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Exercise Physiology Laboratory, School of Education, The Flinders University of South Australia, Adelaide, South Australia 5001, Australia
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
FOOTNOTES
REFERENCES
ABSTRACT 
Laforgia, J., R. T. Withers, N. J. Shipp, and C. J. Gore.
Comparison of energy expenditure elevations after submaximal and
supramaximal running. J. Appl.
Physiol. 82(2): 661-666, 1997.
Although exercise
intensity has been identified as a major determinant of the excess
postexercise oxygen consumption (EPOC), no studies have compared the
EPOC after submaximal continuous running and supramaximal interval
running. Eight male middle-distance runners [age = 21.1 ± 3.1 (SD) yr; mass = 67.8 ± 5.1 kg; maximal oxygen consumption
(
O2 max) = 69.2 ± 4.0 ml · kg
1 ·
min1] therefore
completed two equated treatments of treadmill running (continuous
running: 30 min at 70%
O2 max; interval
running: 20 × 1-min intervals at 105%
O2 max with
intervening 2-min rest periods) and a control session (no exercise) in
a counterbalanced research design. The 9-h EPOC values were 6.9 ± 3.8 and 15.0 ± 3.3 liters (t-test:
P = 0.001) for the submaximal and
supramaximal treatments, respectively. These values represent 7.1 and
13.8% of the net total oxygen cost of both treatments. Notwithstanding the higher EPOC for supramaximal interval running compared with submaximal continuous running, the major contribution of both to weight
loss is therefore via the energy expended during the actual exercise.
excess postexercise oxygen consumption; indirect calorimetry
INTRODUCTION THE ELEVATION in
O2 consumption
( Although there have been improvements in the experimental design of
more recent EPOC studies, only five (7, 14, 18, 25, 33) of them have
examined the Bahr and Sejersted (6) have reported an exponential relationship
between exercise intensity and the EPOC for prolonged exercise.
Furthermore, Gore and Withers (17) demonstrated that exercise intensity
was the major determinant of the EPOC because it explained five times
more of the EPOC variance than either exercise duration or total work
completed. This may be pertinent to athletes who perform supramaximal
exercise (intensity >100% METHODS Table 1.
Weekly training loads
O2) above the resting level
after exercise, which Gaesser and Brooks (15) have called the excess
postexercise oxygen consumption (EPOC), was initially thought to
contribute significantly to the energy cost of exercise (11, 21). This
finding is often used to enhance the attractiveness of exercise as an
integral component of weight-reduction programs. However, neither study
quantified the intensity and duration of the exercise, and there is
minimal information on the controls (24) that should have been observed
when the baseline O2 data were collected. Bahr and Maehlum (4), accordingly, concluded that the
reported large sustained increases in the postexercise O2 may be more an
artifact of the experimental design than the exercise stimulus.
O2 after
quantified weight-bearing exercise by using experimental designs that
accounted for the diurnal variation in resting metabolic rate (RMR).
The study by Gore and Withers (17) is the most comprehensive because
the treatments ranged from a 20-min walk at 30% maximal
O2
(O2 max; 6.8 km/h) to
an 80-min training run at 70%
O2 max (13.4 km/h). The
maximal 8-h EPOC, which occurred after 80 min at 70%
O2 max, was 14.6 liters
(~297 kJ). Withers et al. (33) also reported an 8-h EPOC of 32.4 liters (~594 kJ) after a 35-km road run [~70% O2 max; time = 164.1 ± 14.0 (SD) min], which is by far the most exhausting bout
for any of the EPOC studies. They concluded that even after a 35-km
run, which is well beyond the capacities of sedentary persons, the
contribution of the postexercise increase in metabolism to weight loss
is relatively minor when compared with the net energy expenditure
during the run.
O2 max) during interval
training. Bahr et al. (2) measured the EPOC after supramaximal cycling.
