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Department of Human Biology, Nutrition, Toxicology, and Environmental Research Institute, Maastricht University, 6200 MD Maastricht, The Netherlands
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The present
study investigated the effect of exercise training at different
intensities on fat oxidation in obese men. Twenty-four healthy male
obese subjects were randomly divided in either a low- [40% maximal
oxygen consumption (
O2 max)] or
high-intensity exercise training program (70%
O2 max) for 12 wk, or a nonexercising
control group. Before and after the intervention, measurements of fat
metabolism at rest and during exercise were performed by using indirect
calorimetry, [U-13C]palmitate, and
[1,2-13C]acetate. Furthermore, body composition and
maximal aerobic capacity were measured. Total fat oxidation did not
change at rest in any group. During exercise, after low-intensity
exercise training, fat oxidation was increased by 40%
(P < 0.05) because of an increased non-plasma fatty
acid oxidation (P < 0.05). High-intensity exercise training did not affect total fat oxidation during exercise. Changes in
fat oxidation were not significantly different among groups. It was
concluded that low-intensity exercise training in obese subjects seemed
to increase fat oxidation during exercise but not at rest. No effect of
high-intensity exercise training on fat oxidation could be shown.
low intensity; stable isotopes; acetate correction factor; [13C]palmitate
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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OBESITY IS
ASSOCIATED with an impaired ability to use fat as a fuel. This
may contribute to the development and maintenance of large fat stores.
Upper body obesity is associated with an impaired postabsorptive free
fatty acid (FFA) utilization in skeletal muscle in women
(6). Isoprenaline-induced fat oxidation and skeletal
muscle FFA uptake are impaired in obese men, and no improvement was
found after weight loss (1-3). Lean, formerly obese
women have lower fasting fat oxidation rates compared with lean,
never-obese women (32). Moreover, in Pima Indians, a
population with a high prevalence of obesity, weight gain is
association with a low 24-h fat-to-carbohydrate oxidation ratio
(49). Several explanations have been proposed for this
reduced fat utilization in obesity, such as a low activity of enzymes
of 
-oxidation (50), low skeletal muscle lipoprotein
lipase activity (7), and impaired mobilization of fat
stores (1). Interventions that will increase the capacity of the skeletal muscle to utilize fat may, therefore, make an important
contribution to weight management in obese individuals and individuals
at risk for obesity.
Endurance exercise training is known to increase fat oxidation during submaximal exercise at a fixed workload in lean subjects (14, 17, 23, 30, 38). Cross-sectional studies also report higher fat oxidation during exercise after an overnight fast (18, 20, 21, 40, 45) or with glucose (19, 47) in trained compared with sedentary men. Some studies also found an enhanced resting fat oxidation after endurance training (5, 31, 34). Thus endurance exercise training appears to have the capacity to increase fat oxidation in lean subjects.
However, all studies reporting an effect of exercise training on fat
metabolism involved moderate- to high-intensity (HI) exercise training
[60% maximal oxygen consumption
(O2 max)]. No studies with lower
training intensities have been performed. In the obese population,
low-intensity (LI) exercise training may be preferable to HI exercise
training because of a lower risk of musculoskeletal injuries and better
adherence. The impaired ability for fat mobilization and utilization in
obese subjects might implicate that exercise training has a different
effect on fat oxidation in obese compared with lean subjects. Because, during LI exercise, the proportion of lipids in the fuel mix oxidized is greater than during HI exercise (4), LI exercise
training might improve the ability to oxidize fat more than HI exercise training. Therefore, the hypothesis of the present study is that fat
metabolism of obese subjects can be improved by LI rather than HI
exercise training. The present study compares the effects of LI (40%
O2 max) and HI (70%
O2 max) endurance training on fat
metabolism in obese men. The energy expenditure per training session
was kept the same with LI and HI training, which meant that training
sessions were twice as long in the LI program than in the HI program.
