Effect of duration of exercise
on excess postexercise O2 consumption
ROALD
BAHR,
IVAR INGNES,
ODD VAAGE,
OLE M. SEJERSTED,
AND ERIC A. NEWSHOLME
Institute of Muscle Physiology, 0033 Oslo 1, Norway; and Department
of Biochmzistry,
University of Oxford, South Parks Road, Oxford OX1 3QU, United Kingdom
BAHR, ROALD, IVAR INGNES, ODD VAAGE, OLE M. SE- compare quantitatively the magnitude of EPOC and the
JERSTED, AND ERIC A. NEWSHOLME.
Effect of duration
of total exercise 02 consumption. If EPOC is related to the
exercise on excess postexercise O2 consumption. J. Appl. Physiol.
utilization of some energy store during exercise, the
62(2): 48%490,1987.-This
study was undertaken to determine
magnitude of EPOC would be expected to be closely
the effect of exercise duration on the time course and magnitude
related to the total work performed. In this study the
of excess postexercise
O2 consumption
(EPOC). Six healthy
previous work of Hermansen et al. (16) has been exmale subjects exercised on separate days for 80,40, and 20 min
tended to investigate the effect of 20, 40, and 80 min of
at 70% of maximal O2 consumption
on a cycle ergometer. A
exercise on EPOC.
control experiment without exercise was performed. O2 uptake,
respiratory exchange ratio (R), and rectal temperature
were
MATERIALS
AND
METHODS
monitored while the subjects rested in bed 24 h postexercise.
An increase in O2 uptake lasting 12 h was observed for all
Subjects. Six male subjects participated in the study.
exercise durations, but no increase was seen after 24 h. The
Their physical characteristics are shown in Table 1. After
magnitude of 12-h EPOC was proportional
to exercise duration
a medical examination, they were fully informed about
and equaled 14.4 t 1.2, 6.8 t 1.7, and 5.1 t 1.2% after 80, 40,
all procedures before written consent was obtained. All
and20 min of exercise, respectively. On the average, 12-h EPOC
subjects were physically active, but not engaged in enequaled 15.2 _t 2.0% of total exercise 0, consumption
(EOC).
durance training. Their maximal 0, uptake values are
There was no difference in EPOC:EOC
for different exercise
similar to those reported as high average for Norwegian
durations. A linear decrease with exercise duration was observed in R between 2 and 24 h postexercise. No change was
males (15).
observed in recovery rectal temperature.
It is concluded that
Testing procedures. Before the testing started the subEPOC increases linearly with exercise duration
at a work
jects were familiarized with bicycle exercise at a constant
intensity of 70% of maximal O2 consumption.
pedalling rate and with breathing through the mouthrespiratory
humans
exchange
ratio; rectal temperature;
weight
control;
IT IS WELL-ESTABLISHED that O2 consumption remains
elevated for some period of time after exercise and the
phenomenon has recently been termed excess postexercise O2 consumption (EPOC) (11). Several aspects of the
EPOC are still debated: i.e., estimations of its duration
vary from 30 to 72 h (3, 4, 9, 11, 13, 14, 24, 30) and
variations in experimental design makes it impossible to
draw any conclusions as to the magnitude of the EPOC.
Furthermore, it is known that food intake enhances O2
consumption- the thermic effect of food-but
whether
previous exercise enhances this thermic effect is controversial (4, 18, 27, 28, 31). Recently, it was shown that
prolonged exercise (-90 min) at 70% of maximal aerobic
capacity not only increased 02 consumption after exercise by 14% over a period of 12 h but also increased the
thermic response to a meal (18). Other recent studies (5,
10, 21) have failed to show any prolonged thermogenic
effect from less intensive exercise (3555% of maximal
aerobic capacity).
From previous studies it has not been possible to
0161-7567/87 $1.50 Copyright
0
piece and the breathing valve used in all metabolic measurements. All testing and experimental exercise procedures were performed on a modified Krogh cycle ergometer. About 2 wk before the experiment started maximal
O2 uptake was measured using the criteria of Taylor et
al. (29). These results were used to predict a work load
corresponding to 70% of maximal O2 uptake in each
subject. Finally, this work load was used in a lo-min trial
run to familiarize the subjects with their subsequent work
intensity. The results from the tests are shown in Table
1.
