Exercise intensity: effect on postexercise 0, uptake in trained and untrained women KAREN Department
E. CHAD
AND
BRIAN
M. QUIGLEY
of Human Movement Studies, University of Queensland, Brisbane, Queensland 4607, Australia
CHAD,KARENE., ANDBRIANM. QUIGLEY.Exerciseintensity: effect on postexercise O2 uptake in trained and untrained women. J. Appl. Physiol. 70(4): 1713-1719, 1991.-Despite many reports of long-lasting elevation of metabolismafter exercise,little is known regardingthe effects of exerciseintensity and duration on this phenomenon.This study examined the effect of a constant duration (30 min) of cycle ergometer exercise at varied intensity levels [50 and 70% of maximal -0, co.nsumption (vo2,,)] on 3-h recovery of oxygen uptake (VO,). VO, and respiratory exchange ratios were measuredby open-circuit spirometry in five trained female cyclists (age25 t I..7 yr) and five untrained females(age27 k 0.8 yr). PostexerciseVO, measured at intervals for 3 h after exercise was greater (P < 0.01) after exercise at 50% V02- in trained (0.40 t 0.01 Urnin) and untrained subjects(0.39 k 0.01 l/min) than after 70% VO,,, in trained (0.31 t 0.02 l/min) and untrained subjects(0.29 t 0.02 Urnin). The lower respiratory exchange ratio values (P < 0.01) after 50% Oo,, in trained (0.78 & 0,Ol) and untrained subjects (0.80t 0.01) comparedwith 70% VO,,, in trained (0.81 t 0.01) and untrained subjects (0.83 t 0.01) suggestthat an increasein fat metabolism may be implicated in the long-term elevation of metabolism after exercise. This was supported by the greater estimated fatty acid oxidation (P < 0.05) after 50% % maxin trained (147 * 4 mg/min) and untrained subjects (133 t 9 mg/min) comparedwith 70%VO, mBx in trained (101 t 6 mg/min) and untrained subjects (85 t 7 mg/min). metabolism;metabolic rate; postexercise recovery; oxygen uptake; oxygen debt; respiratory exchange ratio; energy cost
theenergycostofexercise is generally assessed from the 0, uptake (VO,) during the activity, with the well-documented elevation of metabolism during recovery, variously referred to as 0, debt (22), recovery 0, (37), or, more recently, excess postexercise 0, consumption (EPOC) (17) ignored. Hill et al. (22) and Margaria et al. (28) found increased resting metabolism for several hours after exercise but considered the long-term effect to be something other than the recovery process and eliminated it from their recovery 0, measurements. Research on 0, debt since then has concentrated on the two phases described by Margaria et al. (28) as the rapid alactacid phase and the slower lactacid phase, which was purportedly due to the removal of lactic acid and resynthesis of glycogen. Other authors have since ascribed at least part of the EPOC to the increase in rate of chemical reaction for each 10°C increase in temperature (QJ effect of elevated body temperatures (7, 19). None of these studies, however, has considered the long-term elevation of metabolism reIN~EIGHTREDUCTIONPROGRAMS
ferred to by Hill et al. (22) and confirmed by many other authors (3, 6, 13-15, 20, 27, 34). Little is known about the factors associated with the prolonged elevation of metabolism after exercise. In the past, studies have found that resting metabolic rate (RMR) was restored within 1 h after 3-2q min of exercise at 3045% of maximal 0, consumption (VO, ,,) (33,36), after 40 min of exercise at ventilatory threshold (16), or after exercise to exhaustion at 90% VO, mw (1). However, other investigators (3, 6, 20, 27) have shown that metabolic rate after l-3 h of exercise at 50-75% Vozmax was still significantly elevated above rest 5-12 h after completion of exercise. It would appear from these studies that if exercise duration is too short (even with high intensity) or intensity is too low, no long-lasting calorigenie effect of exercise is observed. Moderate exercise maintained for a sufficient period of time may be more successful in elevating postexercise metabolic rate hours after exercise cessation (11). Chad and Wenger (10, 11) found that when exercise intensity or total work was equated, elevation of postexercise metabolism was related to exercise duration. Core temperatures returned to resting levels within 2 h, whereas Vo2 remained elevated for 2-8 h. Since then a recent study has been published indicating that, in untrained males, 3-h recovery of VO, was positively