Because fat oxidation (in g/min) is approximately the same during
exercise at 40 and 70% O2 max (16), total fat oxidation during the LI exercise sessions
was twice that of the HI exercise sessions. The study was advertised as
a training study, not as a weight-loss or weight-management study, in
an attempt to prevent weight and body composition changes that might
interfere with the effects of training on fat metabolism.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects
Twenty-four obese male subjects participated in this study. Physical characteristics are indicated in Table 1. All subjects were in good health, as assessed by medical history and physical examination. They did not take medication known to influence the variables measured and had a stable body weight (<3 kg change) during 2 mo before selection. Subjects did not spend more than 2 h/wk in sports activities and had no physically demanding jobs. Subjects were matched in groups of three for age, body mass index, fat percentage, andO2 max
per kilogram fat-free mass. Members of each group were subsequently
randomly divided into three groups: the LI or HI exercise training
group or the control (C) group. Subjects were requested to maintain
their dietary habits during the study. The study protocol was approved
by the Ethics Committee of Maastricht University. Written, informed
consent was obtained from all subjects.
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Experimental Design
Two of the three groups participated in an exercise-training intervention of 12 wk. The third group served as a nontraining C group. Measurements of body composition,O2 max, and fat metabolism were made
before the start of the exercise-training program and repeated within 2 wk after 12 wk of exercise training. The exercise training program was
continued until all measurements were performed.
Exercise Training
The exercise training program consisted of cycling on an ergometer (Bodyguard Cardiocycle, Sandnes, Norway, or Excalibur, Lode, Groningen, The Netherlands) at either LI (40% of predeterminedO2 max) or HI (70% of predetermined
O2 max). Eight subjects participated in
the LI and eight subjects in the HI training program. Subjects trained
during 12 wk, three times per week. Energy expenditure of each subject
in each training session was 5 kcal/kg fat free mass (~350 kcal).
Training duration for subjects in the LI and HI training program was
57.1 ± 8.0 and 32.8 ± 2.5 min, respectively. Heart rate was
monitored continuously during the training sessions (Polar Electro, Oy,
Finland). After 4 and 8 wk of exercise training, a
O2 max exercise test was performed, and
the training workload and duration were adjusted if necessary. All
training sessions took place at the laboratory under the supervision of
a professional instructor.
Measurements
Body composition. Subjects were weighed on a digital balance accurate to 0.1 kg (Sauter D-7470, Ebingen, Germany). Height was measured to the nearest 0.1 cm by using a wall-mounted stadiometer (Seca, model 220, Hamburg, Germany). Body density was measured by hydrostatic weighing, with correction for residual lung volume measured by helium dilution with a spirometer (Volugraph 2000, Mijnhardt, The Netherlands) at the moment of underwater weighing. Body composition was calculated according to the formula of Siri (41).
O2 max.
O2 max for each subject was determined
by an incremental exercise test on an electromagnetically braked cycle
ergometer (Excalibur, Lode). After a warming-up period of 5 min at 100 W, workload was increased every 4 min by 40 W until exhaustion. During the experiment, ventilatory and gas exchange responses were measured continuously by using indirect calorimetry (Oxycon , Mijnhardt, The
Netherlands). Heart rate was recorded continuously by an
electrocardiogram. The highest oxygen uptake achieved over 30 s
was taken as O2 max.
Measurements of fat oxidation and rate of appearance of FFA during rest and exercise. Fat metabolism was studied by means of indirect calorimetry and stable isotope tracer methodology. To study fat metabolism, all subjects participated in two tracer tests before and after the training intervention, in which palmitate and acetate, respectively, were infused. The acetate-infusion test was performed to obtain a correction factor for the loss of 13C label in the tricarboxylic acid cycle. Tracer tests were separated by a week to prevent carry over of the label. The sequence of the tracer tests was random. Subjects filled in a food and exercise questionnaire 3 days before the first tracer test. They were instructed to adjust to the same food and exercise habits 3 days before the second tracer test and the tracer tests after the training intervention to exclude bias by these factors.
[U-13C]palmitate Infusion
This experiment was performed at least 36 h after the last exercise bout. Subjects were asked to refrain from consuming naturally 13C-enriched food products for 1 wk before the experiment. After an overnight fast, subjects came to the laboratory by car or bus. Subjects remained in semi-supine position throughout the first 2.5 h of the experiment. Catheters were inserted in an arm vein for infusion of the palmitate tracer and retrogradely into a contralateral dorsal hand vein for blood sampling. The cannulated hand was placed in a hot box, in which warm air of 60°C circulated, to obtain arterialized venous blood. A baseline arterialized blood sample was taken after 30 min. Baseline expired breath was sampled in a 15-ml vacutainer tube (Becton Dickinson, Meyland Cedex, France) to determine background enrichment.Immediately after baseline samples were obtained, subjects were given
an intravenous dose of 1.0 µmol/kg NaH13CO3
to prime the bicarbonate pool. A constant infusion 0.0053 µmol · kg
1 · min1
[U-13C]palmitate was then started [time
(t) = 0] by using IVAC pumps (IVAC Medical,
Amersfoort, The Netherlands). These infusions were continued for 120 min with the subjects in a semi-supine position. Subsequently, subjects
started to exercise in a sitting position for 1 h at 50% of
pretraining O2 max on a cycle ergometer (Excalibur, Lode). The infusion rate during exercise was doubled to
minimize changes in isotopic enrichment.
