Sports Med 2003; 33 (14): 1037-1060

REVIEW ARTICLE 0112-1642/03/0014-1037/$30.00/0

 Adis Data Information BV 2003. All rights reserved.

Effect of Exercise Intensity, Duration

and Mode on Post-Exercise
Oxygen Consumption
Elisabet Børsheim and Roald Bahr
Norwegian University of Sport and Physical Education, Oslo, Norway

Contents
Abstract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1037
1. Excess Post-Exercise Oxygen Consumption (EPOC) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1038
2. Early Studies on EPOC . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1039
3. Methodological Considerations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1039
4. Effect of Intensity and Duration of Aerobic Exercise on EPOC . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1040
5. Effect of Split Exercise Sessions on EPOC . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1047
6. Effect of Supramaximal Exercise on EPOC . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1048
7. Effect of Aerobic Exercise Mode on EPOC . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1048
8. Effect of Resistance Exercise on EPOC . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1049
9. Effect of Training Status on EPOC . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1051
10. Effect of Sex on EPOC . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1052
11. Possible Mechanisms for the Rapid EPOC Component . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1053
12. Possible Mechanisms for the Prolonged EPOC Component . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1053
13. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1056

Abstract In the recovery period after exercise there is an increase in oxygen uptake
termed the ‘excess post-exercise oxygen consumption’ (EPOC), consisting of a
rapid and a prolonged component. While some studies have shown that EPOC
may last for several hours after exercise, others have concluded that EPOC is
transient and minimal. The conflicting results may be resolved if differences in
exercise intensity and duration are considered, since this may affect the metabolic
processes underlying EPOC. Accordingly, the absence of a sustained EPOC after
exercise seems to be a consistent finding in studies with low exercise intensity
and/or duration. The magnitude of EPOC after aerobic exercise clearly depends
on both the duration and intensity of exercise. A curvilinear relationship between
the magnitude of EPOC and the intensity of the exercise bout has been found,
whereas the relationship between exercise duration and EPOC magnitude appears
to be more linear, especially at higher intensities.
Differences in exercise mode may potentially contribute to the discrepant
findings of EPOC magnitude and duration. Studies with sufficient exercise
challenges are needed to determine whether various aerobic exercise modes affect
EPOC differently. The relationships between the intensity and duration of resis-
tance exercise and the magnitude and duration of EPOC have not been deter-
1038 Børsheim & Bahr

mined, but a more prolonged and substantial EPOC has been found after hard-
versus moderate-resistance exercise. Thus, the intensity of resistance exercise
seems to be of importance for EPOC.
Lastly, training status and sex may also potentially influence EPOC magni-
tude, but this may be problematic to determine. Still, it appears that trained
individuals have a more rapid return of post-exercise metabolism to resting levels
after exercising at either the same relative or absolute work rate; however, studies
after more strenuous exercise bouts are needed. It is not determined if there is a
sex effect on EPOC.
Finally, while some of the mechanisms underlying the more rapid EPOC are
well known (replenishment of oxygen stores, adenosine triphosphate/creatine
phosphate resynthesis, lactate removal, and increased body temperature, circula-
tion and ventilation), less is known about the mechanisms underlying the pro-
longed EPOC component. A sustained increased circulation, ventilation and body
temperature may contribute, but the cost of this is low. An increased rate of
triglyceride/fatty acid cycling and a shift from carbohydrate to fat as substrate
source are of importance for the prolonged EPOC component after exhaustive
aerobic exercise. Little is known about the mechanisms underlying EPOC after
resistance exercise.

1. Excess Post-Exercise Oxygen neutral term ‘excess post-exercise oxygen consump-

Consumption (EPOC)
During exercise, there is an increase in oxygen
uptake (V̇O2) to support the increased energy need.
After exercise, V̇O2 does not return to resting levels
immediately, but may be elevated above resting
levels for some period of time. Originally, the in-
creased V̇O2 after exercise was explained by the
oxygen debt hypothesis. The theoretical basis for
this was formulated by Hill et al.[1-4] They hypothe-
sised that the elevated V̇O2 after exercise was neces-
sary for the repayment of the oxygen deficit incurred
after the start of exercise, and ascribed the oxygen
debt to the oxidative removal of lactate. Margaria et
al.[5] modified the concept, and suggested that the
oxygen debt consisted of a lactacid component
caused by glycogen synthesis from lactate, and an
alactacid component related to other factors. The
lactacid component was considered to be the slower
component. However, the causality implied by the
term ‘oxygen debt’ is contrary to what is currently
known about the biochemical mechanisms underly-
ing the increase in metabolism post-exercise. There-
fore, Gaesser and Brooks[6] introduced the causality
tion’ (EPOC), which also includes the more pro-
longed increase in V̇O2 that may be observed for
hours after exercise.
EPOC consists of several components.[6,7] In this
review, the term ‘rapid component’ will be used to
describe the sum of components that decays within
approximately 1 hour, whereas the prolonged com-
ponent decays monoexponentially with a half-life in
the order of several hours (figure 1). Therefore,
processes active also beyond the first hour post-
exercise must be responsible for the prolonged
EPOC component.
Training (i.e. repetitive bouts of exercise) may
also have a more chronic effect on resting metabolic
rate (RMR). In particular, this seems to be the case
in trained compared with untrained individuals, es-
pecially when combined with high/sufficient energy
intake, resulting in a high energy flux or turnover.[8]
At times it may be difficult to separate this effect
from the EPOC effect. In this review, we will only
include studies of V̇O2 after an acute bout of exer-
cise.

 Adis Data Information BV 2003. All rights reserved. Sports Med 2003; 33 (14)
EPOC and Exercise Intensity and Duration
200
150
EPOC (mL/min)
100
50
0 ing status and sex may potentially contribute to the
0 2 4 6 8 10
Time after exercise (h)
Fig. 1. Time plot of excess post-exercise oxygen consumption
(EPOC) after exhaustive submaximal exercise (71–80 minutes at
69–78% of maximal oxygen uptake; n = 12). The solid line shows
the prolonged EPOC component (reproduced from Bahr,[7] with
permission).
2. Early Studies on EPOC
The first report on an elevated RMR after physi-
cal activity was published by Benedict and Carpen-
ter in 1910.[9] They observed a mean increase in
RMR of 11.1% for their two study participants
during sleep in a respiration calorimeter 7–13 hours
after severe exercise. Initially it was thought that
post-exercise elevation in V̇O2 contributed signifi-
cantly to the energy cost of exercise, and would be
an important factor in daily energy expenditure.
Herxheimer et al.[10] noted that the V̇O2 of five
untrained individuals did not return to baseline until
36–48 hours after exercise, and Edwards et al.[11]
reported a 25% elevation in metabolism 15 hours
after cessation of 2 hours of strenuous football.
Also, Passmore and Johnson[12] found a 15% in-
crease in RMR for 7 hours after a 16km walk at 6.4
km/hour in three males, and deVries and Gray[13]
found a 10% increase in RMR for 6 hours after 1
hour of mixed aerobic exercise. However, in many
cases, the intensity and duration of exercise was not
quantified in these early studies, and they provided
minimal information about the controls. Also, they
did not account for other factors that may influence
RMR, such as time of day, prior uncontrolled exer-
cise, food, temperature, caffeine intake, habituation
and stress.
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1039
Later, more controlled studies have been per-
formed. Some studies have confirmed that there is
an increase in V̇O2 after exercise that may last for
several hours.[14-19] However, other studies have
concluded that EPOC is transient and minimal after
exercise.[20-24] The conflicts in the results may be
resolved if differences in exercise intensity and du-
ration are taken into account, since this may be
expected to affect the metabolic processes underly-
ing EPOC. Also, differences in exercise mode, train-
12
discrepant findings.
3. Methodological Considerations
There are several methodological issues that are
important to consider when studying EPOC. Accu-
rate control over the pre-experimental conditions,
and an excellent reproducibility in the indirect calo-
rimetry measures are prerequisites to be able to
detect small, but potentially important differences.
Only few authors report the precision of the indirect
calorimetry system used to measure V̇O2. The
Douglas bag method is generally considered to be
the most accurate method of expired gas analysis,
but few authors, especially of newer studies, have
used this technique. Instead, automated systems
have been used, often with unknown validity and
reliability.
Furthermore, the pre-experimental conditions
have not always been well controlled. The study
participants should have a stable weight, and food
intake and exercise should be controlled. It is also
advisable for study participants to sleep overnight in
the laboratory before a study to avoid exercise in the
morning; however, an outpatient protocol may give
no different values than an inpatient protocol when
the conditions are controlled and the study partici-
pants are transported to the laboratory.[25,26] Also,
habituation of the study participants to testing proce-
dures is of utmost importance. The experimental
conditions both before and during measurements
need to be strictly controlled. For female study
participants, it may also be necessary to control for
menstrual cycle differences.
Sports Med 2003; 33 (14)
1040
When reviewing even the newer EPOC literature,
it is a problem that the methods for measuring
baseline and EPOC duration are inconsistent among
investigations. In some studies, a separate control
study has been used to control for time effects,
whereas others have used only one pre-exercise
value as baseline. In many studies, only 30 minutes
of rest in the morning has been used and the V̇O2
during the final 10 minutes of this has been taken as
baseline for EPOC. This can lead to falsely high
V̇O2 baseline values in the morning, since a certain
increase because of anticipation may be expected,
which subsequently leads to an underestimation of
EPOC.
In some cases, the baseline and recovery data
have been collected with the individuals in a seated
position, in others in a recumbent position. The
RMR is lower in recumbent position, probably be-
cause it is difficult to avoid fidgeting and relax
completely when sitting for an extended period.
This results in a greater measurement error and a
reduced ability to detect differences between the
baseline and recovery conditions.
Different methods have also been used to deter-
mine when V̇O2 has returned to resting levels. Some
have measured V̇O2 continuously, whereas others
have measured at discrete time points. Furthermore,
some have measured V̇O2 until it has returned to
resting values, others only for a pre-determined time
period.
Finally, because of inter-individual variability in
EPOC, it is important with a high enough number of
study participants to be able to detect differences.
4. Effect of Intensity and Duration of
Aerobic Exercise on EPOC
Table I contains a review of studies on V̇O2 after
aerobic exercise. The absence of a sustained in-
crease in V̇O2 after exercise seems to be a consistent
finding in studies with low exercise intensity and/or
low exercise duration. No EPOC was found beyond
35 minutes of recovery after 5 or 20 minutes cycling
at 50%, 65%, and 80% of maximal oxygen uptake
(V̇O2max),[20] beyond 40 minutes of recovery after
20–40 minutes of treadmill exercise around the ven-
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Børsheim & Bahr
tilatory threshold,[21] and beyond 40 minutes after 4
× 20 minutes of cycle ergometry at 35–55% of
V̇O2max.[22] Only two males and two females took
part in the last study. Brehm and Gutin[23] found a
relationship between EPOC and the intensity of
walking/running, but their intensity was still low,
the highest being 11.3 km/hour in trained individu-
als. After 3.2km running at this intensity, EPOC
amounted to only 71kJ (~3.5L oxygen). Elliot et
al.[24] also found a short lasting (<30 minutes) EPOC
after 10–30 minutes cycling at 80% of V̇O2max.
Finally, Maresh et al.[27] had male study participants
cycle at 60% and 70% of V̇O2max, but only for 20
and 30 minutes, and found an EPOC duration less
than 40 minutes.
Several studies on EPOC have their origin in the
late Lars Hermansen’s laboratory. He started the
series of studies himself by having a male study
participant cycle for 80 minutes at 75% of
V̇O2max.[30] After 12 hours, the size of EPOC was
48L. After 24 hours of recovery, V̇O2 was still
increased by 5.9% compared with a control day.
Mæhlum et al.[15] from the same laboratory, found a
mean EPOC of 26L after 80 minutes cycling (in
periods of 10–30 minutes with 5-minute breaks be-
tween) at an intensity of 70% of V̇O2max using eight
study participants. In accordance with Hermansen et
al.’s case study,[30] they found that V̇O2 was still
increased by 5% as late as 24 hours after the end of
exercise. We followed up with a series of exercise
studies spanning from 20–80 minutes of cycling at
intensities ranging from 30–75% of V̇O2max[16,43]. A
clear relationship was found between the magnitude
of EPOC and both the intensity and duration of
exercise. A curvilinear relationship between the
magnitude of EPOC and the intensity of the exercise
bout was observed (figure 2). No prolonged increase
in recovery V̇O2 was found after 80 minutes at 29%
of V̇O2max. Instead, it appeared that an intensity
above 50–60% of V̇O2max was required in order to
induce an EPOC lasting for several hours after exer-
cise. At exercise intensities at or above this level, a
linear relationship between the magnitude of EPOC
and the duration of the exercise bout was observed
(figure 2). The size of EPOC was 11.1, 14.7 and
Sports Med 2003; 33 (14)
 Adis Data Information BV 2003. All rights reserved.

