Effect of Exercise Intensity, Duration and Mode on Post-Exercise Oxygen Consumption
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 resistance exercise and the magnitude and duration of EPOC have not been determined, but a more prolonged and substantial EPOC has been found after hardversus 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 magnitude, 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, circulation and ventilation), less is known about the mechanisms underlying the prolonged 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.
Excess Post-Exercise Oxygen 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 increased V̇O2 after exercise was explained by the oxygen debt hypothesis. The theoretical basis for this was formulated by Hill et al.[1, 2, 3, 4] They hypothesised that the elevated V̇O2 after exercise was necessary 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. 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 underlying the increase in metabolism post-exercise. Therefore, Gaesser and Brooks introduced the causality neutral term ‘excess post-exercise oxygen consumption’ (EPOC), which also includes the more prolonged 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 component 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, especially when combined with high/sufficient energy intake, resulting in a high energy flux or turnover. 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 exercise.
Early Studies on EPOC
The first report on an elevated RMR after physical activity was published by Benedict and Carpenter in 1910. 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 significantly to the energy cost of exercise, and would be an important factor in daily energy expenditure. Herxheimer et al. noted that the V̇O2 of five untrained individuals did not return to baseline until 36–48 hours after exercise, and Edwards et al. reported a 25% elevation in metabolism 15 hours after cessation of 2 hours of strenuous football. Also, Passmore and Johnson found a 15% increase in RMR for 7 hours after a 16km walk at 6.4 km/hour in three males, and deVries and Gray 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 exercise, food, temperature, caffeine intake, habituation and stress.
Later, more controlled studies have been performed. Some studies have confirmed that there is an increase in V̇O2 after exercise that may last for several hours.[14, 15, 16, 17, 18, 19] However, other studies have concluded that EPOC is transient and minimal after exercise.[20, 21, 22, 23, 24] The conflicts in the results may be resolved if differences in exercise intensity and duration are taken into account, since this may be expected to affect the metabolic processes underlying EPOC. Also, differences in exercise mode, training status and sex may potentially contribute to the discrepant findings.
There are several methodological issues that are important to consider when studying EPOC. Accurate control over the pre-experimental conditions, and an excellent reproducibility in the indirect calorimetry 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 participants are transported to the laboratory.[25,26] Also, habituation of the study participants to testing procedures 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.
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 because 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 determine 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.
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 increase 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), beyond 40 minutes of recovery after 20–40 minutes of treadmill exercise around the ventilatory threshold, and beyond 40 minutes after 4 × 20 minutes of cycle ergometry at 35–55% of V̇O2max. Only two males and two females took part in the last study. Brehm and Gutin 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 individuals. After 3.2km running at this intensity, EPOC amounted to only 71kJ (~3.5L oxygen). Elliot et al. also found a short lasting (<30 minutes) EPOC after 10–30 minutes cycling at 80% of V̇O2max. Finally, Maresh et al. 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. 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. from the same laboratory, found a mean EPOC of 26L after 80 minutes cycling (in periods of 10–30 minutes with 5-minute breaks between) at an intensity of 70% of V̇O2max using eight study participants. In accordance with Hermansen et al.’s case study, 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 exercise. 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 31.9L of oxygen after 20, 40 and 76 minutes at 70% of V̇O2max, respectively. After the longest bout, EPOC duration was at least 10 hours.
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 80-minute run at 70% of V̇O2max. The maximal EPOC was 14.6L oxygen (297kJ) after the longest and hardest bout. In accordance with our studies,[16,43] they found an exponential relationship between exercise intensity and the magnitude of EPOC. They calculated that the intensity explained five times more of EPOC than either exercise duration or total work completed. While intensity accounted for 45.5% of the variation in EPOC, the duration of exercise, and the interaction between intensity and duration accounted only for 8.9% and 7.7%, respectively.
In our studies,[15,16,43] we found much higher EPOC values, and also more prolonged duration of EPOC, compared with Gore and Withers.[18,19] In the study by Mæhlum et al., the response was about twice the response of that observed in the study by Gore and Withers. Even though the measurement period was 4 hours shorter in the latter study, this can still not explain the difference. While we used cycling in our experiments, Gore and Withers used running, and the different exercise modes may be a possible explanation of the discrepancy in results. Another possible explanation, perhaps more likely, is the different training status of the study participants. In the studies by Gore and Withers,[18,19] the participants were well trained, whereas in our studies they were not.