Carbon dioxide consumption (CO2) and
oxygen consumption (O2) were measured by
using an open-circuit ventilated-hood system (Oxycon ). At rest and
during exercise, CO2 and
O2 were measured during 5 min
immediately before taking a breath sample for measurement of
13CO2 enrichment. The accuracy of the
ventilated-hood system for measuring CO2
and O2 was tested regularly to be within
5%. Breath samples were taken at t = 100, 110, and 120 min at rest and at t = 40, 50, and 60 min during exercise.
The exact infusion rate of [U-13C]palmitate was
determined for each experiment by measuring the concentrations of the
infusates (see Sample Analyses). Blood samples were taken at
t = 90, 100, 110, and 120 min of rest and at
t = 30, 40, 50, and 60 min during exercise. Blood
samples were put into an EDTA or heparin and 300-µl glutathione (45 µg/l saline) containing chilled 10-ml tube and immediately
centrifuged at for 10 min at 800 g at 4°C. Plasma was
stored at 
80°C until analyses. EDTA containing blood was used for
analyses of glucose, FFA, insulin, triglyceride (TG), and palmitate
concentrations as well as the plasma enrichment of palmitate. Heparin
and glutathione containing blood was used for analysis of
catecholamines. During rest (t = 0, 90, and 120 min)
and exercise (t = 30 and 60 min), blood was sampled for
the measurement of oxygen saturation (hemoxymeter OSM2, Copenhagen, Denmark) to check that the arterialization was at least 90%. Before infusion, the palmitate tracer (60 mg of potassium salt of
[U-13C]palmitate, enrichment = 98.9%, Cambridge
Isotope Laboratories, Andover, MA) was bound to albumin by dissolving
it in heated (60°C) sterile water and passing it through a 0.2-µm
filter into a 5% warm (60°C) human serum albumin solution to make a
0.670 mM solution.
[1,2-13C]acetate Infusion
Palmitate oxidation rates were corrected for loss of tracer in products of the tricarboxylic acid cycle by using the acetate correction factor previously described by Sidossis et al. (39) and Schrauwen et al. (36). The protocol for the acetate-infusion experiment was the same as for the palmitate-infusion experiment, except that no blood was sampled. The acetate tracer (sodium salt of [1,2-13C]acetate, enrichment = 99%, Cambridge Isotope) was dissolved in 0.9% saline. The acetate infusion rate was 0.0496 µmol · kg1 · min1 at rest
and was doubled during exercise. Before the acetate infusion was
started, an intravenous dose of 1.0 µmol/kg
NaH13CO3 was given to prime the bicarbonate pool.
Sample Analysis
Plasma total FFA, glycerol, and TG concentrations were measured on a COBAS FARA centrifugal spectrophotometer. For analysis of plasma total FFA concentrations, a nonesterified fatty acids (FA) C kit (Wako Chemicals, Neuss, Germany) was used. Plasma glycerol and TG concentrations were analyzed by using a glycerol kit (Boehringer, Mannheim, Germany). Plasma insulin concentrations were measured with a double-antibody radioimmunoassay (insulin RIA 100, Pharmacia, Uppsala, Sweden). Plasma catecholamine concentrations were analyzed by HPLC with electrochemical detection (42).Chemical and isotopic purities (99%) of the palmitate and acetate tracers were checked by 1H- and 13C-NMR and gas chromatography (GC)/mass spectrometry (MS). Breath samples were analyzed for 13C/12C ratio by using a GC-isotope ratio mass spectrometer (GC-IRMS, Finnigan MAT 252, Bremen, Germany). For determination of the plasma palmitate concentration, FFA were extracted from plasma, isolated by thin-layer chromatography, and derived to methyl esters. Palmitate concentration was determined on an analytical GC with flame ionization detection, which used heptadecanoic acid as an internal standard. The isotope tracer-to-tracee ratio (TTR) of palmitate was determined by using GC combustion isotope ratio MS, with correction for the extra methyl group in the derivative.