Experimental protocol. Each subject participated in
four experiments. The subjects reported to the laboratory
at 7:00 A.M. after an overnight fast. They were transported by car, to avoid any physical activity on the
morning of each experiment. They were told not to make
any changes in their dietary or exercise habits, except
that they were asked not to partake in any exercise for 2
days before days of experiment. No tobacco or alcohol
was allowed 24 h before each experiment.
Body weight was measured at the start of each test
session.A thermistor (type DU 3S, Ellas Instruments A/
S, Copenhagen, Denmark) was inserted lo-15 cm into
the rectum. After that the subjects rested in bed until
the exercise period started.
1987 the American
Physiological
Society
485
486
EXERCISE
DURATION
AND
POSTEXERCISE
O2 CONSUMPTION
1. Physical characteristics and exercise data for each subject
TABLE
Subject
No.
Age,
1
2
3
4
5
6
Yr
Ht,
cm
22
21
22
21
26
24
188
181
175
183
197
197
Mean
_t SE
22.7k0.8
Missing
value
for subject
186.8t3.6
Vi0 2 max,
ml - kg-l - min-’
82.3
70.3
71.5
75.5
93.0
92.0
59.4
57.2
52.2
50.2
55.1
50.7
80.8zk4.1
1 is due to an accidental
technical
54.1t1.5
malfunction.
On three separate days the subjects exercised for 80,
40, or 20 min. A control experiment without exercise was
also performed. Otherwise the conditions were identical
to the exercise experiments. Experimental days were
separated by -2 wk and the sequence of the experiments
(80,40, or 20 min of exercise or control) was randomized.
The start of exercise was adjusted so that the recovery
period always started at 9:30 A.M. Three subjects were
unable to complete the BO-min exercise period due to
exhaustion, and their exercise times are shown in Table
1. After exercise the subjects rested in bed for 24 h, but
they were not allowed to sleep for the first 12 h of
recovery.
The subjects were given three meals consisting of
bread, jam, and skimmed milk during the experiment.
The average caloric content per meal was 1,200 kcal. The
.
fl .rst meal was taken 2 h, the second 7 h, and the last 12
h after exercise. All meals were camp leted within 30 min.
For every subject the amount of food taken at each meal
was measured, and he was given an identical diet all four
experiments.
Measurements. O2uptake was measured for the last 15
min of the rest period before exercise and 5 min before
the end of exercise. Postexercise O2uptake was measured
continuously for the 1st h and thereafter for the last 15
min of each hour for the next 11 h. Finally, O2 uptake
was measured 24 h after the end of exercise, i.e., after
the subject had sl.ept in the laboratory overnight. Rectal
temperature was recorded continuously during th .e whole
experimental period except between 12 and 24 h after
exercise.
Expired air was collected by the Douglas bag method,
and volume was measured in a wet spirometer. Analyses
for CO, and O2 were performed on a Scholander apparatus (23).
StatisticaL methods. Results are given as means t SE.
Linear relationships between work time and individual
responses of postexercise OZ consumption or R were
tested by analysis of covariance. Under the null hypothesis that slopes were 0, probability was estimated from F
provided by the deviations mean square (25). Rejection
level was chosen as P 5 0.05.
RESULTS
O2 uptake. On the control day, 02 consumption was
267 t 13 ml/min in the morning, and after the first meal
it was increased to 334 t 13 ml/min. O2 consumption
then fell slowly during the next 5 h but was increased to
Work
Exercise
iTo2,
% of max
80 min
40 min
20 min
Exercise
Duration
on Day I,
min
72
73
71
69
73
70
68
67
69
74
68
70
71
67
62
77
67
80
72
80
75
80
71
71.3t0.7
69.2t1.3
69.0t2.0
Load,
W
240
193
175
175
286
229
216.3t17.8
VOW,,,,
maximum
76.3t1.7
O2 uptake.
approximately the previous value by the second meal
(Fig. 1). Exercise increased the rate of 0, consumption
to 3,219 t 189 ml/min (for 80 min duration of exercise),
3,076 t 231 ml/ min (40 min), and 3,049 t 251 ml/min
(20 min).