In support of a significant EPOC after high-intensity exercise, a 3–7% increase in energy expenditure was found as late as 12–16 hours after intermittent exercise for a total of 71 minutes at 85% of V̇O2max. The most exhaustive bout for any of the EPOC studies was a 35km road run (intensity about 70% of V̇O2max for about 160 minutes). A total EPOC of 32.4L of oxygen, lasting for a total of 8 hours, was found. Furthermore, an EPOC lasting for 3 hours was observed after only 30 minutes treadmill walking at 70% of V̇O2max in young trained women. Also, a comparison of interval-type exercise alternating between 30% and 90% of V̇O2max, with continuous exercise of equal duration (36 minutes) 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.
Sedlock et al. 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 constant (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 duration 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 duration (~2.5L oxygen), even though no difference in EPOC duration (33 versus 28 minutes, respectively) was found. Similar studies with modest exercise protocols have supported the conclusion that exercise 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. found a significantly higher 3-hour EPOC after cycling at 75% versus 50% of V̇O2max (equal work, 500 kcal) in women. Brockman et al. investigated 1-hour EPOC after intense intermittent running (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 conclusion can be drawn.
In contrast to the findings of an intensity-related EPOC, Chad and Wenger did not find any relationship 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 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 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 mentioned 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 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 minutes, respectively. After the most exhaustive bout, EPOC lasted for 7.5 hours. Sedlock, 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 factors. 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 estimated.[15, 16, 17,22,24,30,33,39,40,43, 44, 45, 46, 47,51, 52, 53, 54,56,57,60,63,65,67, 68, 69, 70,72] It should be noted that some of the studies included 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 analysed the interaction effect between exercise intensity and duration on EPOC after treadmill exercise ranging from 20 minutes 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, compared 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 addition, they show that the highest EPOC values have been found when both exercise intensity and duration are substantial.
It appears that the post-exercise increase in energy 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 training. However, there are no studies where EPOC has been measured repeatedly in the same individuals 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, ≥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 expected 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.
In summary, the magnitude of EPOC after aerobic exercise is clearly dependent on both the duration and intensity of exercise. There is a curvilinear relationship between the magnitude of EPOC and the intensity of the exercise bout. At least for cycling, 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.
Effect of Split Exercise Sessions on EPOC
A couple of studies have shown a higher EPOC after split exercise sessions compared with a continuous bout. Kaminsky et al. investigated women during 50 minutes of continuous running versus two 25-minute sessions at 70% of V̇O2max. The combined EPOC after the two split sessions corresponded to ~3.1L versus 1.4L of oxygen after the continuous session. Almuzaini et al. 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 approximately 120% and 40% greater after split sessions 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 expenditure. 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 continuous sessions will be smaller than the difference in EPOC. This was not taken into account in the two studies mentioned.[36,67]
Effect of Supramaximal Exercise on EPOC
Given the relationship between exercise intensity and EPOC, it comes as no surprise that supramaximal exercise stimulates EPOC. We found that brief intermittent bouts of exhaustive supramaximal exercise (1, 2, or 3 × 2-minute bouts of cycling at 108% of V̇O2max, separated by 3-minute rest periods) elevated post-exercise energy expenditure for 4 hours.
Laforgia et al. 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. Interestingly, 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 performed in the latter study.
Few authors have tried to divide EPOC into different components. This is unfortunate, since exercise intensity and duration may affect the short and prolonged components to a different extent. We calculated the short EPOC component as the difference between the observed 1-hour EPOC and the prolonged curve component. By comparing EPOC after 70–80 minutes of cycling at 69–78% of V̇O2max with 3 × 2 minutes at 104–117% of V̇O2max, very similar 1-hour EPOCs were found; 7.6L (submaximal exercise) and 7.8L (supramaximal 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 exhausting exercise stimulates mechanisms also present beyond the first hour of recovery. However, this relationship remains to be fully elucidated.
Effect of Aerobic Exercise Mode on EPOC
A curvilinear relationship between exercise intensity 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 absolute 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 exercise,[75, 76, 77] and it is possible that this influences EPOC. However, in studies where concentric and eccentric exercise have been compared, no differences have been found in EPOC[47,55] or RMR for several days after exercise. Sedlock 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 degrees of eccentric muscular activity. No increase in recovery energy expenditure was found after eccentric 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 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. 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 intensity was found to have a greater effect than duration, but durations were low and within a narrow spectrum in this study. Since exercise duration and intensity 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.