The concentration of the acetate infusate was determined on a COBAS FARA with an enzymatic method kit 148261 (Boehringer). The concentration of the palmitate infusate was determined as described above for plasma samples.
Calculations
Total fat oxidation was calculated by the following equation (8)
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CO2 and
O2 in liters per minute. The value 1.67 is derived from the volumes of oxygen consumed and carbon dioxide produced in oxidation of 1 g of fat.
Because no estimation of protein oxidation is included in this calculation of fat oxidation, fat oxidation will be overestimated. However, because fat oxidation is compared before and after exercise training, this overestimation will not influence the outcome.
Total FA oxidation was determined by converting the rate of total fat oxidation to its molar equivalent, with the assumption that the average molecular weight of TG is 860 g/mol and multiplying the molar rate of TG oxidation by three because each molecule contains 3 mol of FA.
13C enrichment of breath carbon dioxide and plasma
palmitate is expressed as a TTR. TTR was defined as
(13C/12C)sa (13C/12C)bk in which sa is sample
and bk is background.
Fractional recovery of infused acetate 13C label in breath
carbon dioxide (AR) was calculated as
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The rate of [U-13C]palmitate oxidation was calculated as
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CO2 over the last
three time points at rest and during exercise was used.
Total plasma FA oxidation was then calculated by dividing palmitate oxidation by the fractional contribution of palmitate to the total FFA concentration. The average fraction palmitate/FFA was used in this equation, and total plasma FA oxidation per time point was calculated during the rest and exercise period.
Non-plasma-derived FA oxidation (µmol/min), which refers to intramuscular TGs and plasma triacylglycerol, was calculated at rest and during exercise as the average total FA oxidation minus the average plasma FFA oxidation.
Rate of appearance (Ra) of palmitate in plasma, which under
steady-state conditions is equal to the rate of disappearance minus
tracer infusion rate, was calculated as
![R<SUB>a</SUB><IT>=</IT>[(TTR infusate<IT>/</IT>TTR plasma)<IT>−</IT>1]F](/content/vol92/issue3/fulltext/1300/img005.gif)
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Statistics
Data are expressed as means ± SE. Changes within groups were analyzed by using the Wilcoxon signed rank test. Differences in basal values and in changes among groups were tested by the Kruskal-Wallis test. Post hoc testing was done by the Mann-Whitney test. Where appropriate, P values of the post hoc comparisons were corrected according to Bonferroni inequalities. Spearman correlation coefficients (r) were calculated between the changes because of the intervention (LI or HI training or no training) in norepinephrine and epinephrine concentrations during exercise and between the changes in total fat oxidation, Ra FFA and plasma FFA, and glycerol concentrations during exercise. A P value of <0.05 was regarded as statistically significant.| |
RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subject Characteristics
The exercise training intervention did not lead to significant changes in body weight and body composition (Table 1). Both LI and HI exercise training significantly increasedO2 max and
O2 max/free fatty mass (FFM;
P < 0.05), whereas the C group showed no change.
Changes in O2 max and
O2 max/FFM were significantly different
between the HI and C groups (P < 0.05). The absolute
workload during the exercise test (50% of pretraining
O2 max) in the LI, HI, and C groups was
102 ± 33, 104 ± 23, and 92 ± 24 W, respectively.
Workloads were not significantly different among groups. Attendance at
the exercise training sessions was 89.4 ± 7.7% for the LI group
and 92.6 ± 5.5% for the HI group.
Fat Oxidation at Rest
Data from indirect calorimetry showed that relative fat oxidation during the last 20 min of the resting period, expressed as respiratory exchange ratio (RER), was not different after the intervention from before (Table 2). Total FA oxidation (Table 2) and percentage of fat oxidized of total energy expenditure (Fig. 1A) did not change in any of the groups because of the intervention either. Preintervention total and relative fat oxidation were not significantly different between groups. Energy expenditure at rest was slightly lower after the intervention in all groups but was only significantly lower in the HI group (P < 0.05).
