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Substrate metabolism during different exercise intensities in endurance- trained women

  • Rutgers, The State University of New Jersey, USA - Harokopio University, Athens, Greece

Abstract and Figures

We have studied eight endurance-trained women at rest and during exercise at 25, 65, and 85% of maximal oxygen uptake. The rate of appearance (R(a)) of free fatty acids (FFA) was determined by infusion of [(2)H(2)]palmitate, and fat oxidation rates were determined by indirect calorimetry. Glucose kinetics were assessed with [6,6-(2)H(2)]glucose. Glucose R(a) increased in relation to exercise intensity. In contrast, whereas FFA R(a) was significantly increased to the same extent in low- and moderate-intensity exercise, during high-intensity exercise, FFA R(a) was reduced compared with the other exercise values. Carbohydrate oxidation increased progressively with exercise intensity, whereas the highest rate of fat oxidation was during exercise at 65% of maximal oxygen uptake. After correction for differences in lean body mass, there were no differences between these results and previously reported data in endurance-trained men studied under the same conditions, except for slight differences in glucose metabolism during low-intensity exercise (Romijn JA, Coyle EF, Sidossis LS, Gastaldelli A, Horowitz JF, Endert E, and Wolfe RR. Am J Physiol Endocrinol Metab 265: E380-E391, 1993). We conclude that the patterns of changes in substrate kinetics during moderate- and high-intensity exercise are similar in trained men and women.
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Substrate metabolism during different exercise
intensities in endurance-trained women
Department of Endocrinology and Metabolism, Leiden University Medical Center,
2300 RC Leiden, The Netherlands;
Human Performance Laboratory,
Department of Kinesiology and Health, The University of Texas at Austin, Austin 78712;
Metabolism Unit, Shriners Burns Institute, and
Departments of Anesthesiology
and Surgery, University of Texas Medical Branch, Galveston, Texas 77550
Romijn, J.A., E. F. Coyle, L. S. Sidossis, J. Rosenblatt,
and R. R. Wolfe. Substrate metabolism during different
exercise intensities in endurance-trained women. J Appl
Physiol 88: 17071714, 2000.—We have studied eight endur-
ance-trained womenatrestand during exercise at25,65,and
85%ofmaximal oxygenuptake.The rateof appearance(R
free fatty acids (FFA) was determined by infusion of
]palmitate, and fat oxidation rates were determined by
indirect calorimetry. Glucose kinetics were assessed with
]glucose. Glucose R
increased in relation to exercise
intensity. In contrast, whereas FFA R
was significantly
increased to the same extent in low- and moderate-intensity
exercise, during high-intensity exercise, FFA R
was reduced
tion increased progressively with exercise intensity, whereas
the highest rate of fat oxidation was during exercise at 65% of
maximal oxygen uptake. After correction for differences in
lean body mass, there were no differences between these
results and previously reported data in endurance-trained
men studied under the same conditions, except for slight
differences in glucose metabolism during low-intensity exer-
cise (Romijn JA, Coyle EF, Sidossis LS, GastaldelliA, Horow-
itz JF, Endert E, and Wolfe RR. Am J Physiol Endocrinol
Metab 265: E380E391, 1993).We conclude that the patterns
of changes in substrate kinetics during moderate- and high-
intensity exercise are similarin trained men and women.
stable isotopes; body composition; glucose; glycogen; fatty
relatively more suited to endurance exercise than men
because of a greater ability to use fatty acids as energy
substrates during exercise. This notion is supported by
several studies that have found some index of fat
metabolism to be greater in women than in men at
comparable exercise intensity (e.g., Refs. 7, 22). On the
other hand, several other studies have failed to show a
gender difference in substrate metabolism (3, 23). It
has been suggested that the difference in substrate
metabolism between men and women during exercise
becomes less as training status increases (19), but all
data are not consistent with this explanation. For
example, endurance-trained women were found to de-
rive more energy from lipids than endurance-trained
men did when exercising at 65% of maximal oxygen
consumption (V
) (21).
If women are in fact better able to rely on fat during
exercise than men, it may be because women generally
have a higher percentage of body fat than men. This
could theoretically lead to greater availability of fatty
acids during exercise and, inturn, to more fat oxidation
at a given exercise intensity than in a man with less
body fat. In this regard, changes in fatty acid availabil-
ity have been shown to have an effect on fatty acid
oxidation during high-intensity exercise (16). On the
other hand, it may be erroneous to assume that women
have an increased rate of lipolysis because of their
greater amount of body fat. Our laboratory has previ-
ously shown that changes in the percentbody fat result
in altered lipolytic sensitivity that makes individuals
with low body fat better able to mobilize fatty acids
than might be anticipated otherwise. Thus lipolytic
responsiveness is enhanced in subjects with low body
fat (11) and decreased inobese subjects (29).Consistent
with these observations, our laboratory found that
highly trained athletes had higher rates of lipolysis at
rest (18) than untrained controls did. However, it is not
clear whether this reflects a response to training, a
change in body composition, or some other factor. In
trained men, it is difficult to distinguish a training
effect on fat metabolism from a body-composition effect
because body fat is low in all endurance-trained men.
This is not necessarily the case in endurance-trained
women, who may have a relatively large range in body
composition. The purpose of the present study was
therefore twofold: 1) to compare with the previously
reported data from endurance-trained men (15) the
response of glucose and lipid kinetics in endurance-
trained women to three intensities of exercise and 2)to
evaluate the role of bodycomposition on the response of
substrate kinetics to exercise in the trained women. To
accomplish these goals, we have quantified glucose and
fatty acid kinetics by using stable isotopically labeled
tracers at three intensities of exercise in eight endur-
ance-trained women with a range in body composition
from 7.7 to 26.9% body fat.
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J Appl Physiol
88: 1707–1714, 2000.
8750-7587/00 $5.00 Copyright
2000 the American Physiological Society 1707
We studied eight well-trained female cyclists with percent
body fat ranging from 7.7 to 26.9%. Their physical character-
istics are shown in Table 1. All subjects were healthy, as
indicated by medical history and physical examination. They
were consuming a weight-maintaining diet containing at least
300–400 g of carbohydrates daily. They were in energy balance,
documented by their stable weight in the 2 mo preceding the
study. They were studied in the postabsorptive state after a
10- to 12-h fast and did not exercise the day before the
studies.Thesubjects wereeumenorrheicand studied through
a variety of phases of the menstrual cycle. The men we used
for comparison were describedpreviously (15).
Body composition was determined by densitometry by
using the hydrostatic weighing technique with correction for
residual lung volume (25). Relative body fat was estimated
from total body density (26). Assessment of body composition
was performed within 1wk of the isotope-infusion protocol.
had been determined several weeks before the
present protocol while the subjects cycled on a stationary
ergometer (model 819, Monark). V
was determined
during an incremental cycling protocol lasting 710 min. The
study was approved by the institutional review boards of the
University of Texas, Galveston andAustin.
Exercise Protocol
The subjects were studied on 2 consecutive days in the
postabsorptive state. On one occasion, the protocol consisted
of at least 120 min of bed rest, 60 min of exercise at 25% of
on a stationary ergometer (model 819, Monark),
followed by 60 min of bed rest, and, finally, 30 min of exer-
cise at 85% of V
. We have previously shown that the
effects of very-low-intensity exercise (120 min at 25% of
) on glucose and fat metabolism subside within1hof
bed rest (15). On the other day, the protocol consisted of at
least 120minof bed rest followedby60min of exercise at65%
of V
. The order of the two protocols was determined by
random allocation.
