Effect of Intensity
of Exercise
on Excess
Postexercise
0, Consumption
Roald Bahr and Ole M. Sejersted After exercise, there is an increase in 0, consumption termed the excess postexercise 0, consumption (EPOC). In this study, we have examined the effect of exercise intensity on the time course and magnitude of EPOC. Six healthy male subjects exercised on separate days for 80 minutes at 29%. 50%, and 75% of maximal 0, uptake (Vo,max) on a cycle ergometer. 0, uptake, R value, and rectal temperature were measured while the subjects rested in bed for 14 hours postexercise, and the results were compared with those of an identical control experiment without exercise. An increase in 0, uptake lasting for 0.3 IT 0.1 hour (29% exercise), 3.3 2 0.7 hour (50%) and 10.5 2 1.6 hour (75%) was observed. EPOC was 1.3 f 0.46 I(29%), 5.7 t 1.7 I(50%), and 30.1 ? 6.4 I (75%). There was an exponential relationship between exercise intensity and total EPOC, both during the first 2 hours and the next 5 hours of recovery. Hence, prolonged exercise at intensities above 40% to 50% of Vo,max is required in order to trigger the metabolic processes that are responsible for the prolonged EPOC component extending beyond 2 hours postexercise. Copyright 0 1991 by W.B. Saunders Company
A
FTER EXERCISE, 0, consumption remains elevated above resting levels for some period of time. This excess postexercise O? consumption (EPOC) comprises the classic 0, debt, which according to many investigators decays rapidly and does not extend beyond 1 to 2 hours after exercise.‘-5 On the other hand, there are other observations indicating that there is a prolonged EPOC component, detectable for up to 24 hours after strenuous exercise.‘~” An examination of the literature showed marked differences in the exercise stimulus used to elicit EPOC, and led us to the hypothesis that exercise intensity must exceed a certain level in order to trigger a component of EPOC, which lasts for many hours. A recent study shows that EPOC over a period of 8 hours postexercise was quite small when exercise intensity was less than 50% of maximal 0, uptake (Vo?max), but the data did not permit identification of a prolonged EPOC component.‘J Other studies are difficult to interpret, since the effects of exercise duration and intensity cannot be separated as total work was kept constant.‘,“,” Thus, the present study was designed to follow EPOC over 14 hours after exercise so that any prolonged EPOC component could be detected. Exercise duration was kept constant, and the hypothesis was tested by varying intensity of the exercise within the submaximal range. MATERIALS
AND METHODS
Subjects Six male students participated in the study (Table 1). All subjects were physically active, but not engaged in regular training. After a medical examination, they were fully informed dures before written consent was obtained.
about
all proce-
From the Depaament of Physiology National Institute of Occupational Health, Oslo, Norway. R.B. was supported by a grant from the Norwegian Research Councilfor Science and the Humanities (NAVF). Address reprint requests to Roald Bahr, MD, Department of Physiology, National Institute of Occupational Health, PO Box 8149 Dep, N-0033 Oslo 1, Norway. Copyright 0 1991 by W.B. Saunders Company 0026.0495/9114008-0012$03.OOiO
836
Preexperirnental Procedures Before experiments started, all subjects were tamiliarized with bicycle exercise at a constant pedaling rate and with breathing through the mouthpiece and the breathing valve used in all metabolic measurements. All testing and experimental exercise procedures were performed on a modified J$ogh cycle ergometer. About 2 weeks before the experiments, Vo,max was measured using the criteria of Taylor et al.‘” These results were used to predict work loads corresponding to 29%. 50%. and 75r7r of Vo,max in each subject.
Experimental Protocol Each subject participated in four experiments. Experiments were separated by 2 weeks and the sequence of the experiments was randomized. The subjects reported to the laboratory at 7:00 AM after an overnight fast, They were transported there by car to avoid unnecessary physical activity before each experiment. The subjects were told not to partake in any exercise for 2. days before an experiment and not to make any changes in their dietary or exercise habits, No tobacco or alcohol was allowed for 24 hours before each experiment. The urinary bladder was emptied, body weight was measured, and a thermistor (type DU3S. Ellas Instruments A/S. Copenhagen. Denmark) was inserted 10 to 15 cm into the rectum. and a plastic cannula was inserted into the antecubital vein. The subjects were connected to an electrocardiograph, Thereafter, the subjects rested in bed until the exercise period started. On 3 separate days. the subjects exercised at a constant pedaling rate of 75 rpm for 80 minutes at 39%. 50’%, and 75% of Vo?max (Table 1). They were allowed a S-minute rest period every 20th minute. After exercise. the subjects rested in bed for 14 hours. A control experiment without exercise was also performed and the conditions were identical to the resting period of the exercise experiment. The start of exercise was adjusted so that the recovery period always started at 9:30 AM. After exercise. the subjects rested in bed until 11:30 PM. and they were not allowed to sleep during this period. The subjects were given three meals consisting of bread (3 g/kg body weight), jam (7 gkg body weight), and skimmed milk (0.5 L) during the experiment. The average energy content per meal was 4.5 MJ (5% fat. Xl’_; carbohydrate, 14% protein). The first meal was taken 2 hours. the second 7 hours, and the last I7 hours after exercise. All meals were completed within 30 minutes.
Measurements 0: uptake was measured for the last 15 minutes of the rest period before exercise and from 15 to 18. 35 to 38, 55 to 58. and 75 to 78 minutes during the prolonged exercise bouts. Postexercise 0:
Metabo//sm,
Vol 40, No 8 (August), 1991: pp 836-841
a37
EXERCISE INTENSITY AND POSTEXERCISE 0, CONSUtiPTlON
Table 1. Physical Characteristics
29%
50%
75%
1
25
189
80
58.5
28
52
77
Subject No.
Age (vr)
Height (cm)
Weight (kg)
and Exercise Data for All Subjects
&,max
(mL
kg-’
min.‘)
2
23
47.4
27
47
77
24
187 185
a7
3
71
50.6
26
50
74
4
24
186
79
44.4
30
50
72
5
20
75
46.1
31
50
78
6
23
la3 178
58
49.0
29
51
70
Mean
23
185
75
49.9
29
50
75
SE
0.6
1.4
3.7
was measured continuously for the first hour and thereafter for the last 15 minutes of every hour for the next 14 hours. Rectal temperature and heart rate were recorded continuously during the whole experimental period. Heparinized blqod samples were drawn according to the same schedule as the Vo, measurements, transferred immediately to 0.4 mmol/L PCA stored on ice and analyzed for lactate concentration.” Expired air was collected in Douglas bags, and volume was measured in a wet spirometer. The bags and spirometer were checked for leaks. Fractions of 0, and CO, were determined on an automatic system (0,, s3A/I Ametek, Pittsburgh, PA; CO,, CO,analysator, Simrad Optronics, Oslo, Norway). The gas analyzers were calibrated against gases of known 0, and CO, concentrations before every bag was emptied. All gas volumes were expressed as STPD. uptake
Calculations and Statistical Methods The EPOC was calculated as the time integral of the difference in Oz uptake between the exercise and control experiments for the corresponding time periods until the postexercise 0, uptake was equal to or less than control values. Similarily, the duration of EPOC was estimated for each subject in each experiment as the time 0, uptake was increased after exercise compared with the corresponding values from the control experiment in that subject. The results are presented as mean +- SE. The postexercise period was divided into four intervals for statistical analysis. The first interval lasts from the end of the exercise period until the first meal (0 to 2 hours). The analysis of this interval provides information on the exclusive effect of exercise on EPOC. The data obtained during the next interval (2 to 7 hours) are influenced not only by exercise, but also by the thermic effect of food. The third (7 to 12 hours) and fourth (12 to 14 hours) intervals are comparable to the second, except that they are an additional 5 hours and 10 hours removed from the exercise period. The relationship between work intensity and individual responses of postexercise 0, consumption or R was tested by regression analysis. Paired comparisons were performed using a t test. Rejection level was chosen as P < .05.