EPOC and Exercise Intensity and Duration

Table I. Studies on the effect of aerobic exercise on post-exercise V̇O2a
Study Year Study Exercise mode, duration and intensity EPOC size and duration Commentsc
participantsb
Passmore & Johnson[12] 1960 3M TM: 16km, 6.4 km/h RMR 14–18%↑ for 6h, >7h Rest position not reported. NC
deVries & Gray[13] 1963 2M Cycling, bench step, run/walk: 45 min ~1.9L (57 kcal) NC
(effective time 25 min)
Knuttgen[28] 1970 5F, 7M Cycling: 45–98%, 15–55 min ≤5L, duration NA Bed rest. NC. EPOC magnitude
related to intensity and duration
Segal & Brooks[29] 1979 11M Cycling: 55 and 95%, 2 min ≤4L, duration NA Seated. NC. EPOC magnitude
related to intensity
Hagberg et al.[20] 1980 18M Cycling: 50%, 65% and 80%, 5 and 20 ≤5L, duration NA Moderate cycling (used as
min base-line). NC. EPOC
measured for 15 min
Hermansen et al.[30] 1984 1M Cycling: 75%, 80 min 12h EPOC: 48L. At 24h: V̇O2↑ Bed rest. C
5.9%
Bielinski et al.[14] 1985 10M (T) TM: 50%, 3h RMR↑ 9% for 4.5h. At 18h: Seated/respiratory chamber. C.
RMR↑ 4.7% Food given 30 min post-
exercise
Pacy et al.[22] 1985 2F, 2M (T) Cycling: 35–55% for 20 min × 4 (40 <2.2L, <60 min Supine. C
min break)
Freedman-Akabas et 1985 13F, 10M (UT TM: Anaerobic threshold, 20 min <4.2L, <40 min Recumbent. C
al.[21] + T)
Chad and Wenger[31] 1985 (a) 3F, 3M; (b) Cycling: (a) 70%, 15 and 30 min; (b) Magnitude and duration not Seated. C. (a) EPOC↑ after 30
6M 70% for 30 min and 50% for 38 min given vs 15 min; (b) EPOC↑ after
(equal work) 50% vs 70%
Brehm & Gutin[23] 1986 8F, 8M (UT + TM: 18–68%, 17–60 min. Incremental 1h EPOC: ≤8L, >1h after max Seated. NC. EPOC measured
T) max test test for 1h. EPOC curvilinear related
to intensity
Devlin & Horton[32] 1986 6M Cycling: 85%, 71 min. Intermittent At 12–16h: RMR↑ 3–7% Rest position not reported. C
Mæhlum et al.[15] 1986 4F, 4M Cycling: 70%, 80 min (10–30 min bouts 12h EPOC: 26L. At 24h: RMR↑ Bed rest. C
with 5 min break) 5%
Bahr et al.[16] 1987 6M Cycling: 70%, 20, 40 and 76 min (20 V̇O2↑ 5.1%, 6.8%, 14.4% over Bed rest. C. EPOC magnitude
min bouts with 5 min break) 12h. 76 min: 12h EPOC: 31.9L, linearly related to duration
≥12h
Elliot et al.[24] 1988 3F, 3M Cycling: 80%, 10 and 30 min ~2.37L (11.4 kcal), 30 min. Supine. C
Chad and Wenger[17] 1988 3F, 3M Cycling: 70%, 30, 45, 60 min 6.6, 14.9, 33L. 128, 204, 455 Seated. NC
min
Sedlock et al.[33] 1989 10M (T) Cycling: (a) 75%, 20 min; (b) 50%, 30 (a) ~6.2L (29.4 kcal); (b) ~3.0L Seated. NC
Sports Med 2003; 33 (14)

min; (c) 50%, 60 min (14.3 kcal); (c) 2.5L (12.1 kcal)
Chad and Quigley[34] 1989 5F TM: 55%, 90 min EPOC magnitude NA. At 1h: Seated. NC. EPOC measured
V̇O2↑ 54%. >1h for 1h

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1041
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1042
Table I. Contd
Study Year Study Exercise mode, duration and intensity EPOC size and duration Commentsc
participantsb
Poehlman et al.[35] 1989 6M Cycling: 50%, 90 min <24h C. RMR measured at 24 and
48h
Kaminsky et al.[36] 1990 6F TM: 70%, 50 min vs 2 × 25 min 1.4L (continuous), <30 min. Seated. NC
3.1L (split), <30 min
Gore & Withers[18,19] 1990 9M TM: 30%, 50% and 70%. 20, 50 and 80 8h EPOC: 30%: 1.0L, 1.4L, Bed rest. C. EPOC magnitude
min 1.0L, all <1h; 50%: 3.1L (<1h), linearly related to duration
5.2L (<1h), 6.1L (<2h); 70%: when intensity >50%. Intensity
5.7L (<1h); 10.0L (<4h), 14.6L major determinant of EPOC
(<8h)
Bahr et al.[37] 1990 6M Cycling: 51%, 120 min 3.5h EPOC: 7.8L, >3.5h Bed rest. C. EPOC measured
for 3.5h
Chad and Quigley[38] 1991 10F (5UT + 5T) Cycling: 50% and 70%, 30 min Unclear magnitude, but 50%↑ Seated. NC. EPOC measured
vs 70%, >3h for 3h
Sedlock[39] 1991 4F, 4M Arm crank + cycling: 60% mode- Arm: ~1.9L (9.2 kcal), 23 min. Seated. NC
specific, 20 min Cycle: ~2.2L (10.4 kcal), 24 min
Sedlock[40] 1991 7F Cycling: 40% and 60% until 850kJ 40%: ~6.2L (30kJ), 28 min. Seated. NC
60%: ~7.5L (36kJ), 18 min
Berg[41] 1991 5F, 5M (T) TM: 40%, 30 min M: ~1.4L (6.7 kcal), ~1h. F: Seated. C. EPOC measured for
~2.2L (10.6 kcal), ~1h 1h
Withers et al.[42] 1991 8M (T) TM: 70%, 164 min 24h EPOC: 32.4L, >8h, <24h Supine. C
Bahr & Sejersted[43] 1991 6M Cycling: 29%, 50%, 75%. 80 min (20 1.3, 5.7, 30.1L; 0.3, 3.3, 10.5h Bed rest. C. EPOC curvilinear
min bouts with 5 min breaks) related to intensity
Bahr & Sejersted[44] 1991 6M Cycling: 75%, 80 min 7h EPOC: 20.9L (fasted), 21.1L Bed rest. C
(fed), >7h
Bahr et al.[45] 1992 6M Cycling: 108%, 1, 2, or 3 × 2 min with 3 5.6, 6.7, 16.3L; 30, 60 min, 4h Bed rest. C
min breaks
Elliot et al.[46] 1992 5F, 4M Cycling: 80% of max heart rate. 40 min ~6.7L (32 kcal), <30 min Supine. C
Sedlock[47] 1992 7M Cycling & TM: 60–65% of mode- Cycling: ~3.1L (15 kcal), 31 Seated. NC
specific, 30 min min; TM: ~3.5L (17 kcal), 34
min
Maresh et al.[27] 1992 8M Cycling: 60% and 70%. 20 and 40 min Magnitude NA, <40 min Seated. NC. NS between
sessions
Donelly & 1992 6F Cycling: 55%, 90 min Magnitude NA, >60 min Rest position not reported. NC
McNaughton[48]
Brockman et al.[49] 1993 5F (T) TM: (a) 25%, 2h; (b) 81%, 10 min; (c) 1h mean V̇O2↑: (a) 12%, 40 Seated. C. EPOC measured for
89%, 7 × 2 min with 2 min break min; (b) 23%, >1h; (c) 44%, 1h: intermittent run >
Sports Med 2003; 33 (14)