Indirect Calorimetry
Indirect calorimetry was performed at rest for at least 15
min continuously during the first 30 min of exercise (all 3
levels of exercise) and for 510 min at 15-min intervals
throughout the remainder of the exercise periods at 25 and
65% of V
. The values obtained from 20 to 30 min of
exercise were used to calculate and compare substrate oxida-
tion rates among the three levels of exercise. Our laboratory
(14) has previously shown that indirect calorimetry is a valid
method to measure substrate oxidation rates in trained
subjects during cycling exercise at 8085% of V
ofthe relativephysiological state(i.e., constantlactate concen-
tration, heart rate, and so forth) over this time interval. The
restingvalueswere obtained afterthesubjects hadbeenlying
on a bed for at least 1 h. Inspired volumes of air were
measured with a dry-gas meter (model CD-4, Parkinson-
Cowan). Aliquots of expired gas were sampled from a mixing
chamber for O
(model S3A, Applied Electrochemistry) and
(model LB-2, Beckman). Analog outputs from the gas
analyses and gas meter were directed to a laboratory com-
puter for calculation of oxygen uptake and carbon dioxide
Isotope Infusion
Teflon catheters were placed percutaneously in an antecu-
bital vein, and a sampling catheter was inserted in a dorsal
hand vein of the contralateral side. The heated hand tech-
nique was used to obtain arterialized blood samples. The
subjects lay on a bed for 1 h after catheter placement. Then,
after a blood sample was drawn to determine background
enrichment, primed, constant infusions of [6,6-
(99% enriched, Merck, Rahway, NJ; 0.22 µmol·kg
priming dose 17.6 µmol/kg) and [
]palmitate (0.04 µmol·
; no priming dose) were started by using cali-
brated syringe pumps (HarvardApparatus, Natick,MA). The
exact infusion rates in each experiment were determined by
measuring the concentrations in the infusates. The palmitate
tracer (99% enriched) was purchased from Tracer Technolo-
gies (Newton, MA). Palmitate was bound to albumin (Cutter
Biological, Berkeley, CA) by following previously described
procedures (27). After2hofinfusion at rest, exercise was
started and the rate of isotope administration was doubled
for palmitate (25 and 65% of V
) and glucose (65% of
) and tripled for glucose (85% of V
) to minimize
changes in substrate isotopic enrichment. These changes in
isotope infusion rates were determined from results of a
previousstudyon metaboliceffectsof similarexerciseintensi-
tiesinmen (15).Duringthe intervalbetween theexperiments
with exercise at 25 and 85%, the isotope infusions were
continued at the basalrates.
Blood Sampling
The first blood samples were drawn before the isotope
infusion was started to determine background enrichment.
Blood was also taken 110, 115, and 120 min after the
beginning of infusion to measure resting kinetics. During
high-intensity exercise, blood was drawn after 5, 10, 15, 20,
25, and 30 min of exercise. In moderate- and low-intensity
exercise, samples were drawn every 10 min for 60 min. All
samples were collected in 10-ml vacutainers containing
lithium heparin and were placed on ice. Plasma was sepa-
rated by centrifugation within 5 min of sampling and subse-
quently frozen until furtherprocessing.
Sample Analysis
Plasma glucose concentration was measured on a glucose
analyzer (Beckman Instruments) by use of the glucose oxi-
dase method. The enrichment of [6,6-
]glucose in plasma
was determined as previously described (27). Briefly, plasma
was deproteinated with barium hydroxide and zinc sulfate
solutions. Glucose was extracted by mixed-bed anion-cation
exchange chromatography (AG-1-X8 and AG 5OW-X8, Bio-
Rad Laboratories, Richmond, CA) and reacted with acetic
anhydride and pyridine to form the pentaacetate derivative.
Isotopic enrichment was determined by using gas chromato-
Table 1. Physical characteristics of study subjects
1 31 48 1.65 44 7.7 2.75
2 27 49 1.63 42 13.4 2.75
3 29 55 1.60 47 14.8 3.30
4 26 63 1.66 52 17.8 3.60
5 28 64 1.65 53 18.4 3.83
6 25 69 1.78 55 20.5 3.90
7 29 65 1.65 51 21.6 4.15
8 18 72 1.77 53 26.9 3.65
Mean6SE 276 16163 1.6760.02 5062 17.662 3.496 0.2
, maximal oxygen uptake.
graph-mass spectrometry (model 5985B, Hewlett-Packard,
Fullerton, CA) with electronic-impact ionization, selectively
monitoring ions at mass-to-charge ratio (m/z) 202, 201, and
200. Correction was made for the contribution of singly
labeled molecules (m/z 201) to the apparent enrichment at
m/z 202 (27).
FFA were extracted from plasma, isolated by thin-layer
chromatography, and derivatized to their methyl esters.
Palmitate and total free fatty acid (FFA) concentrations were
determined by gas chromatography (model 5890, Hewlett-
Packard)byusing heptadecanoicacidas an internalstandard
(27). Isotopic enrichment of palmitate was measured by gas
chromatograph-mass spectrometry analysis of the methyl
ester derivatives (model 5992, Hewlett-Packard). Ions of m/z
270 and 272 wereselectively monitored.
Indirect calorimetry. Carbohydrate and fat oxidation rates
were calculated by using stoichiometric equations (4). Nitro-
gen excretion rate was assumed to be 135 µg·kg
This average value was taken from the measured values
determined in another study performed in our laboratory (1).
A 30% error in this assumed value (which exceeds the total
range of values in the previous study) would have no signifi-
cant effect on the calculated values of fat and carbohydrate
oxidation in exercise in the present study. Fatty acid oxida-
tion was determined by converting the rate of triglyceride
oxidation (g·kg
) to its molar equivalent, assuming
the average molecular mass of triglyceride is 860 g/mol (4)
and multiplying the molar rate of triglyceride oxidation by
three because each moleculecontains 3 mol of fatty acids.
Rates of appearance. Rate of appearance (R
) and, when
appropriate, rate of disappearance (R
5 tissue uptake) of
glucose and palmitate at rest were calculated by using the
equation of Steele (20), as modified for use with stable
isotopes (27). During exercise and the first 30 min ofrecovery,
the non-steady-state approximation of Steele was used in
conjunction with a spline-fitting program to smooth the raw
data(24).The effectivevolume of distributionwasassumed to
be165ml/kg forglucose and40ml/kg forpalmitate. Thevalue
for palmitate was chosen because acute changes in palmitate
concentration are essentially restricted to plasma (because
FFA are bound to albumin). The FFA R
was calculated by
dividing the palmitate R
by the fractional contribution of
palmitate to the total FFA concentration, as determined by
gas chromatography.
Statistical Analysis
The results obtained during 2030 min of exercise were
used for comparison of the subjects of the three levels of
exercise. The effect of time on the response within each
exercise level was analyzed by two-way analysis of variance
for a randomized block, with the subjects as blocks and time
as treatment. If necessary, the time effects were compared by
Fisher’s least significant difference test. The results of the
three exercise intensifies were compared by two-way analysis
ofvarianceforrandomized block design,inwhich the subjects
are blocks and the three exercise levels are treatments. If
necessary, the analysis of variance wasfollowedbyamultiple
comparison to detect differencesamong groups.