1.4
0.7
0.6
1.3
Total EPOC was 1.3 2 0.46 1 (29%), 5.7 2 1.7 1 (50%), and 30.1 2 6.4 1 (75%). Individual EPOC values for different exercise intensities are shown in Fig 2. We observed considerable individual variation, but there is a monoexponential increase in EPOC (y) with increasing exercise intensity (x): y = 0.129 . 1Oo.o3o5” (Z’ < .OOOS). Hence, a threshold intensity of approximately 50% of Vo,max appears to exist, below which EPOC is small and mainly restricted to the rapid component. This threshold intensity may correspond to the lactate threshold, defined as the beginning of an increase in blood lactate above resting level, which in untrained indi.viduals usually occurs at an intensity slightly above 50% of Vo,max. A further analysis of mean 0, consumption in four consecutive time intervals after the exercise period is shown in Fig 3. A significant monoexponential increase in resting 0, consumption was observed with increasing exercise intensity in the first two postexercise intervals (0 to 2 hours and 2 to 7 hours). After 7 hours, this correlation was no longer significant, but 0, consumption was sjgnificantly elevated above control after exercise at 75% of Vo,max. R Value R value increased from 0.79 ? 0.02 (morning value in the control experiment) to 0.84 ? 0.02 (29%), 0.86 2 0.02 (50%) and 0.90 ? 0.02 (75%) during the last minute of the exercise periods (Fig 4). After exercise, there was a rapid
I ‘I’ t
I
II’
”
”
0
2
4
”
”
”
”
’
6
6
10
12
14
I
RESULTS 0, Uptake
After exercise, there was an initial rapid decline in 0, consumption, but 0, uptake remained above the level of the control experiment for 0.3 f 0.1 hours (29%), 3.3 f 0.7 hours (50%), and 10.5 ? 1.6 hours (75%) (Fig 1). Hence, no prolonged EPOC component.was observed after 80 minutes of exercise at 29% of Vo,max, the least strenuous exercise protocol.
-2
Time (h) Fig 1. Time plot of mean 0, uptake (n = 6) for the control day and the prolonged exercise days. Error bars (SE) have been omitted.
a38
BAHR AND SEJERSTED
40 30 20 10
0.7 -2
0
4
2
6
10
6
12
14
Time (h)
0 II
I
11
II
20
0
11
40
Fig 4. omitted.
I
60
80
Time plot of mean R value (n = 6). Error bars (SE) have been
Rectul Temperatures
Exercise
intensity
(%)
Rectal temperature increased from 36.7 -+-0.05”C (mean morning value for all experiments) to 37.2 * 0.07”C (29% ), 37.8 2 0.08”C (50%) and 38.8 * O.ll”C (75% ) at the end of the exercise period. The temperature decreased rapidly and reached control values in less than 1 hour on all exercise days. Thereafter, no significant differences were observed between the postexercise and control experiments.
Fig 2. Plot of EPOC versus exercise intensity. Different symbols are used for each subject. There was an exponential relationship between exercise intensity(x) and total EPOC (y): y = 0.129. 10°olOs’(P < .0005).
decrease in R value to or below the level of the control experiment, followed by a transient increase. After the first meal (2 to 7 hours), R value was lower following exercise at 75% of Vo,max when compared with the other conditions. The same tendency was present after the second (7 to 12 hours) and third (12 to 14 hours) meals.
Blood Luctute Concentration Blood lactate concentration was 0.79 i 0.06 mmol/L during rest before exercise (mean for all exercise experiments) and it was 0.87 -+ 0.11 mmol/L (29%) 1.10 ? 0.07 mmol/L (50%) and 3.83 +- 0.39 mmol/L (75%) at the end of exercise. There was no progressive increase in blood lactate concentration during exercise. Thus, none of the subjects appeared to be above the lactate threshold, even at exercise intensities ranging from 70% to 78% of Vo,max (Table 1). The range of blood lactate concentrations after 80 minutes of exercise at this intensity was 2.33 to 5.24 mmol/L. WC observed a weak relationship between individual blood
Heart Rate Heart rate increased during exercise to 100 ? 3 bpm (29%). 144 * 5 bpm (50%) and 180 -+ 4 bpm (75%). There was a slow return of heart rate to control levels during recovery, and the changes in heart rate parallelled the changes in 0: consumption. Heart rate returned to within 2 bpm above control levels in 1.2 2 0.40 hours (29%) 4.2 + 1.2 hours (50%) and 13.0 +- 0.75 hours (75%).
4oo ”
O-2h
2ool
I,,
0
I
” ”
I
20
I
40
I
I
60
I
2
I
I
I
1
I
I
I
I
I
I
I
I
II, 80
I!
0
Exercise
I
20
I
I
I
I
I
I
I
I
I
7-12h
2-7h
I
40
I
I
60
intensity
,I,
I
80
0
20
I
I
I
I
I
I
I
I
I
I
I
I
400
I
l2oo
12-14h
40
(% of maximal
60
0,
80
I
0
I
20
I
40
60
80
uptake)
Fig 3. 0, uptake versus exercise intensity (n = 6) in four time intervals: between exercise and first meal (0 to 2 hours), between first and second meals (2 to 7 hours), between second and third meals (7 to 12 hours), and after third meal (12 to 14 hours). A monoexponential relationship was observed between exercise intensity and mean 0, uptake in the first two time intervals (0 to 2 hours and 2 to 7 hours, P values am given in the figure). Different symbols are used for each subject.