>1h continuous. Run > walk

Kaminsky & Whaley[50] 1993 10F (5 obese + TM: (a) Alternating 3 min bouts at 30% (a) ~3.6L (17.4 kcal), 37.5 min; Seated. NC. NS between

Børsheim & Bahr

5 lean) and 90%, 36 min; (b) 60%, 36 min (b) ~1.9L (9.0 kcal), 16.5 min obese and lean

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 Adis Data Information BV 2003. All rights reserved.

EPOC and Exercise Intensity and Duration

Table I. Contd
Study Year Study Exercise mode, duration and intensity EPOC size and duration Commentsc
participantsb
Smith & McNaughton[51] 1993 8F, 8M Cycling: 40%, 50%, 70%, 30 min M: 16.3, 22.1, 28.1L for 31.2, Rest position not reported. NC.
42.1, 47.6 min. F: 12.1, 20.8, EPOC duration increased with
24.3L for 26.9, 35.6, 39.1 min intensity
Neary et al.[52] 1993 7M (T) Swimming & cycling: 65% of mode- Swim: 5.3, 5.6, 5.6L; 8.1, 10.1, Seated. NC. Relationship
specific, 30, 45, 60 min 9.4 min. Cycling: 8.2, 9.9, between core temperature and
10.0L; 18.3, 20.4, 22.9 min EPOC
Frey et al.[53] 1993 13F (7UT + 6T) Cycling: 65% and 80%. 24–45 min UT: 4.0, 5.9L, >1h. T: 4.7L, 50 Seated. NC
(until 300 kcal) min; 5.6L, 40 min
Børsheim et al.[54] 1994 6M Cycling: 78%, 60 min 6.5h EPOC: 14.4L, ≥6.5h Bed rest. C. EPOC measured
for 6.5h
Thomas et al.[55] 1994 7M Cycling, jog and downhill jog: 60%, 60 Magnitude NA, <9h Semi-reclined. C. EPOC
min measured for 2h, and again at
9, 24 and 48h. NS between
modes
Sedlock[56] 1994 10M (5UT + Cycling: 50%, ~300 kcal UT: ~2.5L (12.2 kcal), 20.4 min. Seated. NC
5T) T: ~2.5L (12.2 kcal), 16.6 min
Gilette et al.[57] 1994 10M Cycling: 52%, 64 min ~5.6L (27 kcal), 5h Supine. C
Quinn et al.[58] 1994 8F (T) TM: 70%. 20, 40, 60 min 3h EPOC: 8.6, 9.8, 15.2L; >3h Seated. C. EPOC measured for
3h
Harms et al.[59] 1995 16M TM: 70%. 20 min Magnitude unclear, <30 min Supine. NC. EPOC negatively
related with body fat mass
Dawson et al.[60] 1996 8F Cycling: (a) 67%, 34 min; (b) 55%, 41 (a) 3.6L, 13.9 min; (b) 2.6L, Bed rest. NC. Intensity effect
min; (c) 45%, 49 min (same work) 14.1 min; (c) 2.4L, 13.2 min on EPOC magnitude
Short et al.[61] 1996 5M, 5F Arm crank ergometer: (a) 35%, 15 min; (a) 0.46L, 5.7 min; (b) 0.5L, 5.5 Seated. NC. Intensity more
(b) 35%, 30 min; (c) 70%, 15 min min; (c) 1.4L, 14 min important than duration
Trost et al.[62] 1997 5M (T) Cycling: 65%, 60 min 1h EPOC: 5.5L, >1h Seated. NC
Phelain et al.[63] 1997 8F (T) Cycling: (a) 50%, 78 min; (b) 75%, 51 3h EPOC: (a) 4.8L, <3h; (b) Seated + bed rest. C. EPOC
min (500 kcal) 9.0L, >3h measured for 3h
Laforgia et al.[64] 1997 8M (T) TM: (a) 70%, 30 min; (b) 105%, 20 × 1 (a) 6.9L, 1h; (b) 15L, 8h Bed rest. C
min with 2 min break (equal work)
Short & Sedlock[65] 1997 11F, 11M Cycling: (a) 70%, 30 min; (b) 1.5L (a) UT: 3.5L, 50 min; T: 3.2L, Seated. NC. EPOC duration
(10UT + 12T) oxygen/min, 30 min 40 min; (b) UT: 2.4L, 39 min; T: shorter in T
1.5L, 21 min
Burleson et al.[66] 1998 15M TM: 45%, 27 min ~3.4L, <30 min Supine. NC
Almuzaini et al.[67] 1998 10M Cycling: 70%, 30 vs 2 × 15 min 5.3L (cont); 7.4L (split), Supine. C. EPOC measured for
Sports Med 2003; 33 (14)

duration NA 40/2 × 20 min

Børsheim et al.[68] 1998 7M Cycling: 58%, 90 min 4.5h EPOC: 7.5L, >4.5h Bed rest. C. EPOC measured
for 4.5h

Continued next page

1043
1044 Børsheim & Bahr

31.9L of oxygen after 20, 40 and 76 minutes at 70%

for estimate; NC = no rest control experiment, but pre-exercise values used as baseline instead; NS = not significant; RMR = resting metabolic rate; T = trained; TM = treadmill;
C = separate rest control experiment; cont = continuous; EPOC = excess post-exercise oxygen consumption; F = females; M = males; max = maximum; NA = data not available
Bed rest. C. EPOC measured

Rest position not reported. C.

of V̇O2max, respectively. After the longest bout,

EPOC duration was at least 10 hours.
EPOC measured for 6h

Similar comprehensive studies have been done

by Gore and Withers.[18,19] Their treatments ranged
from a 20-minute walk at 30% of V̇O2max to an
Supine. NC
Commentsc

Bed rest. C

80-minute run at 70% of V̇O2max. The maximal

for 4.5h

EPOC was 14.6L oxygen (297kJ) after the longest

and hardest bout. In accordance with our stud-
ies,[16,43] they found an exponential relationship be-
7h EPOC: 8.6L (follicular); 8.9L
Magnitude NA. (a) 10 min; (b)

tween exercise intensity and the magnitude of

12.3L (luteal), duration NA
6h EPOC: 8.4L (follicular);

All studies are in young people. Exercise is shown in percentage of V̇O2max or V̇O2peak. EPOC size is given in litres of oxygen.
EPOC size and duration

EPOC. They calculated that the intensity explained

4.5h EPOC: 8.1L, >4.5h

UT = untrained; V̇O2 = oxygen uptake; V̇O2max = maximal oxygen uptake; V̇O2peak = peak oxygen uptake; ↑ indicates increase.

five times more of EPOC than either exercise dura-

(luteal), duration NA

tion or total work completed.[18] While intensity

accounted for 45.5% of the variation in EPOC, the
duration of exercise, and the interaction between
30 min

intensity and duration accounted only for 8.9% and

7.7%, respectively.
In our studies,[15,16,43] we found much higher
TM: (a) 40%, 40 min; (b) 85%, 20 min
Exercise mode, duration and intensity

EPOC values, and also more prolonged duration of

EPOC, compared with Gore and Withers.[18,19] In the
study by Mæhlum et al.,[15] the response was about
twice the response of that observed in the study by
Cycling: 56%, 90 min

Cycling: 60%, 60 min

Cycling: 70%, 60 min

Gore and Withers.[18] Even though the measurement

period was 4 hours shorter in the latter study, this
can still not explain the difference. While we used
Individuals’ position during measurements of resting V̇O2 is given first.

cycling in our experiments, Gore and Withers used

If nothing is mentioned, individuals were untrained/medium trained.

running, and the different exercise modes may be a

possible explanation of the discrepancy in results.
Another possible explanation, perhaps more likely,
participantsb

is the different training status of the study partici-

pants. In the studies by Gore and Withers,[18,19] the
Study

10M

participants were well trained, whereas in our stud-

8M

7F

5F

ies they were not.