To analyze the effects of body composition and gender on
different metabolic responses (e.g., glucose production) we
used the repeated-measures analysis of covariance. Letting
denote the measured metabolic response from subject(s)
[person(s)] exercising at intensity level e, with body composi-
tion parameter f, the model is Y
5 S
1 E
1 f(FE)
, in which the error terms are assumed to be indepen-
dent, identically distributed, normal random variables with
mean value 0 and common SD
. The body composition factor
was either fat mass (FM), fat free mass (FFM), or the ratio
FM/FFM. Thus the repeated-measures aspect is included via
the subject effect S
, and the effect of body composition is
accounted for by the f(FE) term. To ensure unique estimates,
the baseline constraints E
5 0 and (FE)
5 0 were imposed.
In this case, E
and (FE)
represent the rise over baseline
levels of intercept and slope, respectively. The effect of body
composition at baseline, along with any other baseline vari-
teristics of subjects, is embodied in the S
. If the body
composition were the only such factor, the values of the S
would specify the average effect of body composition on the
baseline metabolic response. Simultaneously, 0.95level confi-
dence intervals for the parameters E
and (FE)
were gener-
ated in association with a repeated-measures analysis of
covariance F-test of the hypothesis H
5 0, (FE)
5 0, e 5
2,3,4. Data fromaprevious paper (15)fromour laboratory, in
which the exact same experimental procedures were used in
trained male subjects, were used for evaluation of gender
Resting State
At rest, there were no differences in concentrations,
, or oxidation rates of FFAor glucose before the three
levels of exercise. Themeanvalues are showninTable 2.
Lactate concentrations. Lactateconcentrationdid not
change during low-intensity exercise and increased
from 0.84 6 0.03 to 1.68 6 0.18 mmol/l (P , 0.05)
during moderate exercise intensity. During high-
was maintained. This was reflected in plasma lactate
concentrations over the last 15 min of exercise (0 min:
0.84 6 0.03, 15 min: 7.92 6 0.17, 30 min: 7.30 6 0.71
Glucose metabolism. Tracer-to-tracee ratios and sub-
strate kinetics are shown in Figs. 1 and 2, respectively.
During low-intensity exercise, plasma glucose concen-
tration and glucose R
did not change from the resting
values. In contrast, during moderate- and high-intensity
exercise, plasma glucose concentration and glucose R
increased significantly in relation to exercise intensity
(Tables 2 and 3).
ally during low-intensity exercise, whereas they tran-
siently decreased and subsequently increased during
moderate exercise intensity [not significant (NS) vs.
low-intensity exercise]. During high-intensity exercise,
FFA concentrations were considerably decreased com-
pared with the values obtained at rest and during
low-intensity exercise (P, 0.05; Table 3). Palmitate R
, and FFAuptake were significantly increased to
the same extent in low- and moderate-intensity exer-
palmitate R
and FFA uptake were significantly
lower than the values during the two lower exercise
intensities (P, 0.05; Fig. 2, Tables 2 and 3).
Substrate oxidation rates. Substrate oxidation rates
are given in Tables 2 and 3. During moderate-intensity
exercise, carbohydrate oxidation rates increased above
the value during low-intensity exercise, and carbohy-
drate oxidation was the highest during high-intensity
exercise. The highest rate of fat oxidation was during
exercise at 65% of V
(Table 3), whereas there was
no significant difference between low- and high-intensity
During exercise at 25% of V
, FFA uptake and
FFA oxidation rates, expressed in fatty acid equiva-
lents, were similar (Table 2), indicating that plasma
could transport adequate amounts of FFAfor oxidation
from adipose tissue. However, during moderate and
high exercise intensity, fatoxidation ratesexceeded the
maximal amounts that could be obtained from plasma,
the differencebeing the minimal contribution of muscle
triglycerides toenergy requirements (Fig. 3). From Fig.
3,itisalsoevident thatthemaximalcombinedcontribu-
tion of plasma glucose and FFA to oxidation rates
hardly differs between the three levels of exercise.
Apparently, the decrease in FFA R
during high-
intensity exercise more or less balances the increase in
glucose R
Relationship of Results to Gender
Table 2 shows the comparison between the women
and the previously described men. V
, expressed
per kilogram of lean body mass, was similar in both
groups. In addition, respiratory exhange ratio (RER)
values obtained during different exercise intensifies
were not different. Despite decreased glucose R
increased rate of carbohydrate oxidation during low-
intensity exercise in the women, there were no differ-
ences in glucose and fat metabolism between men and
women after correction for differences in lean body
mass. The minimal contribution of muscle triglycerides
to energy requirements were 0 vs. 9% (men vs. women)
at 25% of V
(P , 0.05), 23 vs. 25% at 65% ofV
(NS) and 11 vs. 17% at 85% of V
(NS). Muscle
glycogen contributed minimally, 0 vs. 9% (men vs.
women) at 25% of V
(P , 0.05), 41 vs. 34% at 65%
of V
(NS), and 63 vs. 58% at 85% of V
The results of this study indicate that substrate
metabolisminendurance-trainedwomen respondssimi-
larly to moderate- and high-intensity exercise, as our
laboratory has previously reported in endurance-
trained men (15). A greater relative amount of body fat
in women is a potential basis for expecting a difference
in substrate metabolism between trained men and
women. In this study, we were able to assess the effect
ofbodycompositionon substratemetabolismbycompar-
ing men and women with comparable training status
but with different body composition. Because we found
no metabolic effect of gender, substrate metabolism
during exercise is determined by energy requirements
of lean body mass, rather than by gender or body
Therewas a slight differenceinstudydesignbetween
the present study and the previous study in men (15).
In the present study in women, exercise at 85% of
was performed on the same day as the exercise
study at 25% V
. The two exercise studies were
separated by an interval of 1 h. In the study in men, we
performed the three exercise protocols on 3 separate
days. One might argue that this difference in design
affects our conclusion as to the comparison of the
results at 85% of V
. However, there was no gender
effect after correction for differences in lean body mass.
Moreover, in the study in men, we documented that all
changes induced by exercise at 25% of V
within the first hour of recovery. Finally, exercise at
25% of V
in trained subjects only involves cycling
withoutanyresistance. This very low exerciseintensity
is not reflected in any change in glucose R
. Therefore,
Table 2. Comparison of anthropometric values and
substrate metabolism at rest and after 2030 min of
exercise at different exercise intensities in
endurance-trained men and women
(n5 5)
(n5 8)
Weight 75.263.6 60.663.2 ,0.02
Height 1.7860.03 1.6760.02 ,0.05
Lean body mass 68.263.3 49.561.6 ,0.01
Fat mass 8.160.2 11.16 1.7 NS
l/min 5.0160.3 3.560.2 ,0.05
ml/kg lean body mass 73.66 3.5 70.16 2.0 NS
Rest 0.7860.01 0.7660.01 NS
25% 0.7360.01 0.7560.01 NS
65% 0.8160.02 0.8160.01 NS
85% 0.9160.01 0.9060.01 NS
FFAuptake, µmol·kg lean
body mass
Rest 17.061.4 15.961.9 NS
25% 29.062.9 26.661.6 NS
65% 25.262.5 29.463.0 NS
85% 19.063.7 15.661.5 NS
Fatty acid oxidation,
µmol·kg lean body
Rest 6.760.5 5.860.5 NS
25% 26.161.6 30.161.7 NS
65% 47.064.6 53.363.5 NS
85% 33.465.0 36.863.9 NS
glucose, µmol·kg lean
body mass
Rest 11.56 0.4 11.66 0.4 NS
25% 14.360.4 11.26 0.6 ,0.01
65% 24.561.2 28.562.7 NS
85% 56.962.1 51.7611.7 NS
Carbohydrate oxidation,
µmol·kg lean body
Rest 6.460.9 6.261.2 NS
25% 11.56 3.4 22.26 3.7 ,0.01
65% 150.9630.0 130.7612.7 NS
85% 331.1617.5 285615.5 NS
Values are means 6 SE; n, no. of subjects. RER, respiratory
exchange ratio; FFA, free fatty acid; R
, rate of disappearance; NS,
not significant.
it seems unlikely that the slight differences in study
design between the two studies affect our conclusion to
a considerable extent.