EXERCISE INTENSITY
AND POSTEXERCISE
839
0, CONSUMPTION
lactate concentrations at the end of exercise at 75% of (x, mmol/L) and EPOC (y, L): y = 10.5 . x - 10.1 (r = .65, P < .lO). This observation should be interpreted with caution, since correlational analysis with only six subjects lacks statistical power. Lactate concentrations not different from resting values were reached in 5 to 60 minutes after all intensities. ~~,max
DISCUSSION
The main finding of this study is that there is a curvilinear relationship between exercise intensity and the magnitude of the EPOC. There is a sharp increase in EPOC for exercise intensities exceeding approximately 50% of Vo,max. The reason for this, in part, is that the prolonged EPOC component (beyond 1 hour) is not detectable after lowintensity exercise. Relationship Between EPOC and Exercise Intensity After exercise at or below 50% of Vo,max, we observed a small and short-lasting increase in postexercise OZconsumption. The highest exercise intensity (75% of Vo,max) produced the greatest EPOC. However, there was considerable variation in individual EPOCs, from approximately 5 Wmin to above 50 L/.min (Fig 2). We have defined exercise intensity relative to Vo,max. It is likely that the magnitude of EPOC is related to the amount of stress put on specific metabolic processes during exercise, such as the anaerobic metabolism or the rate of mobilization and oxidation of fatty acids (see below). Activation of the sympathetic nervous system probably plays a regulatory role. Thus, expressing exercise intensity relative to the extent of activation of these processes would perhaps give a better correlation with the magnitude of EPOC. Some early investigators reported a prolonged increase in energy expenditure after strenuous exercise.“” However, the interpretation of these studies is difficult, since the number of subjects was limited, the methods for indirect calorimetry were less precise, and the experimental conditions (resting activity level and food intake) were not always controlled. Still, several more recent and better controlled studies provide convincing evidence confirming that there is a significant prolonged EPOC component after exercise exceeding 50% of Vo,max. Two recent studies from this laboratory have shown that exercise at 70% of VoZmax for 80 minutes results in a mean increase in OZ uptake of approximately 14% for a 12-hour recovery period, compared with an identical control experiment without exercise.6.7 Bielinski et al observed an increase in energy expenditure for 5 hours after 3 hours exercise at 52% of VoZmax,’ and Chad and Wenger reported a significant increase in 0, consumption for 7.5 hours after 60 minutes exercise at 67% of VoZmax.9 Devlin and Horton had subjects undergo a protocol of intermittent exercise at 85% of Vo,max for a total of 71 minutes, and observed a 3% to 7% increase in energy expenditure as late as 12 to 16 hours Finally, Gore and Withers in a wellpostexercise.” controlled study have recently concluded that exercise intensity is the major determinant of EPOCt4,”
Also in agreement with the present data, several investigators have concluded that the increase in postexercise energy expenditure after low-intensity exercise is transient and minimal.‘-’ Thus, it appears that the controversy regarding the duration and magnitude of EPOC may be resolved if differences in exercise intensity and duration are taken into account. Based on data from the present and previous studies, the duration of EPOC appears to be less than 30 minutes after light exercise (intensity at < 50% of Vo,max and duration < 1 hour) and the contribution of EPOC to total energy consumption is small.‘-’ Even after moderate exercise (intensity at N 50% of VO,max and lasting > 1 hour), the duration of EPOC is only a few hours (Figs 1 and 3) and the addition to the energy expenditure during exercise is moderate.8.‘3 It is possible that prolonged durations (2 to 4 hours) may result in a prolonged EPOC even at this intensity. Only after strenuous exercise (intensities of 70% or more) is there any prolonged increase in recovery 0, uptake, contributing significantly to total energy expenditure.6.7.‘.” At this exercise intensity, EPOC is linearly related to exercise duration, equaling approximately 15% of total exercise 0, consumption.’ The prolonged EPOC component is the major reason for this effect. So far the prolonged component has not been examined after intensities exceeding 75% of Vo,max. Of course, time to exhaustion will decline rapidly as intensity is increased, so that the interaction between duration and intensity may be difficult to assess. Metabolic Bases of EPOC Exercise triggers a multitude of processes that must return to a basal turnover rate during the recovery period. It appears that other tissues, as well as muscle, must be involved, since whole body EPOC is much greater than can be accounted for by local muscle events.” The classic O2 debt, or rapid EPOC component ( < 1 hour postexercise), is believed to be caused by replenishment of O1 stores in blood and muscle, resynthesis of adenosine triphosphate and creatine phosphate, and lactate remova1.‘“~“~“‘~‘5 Also, quantitatively more important in the early recovery phase is increased ventilation and a higher heart rate. We presently show that any increase in 0, consumption associated with higher body temperature subsides within 1 hour. Clearly, all these processes are to some degree dependent on exercise intensity, which partly explains the strong effect of intensity on EPOC over the first 2 hours of recovery. However, the metabolic explanation for the prolonged EPOC component is less clear, since most of the processes mentioned above are known to be limited to the first few minutes or hours. Apparently, more strenuous exercise triggers other energy-consuming events that persist for hours during recovery from exercise. Sejersted and Vaage pointed out that during the first hour after exercise there is a large EPOC component dependent on exercise duration, in excess of and unaccounted for by the traditional rapid lactacid or alactacid components.‘” More recently Bangsbo et al have shown in the functionally isolated human quadriceps muscle that there is a large unexplained OL consumption over the first 60 minutes postexercise.’
BAHR AND SEJERSTED
840
We now show that blood lactate returns to resting levels within 1 hour, and it appears that the contribution to EPOC from the energy cost of lactate removal is limited to this time period. Even so, the magnitude of the prolonged EPOC component may be related to the activation of anaerobic metabolism during exercise. Exercise at intensities above the lactate threshold or maximum intensity at which there is a steady-state concentration of blood lactate results in non-steady-state behavior of metabolic processes during exercise, ie, an increase in O2 consumption.‘6~‘8 It is possible that exercise above this threshold triggers energyconsuming processes that persist for several hours during recovery. Our lactate data show that all experiments were performed using exercise intensities at or below the maximum steady state for lactate. After exercise at 75% of Vozmax, there was a weak relationship between blood lactate at the end of exercise and the resulting EPOC, which supports the suggestion that the magnitude of EPOC could be better related to the relative activation of specific metabolic processes other than the 0, uptake. Resynthesis of glycogen from carbohydrate supplied in the food has been claimed to account for a large fraction of the prolonged EPOC component.’ However, fasting experiments show that there is no change in EPOC whether food is given during recovery or not.” It may be that feeding results in an increase of some energy-requiring processes (such as glycogen synthesis) and a decrease in other (such as gluconeogenesis). Nevertheless, it appears that EPOC is the same whether the rate of glycogen synthesis is high or low.‘y Exercise at high intensities results in activation of the sympathetic nervous system with elevated concentrations of plasma catecholamines.“’ Triglyceride-fatty acid (TG-FA) cycling, which consumes ATP, is among the many metabolic processes stimulated by catecholamines.31 Two recent studies have demonstrated that the rate of TG-FA cycling is elevated for at least 3 hours after exercise.“,2’ The increase in the rate of TG-FA cycling was estimated to account for a 4% to 5% increase above resting energy expenditure during 2 hours of recovery from 4 hours of exercise at 40% of Vo2max,3Z and at 3 hours after 2 hours of exercise at 50% of Vo,max.” It is possible that the prolonged EPOC component is dependent on sympathetic activation of TG-FA substrate cycling, and there is some evidence that a shift in substrate utilization from carbohydrate to fat is accompanied by an increased cycling rate.‘” This is supported by the recent finding that EPOC is increased when fatty acid mobilization and oxidation is stimulated by caffeine ingestion before exercise.‘3 In the present study, the R values
after exercise at 75% of Vozmax were reduced, indicating an increased reliance on FA oxidation and possibly an increased rate of TG-FA cycling. Other hormones than catecholamines may also play a role in stimulating metabolic rate after exercise. Using a similar protocol to the present, Maehlum et al have shown that there are no changes in plasma levels of insulin, cortisol, and free thyroxine.” There is a need for information on plasma catecholamines or growth hormone from similar controlled recovery studies. We have no complete explanation for the prolonged EPOC component. It is possible that the efficiency of ATP production or ATP consumption is altered during recovery from exercise. In this respect it is interesting to note that exercise efficiency is reduced during recovery from prolonged. strenuous exercise? Practical Implications The main controversy in relation to the practical implications of EPOC is whether exercise has any significant impact on energy balance. Exercise at or around 70% of Vo:max will probably be beyond the tolerance level of the average obese or untrained individual. Therefore, we conclude that the amount and intensity of exercise likely to be tolerated by people embarking on a weight loss program is unlikely to cause any prolonged increase in recovery energy expenditure. However. those who would like to benefit from the additional energy expenditure caused by EPOC should be encouraged to exercise intensities above 50% of Vo,max, perhaps using intermittent-type interval training to increase tolerance. Conclusions This study demonstrates that there is an exponential relationship between exercise intensity and the EPOC after exercise for 80 minutes. After exercise at intensities below 50% of Vo:max, we observed no prolonged EPOC component. Hence, there appears to exist a threshold exercise intensity, possibly equal to the lactate threshold, to exceed in order to trigger the metabolic processes causing the prolonged EPOC component. ACKNOWLEDGMENT The authors thank Ada Ingvaldsen. Svein Nondal. Bjerg I. Selberg, and Jorid Thrane Stuemes for skillful technical assistance. We acknowledge the advice and support from all colleagues at the Department of Physiology at the National Institute of Occupational Health. We thank the subjects who participated in the experiments.