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Plasma palmitate enrichment was at plateau (change = 2.5%)
during the last 20 min of the resting period. Therefore, tracer calculations of plasma palmitate oxidation were made with the use of
the values of plasma palmitate enrichment measured over the 100- to
120-min period. These tracer calculations were corrected by acetate
recovery factors, which were measured and calculated over the same time
points. The fractional recovery of acetate increased gradually at rest
from 22.3 ± 2.5% at 100 min to 25.4 ± 2.9% at 120 min
after the start of the tracer infusion. Exercise training did not
influence the acetate recovery factor significantly.
Plasma FFA oxidation at rest was significantly decreased in the HI
training group after training (P < 0.05) (Fig.
1C), whereas in the LI and C groups there was no change. The
change in the HI group was significantly different from the LI and C
groups (P < 0.05). Non-plasma-derived FA oxidation
(plasma triacylglycerol and intramuscular TGs; calculated as total FA
oxidation plasma FFA oxidation) at rest was not significantly
different from zero before as well as after exercise training (Fig.
1E).
Ra of FFA at rest was significantly higher after training
in the LI group (P < 0.05) (Fig.
2A). The change was
significantly different from the HI group (P < 0.05).
FFA oxidation as a percentage of the Ra of FFA did not
change because of the intervention (Fig. 2A, numbers in
parentheses). Plasma concentrations of FFA (Fig. 3A) and glycerol (Fig.
3B) were not significantly different after the intervention
from before. Plasma TG concentrations were significantly reduced in the
HI group after the intervention (P < 0.05) (Fig. 3C). Average plasma FFA, glycerol, and TG concentrations,
calculated over the last 20 min of rest and exercise, before the
intervention were not significantly different between groups. Plasma
insulin, epinephrine, and norepinephrine concentrations were not
changed after the intervention (Table 3).
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Fat Oxidation During Exercise
During the last 20 min of exercise, RER was significantly decreased in the LI group after exercise training, whereas, in the HI and C groups, RER did not change. In addition, total fat oxidation over the last 20 min was significantly increased in the LI group after training compared with before training (P < 0.05; Table 2). Fat oxidation as percentage of total energy expenditure was also increased in the LI group after the exercise intervention (Fig. 1B). However, the change in fat oxidation due to the intervention (LI or HI exercise training or no training) was not significantly different among groups. Preintervention fat oxidation rates were not significantly different among the groups.Plasma palmitate enrichment was at semi-plateau (change = 3.6%)
during the last 20 min of the exercise period. The acetate correction
factor increased gradually during exercise from 69.0 ± 8.2%
after 40 min to 72.2 ± 8.3% after 60 min of exercise at 50%
O2 max before the intervention. The
intervention did not change the acetate recovery factor. Plasma FFA
oxidation during exercise was significantly decreased in the HI group
(P < 0.05) after training whereas there were no
changes in the LI and C groups (Fig. 1D). Plasma FFA
oxidation before the intervention was not significantly different among
the groups. Non-plasma FA oxidation was significantly increased in the
LI group (P < 0.05) but not in the HI and C groups
(Fig. 1F). The changes were not significantly different
among groups. Non-plasma FA oxidation before the intervention was not
significantly different from zero.
Ra of FFA was significantly decreased in the HI group after
training (P < 0.05) but did not change in the LI and C
groups, and changes were not significantly different among groups. The percentage of FFA oxidized from the Ra of FFA was not
changed after the intervention (Fig. 2B, numbers in
parentheses). Plasma FFA, glycerol, and TG concentrations after
exercise training were significantly reduced from before exercise in
the HI group (P < 0.05; Fig. 3). However,
concentrations before the intervention were not significantly different
among the groups. Interindividual differences in TG concentrations were
high in the LI group (Fig. 3C). However, excluding a subject
with TG concentrations over 4,000 µmol/l did not change the
statistical outcome. After exercise training, plasma epiniphrine
concentrations were significantly decreased in all groups during
exercise (P < 0.05; Table 3). Plasma norepinephrine
was significantly decreased during exercise in the HI and C groups
(P < 0.05; Table 3). The LI group showed a similar
tendency. Changes in plasma norepinephrine concentrations during
exercise did not significantly correlate with changes in total fat
oxidation (r = 0.33, P = 0.12),
Ra FFA (r = 0.31, P = 0.14), plasma FFA (r = 0.12, P = 0.60),
and glycerol concentrations (r = 0.30, P = 0.16) during exercise. In addition, changes in plasma epinephrine concentrations during exercise did not significantly correlate with changes in total fat oxidation (r = 0.22, P = 0.30), Ra FFA
(r = 0.13, P = 0.55), plasma FFA
(r = 0.20, P = 0.93), and glycerol
concentrations (r = 0.04, P = 0.85)
during exercise. Plasma insulin concentrations were not different after the intervention for all groups (Table 3).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Many studies have shown that moderate-intensity to HI exercise
training (>60% O2 max) increases
total fat oxidation during exercise in lean subjects (14, 17, 23,
30, 38). The results of the present study show that exercise
training in obese men is effective in increasing total fat oxidation
when exercise training is executed at LI (40%
O2 max). Exercise training at HI (70%
O2 max) does not significantly increase total fat oxidation during moderate-intensity exercise. In contrast to
the findings during exercise, no changes in fat metabolism because of
exercise training were found under resting conditions.