related to both duration and intensity of exercise (18). The effect of exercise intensity, independent of duration, on the extended EPOC has not been studied in women. This study investigated the effect of constant duration and varying intensity (and thereby total work) on the postexercise metabolic rate. The effects of 30 min of cycling at 50 and 70% Vogrnax on 3-h recovery of VO, were determined. Exercise intensity and duration were chosen as typical of recommendations for aerobic conditioning (2). Because training status influences the intensity of exercise that can be maintained for a given duration, trained female cyclists and untrained females were compared. METHODS Subjects. Five trained female cyclists (age 25.2 t 1.72 yr) and five untrained females (age 27.2 t 0.75 yr) volunteered to participate in the study. The cyclists averaged at least 300 km/wk, and the untrained individuals did no formal exercise. All subjects were eumenorrheic and were not in the menstrual phase of the female cycle during the time of the experiment. Before participation, all subjects
0161-7567/91 $1.50 Copyright 0 1991 the American Physiological Society
1713
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1714
EXERCISE
INTENSITY
completed an informed voluntary consent form and a medical history questionnaire. The procedures were approved by the Human Experimentation Ethical Review Committee of the University of Queensland. Experimental protocol. One week before the 1st day of testing, height and skinfold measurements were taken. Seven skinfold sites (triceps, subscapular, suprailiac, umbilical, biceps, thigh, and medial midcalf) were measured to the nearest 0.1 mm with Harpenden calipers, with the sum of the seven being recorded for each subject (38). The weight of each subject was measured on a beam scale and recorded to the nearest 0.1 kg before commencement of each testing session. Before the testing, the subjects were also familiarized with cycle ergometer exercise at a constant pedaling rate while breathing through a mouthpiece and valve that were to be used in all metabolic measurements. All subjects performed a stepwise incremental test (39) to measure VO, max. The VO, maxtest, performed on a Monark cycle ergometer, consisted of a 5-min warm-up at 100 (trained) or 50 W (untrained), after which time the load was increased by 25 W every 2 min. Pedaling speed was constant at 90 and 60 revolutions/min (trained and untrained, respectively) (39). Verbal encouragement was given to each subject to attain maximal values. Attainment of VO 2maxwas based on the following criteria: 1) a plateau or change of l.OO. Pulmonary ventilation, VO, and CO, output were measured an< recorded during the last minute of every 2-min stage. VO, was then plotted against power output to determine the work rates at 50 and 70% Vo2max for each subject. This estimation was confirmed by measurement of vo2 at that power output during a lo-min pretest conducted 2 days later. One week after the confirmation of test work rates, each subject was tested at approximately the same time of day for two trials scheduled 1 wk apart. The protocols for the 2 days of testing were identical with the exception of . the exercise intensity (1 at 50% 00, m8Xand 1 at 70% vo 2max ) 7 with duration held constant at 30 min. Once they reported to the laboratory (after a 12-h fast), the subjects consumed no food or beverage, with the exception of water, until the test was completed. All subjects were requested to maintain a mixed diet 1 wk before and throughout the experiment. This was confirmed from dietary records. RMR was determined by taking the mean of six 5-min VO, measurements, which were sampled over a continuous period of 30 min to ensure stability of the baseline. The subjects sat quietly on a chair for 1 h before this measurement. They were allowed to read, write, or watch television during this rest period. After RMR was established each day, the subject exercised at either 50 or 70% . vo 2maxfor 30 min. The order of the treatments was counterbalanced. After exercise, subjects returned to the sitting position to read, write, or watch television as in the preexercise phase for a period of 3 h. Subjects were dressed in shorts and T-shirts and wore running shoes throughout the test. The laboratory was air conditioned and held at a constant temperature of 22 t 0.5OC.