REFERENCES 1. Hagberg JM, Mullin JP, Nagle FJ: Effect of work intensity and duration on recovery 0,. J Appl Physiol48:540-544, 1980 2. Freedman-Akabas S, Colt E, Kissileff HR. et al: Lack of sustained increase in Vol following exercise in fit and unfit subjects. Am J Clin Nutr 41:545-549, 1985 3. Pacy PJ, Barton N, Webster JD, et al: The energy cost of aerobic exercise in fed and fasted normal subjects. Am J Clin Nutr 421764768, 1985 4. Brehm BA, Gutin B: Recovery energy expenditure for steady
state exercise in runners and non-exercisers. Med Sci Sports Exert 18205-210, 1986 5. Elliot D. Goldberg L, Kuehl KS: Does aerobic conditioning cause a sustained increase in the metabolic rate? Am J Med Sci 296249-251, 1989 6. Maehlum S. Grandmontagne M. Newsholme EA. et al: Magnitude and duration of excess postexercise oxygen consumption in healthy young subjects. Metabolism 35:425-429. 1986 7. Bahr R, Ingnes I, Vaage 0, et al: Effect of duration of
EXERCISE INTENSITY
AND POSTEXERCISE
0, CONSUMPTION
exercise on excess postexercise 0, consumption. J Appi Physiol 62:485-490, 1987 8. Bielinski R, Schutz Y, Jequier E: Energy metabolism during the postexercise recovery in man. Am J Clin Nutr 42:69-82,198s 9. Chad KE, Wenger HA: The effect of exercise duration on the exercise and post-exercise oxygen consumption. Can .I Sports Sci 13:204-207,1989 10. Sejersted OM, Vaage 0: Components of oxygen debt in man analysed on the basis of its dependence on exercise duration. J Physiol390:182P, 1987 (abstr) 11. Devlin JT, Horton ES: Potentiation of the thermic effect of insulin by exercise: Differences between lean, obese and noninsulindependent diabetic men. Am J Clin Nutr 43:884-890,1986 12. Chad KE, Wenger HA: The effects of duration and intensity on the exercise and post exercise metabolic rate. Aust J Sci Med Sport 17:14-18.1985 13. Bangsbo J, Gollnick PD, Graham TE, et al: Anaerobic energy production and 0, deficit-debt relationship during exhaustive exercise in humans. J Physiol422:539-559, 1990 14. Gore CJ, Withers RT: The effect of exercise intensity and duration on the oxygen deficit and excess post-exercise oxygen consumption. Eur J Appl Physiol60:169-174, 1990 15. Sedlock DA, Fissinger JA, Melby CL: Effect of exercise intensity and duration on postexercise energy expenditure. Med Sci Sports Exert 21:662-666,1989 16. Taylor HL, Buskirk E, Henschel A: Maximal oxygen intake as an objective measure of cardio-respiratory performance. J Appl Physiol55:73-80,1955 17. Lowry OH, Passonneau JV: A Flexible System of Enzymatic Analysis. San Diego, CA, Academic, 1972 18. Benedict FG, Carpenter TH: The Metabolism and Energy Transformations of Healthy Man During Rest. Washington, DC, Carnegie Institution, 1910, pp 182-193 19. Edwards HT, Thorndike A Jr, Dill DB: The energy requirement in strenuous muscular exercise. N Engl J Med 213:532-535, 1935 20. Passmore R, Johnson RE: Some metabolic changes following prolonged moderate exercise. Metabolism 9:452-455, 1960 21. deVries HA, Gray DA: Aftereffects of exercise upon resting metabolic rate. Res Q 34:314-321, 1963
841
22. Gore CJ, Withers RT: Effect of exercise intensity and duration on postexercise metabolism. J Appl Physiol68:2362-2368, 1990 23. Bahr R, Hansson P, Sejersted OM: Triglyceride/fatty acid cycling is increased after exercise. Metabolism 39:993-999,199O 24. Gaesser GA, Brooks GA: Metabolic bases of excess postexercise oxygen consumption: A review. Med Sci Sports Exert 16:29-43,1984 25. Hermansen L, Grandmontagne M, Maehlum S, et al: Postexercise elevation of resting oxygen uptake: Possible mechanisms and physiological significance, in Marconnet P, Hermansen L (eds): Physiological Chemistry of Training and Detraining. Basel, Switzerland, Karger, 1984, pp 119-129 26. Henson LC, Poole DC, Whipp BJ: Fitness as a determinant of oxygen uptake response to constant-load exercise. Eur J Appl Physiol59:21-28, 1989 27. Poole DC, Ward SA, Whipp BJ: The effects of training on the metabolic and respiratory profile of high-intensity cycle ergometer exercise. Eur J Appl Physiol59:421-429, 1990 28. Poole DC, Ward SA, Gardner GW, et al: Metabolic and respiratory profile of the upper limit for prolonged exercise in man. Ergonomics 31:1265-1279,1988 29. Bahr R, Sejersted OM: Effect of feeding and fasting on the excess postexercise 0, consumption. J Appl Physiol 1991 (submitted) 30. Galbo H, Holst J, Christensen NJ: Glucagon and plasma catecholamine responses to graded and prolonged exercise in man. J Appl Physiol38:70-76, 1975 31. Miyoshi H, Shulman GI, Peters EJ, et al: Hormonal control of substrate cycling in humans. J Clin Invest 81:1545-1555, 1988 32. Wolfe RR, Klein S. Carraro F. et al: Role of triglyceridefatty acid cycle in controlling fat metabolism in humans during and after exercise. Am J Physiol258:E382-E389,1990 33. Chad K, Quigley B: The effects of substrate utilization, manipulated by caffeine, on post-exercise oxygen consumption in untrained female subjects. Eur J Appl Physiol59:48-54, 1989 34. Bahr R. Opstad PK, Sejersted OM: Acute overtraining elevates resting metabolic rate and causes reduced mechanical efficiency. Acta Physiol Stand (in press)
of Exercise
on Excess
Postexercise
0, Consumption
Roald Bahr and Ole M. Sejersted After exercise, there is an increase in 0, consumption termed the excess postexercise 0, consumption (EPOC). In this study, we have examined the effect of exercise intensity on the time course and magnitude of EPOC. Six healthy male subjects exercised on separate days for 80 minutes at 29%. 50%, and 75% of maximal 0, uptake (Vo,max) on a cycle ergometer. 0, uptake, R value, and rectal temperature were measured while the subjects rested in bed for 14 hours postexercise, and the results were compared with those of an identical control experiment without exercise. An increase in 0, uptake lasting for 0.3 IT 0.1 hour (29% exercise), 3.3 2 0.7 hour (50%) and 10.5 2 1.6 hour (75%) was observed. EPOC was 1.3 f 0.46 I(29%), 5.7 t 1.7 I(50%), and 30.1 ? 6.4 I (75%). There was an exponential relationship between exercise intensity and total EPOC, both during the first 2 hours and the next 5 hours of recovery. Hence, prolonged exercise at intensities above 40% to 50% of Vo,max is required in order to trigger the metabolic processes that are responsible for the prolonged EPOC component extending beyond 2 hours postexercise. Copyright 0 1991 by W.B. Saunders Company
A