The increase in fat oxidation during moderate-intensity exercise in the LI training group is in agreement with a comparable study in upper-body obese women (46). In this study, relative fat oxidation increased significantly in upper body obese women after executing the same LI exercise training protocol as the upper- body obese men in the present study. The percentage of total energy expenditure coming from fat oxidation during exercise increased from 35 to 52% (P < 0.05) in the LI training group. This is similar to data reported in upper-body obese women after LI exercise training (46) and lean men after HI exercise training (17).
The significant increase in total fat oxidation in the LI group during exercise (P < 0.05) is not explained by an increased plasma FFA oxidation but rather by an increase in non-plasma FA oxidation (P < 0.05). In the HI group, total fat oxidation during exercise failed to increase. Although, in this group, non-plasma FA oxidation increased slightly but not significantly, this was just enough to compensate for the significant decrease of the plasma FFA oxidation (P < 0.05). The decrease in plasma FFA oxidation in the HI group by exercise is paralleled by a significant decrease of the Ra of FFA in plasma. Together with the decrease of plasma FFA and glycerol concentration seen after exercise training (P < 0.05), this seems to point to a reduced rate of adipose tissue lipolysis in the HI group (15).
A reduction in plasma catecholamine concentrations during exercise has been found in all groups. This reduction can be explained by habituation to the exercise experiment because this effect has been found in the C as well as in the exercise-training groups. The changes in catecholamine concentrations during exercise after 12 wk show no correlation with changes in total fat oxidation, Ra of FFA and plasma FFA, and glycerol concentrations. Therefore, the changes in catecholamine concentrations are not likely to affect the outcome of the present study with respect to substrate use.
The increase in non-plasma FA oxidation after exercise training can either implicate an increase in intramuscular triglycerides (IMTG) oxidation and/or an increase in very low-density lipoprotein (VLDL)-TG oxidation. However, the data in the present study are not able to distinguish between the two. No consistent data on training effects on VLDL-TG or IMTG oxidation are available in the literature. Some studies reported an increased IMTG oxidation by exercise training (18, 30), whereas another study showed no change (20). IMTG content does not appear to be correlated with obesity in humans (11, 29) but does correlate with obesity in rats (43). IMTG content is increased in trained compared with untrained human muscle (20, 24). Data on the contribution of VLDL-TG to fat oxidation during exercise in the literature are not consistent (13, 20, 26). An exercise-induced TG clearance from the circulation is suggested because lipoprotein lipase enzyme activity is increased in skeletal muscle by exercise (28, 37). This is in agreement with the decreased plasma TG concentrations after exercise training in the HI group, but this decrease is not seen in the LI group. The cleared plasma TG may be used as fuel in the muscle.
Despite significant changes in plasma FFA oxidation, the percentage of
FFA oxidized from the FFA released in plasma did not change because of
exercise training and was ~40% at rest and 73% during exercise.
This indicates that the Ra of FFA is not rate limiting in
plasma fat oxidation. In lean, untrained men, comparable data were
reported at rest (30%) and during exercise at 40%
O2 max (75%) (48). At
60% maximum external power, the percentage of plasma FFA oxidation was
found to be 76% (45), with no difference after exercise
training. Friedlander et al. (9), however, showed a
significantly increased percentage of FFA oxidized from FFA released in
plasma after exercise training (from 51 to 61% at 65% pretraining
O2 max). In all of these studies,
corrections were made for the loss of 13C or
14C label by using the bicarbonate correction factor rather
than the acetate recovery factor, as in the present study.