Effect of Resistance Exercise on EPOC
EPOC has also been compared between aerobic and resistance exercise. Elliot et al. 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 energy cost or similar exercising V̇O2 have been used to equate continuous aerobic exercise and intermittent resistance exercise, have indicated that resistance exercise produces a greater EPOC response. A higher EPOC was found after hard resistance 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). RMR was still elevated 14.5 hours after the resistance exercise compared with a resting control experiment.
Burleson et al. compared weight training exercise (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 exercise, 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 duration 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 and Dolezal et al. 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, 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. 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 repetitions at 70% of 1RM).
After more moderate resistance exercise (three sets of seven exercises, ten repetitions at 12RM), a smaller EPOC was found, but the V̇O2 was measured for only 1 hour after exercise, and was still elevated at this time point. Binzen et al. found an EPOC shorter than 2 hours after three sets of ten exercises with ten repetitions at 10RM (1 minute of rest between sets) in resistance-trained women.
Murphy and Swartzkopf compared two different 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 compared high- and low-intensity resistance exercise with equated work volume, 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 investigated the effect of high- and low-intensity resistance exercise of similar work volume on EPOC. The exercise bouts consisted of two sets of nine exercises. In the high-intensity bout, eight repetitions at 85% of 8RM of each exercise were performed, 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 exercise 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 diversity in the protocols commonly employed in this research, for example, type (i.e. circuit training or 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 training is similar to interval training and split sessions of aerobic exercise in that each session or set of resistance exercise will have an EPOC of its own during the recovery period between exercises. To determine 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.
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 magnitude 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 exercise intensity level means that trained are working at a lower relative intensity, which has been shown to influence EPOC. Furthermore, if trained and untrained 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 found similar values for EPOC in runners versus non-exercisers following a 3.2km walk at 6.4 km/hour (i.e. same absolute intensity), but the exercise intensity may have been too low to detect a difference. Sedlock 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 duration or magnitude was found, but again, the exercise challenge was low. Finally, in a study of treadmill exercise at approximately the anaerobic threshold, it was concluded that fitness level does not significantly 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.
In contrast to these studies, Chad and Quigley found a higher 3-hour EPOC in trained female cyclists versus untrained women after 30 minutes cycling 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 untrained. V̇O2 was still increased 3 hours after exercise, and no definite EPOC magnitude could be determined.
Frey et al. 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 significantly 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. Following 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 significant 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-intensity, respectively, in the trained group. Thus, EPOC duration was shorter in the trained.
Short and Sedlock 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 significantly shorter duration of EPOC whether compared at the same absolute or relative intensity, but in all situations EPOC lasted less than 1 hour. Furthermore, the magnitude of EPOC was not different between groups after exercise at the same relative intensity (3.2L oxygen in trained versus 3.5L oxygen 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 untrained group had higher EPOC (2.4L oxygen) versus 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 metabolism 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.
Effect of Sex on EPOC
Sex is also a factor that can potentially influence EPOC, as well as have implications for study design. Energy expenditure at rest or during exercise may vary with menstrual phase,[92, 93, 94, 95] and this has not always been taken into consideration when studying EPOC. Basal metabolic rate has been shown to be at its lowest level 1 week before ovulation. Webb found an 8–16% increase in 24-hour energy expenditure during the 14-day luteal phase following ovulation. Accordingly, Matsuo et al. 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. 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 compared after absolute or relative workloads? Berg measured V̇O2 for 1 hour after 30 minutes of exercise at 40% of V̇O2max in active men and women. A higher post-exercise energy expenditure was found among men. However, the calculations are somewhat unclear, since the data are not compared with control resting values, and hence it is the absolute levels rather than the increase in energy expenditure after exercise that is compared.
Smith and McNaughton compared trained men and women after 30 minutes of exercise at 40%, 50% and 70% of V̇O2max. In all three conditions, 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 magnitude 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 menstrual cycle appears to be important in studies with women.
Possible Mechanisms for the Rapid EPOC Component
EPOC is the sum of many underlying mechanisms, 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 ventilation.[6,7,43,97] Thus, the classic oxygen debt hypothesis is one of several factors explaining the rapid component.
Possible Mechanisms for the Prolonged EPOC Component
The mechanisms for the prolonged EPOC component are less well understood. A sustained increased ventilation, circulation and body temperature may contribute; however, the cost of this is low (<1L oxygen).
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 exercise.[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 and substrate control. The energy cost associated with the increase in TG/FA cycling can account for a significant part of EPOC after prolonged steady-state exercise.