FTER EXERCISE, 0, consumption remains elevated above resting levels for some period of time. This excess postexercise O? consumption (EPOC) comprises the classic 0, debt, which according to many investigators decays rapidly and does not extend beyond 1 to 2 hours after exercise.‘-5 On the other hand, there are other observations indicating that there is a prolonged EPOC component, detectable for up to 24 hours after strenuous exercise.‘~” An examination of the literature showed marked differences in the exercise stimulus used to elicit EPOC, and led us to the hypothesis that exercise intensity must exceed a certain level in order to trigger a component of EPOC, which lasts for many hours. A recent study shows that EPOC over a period of 8 hours postexercise was quite small when exercise intensity was less than 50% of maximal 0, uptake (Vo?max), but the data did not permit identification of a prolonged EPOC component.‘J Other studies are difficult to interpret, since the effects of exercise duration and intensity cannot be separated as total work was kept constant.‘,“,” Thus, the present study was designed to follow EPOC over 14 hours after exercise so that any prolonged EPOC component could be detected. Exercise duration was kept constant, and the hypothesis was tested by varying intensity of the exercise within the submaximal range. MATERIALS
AND METHODS
Subjects Six male students participated in the study (Table 1). All subjects were physically active, but not engaged in regular training. After a medical examination, they were fully informed dures before written consent was obtained.
about
all proce-
From the Depaament of Physiology National Institute of Occupational Health, Oslo, Norway. R.B. was supported by a grant from the Norwegian Research Councilfor Science and the Humanities (NAVF). Address reprint requests to Roald Bahr, MD, Department of Physiology, National Institute of Occupational Health, PO Box 8149 Dep, N-0033 Oslo 1, Norway. Copyright 0 1991 by W.B. Saunders Company 0026.0495/9114008-0012$03.OOiO
836
Preexperirnental Procedures Before experiments started, all subjects were tamiliarized with bicycle exercise at a constant pedaling rate and with breathing through the mouthpiece and the breathing valve used in all metabolic measurements. All testing and experimental exercise procedures were performed on a modified J$ogh cycle ergometer. About 2 weeks before the experiments, Vo,max was measured using the criteria of Taylor et al.‘” These results were used to predict work loads corresponding to 29%. 50%. and 75r7r of Vo,max in each subject.
Experimental Protocol Each subject participated in four experiments. Experiments were separated by 2 weeks and the sequence of the experiments was randomized. The subjects reported to the laboratory at 7:00 AM after an overnight fast, They were transported there by car to avoid unnecessary physical activity before each experiment. The subjects were told not to partake in any exercise for 2. days before an experiment and not to make any changes in their dietary or exercise habits, No tobacco or alcohol was allowed for 24 hours before each experiment. The urinary bladder was emptied, body weight was measured, and a thermistor (type DU3S. Ellas Instruments A/S. Copenhagen. Denmark) was inserted 10 to 15 cm into the rectum. and a plastic cannula was inserted into the antecubital vein. The subjects were connected to an electrocardiograph, Thereafter, the subjects rested in bed until the exercise period started. On 3 separate days. the subjects exercised at a constant pedaling rate of 75 rpm for 80 minutes at 39%. 50’%, and 75% of Vo?max (Table 1). They were allowed a S-minute rest period every 20th minute. After exercise. the subjects rested in bed for 14 hours. A control experiment without exercise was also performed and the conditions were identical to the resting period of the exercise experiment. The start of exercise was adjusted so that the recovery period always started at 9:30 AM. After exercise. the subjects rested in bed until 11:30 PM. and they were not allowed to sleep during this period. The subjects were given three meals consisting of bread (3 g/kg body weight), jam (7 gkg body weight), and skimmed milk (0.5 L) during the experiment. The average energy content per meal was 4.5 MJ (5% fat. Xl’_; carbohydrate, 14% protein). The first meal was taken 2 hours. the second 7 hours, and the last I7 hours after exercise. All meals were completed within 30 minutes.
Measurements 0: uptake was measured for the last 15 minutes of the rest period before exercise and from 15 to 18. 35 to 38, 55 to 58. and 75 to 78 minutes during the prolonged exercise bouts. Postexercise 0:
Metabo//sm,
Vol 40, No 8 (August), 1991: pp 836-841
a37
EXERCISE INTENSITY AND POSTEXERCISE 0, CONSUtiPTlON
Table 1. Physical Characteristics
29%
50%
75%
1
25
189
80
58.5
28
52
77
Subject No.
Age (vr)
Height (cm)
Weight (kg)
and Exercise Data for All Subjects
&,max
(mL
kg-’
min.‘)
2
23
47.4
27
47
77
24
187 185
a7
3
71
50.6
26
50
74
4
24
186
79
44.4
30
50
72
5
20
75
46.1
31
50
78
6
23
la3 178
58
49.0
29
51
70
Mean
23
185
75
49.9
29
50
75
SE
0.6
1.4
3.7
was measured continuously for the first hour and thereafter for the last 15 minutes of every hour for the next 14 hours. Rectal temperature and heart rate were recorded continuously during the whole experimental period. Heparinized blqod samples were drawn according to the same schedule as the Vo, measurements, transferred immediately to 0.4 mmol/L PCA stored on ice and analyzed for lactate concentration.” Expired air was collected in Douglas bags, and volume was measured in a wet spirometer. The bags and spirometer were checked for leaks. Fractions of 0, and CO, were determined on an automatic system (0,, s3A/I Ametek, Pittsburgh, PA; CO,, CO,analysator, Simrad Optronics, Oslo, Norway). The gas analyzers were calibrated against gases of known 0, and CO, concentrations before every bag was emptied. All gas volumes were expressed as STPD. uptake
Calculations and Statistical Methods The EPOC was calculated as the time integral of the difference in Oz uptake between the exercise and control experiments for the corresponding time periods until the postexercise 0, uptake was equal to or less than control values. Similarily, the duration of EPOC was estimated for each subject in each experiment as the time 0, uptake was increased after exercise compared with the corresponding values from the control experiment in that subject. The results are presented as mean +- SE. The postexercise period was divided into four intervals for statistical analysis. The first interval lasts from the end of the exercise period until the first meal (0 to 2 hours). The analysis of this interval provides information on the exclusive effect of exercise on EPOC. The data obtained during the next interval (2 to 7 hours) are influenced not only by exercise, but also by the thermic effect of food. The third (7 to 12 hours) and fourth (12 to 14 hours) intervals are comparable to the second, except that they are an additional 5 hours and 10 hours removed from the exercise period. The relationship between work intensity and individual responses of postexercise 0, consumption or R was tested by regression analysis. Paired comparisons were performed using a t test. Rejection level was chosen as P < .05.