In support of a significant EPOC after high-
intensity exercise, a 3–7% increase in energy expen-
diture was found as late as 12–16 hours after inter-
1998

1999

1999

2000
Year

mittent exercise for a total of 71 minutes at 85% of

V̇O2max.[32] The most exhaustive bout for any of the
EPOC studies was a 35km road run (intensity about
70% of V̇O2max for about 160 minutes).[42] A total
Børsheim et al.[69]

Fukuba et al.[72]
Matsuo et al.[70]
Table I. Contd

EPOC of 32.4L of oxygen, lasting for a total of 8

Lee et al.[71]

hours, was found. Furthermore, an EPOC lasting for

3 hours was observed after only 30 minutes tread-
Study

mill walking at 70% of V̇O2max in young trained

a

 Adis Data Information BV 2003. All rights reserved. Sports Med 2003; 33 (14)
EPOC and Exercise Intensity and Duration
a b
50
40
30
EPOC (L)
20
10
0 −10
0 20 40 60
Exercise intensity (%)
Fig. 2. (a) Plot of excess post-exercise oxygen consumption (EPOC) magnitude versus exercise intensity (constant duration of 80 minutes).
(b) Plot of EPOC magnitude versus exercise duration (constant intensity of 70% of maximal oxygen uptake). Different symbols are used for
individual study participants (reproduced from Bahr,[7] with permission).
women.[58] Also, a comparison of interval-type exer-
cise alternating between 30% and 90% of V̇O2max,
with continuous exercise of equal duration (36 min-
utes) at 60% of V̇O2max (equal work) showed a
longer EPOC (38 versus 17 minutes) and higher
EPOC magnitude (~3.6 versus ~1.9L oxygen) after
the interval exercise.[50]
Sedlock et al.[33] also investigated the effect of
exercise intensity and duration on EPOC, but used a
more narrow spectrum of exercise conditions. In one
series of experiments, caloric output was kept con-
stant (300 kcal), whereas intensity was varied (50%
versus 75% of V̇O2max). It took only 30 and 20
minutes, respectively, for the trained male study
participants to finish these work bouts. In another
series, intensity was kept constant (50% of V̇O2max),
whereas duration was varied (30 versus 60 minutes).
Hence, no strenuous exercise was performed, and no
substantial EPOC duration or magnitude was found.
Still, it was concluded that the intensity of exercise
influenced both the magnitude and duration of
EPOC, whereas exercise duration only influenced
EPOC duration. It was also concluded that the dura-
tion of EPOC and the subsequent caloric output was
not necessarily related, since high-intensity exercise
of short duration produced a higher EPOC (~6L
oxygen) than lower intensity exercise of long dura-
tion (~2.5L oxygen), even though no difference in
EPOC duration (33 versus 28 minutes, respectively)
was found. Similar studies with modest exercise
 Adis Data Information BV 2003. All rights reserved.
1045
40
30
20
10
0
80 0 20 40 60 80
Exercise duration (min)
protocols have supported the conclusion that exer-
cise intensity is more important than total work for
EPOC magnitude.[51,60]
There are also some studies of the effect of
intensity on EPOC, where EPOC has been measured
for a specific pre-determined time period. Phelain et
al.[63] found a significantly higher 3-hour EPOC
after cycling at 75% versus 50% of V̇O2max (equal
work, 500 kcal) in women. Brockman et al.[49] inves-
tigated 1-hour EPOC after intense intermittent run-
ning (7 × 2 minutes at 90% of V̇O2max, 2 minutes of
rest between intervals), continuous running for 10
minutes at 81% of V̇O2max, and continuous walking
for 2 hours at 24.5% of V̇O2max. EPOC was higher
after running versus walking and highest after the
highest intensity running. However, since EPOC
was still increased after 1 hour, no definite conclu-
sion can be drawn.
In contrast to the findings of an intensity-related
EPOC, Chad and Wenger[31] did not find any rela-
tionship between exercise intensity and EPOC. They
had one group of individuals cycling for 15 and 30
minutes at 70% of V̇O2max. Another group cycled
for 38 minutes at 50% of V̇O2max and 30 minutes at
70% of V̇O2max (equal total work). They found that
EPOC was highest after the longest duration in both
groups. In another study, Chad and Quigley[38] had
trained and untrained women cycle for 30 minutes at
50% and 70% of V̇O2max, and found a higher EPOC
after the lowest intensity bout. The results of these
Sports Med 2003; 33 (14)
1046 Børsheim & Bahr

50

40
EPOC (L)

30

20

120
10 100
80

k)
or • nsity

ea
2p
60

VO
e
0

int
140

V•O ise
120 40

ax
c
2m
100
80 er
20 Ex
60 of
Exerc 40
ise du
(%

ration 20 0
(min) 0
Fig. 3. Relationship between exercise intensity, exercise duration and excess post-exercise oxygen consumption (EPOC) magnitude. Plot
shows mean EPOC values from studies that have used cycling exercise, and where EPOC values are reported or possible to esti-
mate.[15-17,22,24,30,33,39,40,43-47,51-54,56,57,60,63,65,67-70,72] Note that recovery oxygen uptake was not measured until it had returned to resting control
values in all the included studies (for more details on studies, see table I). V̇O2max = maximal oxygen uptake; V̇O2peak = peak oxygen
uptake.

two studies are somewhat puzzling when compared
with other findings. The authors explain the results
with a lower respiratory exchange ratio (R-value)
after the low intensity bout. It should also be men-
tioned that post-exercise V̇O2 was still elevated at
the end of the experiments 3 hours post-exercise in
the second study, whereas EPOC duration is unclear
in the first study. Also, the experimental conditions
were less rigorously controlled (menstrual cycle
does not appear to be controlled for in the female
participants, participants were sitting during rest and
were allowed to write, watch television and read, the
time of the day for a repeated trial appears to be
slightly different, and V̇O2 was recorded in short
periods).
Chad and Wenger[17] also investigated the effect
of duration (30, 45 and 60 minutes) on EPOC after
cycling at 70% of V̇O2max. They found that EPOC
increased 2.3- and 5.3-fold when exercise duration
was increased from 30 minutes to 45 and 60 min-
utes, respectively. After the most exhaustive bout,
EPOC lasted for 7.5 hours. Sedlock,[40] on the other
hand, did not find any effect of exercise duration on
EPOC, but the intensities used (40% versus 60% of
V̇O2max) were low.
The interaction between exercise intensity and
duration is not completely understood, and it is
difficult to separate the effect of each of these fac-
tors. However, the fact that exercise has to be of a
certain intensity for the linear relationship between
exercise duration and EPOC magnitude to become
apparent, indicates that the interaction between them
is synergistic rather than additive. This is illustrated
in figure 3, which shows mean EPOC values from
studies that have used cycling exercise, and where
EPOC magnitude is presented or can be estimat-
ed.[15-17,22,24,30,33,39,40,43-47,51-54,56,57,60,63,65,67-70,72] It
should be noted that some of the studies included