Several other studies have evaluated the changes in
substrate metabolism in relation to exercise intensity.
Our data extend the observations of Friedlander et al.
(5), which involved the effects of exercise at 52 and
65% of V
in women after 812 wk of endurance
training. They observed that there was no significant
difference in FFAR
between these exercise intensities,
in line with our observation that FFAR
is not different
even between 25 and 65% of V
in trained women.
Fig. 1. Tracer-to-tracee ratios of palmitate (A) and glucose
(B) at rest and during exercise at 25, 65, and 85% of
maximal oxygen uptake. Values are means 6 SE for 8
Fig. 2. Rates of appearance (R
) ofpalmitate (A)and
glucose (B) at rest and during exercise at 25, 65, and
85% of maximal oxygen uptake. Values are means 6
SE for 8 women.
Moreover, our data show for the first time that, in
women, FFAR
at 85% of V
is much lower and not
different from the values obtained at rest, as occurs in
men. In a second study with a similar design, Fried-
lander et al. (6) demonstrated that glucose R
directly related to exercise intensity in trained and
untrained women. Our data arein accordance with this
conclusion over a wider range of exercise intensities.
However, there were also quantitative differences be-
tween the studies of Friedlander et al. and the present
study. For instance, FFA R
and whole body fat oxida-
tion rates were considerably lower in women in the
study of Friedlander et al. (5) than in our study.
Conversely, glucose R
was higher in women after
training in the study of Friedlander et al. (6) than in
our study. These discrepancies are at least in part
related to differences in subject characteristics. For
instance, the women in our study had a lower amount
of body fat than those in the studies of Friedlander et
al. (18 vs. 24%) and a higher V
(70 vs. 54 ml·kg
lean body mass
). These anthropometric values
suggest that the differences in the absolute values
between the studies of Friedlander et al. and our study
are at least in part explained by a differencein training
Several studies have compared substrate metabo-
lism during exercise between men and women. Fried-
lander et al. (6) compared the training-induced alter-
ations of carbohydrate metabolism in men and women.
They found no gender difference in glucose R
exercise in trained men and women,in accordancewith
our data. Moreover, we found no differences in FFA R
between endurance-trained men and women after cor-
rection for differences in lean body mass. In contrast to
our results, however, Friedlander et al. found a gender
a reduction in RER after training, in contrast to men.
In accordance, other authors observed that women
derived more of the total energy expended from fat
oxidation than men did during exercise at 40 or 65% of
(9, 22). The reason for this discrepancy in the
resultsderivedfromindirectcalorimetry betweendiffer-
ent studies is unclear. Most studies evaluate exercising
women in the midfollicular phase (e.g., Refs. 6, 22),
whereas our study was not controlled for the effects of
the menstrual phase. There are indications that the
menstrual cycle affects the metabolic response to exer-
cise. For instance, lipid oxidation during moderate
exercise intensities ishigher in the midluteal phase(8).
Gender differences may, therefore, not be as clear in
women studied throughout all phases of the menstrual
cycle. During submaximal exercise intensity, this gen-
der difference in lipid oxidation disappeared (8). There-
fore, at higher intensities, it is likely that substrate
selection is governed by the exercise itself rather than
by mitigating factors like menstrual cycle.
In this study, we compared five men with eight
women. In this respect, it is appropriate to evaluatethe
statistical power of the comparisons between both
groups. We calculated the detectable difference be-
tween the means as a function of the a-value of 0.05, a
b-value of 0.80, the number of subjects, and the SD of
the observations. Although the detectable difference
varied somewhat between the different variables, the
mean difference between both groups that could be
detected was 15%. Therefore, we cannot exclude the
possibility that there may have been smaller differ-
ences between both groups, which could have been
detected in a study with a larger number of subjects.
However, it is unlikely that this explains the absence of
a difference in RER values between men and women,
Table 3. Substrate concentrations, kinetics, and
oxidation in women after 30 min of exercise
µmol/l 6986103* 7716102* 359668
21.661.7* 25.363.1* 12.661.2
Fat oxidation,
21.561.6† 43.163.5* 30.163.6
Glucose concentration,
mg/dl 8362*† 9566* 141617
9.160.5*† 23.262.0* 41.769.8
Carbohydrate oxida-
18.063.2*† 106.5611.5* 232.16 15.1
Values are means 6 SE for 8 subjects. *P , 0.05 vs. 85% V
P , 0.05 vs.65% V
Fig. 3. Maximal caloric contribution of plasma
free fatty acids (FFA) and glucose and minimal
contribution of muscle triglyceride and glycogen
stores in relation to exercise intensity. Values
represent mean value of 8 endurance-trained
because these values were almost identical in both
In light of the lack of a relationship between relative
fat mass and the lipolytic response, as reflected by FFA
, to exercise, it is appealing to consider the energy
requirements of performing the exercise as the major
determinant of the rate of FFAR
, because it is the rate
of energy utilization that determines the requirement
for substrate oxidation. Nonetheless, several aspects of
our data argue againstthis interpretation.Most impor-
tantly, fatty acid uptake did not increase as the energy
requirement increased. In the absence of a change in
uptake, plasma fatty acid concentrations will not de-
crease, and thus any given peripheral fat cell would
have no direct feedback signal. In any case, there is no
evidence that FFA concentrations influence FFA R
vivo. For example, in short-term fasting the concentra-
tion of FFAincreases two- to threefold, and FFAR
increases (28). Thus there is no direct feedback mecha-
nism whereby FFAconcentration affects FFAR
The absence of a direct link between the energy
utilization of the lean body mass and FFA R
the identification of an alternative mechanism to ex-
plain how the change in energy utilization during
exercise could control lipolysis. Insulin, epinephrine,
and adenosine are the most important short-term
regulators of lipolysis (2), but none provides a link
between energy utilization of lipolysisor FFAR
exercise at different intensities. Thus catecholamines
are only elevated to a great extent during high-
intensity exercise (15), yet in this study [as in previous
studies (10, 15)] fatty acid release was less during
high-intensity exercise than during low intensities.
Insulin concentration is generally suppressed during
exercise (16), and differences in insulin concentration
at different exercise intensities cannot explain the
corresponding rates of lipolysis. Adenosine is a potent
inhibitor of lipolysis in some circumstances (12). How-
ever, because an increase in adenosine will generally
accompany increased ATP turnover, changes in adeno-
sine concentration would not be expected to cause
lipolysis to be positively correlated with energy expen-
diture. In fact, our laboratory (13) has previously
shown that changes in adenosine activity cannot ex-
plain the lipolytic response to exercise. Therefore, it is
impossible to provide a physiological basis for the
notion that energy utilization during exercise controls
lipolysis, either directly or indirectly, through any of
the control mechanisms known to be important in in
vivo regulations of lipolysis.