1.4
0.7
0.6
1.3
Total EPOC was 1.3 2 0.46 1 (29%), 5.7 2 1.7 1 (50%), and 30.1 2 6.4 1 (75%). Individual EPOC values for different exercise intensities are shown in Fig 2. We observed considerable individual variation, but there is a monoexponential increase in EPOC (y) with increasing exercise intensity (x): y = 0.129 . 1Oo.o3o5” (Z’ < .OOOS). Hence, a threshold intensity of approximately 50% of Vo,max appears to exist, below which EPOC is small and mainly restricted to the rapid component. This threshold intensity may correspond to the lactate threshold, defined as the beginning of an increase in blood lactate above resting level, which in untrained indi.viduals usually occurs at an intensity slightly above 50% of Vo,max. A further analysis of mean 0, consumption in four consecutive time intervals after the exercise period is shown in Fig 3. A significant monoexponential increase in resting 0, consumption was observed with increasing exercise intensity in the first two postexercise intervals (0 to 2 hours and 2 to 7 hours). After 7 hours, this correlation was no longer significant, but 0, consumption was sjgnificantly elevated above control after exercise at 75% of Vo,max. R Value R value increased from 0.79 ? 0.02 (morning value in the control experiment) to 0.84 ? 0.02 (29%), 0.86 2 0.02 (50%) and 0.90 ? 0.02 (75%) during the last minute of the exercise periods (Fig 4). After exercise, there was a rapid
I ‘I’ t
I
II’
”
”
0
2
4
”
”
”
”
’
6
6
10
12
14
I
RESULTS 0, Uptake
After exercise, there was an initial rapid decline in 0, consumption, but 0, uptake remained above the level of the control experiment for 0.3 f 0.1 hours (29%), 3.3 f 0.7 hours (50%), and 10.5 ? 1.6 hours (75%) (Fig 1). Hence, no prolonged EPOC component.was observed after 80 minutes of exercise at 29% of Vo,max, the least strenuous exercise protocol.
-2
Time (h) Fig 1. Time plot of mean 0, uptake (n = 6) for the control day and the prolonged exercise days. Error bars (SE) have been omitted.
a38
BAHR AND SEJERSTED
40 30 20 10
0.7 -2
0
4
2
6
10
6
12
14
Time (h)
0 II
I
11
II
20
0
11
40
Fig 4. omitted.
I
60
80
Time plot of mean R value (n = 6). Error bars (SE) have been
Rectul Temperatures
Exercise
intensity
(%)
Rectal temperature increased from 36.7 -+-0.05”C (mean morning value for all experiments) to 37.2 * 0.07”C (29% ), 37.8 2 0.08”C (50%) and 38.8 * O.ll”C (75% ) at the end of the exercise period. The temperature decreased rapidly and reached control values in less than 1 hour on all exercise days. Thereafter, no significant differences were observed between the postexercise and control experiments.
Fig 2. Plot of EPOC versus exercise intensity. Different symbols are used for each subject. There was an exponential relationship between exercise intensity(x) and total EPOC (y): y = 0.129. 10°olOs’(P < .0005).
decrease in R value to or below the level of the control experiment, followed by a transient increase. After the first meal (2 to 7 hours), R value was lower following exercise at 75% of Vo,max when compared with the other conditions. The same tendency was present after the second (7 to 12 hours) and third (12 to 14 hours) meals.
Blood Luctute Concentration Blood lactate concentration was 0.79 i 0.06 mmol/L during rest before exercise (mean for all exercise experiments) and it was 0.87 -+ 0.11 mmol/L (29%) 1.10 ? 0.07 mmol/L (50%) and 3.83 +- 0.39 mmol/L (75%) at the end of exercise. There was no progressive increase in blood lactate concentration during exercise. Thus, none of the subjects appeared to be above the lactate threshold, even at exercise intensities ranging from 70% to 78% of Vo,max (Table 1). The range of blood lactate concentrations after 80 minutes of exercise at this intensity was 2.33 to 5.24 mmol/L. WC observed a weak relationship between individual blood
Heart Rate Heart rate increased during exercise to 100 ? 3 bpm (29%). 144 * 5 bpm (50%) and 180 -+ 4 bpm (75%). There was a slow return of heart rate to control levels during recovery, and the changes in heart rate parallelled the changes in 0: consumption. Heart rate returned to within 2 bpm above control levels in 1.2 2 0.40 hours (29%) 4.2 + 1.2 hours (50%) and 13.0 +- 0.75 hours (75%).
4oo ”
O-2h
2ool
I,,
0
I
” ”
I
20
I
40
I
I
60
I
2
I
I
I
1
I
I
I
I
I
I
I
I
II, 80
I!
0
Exercise
I
20
I
I
I
I
I
I
I
I
I
7-12h
2-7h
I
40
I
I
60
intensity
,I,
I
80
0
20
I
I
I
I
I
I
I
I
I
I
I
I
400
I
l2oo
12-14h
40
(% of maximal
60
0,
80
I
0
I
20
I
40
60
80
uptake)
Fig 3. 0, uptake versus exercise intensity (n = 6) in four time intervals: between exercise and first meal (0 to 2 hours), between first and second meals (2 to 7 hours), between second and third meals (7 to 12 hours), and after third meal (12 to 14 hours). A monoexponential relationship was observed between exercise intensity and mean 0, uptake in the first two time intervals (0 to 2 hours and 2 to 7 hours, P values am given in the figure). Different symbols are used for each subject.