The postexercise period was divided into three intervals for statistical analysis of the data. The first interval
lasts from the end of the exercise period until the first
meal (O-2 h). The analysis of this interval provides
information on the exclusive effect of exercise on EPOC.
The data obtained during the next interval (2-7 h) is
influenced not only by exercise, but also by any change
the exercise period might induce on the thermic effect of
food. The third interval (7-12 h) is identical to the
second, except that it is an additional 5 h removed from
the exercise period.
A linear relationship was observed between exercise
duration and O2 consumption and the increase was statistically significant for all three time intervals (Fig. 2).
No difference was observed between the control and
exercise experiments after 24 h of recovery (P > 0.25).
The total O2consumption for the first 12 h of recovery
was 251.8 t 10.5, 234.6 t 7.7, 231.0 & 8.1, and 219.9 t
8.1 liters for 80, 40, and 20 min of exercise and the
control experiment, respectively. The excesspostexercise
O2 consumption (12-h EPOC) was calculated as the
increase in O2 consumption above control values for the
first 12 h of recovery. Twelve-hour EPOC was 14.4 t
1.2,6.8 t 1.7, and 5.1 t 1.2% (SE) for 80,40, and 20 min
of exercise, respectively. A linear relationship was observed between the magnitude of 12-h EPOC and exercise duration (Fig. 3).
We have also calculated the 12-h EPOC as a percent
of the total exercise 0, consumption (EOC); this value
was 15.2 k 2.0% (mean for all experiments). For different
exercise durations, values of 12-h EPOC were 13.6 t 1.5,
12.2 -c-3.0, and 19.8 t 4.7% of EOC after 80, 40, and 20
min of exercise, respectively (NS).
Respiratory exchange ratio. R increased from 0.78 t
0.01 (mean morning value for all experiments) to 0.92 t
0.04 (80 min period of exercise) and 0.92 t 0.02 (for both
the 40- and 20-min periods of exercise) at the end of the
exercise period. Immediately after exercise, R fell sharply
to those of the control experiment and for the interval
between the end of the exercise period and the first meal
(O-2 h), we observed no significant decrease in R for
different exercise durations (Fig. 4). However, after the
first (2-7 h) and second (7-12 h) meals we observed a
EXERCISE
..............
..............
..............
..............
..............
.............
..............
.............
..............
.............
..............
..............
..............
..............
..:.. ..~.~.~.‘.‘.‘.‘.~.~.~.~.
. .. .. ... .. .1
AND
I
I
O2 CONSUMPTION
0
80
MIN EXERCISE
h
f
MEAL
FIG. 1. Time plot of mean O2 uptake
(n = 6) for all experimental
days. Different symbols are used for 80-, 40-, ZO-min
exercise and control experiments.
2
4
i5
(3
5;
.
300
487
0 CONTROL
W 20 MIN EXERCISE
A 40 MIN EXERCISE
....
350
POSTEXERCISE
I
..............
.............
.
..............
.............
..............
.IT
.............
t
h
;.z
v
w
DURATION
l
0
m
4.
250
.4
I
4
6
TIME
450
( hrs )
.
I
RECOVERY
RECOVERY
INTERVAL
n
.-c
g 400
E
Y
RECOVERY
INTERVAL
-
INTERVAL
2-7h
O-2h
7-12h
FIG. 2. O2 uptake
vs. exercise
duration (n = 6) in 3 time intervals:
between
exercise and 1st meal (O-2 h), between
1st and 2nd meals (2-7 h), and between
the 2nd and 3rd meals (7-12 h). Different
symbols
are used for each subject.
Dashed
mean
regression
line passes
through
mean value of all observations
and slope was obtained
from analysis of
covariance
carried out for each time interval.
e
a
k
3
z
>
g
350
300
t
a
g
0
CJ 250
y
k!
-
269 + 1.36x
p <c 0.001
y=
314+0.58x
p << 0.00
Y = 313 + 0.22x
p < 0.02
1
1
0
40
80
40
0
WORK
TIME
80
0
I
I
40
I
I
80
(min)
linear decrease in R with increasing exercise duration
(Fig. 5). After 24 h there was still a linear decrease in R
as the exercise duration increased (P c 0.05).