An implication of the preceding argument is that the
regulation of lipolysis is not necessarily related to the
rate of energy expenditure. This notion is supported by
empirical data from a variety of circumstances. In the
present study, the maximal lipolytic response was
elicited at 25% of V
(Fig. 2), yet energy expendi-
ture increased severalfold at higher intensities. In
contrast, the response to fasting elicits a doubling or
more in the rate of lipolysis, yet the rate of energy
utilization does not increase (28). Furthermore, the
extra fatty acids supplied by increased lipolysis in
fasting far exceed the decrease in caloric equivalents
due to decreased hepatic glucose production (17). Thus,
in a wide variety of physiological circumstances, the
rate of lipolysis is not directly related to the rate of
energy expenditure. The major hormones regulating
lipolysis, insulin and catecholamines, are primarily
controlled by factors other than availability of fatty
acids. Therefore, direct feedback control of lipolysis via
hormonal control is unlikely.
Because our data indicate that changes in lipolysis
are not primarily responsible for changes in fat oxida-
tion during exercise, it is not surprising that we found
no effect of body composition on any metabolic param-
eter. Differences in fat mass per se should be expected
to affect substrate metabolism by means of differences
in the availability of fatty acids. Because differences in
body composition would be expected to be one of the
major reasons for differences in substrate metabolism
in exercise between men and women, the lack of an
ity inresponses between men and women. On the other
in substrate metabolism in exercise (19). The present
study was not designed to assess the role ofsex steroids
because the phase of the menstrual cycle during which
our subjects were studied was not controlled. It is
unlikely, however, that this affected our conclusion
because the coefficient of variation of the data in the
female subjects in the present study was generally less
than in the male athletes who were studied previously
(15).Consequently,whereasvariationsin theconcentra-
tions of sex steroidsmay have contributed tovariability
of the results, that variability cannot explain the
inability to find significant differences between men
and women. Rather, it is likely that any possible effects
of sex steroids were overshadowed by the effects of
strenuous endurance training.
This work was supported by Shriners of North America Grant
8940 andby NationalInstitute of Diabetes andDigestive andKidney
Diseases Grant DK-46017. J. A. Romijn was supported by a grant
from the Dutch DiabetesFoundation.
Present address of J. A. Romijn: Dept. of Endocrinology and
Metabolism, Leiden University Medical Center, PO Box 9600, 2300
RC Leiden, The Netherlands(E-mail:
Address for correspondence: R. R. Wolfe, Metabolism Unit, Shri-
ners Burns Institute, 815Market St.,Galveston, TX77550.
Received 5 February 1998;accepted infinal form8 December1999.
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... Crossover-Concept der Substratutilisation nach Brooks & Mercier, 1994. In Ruhe und bei niedrigen Belastungsintensitäten (< 25 %V´O2max) ist der Anteil der Fettoxidation am Gesamtumsatz mit über 90 % deutlich dominierend (Romijn et al., 2000). Mit progressiv steigender Die spezifischen physiologischen Ursachen für die abnehmende Fettoxidation bei höheren Intensitäten sind im Detail und besonders in der Gewichtung noch nicht erschöpfend geklärt (Brun et al., 2012). ...
... tor zu sehen, da sich dieses Verhältnis bei zunehmender Intensität und Belastungsdauer deutlich im Vergleich zu Ruhebedingungen verschieben kann(Romijn et al., 2000;van Loon, Greenhaff, Constantin-Teodosiu, Saris & Wagenmakers, 2001). ...
Die Arbeit beleuchtet den Einsatz algorithmischer Datenbearbeitungen bei sportwissenschaftlichen Spiroergometrien aus praktischen und theoretischen Gesichtspunkten. Die aktuelle Verbreitung von algorithmischen Datenbearbeitungen aus Breath-by-Breath Untersuchungen wird über die Ergebnisse eines Fragebogens und einer systematischen Literaturübersicht dargestellt. Zudem erfolgt die Analyse der durch Algorithmen verursachten Messwertvarianzen der Sauerstoffaufnahme in diskontinuierlichen Belastungsuntersuchungen, bei Jugendlichen und im submaximalen Belastungsbereich.
... Given that substrate metabolized to provide energy may vary with exercise constraints such as intensity [105], duration [106], training and sex (e.g. [97,107]), it has been proposed to express RE as gross energy cost [105] in J . kg −1. ...
... In most of the articles focusing on RE responses in females, a qualitative analysis of menstrual cycle is lacking, and this might constitute an important methodological bias in RE evaluation. During endurance exercises, females generally use less CHO and have lower RER values [107,116,117]. These metabolic changes may depend on the phases of the menstrual cycle as well as short-term oral contraceptives and, in turn, affect the RE response in females. ...
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In recent years, there has been a significant expansion in female participation in endurance (road and trail) running. The often reported sex differences in maximal oxygen uptake (VO2max) are not the only differences between sexes during prolonged running. The aim of this narrative review was thus to discuss sex differences in running biomechanics, economy (both in fatigue and non-fatigue conditions), substrate utilization, muscle tissue characteristics (including ultrastructural muscle damage), neuromuscular fatigue, thermoregulation and pacing strategies. Although males and females do not differ in terms of running economy or endurance (i.e. percentage VO2max sustained), sex-specificities exist in running biomechanics (e.g. females have greater non-sagittal hip and knee joint motion compared to males) that can be partly explained by anatomical (e.g. wider pelvis, larger femur-tibia angle, shorter lower limb length relative to total height in females) differences. Compared to males, females also show greater proportional area of type I fibres, are more able to use fatty acids and preserve carbohydrates during prolonged exercise, demonstrate a more even pacing strategy and less fatigue following endurance running exercise. These differences confer an advantage to females in ultra-endurance performance, but other factors (e.g. lower O2 carrying capacity, greater body fat percentage) counterbalance these potential advantages, making females outperforming males a rare exception. The present literature review also highlights the lack of sex comparison in studies investigating running biomechanics in fatigue conditions and during the recovery process.
... However, identifying the precise location of FA origin for this fuel has been difficult. For example, while several studies were unable to identify sex differences in plasma FA utilization during exercise particularly when VO 2max is normalized with lean body mass (Romijn et al., 2000;Beaudry and Devries, 2019), one study identified the increased use of plasma FA (47%) in females after 30 min of cycling . Additionally, the question of whether lipid reliance seen in females is based on intramyocellular lipids (IMCL) content remains controversial within the literature (Beaudry and Devries, 2019). ...
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As the fields of kinesiology, exercise science, and human movement developed, the majority of the research focused on male physiology and extrapolated findings to females. In the medical sphere, basing practice on data developed in only males resulted in the removal of drugs from the market in the late 1990s due to severe side effects (some life-threatening) in females that were not observed in males. In response to substantial evidence demonstrating exercise-induced health benefits, exercise is often promoted as a key modality in disease prevention, management, and rehabilitation. However, much like the early days of drug development, a historical literature knowledge base of predominantly male studies may leave the exercise field vulnerable to overlooking potentially key biological differences in males and females that may be important to consider in prescribing exercise (e.g., how exercise responses may differ between sexes and whether there are optimal approaches to consider for females that differ from conventional approaches that are based on male physiology). Thus, this review will discuss anatomical, physiological, and skeletal muscle molecular differences that may contribute to sex differences in exercise responses, as well as clinical considerations based on this knowledge in athletic and general populations over the continuum of age. Finally, this review summarizes the current gaps in knowledge, highlights the areas ripe for future research, and considerations for sex-cognizant research in exercise fields.