However, the treatment (three 2-min intervals of 108%
O2 max) administered to
their untrained subjects is well below the training loads of
competitive cyclists. There is also scope for their experimental design
to be extended to determine the effect of intensity per se by an
attempt to match the total work performed during the high-intensity
interval training with that accomplished during lower intensity
continuous cycling. No studies were located that examined the EPOC
associated with supramaximal running. The purpose of this research was
therefore to examine the EPOC difference between submaximal continuous
running (30 min at 70%
O2 max) and
supramaximal interval running (twenty 1-min runs at 105%
O2 max with intervening
2-min recovery periods). On the basis of the work by Gore and Withers
(17), it was hypothesized that the EPOC of supramaximal interval
running would be greater than that for the matched work of submaximal
continuous running. If the EPOC difference between these two types of
training is physiologically significant, then this may have
implications for the energy requirements of high-performance athletes
(29) and the design of exercise protocols for weight loss.
O2 max = 69.2 ± 4.0 ml · kg1 ·
min1; height = 174.9 ± 5.3 cm; body fat = 9.1 ± 2.3%] participated in the study.
Table 1 contains the average weekly
training loads during the preceding 12 mo.
Subject
Running, km
Other
MJ
49-60
2 h of
cycling; 2-h weight session
FA
120
SH
60-70
MM
80-90
2.5 km of swimming
MP
25-35
1.25 h of swimming, 2.5 h of cycling
MH
50
2-h weight session
MDH
55
NT
95-100
Listed are average weekly training loads for 12 mo preceding
experiment.
ek et al. (9) equation (%body fat = 497.1/BD 
451.9) was used to estimate percent body fat from BD.
Determination of
O2 max and treatment
workloads.
These measurements were conducted with the automated indirect
calorimetry system described by Sainsbury et al. (27). The Beckman LB-2
CO2 analyzer (Anaheim, CA) and
Ametek S-3A O2 analyzer (Pittsburgh, PA) were calibrated before testing and checked for drift
at the end of the test by using three gases that had been authenticated
by Lloyd-Haldane analyses. Inspired volume was measured by a P. K. Morgan MK2 turbine-volume transducer (Rainham, Kent, UK) that was
calibrated before and after testing by using a 1-liter syringe in
accordance with the manufacturer's instructions. The accuracy of the
turbine had previously been established throughout the range spanning
light to maximum exercise (20). The system was checked daily for leaks.
Before data collection, a
O2 max-reliability trial (n = 6) produced an intraclass
correlation (ICC) of 0.98 and a coefficient of variation (CV) of 1.5%.
Subjects visited the laboratory before the
O2 max test to be
familiarized with running on the Quinton treadmill (model 18-60; Seattle, WA), operating the emergency-stop lever, and breathing through
the Hans Rudolph R2700 respiratory valve (Kansas City, MO) while a
noseclip was attached. A 3-min warmup at 7.5 km/h and 0% grade was
followed by a treadmill speed of either 12 or 15 km/h, with the grade
increased by 2%/min until the subject was unable to continue.
O2 max was held to
occur when the O2 for
successive workloads differed by <2
ml · kg1 · min1.
This criterion is less than two SD for the increments in
O2 that are associated with
the step increments of the protocols. The largest
O2 difference between the
last two increments of the eight
O2 max tests was 1.3 ml · kg1 · min1.
The 70 and 105%
O2 max workloads were
subsequently predicted from the regression of steady-state
O2 at ~40, 50, 70, and
80% O2 max,
respectively, on treadmill speed at 5% elevation.
Recovery and resting
O2.
O2 was measured for the
first 25 min postexercise by using the previously described automated
system. Subsequent RMR, resting O2, and recovery
O2 were
determined by using the Douglas bag method. Douglas bags (150 liter;
Plysu Industrial, Milton Keynes, Buckinghamshire, UK), which had been
previously flushed with the subject's expirate, were connected via a
two-way straight-through valve to the expiratory port of a Hans Rudolph
R2600 respiratory valve. Subjects were connected to the respiratory
valve for 2.5 min before the two-way valve was switched into the
Douglas bag at the end of an expiration. Collection was completed at
the end of an expiration ~10 min later, and the exact collection time was recorded by stopwatch. The volume of expirate was determined by
using a 350-liter Tissot spirometer (Warren Collins, Braintree, MA)
that had been mapped for constant cross-sectional area throughout its
elevation. The preexperimental reliability trials for the resting
O2 of six subjects who were
measured on consecutive days resulted in an ICC of 0.93 and a CV
of 1.8%.