EXERCISE INTENSITY
AND POSTEXERCISE
839
0, CONSUMPTION
lactate concentrations at the end of exercise at 75% of (x, mmol/L) and EPOC (y, L): y = 10.5 . x - 10.1 (r = .65, P < .lO). This observation should be interpreted with caution, since correlational analysis with only six subjects lacks statistical power. Lactate concentrations not different from resting values were reached in 5 to 60 minutes after all intensities. ~~,max
DISCUSSION
The main finding of this study is that there is a curvilinear relationship between exercise intensity and the magnitude of the EPOC. There is a sharp increase in EPOC for exercise intensities exceeding approximately 50% of Vo,max. The reason for this, in part, is that the prolonged EPOC component (beyond 1 hour) is not detectable after lowintensity exercise. Relationship Between EPOC and Exercise Intensity After exercise at or below 50% of Vo,max, we observed a small and short-lasting increase in postexercise OZconsumption. The highest exercise intensity (75% of Vo,max) produced the greatest EPOC. However, there was considerable variation in individual EPOCs, from approximately 5 Wmin to above 50 L/.min (Fig 2). We have defined exercise intensity relative to Vo,max. It is likely that the magnitude of EPOC is related to the amount of stress put on specific metabolic processes during exercise, such as the anaerobic metabolism or the rate of mobilization and oxidation of fatty acids (see below). Activation of the sympathetic nervous system probably plays a regulatory role. Thus, expressing exercise intensity relative to the extent of activation of these processes would perhaps give a better correlation with the magnitude of EPOC. Some early investigators reported a prolonged increase in energy expenditure after strenuous exercise.“” However, the interpretation of these studies is difficult, since the number of subjects was limited, the methods for indirect calorimetry were less precise, and the experimental conditions (resting activity level and food intake) were not always controlled. Still, several more recent and better controlled studies provide convincing evidence confirming that there is a significant prolonged EPOC component after exercise exceeding 50% of Vo,max. Two recent studies from this laboratory have shown that exercise at 70% of VoZmax for 80 minutes results in a mean increase in OZ uptake of approximately 14% for a 12-hour recovery period, compared with an identical control experiment without exercise.6.7 Bielinski et al observed an increase in energy expenditure for 5 hours after 3 hours exercise at 52% of VoZmax,’ and Chad and Wenger reported a significant increase in 0, consumption for 7.5 hours after 60 minutes exercise at 67% of VoZmax.9 Devlin and Horton had subjects undergo a protocol of intermittent exercise at 85% of Vo,max for a total of 71 minutes, and observed a 3% to 7% increase in energy expenditure as late as 12 to 16 hours Finally, Gore and Withers in a wellpostexercise.” controlled study have recently concluded that exercise intensity is the major determinant of EPOCt4,”
Also in agreement with the present data, several investigators have concluded that the increase in postexercise energy expenditure after low-intensity exercise is transient and minimal.‘-’ Thus, it appears that the controversy regarding the duration and magnitude of EPOC may be resolved if differences in exercise intensity and duration are taken into account. Based on data from the present and previous studies, the duration of EPOC appears to be less than 30 minutes after light exercise (intensity at < 50% of Vo,max and duration < 1 hour) and the contribution of EPOC to total energy consumption is small.‘-’ Even after moderate exercise (intensity at N 50% of VO,max and lasting > 1 hour), the duration of EPOC is only a few hours (Figs 1 and 3) and the addition to the energy expenditure during exercise is moderate.8.‘3 It is possible that prolonged durations (2 to 4 hours) may result in a prolonged EPOC even at this intensity. Only after strenuous exercise (intensities of 70% or more) is there any prolonged increase in recovery 0, uptake, contributing significantly to total energy expenditure.6.7.‘.” At this exercise intensity, EPOC is linearly related to exercise duration, equaling approximately 15% of total exercise 0, consumption.’ The prolonged EPOC component is the major reason for this effect. So far the prolonged component has not been examined after intensities exceeding 75% of Vo,max. Of course, time to exhaustion will decline rapidly as intensity is increased, so that the interaction between duration and intensity may be difficult to assess. Metabolic Bases of EPOC Exercise triggers a multitude of processes that must return to a basal turnover rate during the recovery period. It appears that other tissues, as well as muscle, must be involved, since whole body EPOC is much greater than can be accounted for by local muscle events.” The classic O2 debt, or rapid EPOC component ( < 1 hour postexercise), is believed to be caused by replenishment of O1 stores in blood and muscle, resynthesis of adenosine triphosphate and creatine phosphate, and lactate remova1.‘“~“~“‘~‘5 Also, quantitatively more important in the early recovery phase is increased ventilation and a higher heart rate. We presently show that any increase in 0, consumption associated with higher body temperature subsides within 1 hour. Clearly, all these processes are to some degree dependent on exercise intensity, which partly explains the strong effect of intensity on EPOC over the first 2 hours of recovery. However, the metabolic explanation for the prolonged EPOC component is less clear, since most of the processes mentioned above are known to be limited to the first few minutes or hours. Apparently, more strenuous exercise triggers other energy-consuming events that persist for hours during recovery from exercise. Sejersted and Vaage pointed out that during the first hour after exercise there is a large EPOC component dependent on exercise duration, in excess of and unaccounted for by the traditional rapid lactacid or alactacid components.‘” More recently Bangsbo et al have shown in the functionally isolated human quadriceps muscle that there is a large unexplained OL consumption over the first 60 minutes postexercise.’
BAHR AND SEJERSTED
840
We now show that blood lactate returns to resting levels within 1 hour, and it appears that the contribution to EPOC from the energy cost of lactate removal is limited to this time period. Even so, the magnitude of the prolonged EPOC component may be related to the activation of anaerobic metabolism during exercise. Exercise at intensities above the lactate threshold or maximum intensity at which there is a steady-state concentration of blood lactate results in non-steady-state behavior of metabolic processes during exercise, ie, an increase in O2 consumption.‘6~‘8 It is possible that exercise above this threshold triggers energyconsuming processes that persist for several hours during recovery. Our lactate data show that all experiments were performed using exercise intensities at or below the maximum steady state for lactate. After exercise at 75% of Vozmax, there was a weak relationship between blood lactate at the end of exercise and the resulting EPOC, which supports the suggestion that the magnitude of EPOC could be better related to the relative activation of specific metabolic processes other than the 0, uptake. Resynthesis of glycogen from carbohydrate supplied in the food has been claimed to account for a large fraction of the prolonged EPOC component.’ However, fasting experiments show that there is no change in EPOC whether food is given during recovery or not.” It may be that feeding results in an increase of some energy-requiring processes (such as glycogen synthesis) and a decrease in other (such as gluconeogenesis). Nevertheless, it appears that EPOC is the same whether the rate of glycogen synthesis is high or low.‘y Exercise at high intensities results in activation of the sympathetic nervous system with elevated concentrations of plasma catecholamines.“’ Triglyceride-fatty acid (TG-FA) cycling, which consumes ATP, is among the many metabolic processes stimulated by catecholamines.31 Two recent studies have demonstrated that the rate of TG-FA cycling is elevated for at least 3 hours after exercise.“,2’ The increase in the rate of TG-FA cycling was estimated to account for a 4% to 5% increase above resting energy expenditure during 2 hours of recovery from 4 hours of exercise at 40% of Vo2max,3Z and at 3 hours after 2 hours of exercise at 50% of Vo,max.” It is possible that the prolonged EPOC component is dependent on sympathetic activation of TG-FA substrate cycling, and there is some evidence that a shift in substrate utilization from carbohydrate to fat is accompanied by an increased cycling rate.‘” This is supported by the recent finding that EPOC is increased when fatty acid mobilization and oxidation is stimulated by caffeine ingestion before exercise.‘3 In the present study, the R values
after exercise at 75% of Vozmax were reduced, indicating an increased reliance on FA oxidation and possibly an increased rate of TG-FA cycling. Other hormones than catecholamines may also play a role in stimulating metabolic rate after exercise. Using a similar protocol to the present, Maehlum et al have shown that there are no changes in plasma levels of insulin, cortisol, and free thyroxine.” There is a need for information on plasma catecholamines or growth hormone from similar controlled recovery studies. We have no complete explanation for the prolonged EPOC component. It is possible that the efficiency of ATP production or ATP consumption is altered during recovery from exercise. In this respect it is interesting to note that exercise efficiency is reduced during recovery from prolonged. strenuous exercise? Practical Implications The main controversy in relation to the practical implications of EPOC is whether exercise has any significant impact on energy balance. Exercise at or around 70% of Vo:max will probably be beyond the tolerance level of the average obese or untrained individual. Therefore, we conclude that the amount and intensity of exercise likely to be tolerated by people embarking on a weight loss program is unlikely to cause any prolonged increase in recovery energy expenditure. However. those who would like to benefit from the additional energy expenditure caused by EPOC should be encouraged to exercise intensities above 50% of Vo,max, perhaps using intermittent-type interval training to increase tolerance. Conclusions This study demonstrates that there is an exponential relationship between exercise intensity and the EPOC after exercise for 80 minutes. After exercise at intensities below 50% of Vo:max, we observed no prolonged EPOC component. Hence, there appears to exist a threshold exercise intensity, possibly equal to the lactate threshold, to exceed in order to trigger the metabolic processes causing the prolonged EPOC component. ACKNOWLEDGMENT The authors thank Ada Ingvaldsen. Svein Nondal. Bjerg I. Selberg, and Jorid Thrane Stuemes for skillful technical assistance. We acknowledge the advice and support from all colleagues at the Department of Physiology at the National Institute of Occupational Health. We thank the subjects who participated in the experiments.