 Adis Data Information BV 2003. All rights reserved. Sports Med 2003; 33 (14)
EPOC and Exercise Intensity and Duration
probably did not capture the entire EPOC, since
post-exercise V̇O2 was still elevated compared with
resting control values at the end of the measurement
period (for further details on these studies see table
I). Gore and Withers[19] analysed the interaction
effect between exercise intensity and duration on
EPOC after treadmill exercise ranging from 20 min-
utes at 30% of V̇O2max to 80 minutes at 70% of
V̇O2max. They found that the interaction between
exercise intensity and duration accounted for a much
smaller part (7.7%) of the variation in EPOC, com-
pared with exercise intensity alone (45.5%). The
studies illustrated in figure 3 appear to support the
hypothesis that exercise intensity has to be of a
certain size to achieve a significant EPOC. In addi-
tion, they show that the highest EPOC values have
been found when both exercise intensity and dura-
tion are substantial.
It appears that the post-exercise increase in ener-
gy expenditure per se after exercise bouts spanning
from 20 minutes at 30% V̇O2max to 80 minutes at
70% V̇O2max may be negligible in relation to energy
balance and weight loss. However, this may be a
speculative conclusion, since there are no available
data from prolonged studies of the effect of EPOC
on energy balance. Also, it should be noted that
there may be a high inter-individual variability in
EPOC in response to the same relative exercise
stimulus, as can be seen from figure 2. Thus, it can
be hypothesised that there are high, medium and low
responders, corresponding to what has been found
for other parameters in response to exercise train-
ing.[73] However, there are no studies where EPOC
has been measured repeatedly in the same individu-
als under the same conditions. Therefore, it is not
known if the observed variability is the result of
biological variation related to differences in, for
example, body composition or training status, or
whether it is caused by measurement errors. Still, if
we estimate that EPOC amounts to 50–100kJ after
moderate exercise (≥1 hour, approximately 50% of
V̇O2max), this would result in an extra energy loss of
about 11 700kJ per year if training is undertaken
three times per week. This represents only about
311g of fat. After more strenuous exercise (≥1 hour,
 Adis Data Information BV 2003. All rights reserved.
1047
≥70% of V̇O2max), the corresponding values can be
estimated to approximately 700kJ after the exercise
bout, and about 109 200kJ per year (training three
times per week), equivalent to about 2.9kg of fat.
However, such strenuous exercise cannot be expec-
ted to be undertaken by overweight or untrained
individuals. Although overweight may be the result
of a small positive energy balance over a long time,
and EPOC may contribute to the opposite when
strenuous exercise is undertaken regularly, it must
be concluded that EPOC is negligible in relation to
weight loss in the overweight or obese person. It
must be noted that exercise per se has an important
role for weight regulation. Furthermore, EPOC may
have greater implications for elite athletes, who
often have two bouts of exercise on the same day as
a normal training routine. If V̇O2 is elevated from a
previous exercise bout, the mechanical efficiency
may be reduced during the following bout.[74]
In summary, the magnitude of EPOC after aero-
bic exercise is clearly dependent on both the dura-
tion and intensity of exercise. There is a curvilinear
relationship between the magnitude of EPOC and
the intensity of the exercise bout. At least for cy-
cling, it appears that an intensity above 50–60% of
V̇O2max is required in order to induce an EPOC
lasting for several hours. The relationship between
exercise duration and EPOC magnitude appears to
be more linear, especially at higher intensities.
5. Effect of Split Exercise Sessions
on EPOC
A couple of studies have shown a higher EPOC
after split exercise sessions compared with a contin-
uous bout. Kaminsky et al.[36] investigated women
during 50 minutes of continuous running versus two
25-minute sessions at 70% of V̇O2max. The com-
bined EPOC after the two split sessions correspond-
ed to ~3.1L versus 1.4L of oxygen after the continu-
ous session. Almuzaini et al.[67] compared EPOC
after 30 minutes of continuous cycling versus two
15-minute sessions (separated by 6 hours) at 70% of
V̇O2max. In this study, the sum of EPOC after the
split sessions was 7.4L versus 5.3L of oxygen after
the continuous bout. Hence, total EPOC was ap-
Sports Med 2003; 33 (14)
1048
proximately 120% and 40% greater after split ses-
sions compared with a continuous session in these
two studies. It should be noted that even though
EPOC is higher after split sessions, the extra EPOC
is small in relation to the exercise energy expendi-
ture. Thus, prolonging the exercise bout by a few
minutes may make up for the increase in EPOC after
splitting the session. Furthermore, in split sessions,
there will be one oxygen deficit for each session.
This means that the relative difference in energy
expenditure during recovery after split versus con-
tinuous sessions will be smaller than the difference
in EPOC. This was not taken into account in the two
studies mentioned.[36,67]
6. Effect of Supramaximal Exercise
on EPOC
Given the relationship between exercise intensity
and EPOC, it comes as no surprise that supramax-
imal exercise stimulates EPOC. We found that brief
intermittent bouts of exhaustive supramaximal exer-
cise (1, 2, or 3 × 2-minute bouts of cycling at 108%
of V̇O2max, separated by 3-minute rest periods) ele-
vated post-exercise energy expenditure for 4
hours.[45]
Laforgia et al.[64] measured EPOC after
supramaximal (20 × 1 minute runs at 105% of
V̇O2max with 2-minute recovery periods between)
versus submaximal running (30 minutes at 70% of
V̇O2max). A significantly higher 9-hour EPOC was
observed after the supramaximal exercise. Interest-
ingly, the EPOC values in this study were similar to
the values found after 80 minutes of running at 70%
V̇O2max in the study by Gore and Withers,[18,19] even
though more than twice the total work was per-
formed in the latter study.
Few authors have tried to divide EPOC into
different components. This is unfortunate, since ex-
ercise intensity and duration may affect the short
and prolonged components to a different extent. We
calculated the short EPOC component as the differ-
ence between the observed 1-hour EPOC and the
prolonged curve component.[7] By comparing EPOC
after 70–80 minutes of cycling at 69–78% of
V̇O2max with 3 × 2 minutes at 104–117% of
 Adis Data Information BV 2003. All rights reserved.
Børsheim & Bahr
V̇O2max, very similar 1-hour EPOCs were found;
7.6L (submaximal exercise) and 7.8L (supramax-
imal exercise), respectively. Of this, about 4.5L
(submaximal) and 2.0L (supramaximal) could be
attributed to the prolonged curve component, and
about 3.1L (submaximal) and 5.8L (supramaximal)
to the rapid component. Hence, it appears that high-
intensity short exercise affects mainly the rapid
EPOC component, whereas more prolonged ex-
hausting exercise stimulates mechanisms also pre-
sent beyond the first hour of recovery. However, this
relationship remains to be fully elucidated.
7. Effect of Aerobic Exercise Mode
on EPOC
A curvilinear relationship between exercise in-
tensity and EPOC, and a linear relationship between
exercise duration (when intensity is higher than the
break-point) are both shown for cycle exercise[16,43]
and for treadmill exercise.[18,19] However, the abso-
lute EPOC magnitude for a certain exercise intensity
and duration may differ depending on exercise
mode.
Muscle damage is more likely to occur after
eccentric-type exercise than after concentric exer-
cise,[75-77] and it is possible that this influences
EPOC. However, in studies where concentric and
eccentric exercise have been compared, no differ-
ences have been found in EPOC[47,55] or RMR for
several days after exercise.[78] Sedlock[47] compared
30 minutes of cycling and treadmill exercise at an
intensity of 60–65% of mode-specific peak oxygen
uptake (V̇O2peak). No differences could be detected
between modes, but the exercise was moderate, and
hence EPOC was small (15–17 kcal; ~3.5L oxygen).
EPOC has also been compared after 60 minutes of
either jogging, downhill jogging or cycling at 60%
of mode-specific V̇O2max to induce different de-
grees of eccentric muscular activity.[55] No increase
in recovery energy expenditure was found after ec-
centric exercise, but it may be that the detection
level was not sufficient (power = 0.40 for medium
effect size).
To investigate the effect of relative metabolic
rate of the active musculature on EPOC, Sedlock[39]
Sports Med 2003; 33 (14)
EPOC and Exercise Intensity and Duration
compared the effect of 20 minutes of arm crank
exercise versus cycling at 60% of mode-specific
V̇O2peak. V̇O2 during arm crank exercise was about
72% of uptake during cycling in absolute terms. No
difference in EPOC was found between modes, but
again the exercise was short and not very strenuous,
and consequently EPOC lasted less than 25 minutes.
Short et al.[61] have investigated the effect of
intensity and duration of upper body exercise alone
on EPOC, and found a similar pattern as for the
lower body. EPOC was measured after 15 and 30
minutes of arm crank exercise at 35% of V̇O2peak,
and after 15 minutes at 70% of V̇O2peak. The intensi-
ty was found to have a greater effect than duration,
but durations were low and within a narrow spec-
trum in this study. Since exercise duration and inten-
sity did not vary over a range of values, it was not
possible to fully describe the relationships with
EPOC.
In summary, it is not clear whether various
modes of aerobic exercise affect EPOC differently.
Further studies with a sufficient exercise challenge
and adequate statistical power are needed.
8. Effect of Resistance Exercise on EPOC
EPOC has also been compared between aerobic
and resistance exercise. Elliot et al.[46] compared
aerobic cycling (40 minutes at 80% of maximal
heart rate), circuit weight training exercise (4 sets, 8
exercises, 15 repetitions at 50% of one repetition
maximum [1RM]), and heavy resistance exercise (3
sets, 8 exercises, to exhaustion at 80–90% of 1RM).
They found that heavy resistance exercise produced
the biggest EPOC, but it is unclear how the work
volumes related to each other.
Studies in which similar estimated exercise ener-
gy cost[57] or similar exercising V̇O2[66] have been
used to equate continuous aerobic exercise and in-
termittent resistance exercise, have indicated that
resistance exercise produces a greater EPOC res-
ponse. A higher EPOC was found after hard resis-
tance exercise (50 sets of 8–12 repetitions at 70% of
1RM, 2 minutes of rest between sets) compared with
an equated work bout of aerobic cycling (50% of
V̇O2max for 60 minutes).[57] RMR was still elevated
 Adis Data Information BV 2003. All rights reserved.
1049
14.5 hours after the resistance exercise compared
with a resting control experiment.
Burleson et al.[66] compared weight training exer-
cise (two circuit sets of eight exercises at 60% of
1RM for 8–12 repetitions) and treadmill exercise
(27 minutes at 45% of V̇O2max). The weight training
exercise was performed first, and the average V̇O2
was used to determine the intensity for the treadmill
workout. EPOC was found to be higher the first 30
minutes after resistance exercise, but not at 60 and
90 minutes. Even though the V̇O2 volumes were
equated, the resistance exercise was considered to
be of higher intensity activity than the aerobic exer-
cise, and this may explain the higher EPOC after
resistance exercise. Hence, it is difficult to compare
resistance exercise to steady-state exercise, since it
is not easy to precisely quantify the energy cost of
resistance exercise with indirect calorimetry.
The relationship between the intensity and dura-
tion of resistance exercise, and the magnitude and
duration of EPOC has not been determined. Table II
shows a review of studies on the effect of resistance
exercise on EPOC.
Williamson and Kirwan[89] and Dolezal et al.[84]
found that RMR remained elevated for 48 hours
after an acute moderate- to high-intensity bout of
resistance exercise. This was hypothesised to be due
largely to protein turnover and tissue repair. It
should be noted that to avoid eccentric muscle work,
only the concentric phase was used in the study of
Williamson and Kirwan,[89] and still they found a
prolonged effect on recovery metabolic rate. Their
study was done in 59- to 77-year-old men. Similarly,
Melby et al.[81] found that V̇O2 was still increased by
9.4% and 4.7% as late as 15 hours after two hard
resistance exercise work bouts (each 90 minutes of
weight lifting, six sets of ten exercises, 8–12 repeti-
tions at 70% of 1RM).
After more moderate resistance exercise (three
sets of seven exercises, ten repetitions at 12RM),[79]
a smaller EPOC was found, but the V̇O2 was mea-
sured for only 1 hour after exercise, and was still
elevated at this time point. Binzen et al.[86] found an
EPOC shorter than 2 hours after three sets of ten
Sports Med 2003; 33 (14)
 Adis Data Information BV 2003. All rights reserved.