Rectal temperature. Rectal temperature
rose to 38.4 t
0.2”C (80-min period of exercise), 37.8 t 0.3OC (40-min
period of exercise) and 37.5 t O.lOC (20-min period of
exercise) at the end of the exercise period. The temperature decreased rapidly and reached control values in
~30 min on all exercise days. Thereafter,
no significant
difference was observed in rectal temperature
between
postexercise and control experiments.
DISCUSSION
This study shows that the magnitude of 12-h EPOC is
linearly related to the duration of a prolonged submaximal exercise bout. Hence with this kind of exercise 12-h
EPOC is a constant fraction equaling 15% of the total
O2 consumption
during the exercise period.
Because of variability of exercise tasks and differences
in experimental
design, it is difficult to compare previous
findings with those presented in this paper. The present
study confirms the recently published findings of Machlum et al. (18) in which the mean excess postexercise
O2
uptake for 12 h was 14% above the basal after exhaustive
work at a work intensity corresponding
to 70% of maximal aerobic capacity. In other studies there is considerably variability
concerning
the effects of exercise on
postexercise
O2 consumption.
Thus three recent wellcontrolled investigations
(5, 10, 21) failed to show any
prolonged thermic effect of exercise, apparently in conflict with the present study. Since two other reports have
indicated that an increase in severity of exercise (3, 9)
causes an increase in EPOC, the variability
in response
488
EXERCISE
DURATION
AND
POSTEXERCISE
40
y-0.8+0.40x
15
,^ 30
!c
6
cu
T
E
10 5
0
8
5
X
t;
cl
4
20
10
58
%
0
I
I
I
0
20
40
WORK
1
80
0
I
80
TIME (mid
3. Plot of excess postexercise
O2 consumption
for first 12 h of
recovery
(EPOC)
vs. duration
of exercise.
Different
symbols are used
for each subject. Dashed Line, mean regression
as defined in legend to
Fig. 2.
FIG.
may be explained by differences in exercise intensity, as
suggested by Brehm and Gutin (5). The findings of these
latter workers
suggested the existence of a threshold
value of about 50% of maximal aerobic capacity before
any significant
increase in recovery Oz uptake was observed. It should also be noted that in all three studies
(5, 10, 21) O2 uptake was measured for only l-3 h of the
recovery period and in fasting subjects. We were unable
to find in the literature any other study on the effect of
duration of exercise on EPOC. Hence we conclude that
with exercise intensity at approximately
70% of maximal
0, uptake EPOC is clearly demonstrable
for at least 12
h, and linearly related to exercise duration.
It is interesting
to note that EPOC for 12 h is a
constant percent of the total O2 consumption
during
exercise, when exercise duration is varied. However,
in
view of Brehm and Gutin’s finding of a nonlinear rela-
0
2
4
6
TIME
8
( hrs >
O2 CONSUMPTION
tionship between exercise intensity
and EPOC (5), a
study of the effect of intensity of exercise on EPOC could
be of considerable interest.
There is additional controversy
over both the duration
of EPOC and the effect of exercise plus feeding on EPOC.
Previously
it has been found that, even after 31 h of
recovery from exercise, O2 consumption
was 8% above
normal (9). In the present study, we observed an increase
in the 7- to 12-h interval after exercise, but not after 24
h. However, since we have no data for the time period
between 12 and 24 h, our values probably represent a
minimal estimate of the extra energy consumption.
Accordingly, other workers
have suggested that the extra
energy expenditure
after exercise may be considerably
greater than presently
found during a 12-h period (2).
The study of Mzehlum et al. (18) indicated that EPOC
was partly related to an effect of meals. However, other
investigators
have suggested either that exercise has no
effect on the thermic effect of food (27) or that it is only
increased if individuals had overeaten before the exercise
(4, 19, 27, 30). In the present study a considerable part
of the EPOC was observed following the first (2- to 7-h
interval) and second (7- to 12-h interval) meals; 42% of
12-h EPOC was observed after the first meal and 22%
after the second. Proper estimates of the meal effects
will require control studies in which subjects are fasted
after exercise. No such information
is presently available.