Heart rate.
Heart rate (HR) was monitored continuously during all
O2 measurements by an
electrocardiogram (Becton-Dickinson, Sharon, MA) by using a CM-5
electrode placement.
Rectal temperature.
During the treatment and control days, rectal temperature
(Tre) was monitored continuously
by customized equipment (18) that was calibrated before data
collection against a glass thermometer that had been certified by
the National Association of Testing Authorities
(Australia).
Experimental design.
All subjects participated in a control day and two treatment days that
were counterbalanced to eliminate any order effect. Such a design with
eight subjects is sensitive enough to detect (
= 0.05 and power = 0.9) an EPOC difference of 5 liters [excess postexercise energy
expenditure (EPEE) = ~100 kJ] between the two treatments.
Subjects were familiarized with the laboratory on three separate
occasions before the control and treatments. Two of these visits
involved RMR-habituation trials. Subjects ingested a standard dinner
(~5,800 kJ; 70% carbohydrate, 15% fat, 15% protein) by 2000 h
before the control and treatment days, which commenced at 0720, and
they were only permitted to drink water thereafter. On arriving at the
laboratory, subjects were asked to void and empty their bowel before
being weighed. After subjects were weighed, a rectal temperature probe
(18) was inserted and chest electrodes were attached. The subjects then
rested quietly on a bed with their shoulders slightly elevated.
RMR was determined after 50 min of bed rest and was followed by one of
two equated treatments (continuous running: 30 min at 70%
O2 max; interval
running: 20 × 1-min intervals at 105% O2 max with
intervening 2-min rest periods) or a control session (no running). The
treatments were followed by 9 h of bed rest, during which
O2 was measured frequently
during the first hour and thereafter for one 10-min period every hour.
A standardized lunch, which was identical to the dinner on the
preceding evening, was provided at 1230 on both treatment and control
days. The laboratory temperature in the vicinity of the subjects was
maintained at 24.0 ± 0.5°C, and they were covered with a
blanket.
Statistical analyses.
The trapezoidal rule was used to approximate the integral for the
exercise, 9-h postexercise, and control
O2 values over time. This
facilitated the calculation of the net total oxygen cost (NTOC) of
exercise (exercise O2 + 9-h
postexercise O2 exercise and postexercise control
O2) and 9-h EPOC (9-h
postexercise O2 9-h
control O2). Similar
computations determined the 9-h net total energy expenditure (NTEE) and
9-h EPEE after each O2 data point was
converted to an energy equivalent by using the equation of Elia and
Livesey (12). Dependent t-tests
(P 
0.05) were used to locate
statistically significant between-treatment differences for the EPOC
and EPEE data. The O2,
respiratory exchange ratio (RER),
Tre, and HR data were analyzed via
analyses of variance with repeated measures across both time and
treatments/control. In the event of a statistically significant
F-ratio
(P 0.05), differences between
experimental and control conditions for temporally matched variables
were identified via Dunnett's post hoc test (31).
RESULTS
O2.
The postexercise O2 was
significantly greater than the matched control values for 1 and 8 h
after the submaximal and supramaximal treatments, respectively (Fig.
1A).
The ~27% increase in O2 at
4 h for the control and two treatments was ~1 h after the ingestion
of the standard meal.
Figure 1.
Mean postexercise O2 consumption
(O2;
A), respiratory exchange ratio
(B), rectal temperature
(C), and heart rate
(D) after submaximal (
) and
supramaximal (
) running. 
, Control. No control measurements were
made between 0 and 1 h. * Significant difference between
treatment and control means, P 0.05.