1050
Table II. Studies on the effect of resistance exercise on post-exercise V̇O2a
Study Year Study Exercise EPOC size and duration Commentsb
participants
Melby et al.[79] 1992 6M 4 sets of upper and 3 sets of lower body. 7–10 1h EPOC: ~4L (20 kcal), ≥1h Supine. C. EPOC measured for 1h only
reps. 12RM
Elliot et al.[46] 1992 5F, 4M 8 exercises, upper and lower body. (a) 4 sets, 15 (a) ~10.2L (48 kcal); (b) ~10.6L Supine. C. EPOC duration unclear
reps, 50% of 1RM, 30 sec rest; (b) 3 sets, 3–8 (51 kcal). 30 min
reps, 80–90% of 1RM, 30 sec rest
Murphy & 1992 10M 6 exercises, upper and lower body. Circuit: 3 Circuit: 5L, 20 min. Standard: Rest position not reported. NC.
Schwarzkopf[80] times, 8–12 reps, 50% of 1RM, 30 sec rest. 2.7L, 15 min Experiments in the afternoon. 5 min
Standard: 3 sets, reps to exhaustion, 80% of baseline measurement
1RM, 120 sec rest
Melby et al.[81] 1993 (a) 6M; (b) (a) 6 sets of 10 exercises, upper and lower body, (a) 2h EPOC: 7L, ≥15h; (b) 2h Supine. (a) NC; (b) C. EPOC measured
6M ~8–12 reps, 70% of 1RM, 90 min; (b) as (a), but EPOC: 7L, ≥15h for 2h, minus first 5 min post-exercise.
5 sets, and longer rest, 90 min Measured again at 15h
Olds & 1993 7M 2 sets of 7 exercises, upper and lower body, 3.5 (a) 8.2L, <1h; (b) 6.5L, <1h Seated. C
Abernethy[82] min rest. (a) 12 reps, 75% of 1RM; (b) 15 reps,
60% of 1RM
Gilette et al.[57] 1994 10M 5 sets of 10 exercises, upper and lower body, 5h EPOC: 12.6L (51 kcal), Supine. C. Fed study participants. EPOC
8–12 reps, 70% of 1RM, 2 min rest ≥14.5h measured for 5h and again at 14.5h
Burleson et 1998 15M Circuit, 2 times, 8 exercises, upper and lower Magnitude NA, ≥90 min Supine. NC
al.[66] body, 8–12 reps, 60% of 1RM, 1 min rest
Haltom et 1999 7M (a) Circuit, 2 times, 8 exercises, upper and lower 1h EPOC: (a) 10.3L; (b): 7.4L Supine. NC. EPOC measured for 1h.
al.[83] body, 20 reps, 75% of 20RM, 20 sec rest; (b) EPOC↑ for first 5 min after (a) vs (b)
same as (a), but 60 sec rest
Dolezal et 2000 18M (9UT 8 sets of leg press, 6 reps, 6RM, 3 min rest At 24h: RMR↑ 18%. At 48h: Supine. NC
al.[84] + 9T) RMR↑ 11%. UT > T
Osterberg & 2000 7F 5 sets of 10 exercises, upper and lower body, At 3h: V̇O2↑ 13%. At 16h: Supine. NC. EPOC measured for 3h and
Melby[85] 10–15 reps, 12RM or 70% of 1RM, ~2 min rest RMR↑ 4.2% again at 16h
Binzen et 2001 10F 3 sets of 10 exercises, upper and lower body, 10 6.2L, 1h Seated. C
al.[86] reps, 70% of 1RM, 1 min rest
Thornton & 2002 14F 2 sets of 9 exercises, upper and lower body. (a) (a) ~1.1L (5.5 kcal); (b) ~2.3L Seated. C
Potteiger[87] 15 reps, 45% of 8RM, 1 min rest; (b) 8 reps, (11 kcal). <2h
85% of 8RM, 1 min rest
Schuenke et 2002 7M Circuit, 4 times, 3 exercises, upper and lower Mean RMR↑ ~20% for two Supine. C. V̇O2 measured 3×/day.
al.[88] body, 8–12 reps, 10RM, 2 min rest days, ≥38h Exercise in evening. Unclear control
Sports Med 2003; 33 (14)