Although considerable effects of exercise training on fat oxidation in
obese subjects are found during exercise, at rest these effects are
less obvious. Neither after LI nor after HI exercise training were
effects found on fat oxidation. However, other parameters measured
suggest that fat metabolism is more positively influenced by LI
training (significantly increased Ra of FFA) than by HI training (significantly decreased plasma FFA oxidation). In lean subjects, the effects of exercise training on fat metabolism at rest
are not consistent. Some studies reported an increased fat oxidation at
rest after exercise training (5, 30, 31), whereas others
found no change (9, 10, 38). Cross-sectional studies
comparing trained and untrained lean subjects at rest showed higher fat
oxidation rates in trained compared with untrained subjects (21,
33, 44). Obese subjects are known to have a diminished capacity
to mobilize and oxidize FA during -adrenergic stimulation
(1) and have a reduced postabsorptive FFA utilization by
the muscle (6). However, the present study showed that fat oxidation during exercise can be improved by exercise training. Because
the extra FA oxidized in the trained state are mainly coming from
non-plasma FA pools (IMTG and VLDL-TG) rather than from plasma FFA
(lipolysis from adipose tissue), the question can be raised whether
training will help to reduce adipose mass in obese subjects. However,
the depleted non-plasma FA pools after exercise could be restored by
FFA from adipose tissue, which could implicate the importance of
trafficking of substrates between tissues. The IMTG pool is suggested
to be restored by FFA from plasma TG or adipose tissue by activating
muscle lipoprotein lipase after exercise and diminishing the
lipoprotein lipase activity in adipose tissue (22, 25,
27). A study in rats reported that plasma FFA is an important
source for synthesis of IMTG (12). However, whether
exercise training-induced changes in fat utilization during exercise
contribute to the positive/favorable effects of exercise training on
body mass in obese subjects remains to be studied.
Methodological Considerations
The test conditions in the present study did not allow the subjects to exercise 36 h before the test. This implicates that only the more permanent effects of exercise training on fat oxidation were measured and not the acute effects of an exercise bout.Although the present study showed significant differences in FA oxidation and non-plasma FA oxidation, no difference was observed between the exercise groups and the C group. This might be explained by the limited number of subjects in all of the three groups. Furthermore, the slightly, but not significantly, lower RER before the intervention in the HI group, compared with the LI and C groups, might have influenced the outcome in the HI group. These factors should be taken into account in the interpretation of the effect of exercise training on fat oxidation.
In the present study, the acetate recovery factor was used to correct for label loss in the tricarboxylic acid cycle (39) during the palmitate-infusion test. The acetate recovery factor has a high intra-individual reproducibility but varies between subjects (36). The acetate recovery factor is correlated with basal metabolic rate, percentage of body fat, and RER (35). Therefore, measurements of acetate recovery were performed individually both before and after exercise training. At rest, the acetate recovery has a large impact on plasma FFA oxidation rates because only about 25% of 13C label was recovered in expired breath. During exercise, label recovery was ~72%. When the acetate recovery factor was been ignored, plasma palmitate oxidation was underestimated by ~75% at rest and ~28% during exercise. During exercise before the intervention and at rest, calculated non-plasma FFA oxidation rates were not significantly different from zero, although, in some subjects, values were below zero. These negative values may indicate that values for plasma palmitate oxidation rates were over-corrected by using the acetate correction factor. This overcorrection may indicate that more [13C]acetate is trapped in the tricarboxylic acid cycle than [13C]palmitate. Training did not affect the acetate recovery factor. However, it is not known whether exercise training has a different effect on loss of label from acetate or palmitate.
In conclusion, LI exercise training is effective in increasing fat oxidation during exercise but not at rest. No effect of HI exercise training on total fat oxidation could be shown.
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ACKNOWLEDGEMENTS |
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The authors thank Moniek Homan for supervision of the exercise training sessions, Jos Stegen for analytical assistance, and Judith Graat and Vanessa Blokdijk for assistance during the experiments. We also thank Lode BV for providing cycle ergometers.
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FOOTNOTES |
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This study was supported by Netherlands Heart Association Grant 95040.
Address for reprint requests and other correspondence: D. P. C. van Aggel-Leijssen, Maastricht Univ., Dept. of Human Biology, P.O. Box 616, 6200 MD Maastricht, The Netherlands.
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
10.1152/japplphysiol.00030.2001
Received 12 January 2001; accepted in final form 9 November 2001.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
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