[View Larger Version of this Image (15K GIF file)]
EPOC/EPEE. The submaximal and supramaximal treatments resulted in 9-h recovery O2 consumption of 163.8 ± 12.8 and 171.8 ± 13.4 liters, respectively. These values were significantly greater (P < 0.001 for both treatments) than the control day O2 consumption of 156.8 ± 10.9 liters. Table 2 indicates that the differences among the submaximal and supramaximal treatments for EPOC (P = 0.001), NTOC (P = 0.001), EPEE (P = 0.007), and NTEE (P = 0.005) were all statistically significant. When both the EPOC and EPEE values were expressed as percentages of the NTOC and NTEE, respectively, the submaximal treatment comprised 7.1 and 6.6% of the NTOC and NTEE of exercise, respectively, whereas the corresponding values were 13.8 and 11.9% for the supramaximal treatment (Table 2).
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0.05), they
ranged from only 2 to 6 beats/min above the matched controls after 1 h
of recovery. HR returned to control levels after 1 h for the submaximal
treatment.
The HR values for both treatments at 9 h postexercise were not
significantly different from the control value.
DISCUSSION
This is the first study to investigate the relationship between the
EPOC values when supramaximal and submaximal workloads are equated.
Table 2 indicates that the supramaximal work produced a significantly
greater 9-h EPOC compared with that for the submaximal treatment; the
two EPOC values comprised 7.1 and 13.8% of their respective NTOC
values. Furthermore, the energy content of 1 kg of adipose tissue is
approximately equivalent to 1) 215 EPEE and 16 NTEE for the submaximal treatment and
2) 116 EPEE and 14 NTEE for the
supramaximal treatment. Notwithstanding the higher EPEE for
supramaximal interval running compared with submaximal continuous running, the major contribution of both to weight loss is therefore via
the energy expended during the actual exercise. The 135-kJ greater EPEE
for the interval treatment is of little physiological significance to
the energy balance of athletes because this amount of energy is
equivalent to the kilojoules in only 75 ml of orange juice. However,
when exercise for weight loss is utilized, the EPEE would have a
cumulative effect when the exercise is undertaken regularly.
Although the EPEE resultant from supramaximal running in this
study would be associated with a greater cumulative effect, the
exercise intensity and duration involved would be beyond
the capabilities of nonathletes. It has also been reported that
exercise programs utilizing intensities >85%
O2 max are associated
with significant increases in dropout rates and injuries (22).
Few researchers (1, 2, 17, 33) have reported the precision of their
indirect calorimetry system, and this is a key issue underlying our
conclusions. The lack of reliability data, combined with inadequate
controls for the factors known to influence RMR, often confound
comparisons between studies. In the present investigation, temporally
matched measurements of each subject's RMR were conducted on the
control day and before each treatment. These three measurements
produced a CV of 3% and an ICC of 0.88. The smallest difference
between the control and treatment
O2 that achieved statistical
significance was ~5%, which exceeds the precision of our
O2 measurement. Garrow (16)
also reported that the intraindividual biological variability in RMR is
~5%. This value is greater than our precision data, which include
both biological variability and technical or equipment error.
Our results suggest that supramaximal workloads produce more prolonged
elevations in recovery O2
than moderate work intensities (i.e., 70-75%
O2 max). This is in
accordance with the positive linear relationship between submaximal
exercise intensity and EPOC that was reported by Gore and Withers (17).
After the submaximal treatment, postexercise
O2 was generally not
significantly different from control values after 1 h of recovery,
whereas recovery O2 after the
supramaximal treatment did not return to baseline until 9 h
postexercise. The O2 recovery
pattern for the submaximal treatment falls between that obtained by
Gore and Withers (17) for 20 and 50 min of exercise at 70%
O2 max. Quinn
et al. (25) reported a significantly elevated recovery
O2 for 3 h after 30 min of
treadmill walking at 70%
O2 max by young trained
women. In contrast to the earlier work of Bahr et al. (3), Sedlock et
al. (28) reported that O2 was
elevated for only 33 min after the cessation of 20 min of cycling at
74% O2 max. Smith and
McNaughton (30) and Chad and Wenger (10) utilized cycling with young
trained men and women at 70%
O2 max for 30 min and found recovery to be complete within 50 and 128 min, respectively. Bahr
et al. (2) are the only other investigators to use supramaximal interval exercise to investigate recovery
O2. Their untrained young
male subjects completed one, two, and three 2-min bouts of cycling at
108% O2 max, which
were associated with an elevation of recovery
O2 for 30, 60, and 240 min
and with EPOC values of 4.8, 10.4, and 16.6 liters, respectively.