The mechanisms
responsible
for stimulated
O2 consumption after exercise have been discussed by Hermansen et al. (16). Two explanations
were proposed: increased rates of substrate (“futile”)
cycling after exercise
and extra energy required for the synthesis of depleted
glycogen stores.
Exercise at 70% of maximal O2 uptake, as used in the
present study, is known to deplete glycogen stores completely (17). This would, in a subject weighing 80 kg,
0
CONTROL
H
A
20 MIN EXERCISE
40 MIN EXERCISE
0
80 MIN EXERCISE
10
FIG. 4. Time plot of mean respiratory
exchange
ratio (R) (n = 6) for all experimental days. Different
symbols are used
for 80, 40, and 20 min exercise and control experiments.
12
24
EXERCISE
1.0
.
DURATION
AND
POSTEXERCISE
RECOVERY
RECOVERY
INTERVAL
O-2h
O2 CONSUMPTION
489
RECOVERY
INTERVAL
INTERVAL
2-7h
7-12h
FIG. 5. Respiratory
exchange
ratio
(R) vs. exercise duration
(n = 6) in three
time intervals;
between exercise and 1st
meal (O-2 h), between 1st and 2nd meals
(2-7 h), and between
2nd and 3rd meals
(7-12 h). Different
symbols are used for
each subject. Dashed line, mean regression as defined in legend to Fig. 2.
y=O.900-0.000464x
y=O.772-0.000375x
N.S.
0
p c 0.005
80
0
WORK
TIME
I
I
1
0
40
80
(min)
correspond to -1.7 mmol glycosyl units. At an average
R of 0.85, the O2 cost of glycogen resynthesis
would be
-20 liters. However, resynthesis
of muscle glycogen is a
fairly slow process that may take as much as 48 h (22).
In the present study, the average EPOC during the first
12 h of recovery after 80 min exercise was 31.9 liters.
Thus it is unlikely that the extra O2 consumption
would
account for more than half of the EPOC.
There is now considerable indirect evidence to support
the view that an increased rate of substrate (futile) cycles
may be in part responsible for EPOC (6, 8, 16, 18, 20)
and that raised level of catecholamines
could be one
important factor leading to increased cycling rates. The
present findings are consistent with this viewpoint
and,
furthermore,
they suggest that the mobilization
of fat
from the adipose tissue reserves and an increased rate of
cycling between triacylglycerol
and fatty acids may be
responsible for EPOC.
It has been known
for some time that, in normal
subjects, -20 min of exercise is necessary to increase the
plasma levels of fatty acids (7) and, at an exercise intensity of -60% of maximal aerobic capacity, the plasma
fatty acid level increases progressively
over 180 min of
exercise (1). Furthermore,
in this latter study, both the
plasma levels of fatty acids and catecholamines
were
markedly
elevated 40 min after exercise had ceased.
These two factors may be responsible for stimulation
of
the rate of the triacylglycerol-fatty
acid substrate cycle
in adipose tissue. Since one turn of this cycle requires a
net hydrolysis
of eight molecules of ATP to ADP, an
increase in the rate of this cycle would result in a marked
increase in O2 consumption
after exercise. This cycle is
known to occur in adipose tissue of the rat and mouse
(6, 26) and may occur in muscle and liver, and catecholamines can increase the rate of this cycle in vivo (6). The
postexercise decrease in the value of R (Fig. 4) indicates
a greater proportion
of fat being oxidized in our subjects
and hence a higher plasma fatty acid level. Consequently
one factor responsible
for the relationship
between duration of exercise and EPOC may be the gradual increase
in the dependence on fatty acids as a fuel as the duration
of the exercise increases. Once exercise has finished, the
plasma level of fatty acids further increases, and this
increase may be proportional
to the rate of fatty acid
utilization
during the exercise period. One role of the
triacylglycerol-fatty
acid cycle in adipose tissue may be
to decrease gradually and progressively
the rate of fatty
acid mobilization
and, additionally,
in other tissues, it
may act as a system to buffer the intracellular
levels of
fatty acid and fatty acyl-CoA (20). Exercise of insufficient intensity or duration to raise the plasma fatty acid
and/or catecholamine
levels may not result in a marked
EPOC.