The existence of gluconeogenic-glycolytic substrate cycles have also been demonstrated in vivo in humans,[101, 102, 103, 104] but no increase in the rates of these cycles have been found during recovery from exercise.[104,105]
A relative shift from carbohydrate to fat as substrate source is a consistent finding after prolonged exhausting exercise.[37,43,68,69] Since the energy equivalent 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.
The energy cost of glycogen resynthesis has also been suggested as a mechanism for the prolonged EPOC component after aerobic exercise. However, 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. Furthermore, 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 replenishment of muscle and liver glycogen stores compared 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 requires only 5.3%. 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 could not detect any major interaction effects between food and previous aerobic exercise on the V̇O2.
Several hormones are potential stimulants of energy expenditure, including insulin, cortisol, thyroid hormones, growth hormone, adrenocorticotropic hormone (ACTH) and catecholamines. Plasma concentrations of growth hormone and ACTH may increase during exercise, but no sustained increase in secretion has been found after exercise.[111,112] Mæhlum et al. found no changes in plasma insulin and free thyroxine during the recovery period after exhausting endurance exercise, and only a transient increase in the plasma concentration of cortisol. 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 returned to resting levels after aerobic exercise.[68,69] we observed a prolonged depression in arterial plasma insulin concentrations after similar exercise. 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, ACTH, cortisol and growth hormone.
Many authors have suggested that an increased sympathoadrenal activity may be one of the mechanisms underlying EPOC, and of the prolonged component in particular.[6,15,30,37,114, 115, 116, 117] This hypothesis was based on several findings. Firstly, epinephrine and norepinephrine are potent stimulators of the energy metabolism.[118,119] Their calorigenic effect seems to be mediated through the β-adrenoceptors.[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 exercise duration and exponentially with the exercise intensity,[111,122] a similar relationship to that observed between EPOC and exercise duration and intensity, 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-adrenoceptor 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. Hence, there was no effect of β-adrenoceptor 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-adrenoceptor effect on EPOC could not be excluded, but the β3-adrenoceptor does not seem to be of importance for the sympathoadrenal-mediated thermogenesis, 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] The hypothesis was built on observations in vitro of an increased lipolytic response to catecholamine stimulation in human gluteal adipocytes and in suprailiac adipocytes removed immediately after an exercise bout compared with resting samples. However, we have shown that isoprenaline (β-adrenoceptor agonist) stimulated whole body V̇O2 to the same extent during rest with and without previous aerobic exercise. Hence, no increased sensitivity to catecholamines was detected in the post-exercise period. Also, the lipolytic effect of isoprenaline in abdominal adipose tissue was not increased after a prolonged moderate exercise bout, but instead a desensitisation was seen.
Another potential effect of the sympathoadrenal system on EPOC is by stimulation of various processes 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 lipolysis in adipose tissue and in muscles. The catecholamines also influence the release of other hormones, 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 recovery period after exercise. An increased whole body protein synthesis has been demonstrated after 3.75 hours of treadmill running at 50% of V̇O2max, and after 1 hour of cycling at 75% of V̇O2max. Also, an increased muscle protein synthesis has been shown after prolonged exercise, 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 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 turnover 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., leg V̇O2 accounted for only one-third of EPOC in the 60-minute recovery period after exhaustive knee extensor exercise lasting 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 exercise remained to be explained. Non-exercised muscles 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 lactate.[135,136]
The energy efficiency may change during exercise,[97,137] and this may be the case also during recovery from exercise. One potential mechanism for reduced energy efficiency is the activity of uncoupling proteins (UCP). The expression of UCP3 in various organs is consistent with a role in adaptive thermogenesis.[138, 139, 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 ventilation) 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 submaximal exercise. A minor part may be explained by a sustained elevation in circulation, ventilation and temperature. No increased sympathoadrenal activity has been found after such exercise. Little is known about the mechanisms underlying EPOC after resistance exercise.
Much of the conflicting reports of EPOC magnitude and duration may be resolved if differences in exercise intensity and duration are taken into account. 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 observed after more strenuous exercise. The relationship between exercise intensity and EPOC magnitude is curvilinear, whereas at higher intensities there is a linear relationship between exercise duration and EPOC. For resistance exercise, the relationship 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 effects 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 component are more unclear. The sum of the increased rate of TG/FA cycling and the shift from carbohydrate 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.
No sources of funding were used to assist in the preparation of this manuscript. The authors have no conflicts of interest that are directly relevant to the content of this manuscript.
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