Although Brockman et al. (8) also employed interval treadmill running,
their maximum workload was not supramaximal (7 × 2-min
exercise bouts at 90%
O2 max with 2-min
active rest periods). They reported a 12.7% elevation in
recovery O2 after 1 h for their young female distance runners, which is similar to that
found in this study for the supramaximal treatment. The difference in
recovery times between the preceding studies and our treatments could
be attributed to a number of factors, including exercise modality
and/or the greater
O2 max values for our
subjects. Furthermore, some of the investigators (8, 10, 29, 31) used a
resting O2 baseline that was
extrapolated from a pretreatment measure, and different methods have
also been used to determine when
O2 had returned to baseline.
A further consideration, which has not been previously discussed in
studies (2, 8) utilizing interval work, is the contribution to the EPOC
of the increased O2 during
the recovery intervals. When the recovery interval
O2, which is in excess of
both the control day O2 and
O2 deficit incurred during the
work intervals, was added to the 15.0-liter 9-h EPOC determined from
the cessation of the last work interval, then the overall EPOC is 37.2 liters. However, this represents an inflated EPOC estimate because the subjects were standing and moving their legs to prevent venous pooling
during the recovery intervals. It was not feasible to have them lying
down during the recovery intervals to replicate the control day
conditions from which the O2
baseline was derived. In our laboratory, results in two subjects
demonstrated that moving and stretching the legs while standing
required a O2 that was threefold greater than that on the control day (unpublished
observations). Allowance for this elevation led to an
overall EPOC estimate of 17.3 liters, which is not markedly different
from that of 15.0 liters determined from cessation of the last work
interval. However, further work is required with interval treatments
when the corresponding control periods replicate the recovery movement
patterns of the intermittent exercise.
There is good agreement between the 9-h EPOC for our submaximal
treatment and those reported for experiments that measured recovery
O2 until it returned to
baseline. The average EPOC of two previous studies that used treadmill
running and controlled for the diurnal variation in RMR (17, 25) was
7.1 liters compared with our value of 6.9 liters. In the only study of
supramaximal exercise, Bahr et al. (2) reported an EPOC of 16.3 liters
for 14 h postexercise. However, they utilized untrained men who
exercised supramaximally for only 6 min compared with the 20 min used
in our investigation, which was associated with a 9-h EPOC of 15.0 liters. It is interesting to note that the Gore and Withers (17) data
for 80 min of treadmill running at 70%
O2 max, which is over
double the work performed in our supramaximal protocol, produced a
similar 8-h EPOC of 14.6 liters.
The dip in RER values for both treatments before 1 h
postexercise (Fig. 1B) is indicative
of CO2 retention after strenuous exercise to replenish the bicarbonate used to buffer lactic acid. The
more pronounced fall for the interval treatment was probably due to
greater lactate buffering. Recovery RER values were significantly lower
than the control values during the first 4 h of recovery for the
supramaximal treatment. Muscle glycogen stores would have been depleted
to a greater extent during the supramaximal treatment, thereby leading
to a greater reliance on fat metabolism in the recovery period. For the
same O2, fat yields less
energy than carbohydrate: it is therefore logical that the EPOC/NTOC of
13.8% for the supramaximal treatment is greater than the EPEE/NTEE of 11.9% (Table 2). The contribution of elevated fat metabolism toward
the EPOC in this case was estimated to be only 0.8 liter. RER values
were significantly lower than control values for both treatments for
the 1 h postprandial, presumably while repletion of muscle glycogen was
occurring. It has been reported (17) that postprandial glycogen
synthesis may account for ~1 liter of the EPOC. However, Bahr (1) has
suggested that this value should be disregarded because it is probably
less than the O2 consumed in the
control condition when excess carbohydrate is converted to fat as
opposed to glycogen. Only 5.3% of the energy content of ingested
carbohydrate is required to store it as glycogen, compared with
23-24% for conversion to triglyceride (13).