The current findings may be of considerable practical
importance in prevention of obesity and in the treatment
of mild obesity. Thus the importance of exercise depends
on the extra energy utilized due to the physical activitynot only during the activity per se but when the activity
has ceased. Exercise has often been discounted because
of the assumption that very long periods of exercise were
necessary to produce any significant use of energy (12).
The present work demonstrates
that as little as 20 min
of sustained exerci se may be beneficial, since it increases
energy consumption
for a considerable
period of time
after the exercise is stopped. Furthermore,
the thermic
response to food may be increased after exercise and the
subjects oxidized more fat after exercise despite the high
carbohydrate
nature of the diet, suggesting that this fat
must be derived from the adipose tissue. These findings
indicate that a regimen of daily exercise plus an energycontrolled diet should provide a satisfactory,
long-term
treatment for obesity.
In conclusion,
this study demonstrates
a linear increase in EPOC in relation to exercise duration, amounting to -15% of exercise energy expenditure.
In addition
to the obvious practical implications
in relation to obesity, these results indi .cate that the use of tables calculating the energy cost of exercise should be reevaluated
to include the considerable
excess postexercise
energy
expenditure.
This
Science
Institute.
study was supported
and the Humanities
by The Norwegian
Research
Council
for
and by The Norwegian
Building
Research
490
EXERCISE
DURATION
AND
POSTEXERCISE
This study was initiated
and carried out under the inspiring
supervision of the late Dr. Lars Hermansen,
Director
of Research
at the
Institute
of Muscle
Physiology.
The authors
thank
Jorid Thrane
Stuenaes, Bjerg I. Selberg, Kari Heldal, Ada Ingvaldsen,
and Anne Kari
Henanger
for skillful
technical
assistance.
Address
for reprint
requests:
0. M. Sejersted,
Institute
of Muscle
Physiology,
P.O. Box 8149 DEP, 0033 Oslo 1, Norway.
Received
18 November
1985; accepted
in final
form
9 September
1986.
REFERENCES
1. AHLBORG,
G., AND P. FELIG. Lactate and glucose exchange
across
the forearm,
legs and splanchnic
bed during and after prolonged
leg exercise. J. Clin. Invest. 69: 45-54, 1982.
2. ALLEN, D. W., AND B. M. QUIGLEY. The role of physical activity
in the control of obesity. Med. J. Aust. 2: 434-438,
1977.
3. BENEDICT, F. G., AND T. M. CARPENTER.
lrhe Metabolism
and
Energy Transformations
of Healthy
Man During Rest. Washington,
DC: Carnegie
Institution,
1910, p. 182-193.
4. BRAY, G. A., B. J. WHIPP, AND S. N. KOYAL. The acute effect of
food intake on energy expenditure
during cycle ergometry.
Am. J.
Clin. Nutr. 27: 254-259,
1974.
5. BREHM, B., AND B. GUTIN. Recovery energy expenditure
for steady
state exercise in runners
and nonexercisers.
Med. Sci. Sports Exercise 18: 205-210,
1986.
6. BROOKS, B. J., J. R. S. ARCH, AND E. A. NEWSHOLME.
Effect of
some hormones
on the rate of the triacylglycerol/fatty
acid substrate cycle in adipose tissue of the mouse in vivo. Biosci. Rep. 3:
263-267,1983.
7. CARLSON, L. A., L. G. EKELUND,
AND L. ORO. Studies on blood
lipids during exercise. J. Lab. CZin. Med. 61: 724-729,
1963.
8. CHALLISS, R. A. J., J. R. S. ARCH, AND E. A. NEWSHOLME.
The
rate of substrate
cycling between fructose 6-phosphate
and fructose
1,6-bisphosphate
in skeletal
muscle.
Biochem.
J. 221: 153-161,
1984.
9. EDWARDS, H. T., A. THORNDIKE,
JR., AND D. B. DILL. The energy
requirement
in strenuous
muscular
exercise.
New Engl. J. Med.
213: 532-535,
1935.
10. FREEDMAN-AKABAS,
S., E. COLT, H. R. KISSILEFF,
AND X. PISUNYER. Lack of sustained
increase in Voz following
exercise
in
fit and unfit subjects. Am. J. CZin. Nutr. 41: 545-549,
1985.
11. GAESSER, G. A., AND G. A. BROOKS.
Metabolic
bases of excess
postexercise
oxygen consumption:
a review.