conditions between measurements

Børsheim & Bahr

a All studies are in young people. In all studies, except UT, the individuals participated in resistance exercise several times per week. EPOC size is given in litres of oxygen.
b Under Comments, individuals’ position during measurements of resting V̇O2 is given first.
C = separate rest control experiment; EPOC = excess post-exercise oxygen consumption; F = females; M = males; NA = data not available for estimate; NC = no rest control
experiment, but pre-exercise values used as baseline instead; reps = repetitions; RM = repetition maximum; RMR = resting metabolic rate; T = trained (resistance exercise several
times per week); UT = untrained; V̇O2 = oxygen uptake; ↑ indicates increase.
EPOC and Exercise Intensity and Duration
exercises with ten repetitions at 10RM (1 minute of
rest between sets) in resistance-trained women.
Murphy and Swartzkopf[80] compared two differ-
ent protocols of resistance exercise (three sets of six
exercises, repetitions to exhaustion at 80% of 1RM
with 120-second rest periods versus three circuit sets
of the six same exercises, 10–12 repetitions at 50%
of 1RM with 30-second rest periods). Work volume
of each session was similar, but intensity (weight
lifted per unit of time) was greater for the circuit
exercise. The higher intensity session produced
higher EPOC than the standard set exercise (4.9
versus 2.7L oxygen), but the duration of EPOC was
only 20 minutes.
Olds and Abernethy[82] compared high- and low-
intensity resistance exercise with equated work vol-
ume, and found no difference in EPOC. However,
their range of intensities was narrow (12 repetitions
at 75% of 1RM and 15 repetitions at 60% of 1RM),
and may not have been large enough to elicit a
treatment effect. Accordingly, V̇O2 returned to
baseline within 1 hour after exercise. Also, the age
range was wide (22–55 years) and there was a high
inter-individual difference in EPOC (0.7–27L).
In a recent study, Thornton and Potteiger[87] in-
vestigated the effect of high- and low-intensity resis-
tance exercise of similar work volume on EPOC.
The exercise bouts consisted of two sets of nine
exercises. In the high-intensity bout, eight repeti-
tions at 85% of 8RM of each exercise were per-
formed, whereas 15 repetitions at 45% of 8RM were
performed in the low-intensity bout. The rest period
between sets was 2 minutes. The duration was 23
minutes for the high-intensity bout and 26 minutes
for the low-intensity bout, whereas the actual exer-
cise time was 6.9 minutes (high) and 8.3 minutes
(low), respectively. V̇O2 was measured between
0–20, 45–60, and 105–120 minutes post-exercise.
The magnitude of EPOC was higher during each
measurement period after high- versus low-intensity
resistance exercise.
Understanding the effect of resistance exercise
on EPOC is confounded by the considerable diversi-
ty in the protocols commonly employed in this re-
search, for example, type (i.e. circuit training or
 Adis Data Information BV 2003. All rights reserved.
1051
multiple sets), weights, sets, repetitions, and length
of rest periods. These factors will all influence the
energy cost of the exercise, but this effect is difficult
to quantify precisely. Furthermore, resistance train-
ing is similar to interval training and split sessions of
aerobic exercise in that each session or set of resis-
tance exercise will have an EPOC of its own during
the recovery period between exercises. To deter-
mine the total energy expenditure, this has to be
included in the calculations.
All this taken into consideration, it seems likely
that EPOC after resistance exercise is influenced by
the intensity of the exercise, since a more prolonged
and substantial EPOC has been found after hard
versus more moderate exercise. More research is
still needed to elucidate the effect of intensity and
duration of resistance exercise on the magnitude and
duration of EPOC.
9. Effect of Training Status on EPOC
Individuals of different fitness levels have been
used in EPOC studies, and this may also potentially
explain some of the differences observed in magni-
tude and duration of EPOC. The effect of training
status is not easy to study, since comparing groups
of different fitness levels at the same absolute exer-
cise intensity level means that trained are working at
a lower relative intensity, which has been shown to
influence EPOC. Furthermore, if trained and un-
trained are compared at the same relative exercise
intensity, when total work is equal, the untrained
have to work for a longer duration, which may also
influence the results. In other words, there is no
study design available to provide a definite answer
to whether training status affects EPOC.
Brehm and Gutin[23] found similar values for
EPOC in runners versus non-exercisers following a
3.2km walk at 6.4 km/hour (i.e. same absolute inten-
sity), but the exercise intensity may have been too
low to detect a difference. Sedlock[56] compared fit
and unfit males after cycling at 50% of V̇O2peak,
until 300 kcal were used (27 and 35 minutes to
finish, respectively). No difference in EPOC dura-
tion or magnitude was found, but again, the exercise
challenge was low. Finally, in a study of treadmill
Sports Med 2003; 33 (14)
1052
exercise at approximately the anaerobic threshold, it
was concluded that fitness level does not significant-
ly alter magnitude and duration of EPOC, but both
the separation of study participants into groups and
the exercise intensity were somewhat unclear in that
study.[21]
In contrast to these studies, Chad and Quigley[38]
found a higher 3-hour EPOC in trained female cy-
clists versus untrained women after 30 minutes cy-
cling at 50% or 70% of V̇O2max. The difference was
most apparent immediately after exercise, which
was explained by higher absolute exercise intensity,
and thereby a higher V̇O2 in trained versus un-
trained. V̇O2 was still increased 3 hours after exer-
cise, and no definite EPOC magnitude could be
determined.
Frey et al.[53] measured V̇O2 for 1 hour after
cycling at ~65% and ~80% of V̇O2max until 300 kcal
had been expended in trained and untrained women.
No difference in EPOC magnitude was found after
cycling at the highest intensity, but EPOC was sig-
nificantly smaller in the untrained (4.0L oxygen)
versus the trained group (4.7L oxygen) after the
lowest intensity. EPOC decreased rapidly during the
first 10 minutes post-exercise in both groups. Fol-
lowing both intensities, the initial EPOC (first 10
minutes post-exercise) was greater in trained versus
untrained, most likely because of higher V̇O2 during
exercise in this group. While there still was a signif-
icant EPOC at the end of the experiment in the
untrained group, post-exercise V̇O2 was elevated for
only 50 and 40 minutes after low- and high-intensi-
ty, respectively, in the trained group. Thus, EPOC
duration was shorter in the trained.
Short and Sedlock[65] compared EPOC in trained
(V̇O2max: 53 mL/kg/min) versus untrained males
(37 mL/kg/min) after 30 minutes cycling on both
similar absolute (1.5L oxygen/min) and relative
(70% of V̇O2peak) intensities. At a V̇O2 of 1.5 L/
min, the trained group exercised at 45% of V̇O2peak,
while the untrained worked at 61% of V̇O2peak. The
results showed that the trained group had a signifi-
cantly shorter duration of EPOC whether compared
at the same absolute or relative intensity, but in all
situations EPOC lasted less than 1 hour. Further-
 Adis Data Information BV 2003. All rights reserved.
Børsheim & Bahr
more, the magnitude of EPOC was not different
between groups after exercise at the same relative
intensity (3.2L oxygen in trained versus 3.5L oxy-
gen in untrained). The trained group had higher V̇O2
at the end of the exercise bout, and if the data were
normalised to percentage change afterwards, the
trained had a more rapid fall in post-exercise V̇O2.
After exercise of similar absolute intensity, the un-
trained group had higher EPOC (2.4L oxygen) ver-
sus trained (1.5L oxygen). Longitudinal training
studies also support the findings of a faster recovery
in V̇O2 in trained individuals.[90,91]
In summary, it appears that trained individuals
have a more rapid return of post-exercise metabol-
ism to resting levels when exercising at either the
same relative or same absolute work rate, but studies
after more strenuous exercise bouts should be done.
10. Effect of Sex on EPOC
Sex is also a factor that can potentially influence
EPOC, as well as have implications for study de-
sign. Energy expenditure at rest or during exercise
may vary with menstrual phase,[92-95] and this has
not always been taken into consideration when stud-
ying EPOC. Basal metabolic rate has been shown to
be at its lowest level 1 week before ovulation.[92]
Webb[96] found an 8–16% increase in 24-hour ener-
gy expenditure during the 14-day luteal phase fol-
lowing ovulation. Accordingly, Matsuo et al.[70]
found a higher EPOC after 60 minutes cycling at
60% of V̇O2max in the luteal versus the follicular
phase in seven healthy women. On the other hand,
Fukuba et al.[72] did not detect any significant effect
of menstrual cycle on EPOC in five young women
after 60 minutes cycling at 70% of V̇O2max.
When comparing EPOC between men and
women, the same question as for trained versus
untrained must be addressed: should EPOC be com-
pared after absolute or relative workloads? Berg[41]
measured V̇O2 for 1 hour after 30 minutes of exer-
cise at 40% of V̇O2max in active men and women. A
higher post-exercise energy expenditure was found
among men. However, the calculations are some-
what unclear, since the data are not compared with
control resting values, and hence it is the absolute
Sports Med 2003; 33 (14)
EPOC and Exercise Intensity and Duration
levels rather than the increase in energy expenditure
after exercise that is compared.
Smith and McNaughton[51] compared trained
men and women after 30 minutes of exercise at
40%, 50% and 70% of V̇O2max. In all three condi-
tions, the men had a longer EPOC duration than the
women; however, the longest duration observed was
only 47 minutes, at least partly because of the short
exercise duration. In all conditions, EPOC magni-
tude in absolute terms was also higher in men versus
women, but this difference disappeared when EPOC
was adjusted for body mass. Furthermore, there
were no differences between sexes when EPOC was
expressed as a percentage of total energy expended.
In summary, few studies have been conducted to
compare EPOC in men and women. Thus, the sex
effect on EPOC is not fully clarified, but controlling
for changes in energy expenditure during the men-
strual cycle appears to be important in studies with
women.
11. Possible Mechanisms for the Rapid
EPOC Component
EPOC is the sum of many underlying mechan-
isms, some of which are still not known. Hence, the
influence of individual factors on EPOC is via an
effect on the underlying mechanisms. Most of the
studies on mechanisms causing EPOC are done after
cycling protocols, and little is known about EPOC
after resistance exercise.
Some of the metabolic processes believed to be
responsible for the rapid EPOC component are well
defined: replenishment of oxygen stores in blood
and muscle, resynthesis of adenosine triphosphate
(ATP) and creatine phosphate, lactate removal, and
increased body temperature, circulation and ventila-
tion.[6,7,43,97] Thus, the classic oxygen debt hypo-
thesis is one of several factors explaining the rapid
component.
12. Possible Mechanisms for the
Prolonged EPOC Component
The mechanisms for the prolonged EPOC com-
ponent are less well understood. A sustained in-
creased ventilation, circulation and body tempera-
 Adis Data Information BV 2003. All rights reserved.
1053
ture may contribute; however, the cost of this is low
(<1L oxygen).[7]
It has been shown that there is an increase in the
rate of the energy-requiring triglyceride/fatty acid
(TG/FA) cycle after prolonged exhausting exer-
cise.[37,68,69,98] In the TG/FA cycle, FA released
during the process of lipolysis are subsequently re-
esterified into TG rather than oxidised. ATP is
needed for the re-esterification, which can occur
within the adipocyte (intracellular recycling), or the
FA can be released and re-esterified elsewhere, e.g.
in the liver (extracellular recycling). The TG/FA
cycle is under both hormonal[99] and substrate con-
trol.[100] The energy cost associated with the increase
in TG/FA cycling can account for a significant part
of EPOC after prolonged steady-state exercise.[7]
The existence of gluconeogenic-glycolytic sub-
strate cycles have also been demonstrated in vivo in
humans,[101-104] but no increase in the rates of these
cycles have been found during recovery from exer-
cise.[104,105]