Tre for both treatments had returned to control levels within 2 h. It is therefore unlikely that Tre contributed to the significantly greater EPOC associated with the supramaximal treatment. The sum of the Tre differences between the control and treatments over the entire postexercise period for each subject did not correlate significantly with the EPOC. These correlations were 0.30 and 0.13 for the submaximal and supramaximal treatments, respectively. Tre therefore accounted for only 9 and 2% of the EPOC variance. Maehlum et al. (23), Bahr et al. (2), and Gore and Withers (17) also reported that Tre only accounted for a small proportion of the EPOC. It has been suggested (17) that muscle temperature may be more closely correlated with the EPOC, but this was not measured.
Although HR was significantly elevated above control levels for much of
the supramaximal recovery period, the physiological significance of
this is doubtful. All the postexercise HR values after 1 h of recovery
for the supramaximal treatment ranged from 2 to 6 beats/min more than
the matched control values. Given that the heart consumes ~10% of
the resting O2 (19) and the
elevations in HR beyond 1 h of recovery were low (2-6 beats/min),
the contribution of extra myocardial
O2 to the EPOC
would be negligible.
Several other factors have been proposed to contribute to EPOC. These
include the potentiated thermic effect of feeding (TEF), elevated
ventilation (E), lactate metabolism,
hormonal influences, substrate cycling, and glycogen synthesis from
ingested carbohydrate. Bahr and Sejersted (5) reported that a 4.5-MJ
test meal 2 h after cessation of 80-min cycling at 75%
O2 max did
not potentiate the TEF. Hence, it is unlikely that any of the EPOC
differences in this study can be attributed to a 5.8-MJ meal 3 h after
the cessation of exercise. E for the
treatments in this study was elevated above the control
E by ~9% at 1 h postexercise but had
returned to control levels for both treatments by 2 h postexercise. The
O2 of the respiratory
muscles at rest is 1-2% of the RMR (26); it is
therefore likely that the modest elevation in
E before 2 h postexercise would
have a negligible effect on the EPOC. The impact of the other factors
on the EPOC have been reviewed by Bahr (1) and lactate metabolism could
possibly explain some of the EPOC difference between the two treatments
used in this study, but plasma and muscle lactate were not measured.
Bahr et al. (2) estimated that 4 liters of
O2 were required to synthesize glycogen from 50% of the lactate generated from 3 × 2-min bouts of cycling at 108%
O2 max. This value only
represents a little over one-half of the difference between the EPOC
values in our study, but, given our more strenuous (20-min)
supramaximal protocol, it is possible that glycogenesis from lactate
could account for the EPOC difference between the two treatments.
However, estimates of O2 in
relation to lactate metabolism need to be treated with caution. The
determination of lactate kinetics is difficult because plasma lactate
is not indicative of the total lactate produced during exercise.
Furthermore, extrapolation of the lactate concentration in a single
muscle biopsy to the amount of lactate in an estimated active muscle
mass may be erroneous. Moreover, uncertainty exists in relation to what
proportion of lactate is channeled into glycogenesis, which is the
component of lactate metabolism that contributes to the EPOC.
In conclusion, this study has demonstrated that the EPEE is significantly greater for supramaximal running compared with submaximal running when there is an attempt to equate the amounts of work performed. Notwithstanding the higher EPEE for supramaximal interval running, the major contribution of both treatments to weight loss was via the energy expended during the actual exercise. The EPEE is therefore of negligible physiological significance as far as weight loss is concerned, unless the exercise is undertaken regularly when the EPEE would have a cumulative effect.
ACKNOWLEDGEMENTS
We are indebted to Helen Houghton, Peter Sinclair, and David Adams for assistance in preparing this manuscript.
FOOTNOTES
Address for reprint requests: R. T. Withers, Exercise Physiology Laboratory, School of Education, The Flinders Univ. of South Australia, GPO Box 2100, Adelaide, South Australia 5001, Australia.
Received 23 April 1996; accepted in final form 20 September 1996.
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