... The widely adopted idea of polarized training [4,21,22], i.e., a combination of LIT and HIIT, leads us to assume that further adaptations may occur in HSM + LIT. LIT serves as a potent stimulus to enhance fat oxidation and glucose utilization, which are essential for aerobic energy provision during prolonged endurance training [61][62][63][64]. In contrast, HIIT may lead to cardiopulmonary improvements, such as increased stroke and blood volume [2,65]. ...
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Background Performing multiple high-intensity interval training (HIIT) sessions in a compressed period of time (approximately 7–14 days) is called a HIIT shock microcycle (SM) and promises a rapid increase in endurance performance. However, the efficacy of HIIT-SM, as well as knowledge about optimal training volumes during a SM in the endurance-trained population have not been adequately investigated. This study aims to examine the effects of two different types of HIIT-SM (with or without additional low-intensity training (LIT)) compared to a control group (CG) on key endurance performance variables. Moreover, participants are closely monitored for stress, fatigue, recovery, and sleep before, during and after the intervention using innovative biomarkers, questionnaires, and wearable devices. Methods This is a study protocol of a randomized controlled trial that includes the results of a pilot participant. Thirty-six endurance trained athletes will be recruited and randomly assigned to either a HIIT-SM (HSM) group, HIIT-SM with additional LIT (HSM + LIT) group or a CG. All participants will be monitored before (9 days), during (7 days), and after (14 days) a 7-day intervention, for a total of 30 days. Participants in both intervention groups will complete 10 HIIT sessions over 7 consecutive days, with an additional 30 min of LIT in the HSM + LIT group. HIIT sessions consist of aerobic HIIT, i.e., 5 × 4 min at 90–95% of maximal heart rate interspersed by recovery periods of 2.5 min. To determine the effects of the intervention, physiological exercise testing, and a 5 km time trial will be conducted before and after the intervention. Results The feasibility study indicates good adherence and performance improvement of the pilot participant. Load monitoring tools, i.e., biomarkers and questionnaires showed increased values during the intervention period, indicating sensitive variables. Conclusion This study will be the first to examine the effects of different total training volumes of HIIT-SM, especially the combination of LIT and HIIT in the HSM + LIT group. In addition, different assessments to monitor the athletes' load during such an exhaustive training period will allow the identification of load monitoring tools such as innovative biomarkers, questionnaires, and wearable technology. Trial Registration :, NCT05067426. Registered 05 October 2021—Retrospectively registered, . Protocol Version Issue date: 1 Dec 2021. Original protocol. Authors: TLS, NH.
... Free fatty acids originating from the adipocytes and intramuscular triglycerides are used to generate energy. Due to their low energy flow rate, the percentage contribution of fat oxidation to total energy provision is low during short intensive exercises and increases with the duration of the exercise and the decrease in intensity (6). ...
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Consuming low glycemic carbohydrates leads to an increased muscle fat utilization and preservation of intramuscular glycogen, which is associated with improved flexibility to metabolize either carbohydrates or fats during endurance exercise. The purpose of this trial was to investigate the effect of a 4-week high fat low carbohydrate (HFLC-G: ≥65% high glycemic carbohydrates per day; n = 9) vs. high carbohydrate low glycemic (LGI-G: ≥65% low glycemic carbohydrates daily; n = 10) or high glycemic (HGI-G: ≥65% fat, ≤ 50 g carbohydrates daily; n = 9) diet on fat and carbohydrate metabolism at rest and during exercise in 28 male athletes. Changes in metabolic parameters under resting conditions and during cycle ergometry (submaximal and with incremental workload) from pre- to post-intervention were determined by lactate diagnostics and measurements of the respiratory exchange ratio (RER). Additionally, body composition and perceptual responses to the diets [visual analog scale (VAS)] were measured. A significance level of α = 0.05 was considered. HFLC-G was associated with markedly decreased lactate concentrations during the submaximal (−0.553 ± 0.783 mmol/l, p = 0.067) and incremental cycle test [−5.00 ± 5.71 (mmol/l) × min; p = 0.030] and reduced RER values at rest (−0.058 ± 0.108; p = 0.146) during the submaximal (−0.078 ± 0.046; p = 0.001) and incremental cycle test (−1.64 ± 0.700 RER × minutes; p < 0.001). In the HFLC-G, fat mass (p < 0.001) decreased. In LGI-G lactate, concentrations decreased in the incremental cycle test [−6.56 ± 6.65 (mmol/l) × min; p = 0.012]. In the LGI-G, fat mass (p < 0.01) and VAS values decreased, indicating improved levels of gastrointestinal conditions and perception of effort during training. The main findings in the HGI-G were increased RER (0.047 ± 0.076; p = 0.117) and lactate concentrations (0.170 ± 0.206 mmol/l, p = 0.038) at rest. Although the impact on fat oxidation in the LGI-G was not as pronounced as following the HFLC diet, the adaptations in the LGI-G were consistent with an improved metabolic flexibility and additional benefits regarding exercise performance in male athletes.
... The energy requirements of moderate-intensity exercise are provided primarily by the oxidation of carbohydrates and lipids [1]. The relative contribution by the oxidation of carbohydrates and lipids towards the moderate-intensity exercise requirements are affected by dietary intake [2], training status [3], sex [4], exercise modality [5], environmental conditions [6], and supplementation (e.g., caffeine [7], green tea extract [8], Matcha green tea [9], New Zealand blackcurrant [10]). ...
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New Zealand blackcurrant (NZBC) extract enhanced cycling-induced fat oxidation in female endurance athletes. We examined in recreationally active females the effects of NZBC extract on physiological and metabolic responses by moderate-intensity walking and the relationship of fat oxidation changes with focus on body composition parameters. Twelve females (age: 21 ± 2 y, BMI: 23.6 ± 3.1 kg·m−2) volunteered. Bioelectrical bioimpedance analysis was used for body composition measurements. Resting metabolic equivalent (1-MET) was 3.31 ± 0.66 mL·kg−1·min−1. Participants completed an incremental walking test with oxygen uptake measurements to individualize the treadmill walking speed at 5-MET. In a randomized, double-blind, cross-over design, the 30 min morning walks were in the same phase of each participant’s menstrual cycle. No changes by NZBC extract were observed for walking-induced heart rate, minute ventilation, oxygen uptake, and carbon dioxide production. NZBC extract enhanced fat oxidation (10 responders, range: 10–66%). There was a significant correlation for changes in fat oxidation with body mass index; body fat% in legs, arms, and trunk; and a trend with fat oxidation at rest but not with body mass and habitual anthocyanin intake. The NZBC extract responsiveness of walking-induced fat oxidation is body composition-dependent and higher in young-adult females with higher body fat% in legs, arms, and trunk.
... Vollaard and colleagues (46) have demonstrated that individuals with higher V̇O2max, had a significantly lower absolute V̇O2 and HR responses for a given submaximal exercise intensity. In agreement with others (1,37,40), they have suggested that these improvements may be related to better metabolic and hormonal control and greater dependence on lipids metabolism (46). ...