A relative shift from carbohydrate to fat as sub-
strate source is a consistent finding after prolonged
exhausting exercise.[37,43,68,69] Since the energy equi-
valent of oxygen is lower with fat as the substrate
compared with carbohydrates (free fatty acids: ~4.7
mol ATP/mol oxygen; glucose: ~5.1 mol ATP/mol
oxygen), part of EPOC can be explained by this
substrate shift. The substrate shift after exhaustive
submaximal exercise has been calculated to account
for 10–15% of the observed EPOC.[7]
The energy cost of glycogen resynthesis has also
been suggested as a mechanism for the prolonged
EPOC component after aerobic exercise.[30] How-
ever, glycogen resynthesis is low during fasting, and
we did not find any difference in the magnitude of
EPOC in the fed versus the fasted state after 80
minutes of cycling at 75% of V̇O2max.[44] Further-
more, on a biochemical basis, it can be argued that
the oxygen cost of glycogen resynthesis should not
be included as a part of EPOC.[7,44] The rationale for
this is that in situations when food is given, the
energy cost of carbohydrate storage is less after
exercise when the carbohydrates are used for replen-
ishment of muscle and liver glycogen stores com-
Sports Med 2003; 33 (14)
1054
pared with rest where more of the carbohydrates
may be stored as fat. The energy cost of storing
dietary carbohydrates as fat requires 23–24% of the
ingested energy, whereas storage as glycogen re-
quires only 5.3%.[106] On the other hand, emerging
data[107,108] suggest that hepatic de novo lipogenesis
is quantitatively insignificant under most conditions
of carbohydrate overfeeding.
It has been suggested that when food is given in
the recovery period there is a synergistic interaction
of food and exercise on energy expenditure. The
difference in opinion as to whether this interaction
exists[109,110] may be caused by the large intra- and
inter-individual variations in the thermogenic effect
of a standard meal. We[44] could not detect any
major interaction effects between food and previous
aerobic exercise on the V̇O2.
Several hormones are potential stimulants of en-
ergy expenditure, including insulin, cortisol, thyroid
hormones, growth hormone, adrenocorticotropic
hormone (ACTH) and catecholamines. Plasma con-
centrations of growth hormone and ACTH may in-
crease during exercise, but no sustained increase in
secretion has been found after exercise.[111,112]
Mæhlum et al.[15] found no changes in plasma insu-
lin and free thyroxine during the recovery period
after exhausting endurance exercise, and only a tran-
sient increase in the plasma concentration of cor-
tisol. However, in this experiment, food was given
in the recovery period, which may have influenced
the hormonal response. Although we found that
venous plasma insulin concentration rapidly re-
turned to resting levels after aerobic exercise.[68,69]
we observed a prolonged depression in arterial plas-
ma insulin concentrations after similar exercise.[113]
This may be important for the increase in fat
mobilisation during the recovery period. We also
found an increased hormonal response to a repeated
bout of endurance exercise for catecholamines, AC-
TH, cortisol and growth hormone.[112]
Many authors have suggested that an increased
sympathoadrenal activity may be one of the mech-
anisms underlying EPOC, and of the prolonged
component in particular.[6,15,30,37,114-117] This hypo-
thesis was based on several findings. Firstly, epi-
 Adis Data Information BV 2003. All rights reserved.
Børsheim & Bahr
nephrine and norepinephrine are potent stimulators
of the energy metabolism.[118,119] Their calorigenic
effect seems to be mediated through the β-adre-
noceptors.[120,121] Secondly, the sympathoadrenal
system is activated during exercise with elevated
concentrations of plasma catecholamines as a result.
During dynamic exercise, the plasma concentrations
of catecholamines increase linearly with the exer-
cise duration and exponentially with the exercise
intensity,[111,122] a similar relationship to that observ-
ed between EPOC and exercise duration and intensi-
ty, respectively (figure 2). Thirdly, catecholamines
are important regulators of TG/FA cycling and FA
oxidation through stimulation of lipolysis via β-
adrenoceptors. Both processes are increased after
exercise and may account for a significant part of
EPOC.
In early studies on the effect of β-adrenoceptor
blockade on post-exercise V̇O2, antagonists were
administered in dogs before an exercise bout.[114,123]
The results showed that short-term EPOC decreased
after administration of the non-selective β-adre-
noceptor antagonist, propranolol. The results have
been used as an indication of the importance of the
sympathoadrenal system for EPOC, but since
propranolol was administered before the start of the
exercise, the physiological effects of the exercise
bout were different between the control and the
propranolol situation. We have shown that both
propranolol and also the selective β1-adrenoceptor
antagonist, atenolol, reduced V̇O2 to a similar extent
when given intravenously during rest post-exercise
and during rest without previous exercise in
humans.[68] Hence, there was no effect of β-adre-
noceptor blockade on EPOC after aerobic exercise,
and the results do not support the hypothesis that the
prolonged EPOC component is caused by increased
sympathoadrenal activity. A possible β3-adre-
noceptor effect on EPOC could not be excluded, but
the β3-adrenoceptor does not seem to be of impor-
tance for the sympathoadrenal-mediated thermogen-
esis,[121] and thus it seems unlikely that there is any
β3-adrenoceptor effect on EPOC.
An increased sensitivity to catecholamines in the
post-exercise period has also been proposed.[7,124]
Sports Med 2003; 33 (14)
EPOC and Exercise Intensity and Duration
The hypothesis was built on observations in vitro of
an increased lipolytic response to catecholamine
stimulation in human gluteal adipocytes[125] and in
suprailiac adipocytes[126] removed immediately after
an exercise bout compared with resting samples.
However, we have shown[69] that isoprenaline (β-
adrenoceptor agonist) stimulated whole body V̇O2
to the same extent during rest with and without
previous aerobic exercise. Hence, no increased sen-
sitivity to catecholamines was detected in the post-
exercise period. Also, the lipolytic effect of isopren-
aline in abdominal adipose tissue was not increased
after a prolonged moderate exercise bout, but in-
stead a desensitisation was seen.[113]
Another potential effect of the sympathoadrenal
system on EPOC is by stimulation of various pro-
cesses during the exercise bout, which are reversed
slowly after the end of the exercise bout, even if
there is no increased sympathoadrenal activity in
this period. During an exercise bout, catecholamines
stimulate both the heart rate, the contractility of the
heart, glycogenolysis, gluconeogenesis, and lipoly-
sis in adipose tissue and in muscles.[127] The cat-
echolamines also influence the release of other hor-
mones, e.g. insulin and renin. During exercise,
blood flow in some tissues is decreased through α-
adrenoceptors, which may be of importance for
blood flow and V̇O2 in the tissues after exercise.
Hence, the influence of catecholamines on various
processes during exercise may in turn influence
EPOC. This is in agreement with the finding of a
reduced EPOC when propranolol was administered
in dogs before exercise.[114,123]
An elevated rate of both protein breakdown and
protein synthesis has been demonstrated in the re-
covery period after exercise.[128] An increased whole
body protein synthesis has been demonstrated after
3.75 hours of treadmill running at 50% of
V̇O2max,[129] and after 1 hour of cycling at 75% of
V̇O2max.[130] Also, an increased muscle protein syn-
thesis has been shown after prolonged exercise,[131]
whereas studies of the breakdown of muscle protein
after such exercise is lacking. Resistance exercise
also stimulates protein synthesis in the post-exercise
period.[132,133] Synthesis of protein is energetically
 Adis Data Information BV 2003. All rights reserved.
1055
expensive, and thus it seems reasonable to speculate
that the energy cost associated with an accelerated
rate of protein synthesis in the post-exercise state
can contribute to higher energy expenditure. Further
studies on the importance of increased protein turn-
over and adaptive protein synthesis on EPOC after
different types of exercise are necessary. To our
knowledge, EPOC and protein turnover have not
been measured in the same study.
Both whole body (pulmonary) and muscle V̇O2
should be measured to determine the quantitative
contribution of muscle metabolism to EPOC. In a
study by Bangsbo et al.,[134] leg V̇O2 accounted for
only one-third of EPOC in the 60-minute recovery
period after exhaustive knee extensor exercise last-
ing 3 minutes. Only a minor fraction (26%) of the
excess leg V̇O2 could be attributed to the oxygen
requirements for resynthesis of substrate. Hence, a
large part of the increase in muscle V̇O2 after exer-
cise remained to be explained. Non-exercised mus-
cles may also contribute to EPOC, as both in vitro
and in vivo studies have shown an increased V̇O2 in
inactive muscles perfused with blood high in lac-
tate.[135,136]
The energy efficiency may change during exer-
cise,[97,137] and this may be the case also during
recovery from exercise. One potential mechanism
for reduced energy efficiency is the activity of un-
coupling proteins (UCP). The expression of UCP3
in various organs is consistent with a role in adaptive
thermogenesis.[138-140] It remains to be determined if
the cellular milieu during exercise stimulates the
activity of UCP, and if changes in energy efficiency
during and after exercise may explain part of EPOC.
In summary, whereas several of the metabolic
processes believed to be responsible for the rapid
EPOC component are well known (replenishment of
oxygen stores in blood and muscle, resynthesis of
ATP and creatine phosphate, lactate removal, and
increased body temperature, circulation and ventila-
tion) the mechanisms underlying the prolonged
component are less well understood. An increased
TG/FA cycling, and a shift from carbohydrate to fat
as substrate source, may explain a substantial part of
the prolonged EPOC component after exhaustive
Sports Med 2003; 33 (14)
1056
submaximal exercise. A minor part may be ex-
plained by a sustained elevation in circulation, ven-
tilation and temperature. No increased
sympathoadrenal activity has been found after such
exercise. Little is known about the mechanisms un-
derlying EPOC after resistance exercise.
13. Conclusions
Much of the conflicting reports of EPOC magni-
tude and duration may be resolved if differences in
exercise intensity and duration are taken into ac-
count. Thus, a small and short-lasting EPOC has
typically been observed in studies with low exercise
intensity and/or low exercise duration, whereas a
more prolonged and substantial EPOC can be ob-
served after more strenuous exercise. The relation-
ship between exercise intensity and EPOC magni-
tude is curvilinear, whereas at higher intensities
there is a linear relationship between exercise dura-
tion and EPOC. For resistance exercise, the relation-
ship between exercise intensity, duration and EPOC
is less clear, but a more prolonged and substantial
EPOC has been found after hard versus moderate
resistance exercise. Furthermore, the individual ef-
fects of exercise mode, training status and sex on
EPOC are unclear, partly because of difficulties in
designing appropriate protocols to investigate these
effects. Still, it appears that trained individuals have
a more rapid return of V̇O2 to resting levels after
exercising at either the same relative or the same
absolute work rate, but studies after more strenuous
exercise bouts should be done. Finally, while some
of the mechanisms underlying the more rapid EPOC
after strenuous aerobic exercise are well known, the
mechanisms underlying the prolonged EPOC com-
ponent are more unclear. The sum of the increased
rate of TG/FA cycling and the shift from carbohy-
drate to fat as substrate source has been suggested to
account for more than half of the prolonged EPOC
component, but there is still a significant part that
remains to be explained. It is hypothesised that
increased protein turnover and/or a change in energy
efficiency in the recovery period may explain some
of this.
 Adis Data Information BV 2003. All rights reserved.
Børsheim & Bahr
Acknowledgements
No sources of funding were used to assist in the prepara-
tion of this manuscript. The authors have no conflicts of
interest that are directly relevant to the content of this manu-
script.
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