REFERENCES 1. Hagberg JM, Mullin JP, Nagle FJ: Effect of work intensity and duration on recovery 0,. J Appl Physiol48:540-544, 1980 2. Freedman-Akabas S, Colt E, Kissileff HR. et al: Lack of sustained increase in Vol following exercise in fit and unfit subjects. Am J Clin Nutr 41:545-549, 1985 3. Pacy PJ, Barton N, Webster JD, et al: The energy cost of aerobic exercise in fed and fasted normal subjects. Am J Clin Nutr 421764768, 1985 4. Brehm BA, Gutin B: Recovery energy expenditure for steady
state exercise in runners and non-exercisers. Med Sci Sports Exert 18205-210, 1986 5. Elliot D. Goldberg L, Kuehl KS: Does aerobic conditioning cause a sustained increase in the metabolic rate? Am J Med Sci 296249-251, 1989 6. Maehlum S. Grandmontagne M. Newsholme EA. et al: Magnitude and duration of excess postexercise oxygen consumption in healthy young subjects. Metabolism 35:425-429. 1986 7. Bahr R, Ingnes I, Vaage 0, et al: Effect of duration of
EXERCISE INTENSITY
AND POSTEXERCISE
0, CONSUMPTION
exercise on excess postexercise 0, consumption. J Appi Physiol 62:485-490, 1987 8. Bielinski R, Schutz Y, Jequier E: Energy metabolism during the postexercise recovery in man. Am J Clin Nutr 42:69-82,198s 9. Chad KE, Wenger HA: The effect of exercise duration on the exercise and post-exercise oxygen consumption. Can .I Sports Sci 13:204-207,1989 10. Sejersted OM, Vaage 0: Components of oxygen debt in man analysed on the basis of its dependence on exercise duration. J Physiol390:182P, 1987 (abstr) 11. Devlin JT, Horton ES: Potentiation of the thermic effect of insulin by exercise: Differences between lean, obese and noninsulindependent diabetic men. Am J Clin Nutr 43:884-890,1986 12. Chad KE, Wenger HA: The effects of duration and intensity on the exercise and post exercise metabolic rate. Aust J Sci Med Sport 17:14-18.1985 13. Bangsbo J, Gollnick PD, Graham TE, et al: Anaerobic energy production and 0, deficit-debt relationship during exhaustive exercise in humans. J Physiol422:539-559, 1990 14. Gore CJ, Withers RT: The effect of exercise intensity and duration on the oxygen deficit and excess post-exercise oxygen consumption. Eur J Appl Physiol60:169-174, 1990 15. Sedlock DA, Fissinger JA, Melby CL: Effect of exercise intensity and duration on postexercise energy expenditure. Med Sci Sports Exert 21:662-666,1989 16. Taylor HL, Buskirk E, Henschel A: Maximal oxygen intake as an objective measure of cardio-respiratory performance. J Appl Physiol55:73-80,1955 17. Lowry OH, Passonneau JV: A Flexible System of Enzymatic Analysis. San Diego, CA, Academic, 1972 18. Benedict FG, Carpenter TH: The Metabolism and Energy Transformations of Healthy Man During Rest. Washington, DC, Carnegie Institution, 1910, pp 182-193 19. Edwards HT, Thorndike A Jr, Dill DB: The energy requirement in strenuous muscular exercise. N Engl J Med 213:532-535, 1935 20. Passmore R, Johnson RE: Some metabolic changes following prolonged moderate exercise. Metabolism 9:452-455, 1960 21. deVries HA, Gray DA: Aftereffects of exercise upon resting metabolic rate. Res Q 34:314-321, 1963
841
22. Gore CJ, Withers RT: Effect of exercise intensity and duration on postexercise metabolism. J Appl Physiol68:2362-2368, 1990 23. Bahr R, Hansson P, Sejersted OM: Triglyceride/fatty acid cycling is increased after exercise. Metabolism 39:993-999,199O 24. Gaesser GA, Brooks GA: Metabolic bases of excess postexercise oxygen consumption: A review. Med Sci Sports Exert 16:29-43,1984 25. Hermansen L, Grandmontagne M, Maehlum S, et al: Postexercise elevation of resting oxygen uptake: Possible mechanisms and physiological significance, in Marconnet P, Hermansen L (eds): Physiological Chemistry of Training and Detraining. Basel, Switzerland, Karger, 1984, pp 119-129 26. Henson LC, Poole DC, Whipp BJ: Fitness as a determinant of oxygen uptake response to constant-load exercise. Eur J Appl Physiol59:21-28, 1989 27. Poole DC, Ward SA, Whipp BJ: The effects of training on the metabolic and respiratory profile of high-intensity cycle ergometer exercise. Eur J Appl Physiol59:421-429, 1990 28. Poole DC, Ward SA, Gardner GW, et al: Metabolic and respiratory profile of the upper limit for prolonged exercise in man. Ergonomics 31:1265-1279,1988 29. Bahr R, Sejersted OM: Effect of feeding and fasting on the excess postexercise 0, consumption. J Appl Physiol 1991 (submitted) 30. Galbo H, Holst J, Christensen NJ: Glucagon and plasma catecholamine responses to graded and prolonged exercise in man. J Appl Physiol38:70-76, 1975 31. Miyoshi H, Shulman GI, Peters EJ, et al: Hormonal control of substrate cycling in humans. J Clin Invest 81:1545-1555, 1988 32. Wolfe RR, Klein S. Carraro F. et al: Role of triglyceridefatty acid cycle in controlling fat metabolism in humans during and after exercise. Am J Physiol258:E382-E389,1990 33. Chad K, Quigley B: The effects of substrate utilization, manipulated by caffeine, on post-exercise oxygen consumption in untrained female subjects. Eur J Appl Physiol59:48-54, 1989 34. Bahr R. Opstad PK, Sejersted OM: Acute overtraining elevates resting metabolic rate and causes reduced mechanical efficiency. Acta Physiol Stand (in press)
