and mitochondrial DNA (mtDNA). The exercise intensity for Fatmax was significantly lower in the T2DM group (34.19% maximal oxygen uptake [VO2 max]) than the control group (51.80% VO2 max). Additionally, the rate of fat oxidation during exercise (P<0.05) and mtDNA (P<0.05) were significantly lower in the T2DM group than the control group. The VO2 max level (P<0.001) and the insulin level (P<0.05) were positively correlated with the rate of fat oxidation. The results of this study suggest lower exercise intensity that achieves Fatmax is recommended for improving fat oxidation and enhancing fitness levels in Korean women with T2DM. Our data could be useful when considering an exercise regimen to improve health and fitness.
    Full-text · Article · Aug 2015 · Diabetes & metabolism journal
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    • "Lipid oxidation was lower in T2D. Maximal lipid oxidation point and the crossover point were lower in T2D Lima et al [26] T2D = 9 CG = 11 20 min of cycle ergometer at 90% LT, increasing exercise intensity and control session T2D have a better fat oxidation after high-intensity exercise than moderate exercise. T2D had less fat oxidation than CG after moderate exercise Motta et al [ Resistance exercise circuit at 43% and 23% 1RM (approximately 25 min), and control session 43% 1RM promoted PEH, whereas the 23% did not "
    [Show abstract] [Hide abstract] ABSTRACT: The literature has shown the efficiency of exercise in the control of type 2 diabetes (T2D), being suggested as one of the best kinds of non-pharmacological treatments for its population. Thus, the scientific production related to this phenomenon has growing exponentially. However, despite its advances, still there is a lack of studies that have carried out a review on the acute effects of physical exercise on metabolic and hemodynamic markers and possible control mechanisms of these indicators in individuals with T2D, not to mention that in a related way, these themes have been very little studied today. Therefore, the aim of this study was to organize and analyze the current scientific production about the acute effects of physical exercise on metabolic and hemodynamic markers and possible control mechanisms of these indicators in T2D individuals. For such, a research with the following keywords was performed: -exercise; diabetes and post-exercise hypotension; diabetes and excess post-exercise oxygen consumption; diabetes and acute effects in PUBMED, SCIELO and HIGHWIRE databases. From the analyzed studies, it is possible to conclude that, a single exercise session can promote an increase in the bioavailability of nitric oxide and elicit decreases in postexercise blood pressure. Furthermore, the metabolic stress from physical exercise can increase the oxidation of carbohydrate during the exercise and keep it, in high levels, the post exercise consumption of O², this phenomenon increases the rate of fat oxidation during recovery periods after exercise, improves glucose tolerance and insulin sensitivity and reduces glycemia between 2-72 h, which seems to be dependent on the exercise intensity and duration of the effort.
    Full-text · Article · Oct 2014
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    • "Après lissage de la courbe en cloche entre la puissance de l'exercice (en % de PMA) et l'oxydation lipidique (Lox), on peut calculer la puissance pour laquelle l'utilisation des lipides est maximale (débit d'oxydation maximale lipidique ), qui est le point o` u la dérivée de cette courbe s'annule (Ghanassia, Brun, Fedou, Raynaud, & Mercier, 2006) (Fig. 2). "
    Full-text · Article · Jan 2014 · Movement and Sports Sciences - Science et Motricite
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