Med. Sci. Sports Exercise 16: 29-43, 1984.
12. GARROW, J. S. The regulation
of energy expenditure
in man. In:
Recent Advances
in Obesity Research.
London:
Newman,
1978, p.
200-210.
13. GLICK, Z., E. SHVARTZ, AND M. MODAN. Absence of increased
thermogenesis
during short-term
overfeeding
in normal
and over-
O2 CONSUMPTION
weight women. Am. J. Clin. Nutr. 30: 1026-1035, 1977.
14. HANSON,
J. S. Exercise
responses
following
production
of experimental obesity. J. Appl. Physiol. 35: 587-591,
1973.
15. HERMANSEN,
L. Oxygen
transport
during exercise in human subjects. Acta Physiol. Stand. Suppl. 399: 53-68, 1973.
L., M. GRANDMONTAGNE,
S. M~HLUM,
AND I.
16. HERMANSEN,
INGNES. Postexercise
elevation
of resting oxygen uptake:
possible
mechanisms
and physiological
significance.
In: Physiological
Chemistry of Training
and Detraining.
Basel: Karger,
1984, p. 119-129.
17. HERMANSEN,
L., E. HULTMAN,
AND B. SALTIN. Muscle glycogen
during prolonged
severe exercise. Acta Physiol. Stand. 71: 129-139,
1962.
18. MLEHLUM,
S., M. GRANDMONTAGNE,
E. A. NEWSHOLME,
AND 0.
M. SEJERSTED.
Magnitude
and duration
of excess post-exercise
oxygen
consumption
in healthy
young subjects.
Metabohsm.
35:
425-429,1986.
19. MILLER,
D. S., P. MUMFORD,
AND M. J. STOCK. Gluttony.
2.
Thermogenesis
in overeating
man. Am. J. Clin. Nutr.
20: 12231229,1967.
20. NEWSHOLME,
E. A. Substrate
cycles: their metabolic,
energetic
and thermic
consequences
in man. Biochem.
Sot. Symp. 43: 183-
205,1978.
21. PACY, P. J., N. BARTON,
J. WEBSTER, AND J. S. GARROW.
The
energy cost of aerobic exercise in fed and fasted normal subjects.
Am. J. Clin. Nutr. 42: 764-768, 1985.
22. PIEHL, K. Time course for refilling
glycogen
stores in human
muscle fibers following
prolonged
moderate
exercise. Acta PhysioZ.
Stand. 90: 297, 1974.
23. SCHOLANDER,
P. F. Analyzer
for accurate estimating
of respiratory
gases in one-half
cubic centimeter
samples.
J. BioZ. Chem. 167:
235-249,1947.
24. SEGAL, K. R., AND B. GUTIN. Thermic effect of food and exercise
in lean and obese women. Metabohsm
32: 581-589, 1983.
25. SNEDECOR, G. W., AND W. G. COCHRAN.
StatisticaL
Methods.
Ames: Iowa State Univ. Press, 1980.
26. STEINBERG, D. Fatty acid mobilization-mechanisms
of regulation
and metabolic
consequences.
Biochem.
Sot. Symp. 24: 111-144,
1963.
27. STOCK, M. J. Effects of fasting and refeeding
on the metabolic
response to a standard
meal in man. Eur. J. Appl. Physiol. Occup.
Physiol. 43: 35-40, 1980.
Y. A. The influence
of activity
and size of meals on
28. SWINDELLS,
caloric response in women. Br. J. Nutr. 27: 65-73, 1973.
29. TAYLOR, H. L., E. BUSKIRK,
AND A. HENSCHEL.
Maximal
oxygen
intake as an objective
measure of cardio-respiratory
performance.
J. Appl. Physiol. 8: 73-80, 1955.
30. WHIPP, B. J., G. A. BRAY, AND S. N. KOYAL. Exercise energetics
in normal
man following
acute weight gain. Am. J. CZin. Nutr. 26:
1284-1286,1973.
31. ZAHORSKA-MARKIEWICZ,
obesity.
Eur.
J. Appl.
B. Thermic
Physiol. Occup.
effect of food and exercise in
Physiol. 44: 231-235, 1980.