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International Journal of Exercise Science 15(2): 113-124, 2022. Although several studies investigated heart rate (HR) and metabolic responses to preferred walking speed (PWS), there is a limited amount of data on PWS responses during varying inclines. Further, there is no data pertaining to the impact of PWS at various inclines on postural control. The purpose of the study was to measure cardiovascular, metabolic, perceptual, and postural impacts of walking at PWS at various inclines. Twenty-one participants completed two lab sessions, seven days apart. On day one, PWS on the treadmill and maximal oxygen consumption (V̇O2max) were established for each participant. On day two, using a counter balanced design, participants completed three, 15-minute walking sessions at their PWS at 0, 4, and 8% inclines. During the sessions, HR, V̇O2, rating of perceived exertion (RPE), V̇O2 reserve (V̇O2R) and HR reserve (HRR) were measured and recorded. Center of Pressure (COP) motion was recorded while standing upon a force plate immediately following each walking bout with eyes closed (EC) and eyes open (EO). The results of the study demonstrated a significant difference (p < .05) in the independent variables across the different inclines excluding HR, RPE and HRR at 4% incline. While there were no significant differences in sway amplitude between the different walking bouts, there was a significant increase in sway with EC compared to EO vision condition (p < .05). Still, Approximate Entropy values decreased (increased regularity) from baseline measures (p < .05). These findings suggest that PWS at different inclines impact measures of exertion and signal regularity but not sway amplitude or velocity.
... Several studies have found that fat oxidation rates increase from low-to moderate-intensity exercises and are reduced when the intensity increases (Romijn et al., 2000;Skovgaard et al., 2016). The maximal fat oxidation rate (FATmax) occurs near 40-55% of the maximal oxygen uptake (V̇O2max) (Maunder, Plews and Kilding, 2018) and is commonly prescribed as the intensity for Moderate-Intensity Continuous Exercise (MICT), especially when the goal is fat loss (Achten, Gleeson and Jeukendrup, 2002). ...
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To assess the physiological demand of including high-intensity efforts during continuous exercise, we designed a randomized crossover study, where 12 physically active young males executed three different exercises in random order: FATmax - continuous exercise at the highest fat oxidation zone (FATmax); 2min-130% - FATmax interspersed by a 2-min bout at 130% of the maximal oxygen uptake associated intensity (iV̇O2max); and 20s:10s-170% - FATmax interspersed by four 20-s bouts at 170%iV̇O2max interpolated by 10s of passive recovery. We measured oxygen uptake (V̇O2), blood lactate concentration ([LAC]), respiratory exchange rate (RER), fat and carbohydrate (CHO) oxidation. For statistical analyses, repeated measures ANOVA was applied. Although no differences were found for average V̇O2 or carbohydrate oxidation rate, the post-exercise fat oxidation rate was 37.5% and 50% higher during 2min-130% and 20s:10s-170%, respectively, compared to FATmax, which also presented lower values of RER during exercise compared to 2min-130% and 20s:10s-170% (p<0.001 in both), and higher values post-exercise (p=0.04 and p=0.002, respectively). The [LAC] was higher during exercise when high-intensity bouts were applied (p<0.001 for both) and higher post-exercise on the intermittent one compared to FATmax (p=0.016). The inclusion of high-intensity efforts during moderate-intensity continuous exercise promoted higher physiological demand and post-exercise fat oxidation. Novelty bullets • The inclusion of 2-min efforts modifies continuous exercise demands • Maximal efforts can increase post-exercise fat oxidation • 2-min maximal efforts, continuous or intermittent, presents similar demands.
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For centuries, regular exercise has been acknowledged as a potent stimulus to promote, maintain, and restore healthy functioning of nearly every physiological system of the human body. With advancing understanding of the complexity of human physiology, continually evolving methodological possibilities, and an increasingly dire public health situation, the study of exercise as a preventative or therapeutic treatment has never been more interdisciplinary, or more impactful. During the early stages of the NIH Common Fund Molecular Transducers of Physical Activity Consortium (MoTrPAC) Initiative, the field is well-positioned to build substantially upon the existing understanding of the mechanisms underlying benefits associated with exercise. Thus, we present a comprehensive body of the knowledge detailing the current literature basis surrounding the molecular adaptations to exercise in humans to provide a view of the state of the field at this critical juncture, as well as a resource for scientists bringing external expertise to the field of exercise physiology. In reviewing current literature related to molecular and cellular processes underlying exercise-induced benefits and adaptations, we also draw attention to existing knowledge gaps warranting continued research effort. © 2021 American Physiological Society. Compr Physiol 12:3193-3279, 2022.
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The article considers the issue of the relationship between the phenomenon of procrastination and creative thinking. One of the most common factors that hinder personal and professional effectiveness is procrastination. There is a hypothesis that people with high levels of procrastination have correspondingly well-developed creative thinking, which endows them with the ability to solve problems outside the box and quickly adapt to situations.1 We consider procrastination as a psychological pattern of behavior characterized by person's delaying planned actions or decision-making followed by negative emotional experiences. Literature analysis has shown that procrastination influences creative activity, which leads to the assumption that people with higher levels of procrastination have a higher level of creativity. Upon conducting our research, we uncovered the following pattern: students with a high level of procrastination are more inclined to such factors as risk-taking and fantasy; students with a low level are more likely to present curiosity and task complexity; and students with an average level of procrastination are equally likely to present both factors.
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A new stable isotope method for the determination of substrate oxidation rates in vivo is described and compared with indirect calorimetry at rest and during high-intensity exercise (30 min at 80-85% maximal O2 uptake capacity) in six well-trained cyclists. This method uses the absolute ratios of 13C/12C in expired air, endogenous glucose, fat, and protein in addition to O2 consumption and is independent of CO2 production (VCO2). Carbohydrate and fat oxidation rates at rest, calculated by both methods, were not significantly different. During exercise the breath 13C/12C ratio increased and reached a steady state after 15-20 min. Carbohydrate oxidation rates during exercise were 39.4 +/- 5.2 and 41.7 +/- 5.7 [not significant (NS)], and fat oxidation rates were 7.3 +/- 1.3 and 6.9 +/- 1.2 (NS), using indirect calorimetry, and the breath ratio method, respectively. We conclude that the breath 13C/12C ratio method can be used to calculate substrate oxidation under different conditions, such as the basal state and exercise. In addition, the results obtained by this new method support the validity of the underlying assumption that indirect calorimetry regards VCO2 as a reflection of tissue CO2 production, during exercise in trained subjects, even up to 80-85% maximal O2 uptake.
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Previous studies using indirect means to assess the response of protein metabolism to exercise have led to conflicting conclusions. Therefore, in this study we have measured the rate of muscle protein synthesis in normal volunteers at rest, at the end of 4 h of aerobic exercise (40% maximal O2 consumption), and after 4 h of recovery by determining directly the rate of incorporation of 1,2-[13C]leucine into muscle. The rate of muscle protein breakdown was assessed by 3-methylhistidine (3-MH) excretion, and total urinary nitrogen excretion was also measured. There was an insignificant increase in 3-MH excretion in exercise of 37% and a significant increase (P less than 0.05) of 85% during 4 h of recovery from exercise (0.079 +/- 0.008 vs. 0.147 +/- 0.0338 for rest and recovery from exercise, respectively). Nonetheless, there was no effect of exercise on total nitrogen excretion. Muscle fractional synthetic rate was not different in the exercise vs. the control group at the end of exercise (0.0417 +/- 0.004 vs. 0.0477 +/- 0.010%/h for exercise vs. control), but there was a significant increase in fractional synthetic rate in the exercise group during the recovery period (0.0821 +/- 0.006 vs. 0.0654 +/- 0.012%/h for exercise vs. control, P less than 0.05). Thus we conclude that although aerobic exercise may stimulate muscle protein breakdown, this does not result in a significant depletion of muscle mass because muscle protein synthesis is stimulated in recovery.
Bipsies were obtained from the gastrocnemius muscle of 13 male and 12 female distance runners and analyzed for [14C]palmitoyl-CoA oxidation, fiber composition, and the activities of selected enzymes. The male and female runners were similar in terms of maximal oxygen uptake (VO2max), training mileage, fiber compositions, and data collected during a 60-min treadmill run at 70% VO2max. Muscle succinate dehydrogenase and carnitine palmitoyl transferase activities were, however, significantly greater (P less than 0.05) in the male than in female runners. In addition, the male runners' muscle also showed a greater capacity to oxidize palmitoyl CoA. Little relationship, however, was found between muscle lipid metabolism, enzyme activities, and the calculated (respiratory exchange) fraction of energy derived from fat during 60 min of running at 70% VO2max. Although these data support the concept that endurance training (80-115 km/wk) markedly enhances the capacity of muscles to metabolize fats, the factors that regulate the usage of lipids during prolonged exercise do not appear to be limited by the capacity of the fibers to oxidize fatty acids, as determined by in vitro measurements.
We investigated the hypothesis that the increase in lipolysis that occurs in short-term (86-h) fasting is due to a decreased inhibitory influence of adenosine. In normal volunteers who fasted for 14 and 86 h, the response to adenosine receptor blockade was assessed by the infusion of theophylline at a rate sufficient to produce plasma concentrations (30 microM) that blocked adenosine receptors but that were well below the threshold for inhibition of phosphodiesterase. Lipolysis was assessed by determining the rate of appearance of glycerol using D-5-glycerol infusion. Fatty acid flux was also determined by means of [1-13C]palmitate infusion, and total fatty acid oxidation was determined by indirect calorimetry. There was a mild stimulatory effect of theophylline on lipolysis at 14 h. After the subjects fasted for 86 h, theophylline infusion caused a much greater increase in both lipolysis and fatty acid oxidation. These results suggest that the inhibitory effect of adenosine on lipolysis is increased during short-term fasting.
To evaluate the metabolic consequences of short-term (i.e., less than 24 hours) starvation, glucose and fat metabolism were studied in eight healthy subjects and in eight patients with stable cirrhosis after 16-hour and again after 22-hour starvation by 3-[3H]glucose and [14C]palmitate turnover and by indirect calorimetry. Although patients and controls showed significant increases in free fatty acid concentration (respectively, 48% +/- 12% and 53% +/- 17%) and turnover (55% +/- 14% and 71% +/- 21%) during short-term starvation, the values after 16- and after 22-hour starvation were higher in cirrhosis. Fat oxidation was enhanced in the patients, but did not increase during fasting in contrast to controls (increase 19% +/- 17%, P less than 0.05). Net glucose oxidation was decreased in postabsorptive cirrhotics (P less than 0.05). Although postabsorptive glucose turnover was not different from controls, starvation induced a greater decrease in glucose turnover in the patients (25% +/- 3% vs. 10% +/- 3%, P less than 0.05). This was not reflected in plasma glucose concentrations. In conclusion, the effects of starvation on glucose and fat metabolism are enhanced in cirrhosis; fasting hypoglycemia is prevented by decreased use of glucose. It remains to be established whether these changes are merely explained by defective liver function, per se.
The effects of gender on substrate utilization during prolonged submaximal exercise were studied in six males and six equally trained females. After 3 days on a controlled diet (so that the proportions of carbohydrate, protein, and fat were identical), subjects ran on a treadmill at a velocity requiring an O2 consumption of approximately 65% of maximal. They ran a total "distance" of 15.5 km with a range in performance time of 90-101 min. Plasma glycerol, glucose, free fatty acids, and selected hormones (catecholamines, growth hormone, insulin, and glucagon) were measured throughout and after the run by sampling from an indwelling venous catheter, and glycogen utilization was calculated from pre- and postexercise needle biopsies of vastus lateralis. Exercise protein catabolism was estimated from 24-h urinary urea nitrogen excretion over the test day and a nonexercise day. The males were found to have significantly higher respiratory exchange ratios (mean 0.94 vs. 0.87), greater muscle glycogen utilization (by 25%), and greater urea nitrogen excretion (by 30%) than the females. No gender differences were evident in the hormonal response to the exercise with the exception of a lower insulin concentration and a higher epinephrine concentration in the males. We conclude that, during moderate-intensity long-duration exercise, females demonstrate greater lipid utilization and less carbohydrate and protein metabolism than equally trained and nourished males.
Whole-body lipolytic rates and the rate of triglyceride-fatty acid cycling (reesterification of fatty acids released during lipolysis) were measured with stable isotopic tracers in the basal state and during beta-adrenergic blockade with propranolol infusion in five cachectic patients with squamous cell carcinoma of the esophagus, five cachectic cancer-free, nutritionally-matched control patients, and 10 healthy volunteers. Resting energy expenditure and plasma catecholamines were normal in all three groups. The basal rate of glycerol appearance in blood in the patients with cancer (2.96 +/- 0.45 was similar to that in the nutritionally matched controls (3.07 +/- 0.28, but 48% greater than in the normal-weight volunteers (2.00 +/- 0.16 (P = 0.028). The antilipolytic effect of propranolol and the rate of triglyceride-fatty acid cycling in the patients with cancer were also similar in the cachectic control group and approximately 50% greater than in the normal-weight volunteers, but the differences were not statistically significant because of the variability in the data. We conclude that the increase in lipolysis and triglyceride-fatty acid cycling in "unstressed" cachectic patients with esophageal cancer is due to alterations in their nutritional status rather than the presence of tumor itself. Increased beta-adrenergic activity may be an important contributor to the stimulation of lipolysis.
The hepatic glucose cycle involves the production of plasma glucose from glucose 6-phosphate and the simultaneous conversion of glucose back to glucose 6-phosphate. We have evaluated the role of the glucose cycle in the regulation of plasma glucose concentration during exercise at 70% of maximal O2 uptake and during recovery in five normal volunteers. Total glucose flux was measured by use of [2-2H]glucose (Ra2), net glucose flux through the glucose cycle was determined with [6,6-2H2]glucose (Ra6), and the rate of glucose cycling was determined by Ra2 - Ra6. Gas chromatography-mass spectrometry was used for analysis of isotopic enrichment. At rest, 33% of total glucose flux was recycled. In exercise, total flux increased 300%, but so did glucose cycling, which means that there was no change in the percentage of flux recycled. In recovery, both total flux and the rate of recycling returned rapidly to the resting value. We therefore conclude that whereas total glucose production can respond extremely quickly to large changes in energy requirements caused by exercise, thereby enabling maintenance of a constant blood glucose concentration, glucose cycling does not have an important role in amplifying the control of net hepatic glucose flux through the glucose cycle.
In this study the rate of lipolysis (fatty acid and glycerol release into blood) has been quantified in both normal weight and obese volunteers after both 15 and 87 h of fasting. In each study, the basal rate and subsequent response to epinephrine infusion (0.015 microgram X kg-1 X min-1) were determined. The rate of appearance (Ra) of free fatty acids (FFA) and glycerol were quantified by infusion of [1-13C]palmitate and D-5-glycerol, respectively. Substrate flux rates per unit of body fat mass and lean body mass were calculated from total body water measurements using H2(18)O dilution. In normal volunteers, the basal Ra FFA and Ra glycerol rose markedly with 87 h of fasting, whereas the increases were more modest in the obese subjects. However, the rate of mobilization of fat, in relation to the lean body mass, was higher in the obese subjects than in the normal subjects after 15 h of fasting, and the values were similar in both groups after 87 h of fasting. There was an increased lipolytic response to epinephrine after fasting in both groups. This increased sensitivity may have resulted from the enhancement of fatty acid-triglyceride substrate cycling that occurred after fasting.