AND
POSTEXERCISE
ire,
All ventilatory measurements were made by standard open-circuit spirometry. For at least 5 min before sampling, subjects wore noseclips and breathed through a Hans Rudolph low-resistance low-dead-space valve (model 2700) that was connected to a mixing chamber via lightweight tubing. The volume of air inspired during measurement periods was measured by a turbine ventilometer (Morgan Mark 2). Volume of expired air was calculated from this measurement by use of the Haldane transformation. All volumes were corrected to STPD. Morgan CO, (infrared type 901 MK2) and 0, (paramagnetic model OA 500D) analyzers were used for measurement of respiratory gases. Calibration of the gas analyzers by use of certified gravimetric calibration gas and the ventilometer was conducted before and after the preexercise phase, 15 min after exercise, and, thereafter, immediately before each postexercise measurement. The Monark cycle ergometer was calibrated before each exercise bout. Heart rate was recorded from chest electrodes by a Rigel cardiac monitor (model 302). Five-minute ventilatory measurements were taken during the rest (preexercise) and exercise periods. In the postexercise phase, a 5-min ventilatory sample was taken from 10 to 15 min and, thereafter, every 40-45 min for the next 3 h, which was selected as the predetermined recovery period because of fasting and time constraints. To seek an explanation for the unexpected results, R values were subsequently used to estimate the proportional contribution from fat and carbohydrate in total energy yield. Absolute fat metabolism was also estimated. Because the work performed was predominantly aerobic, the proportions of 0, consumed in the oxidation of fatty acids and carbohydrate were calculated with a nonprotein R assumed and by use of the accepted values for fatty acid (R = 0.70) and carbohydrate (R = 1.00): %fatty acid = (1 - R)/0.3 X 100% and %carbohydrate = (R - 0.7)/0.3 X 100%. By use of palmitic acid as a typical fatty acid, yielding an R = 0.7, the absolute quantity of fatty acid oxidized may be calculated from the equation palmitic acid + 130 phosphate + 130 ADP + 23 0, + 16 CO, + 146 H,O + 130 ATP. Oxidation of 1 mol of fatty acid requires 23 mol of 0, or (23 X 22.4) liters because 1 mol of a gas occupies 22.4 liters (STPD). One liter of O,, therefore, accounts for the oxidation of 1000/(23 X 22.4) liters or 1.94 mmol of fatty acid. Millimoles of fatty acid are converted to milligrams by multiplying by the gram molecular weight, in this case 256, yielding ~500 mg fatty acid/l 0, consumed in the oxidation of fatty acid. Data analysis. The physical characteristics of the trained and untrained subjects were compared by Student’s t test for unpaired samples. For resting and exercise VO, and R values differences between means of six 5-min samples were analyzed across fitness group (trained vs. untrained) and test day (50% v02max vs. 70% vo 2max)by a two-way analysis of variance with repeated measures on test day. Postexercise comparisons were made by three-way analysis of variance across fitness level, exercise intensity, and time into recovery (15, 60, 105, 150, and 180 min), with repeated measures on exercise intensity and time. Differences between trained and untrained groups, between exercise intensities at each individual sampling
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EXERCISE
1. Physical characteristics
TABLE Subj
No.
INTENSITY
AND
POSTEXERCISE
1715
ire,
of untrained and trained subjects
Age, yr
Ht, m
28 28 26 27 27
1.73 1.52 1.54 1.67 1.64
59.0 59.5 60.0 67.5 62.5
124.0 130.4 145.3 186.3 152.7
1.73 1.74 1.80 1.96 1.60
27.2kO.75
1.62kO.08
61.7k3.14
147.9t21.65
1.77kO.12
1.70 1.65 1.72 1.73 1.64
54.0 60.0
80.5 107.0
2.95
7 8 9 70
24 23 28 25 26
59.0
92.0
2.98
57.0 55.5
85.0 98.3
3.10 3.31
Mean -t SD
25.2k1.72
1.69kO.04
57.1t2.20
W
kg
Sum of Skinfolds,
mm
VO
2mex, l/min
Untrained
Mean + SD
Trained
92.68k9.33
3.21
3.11-to.13
n = 10 women.
time in recovery, and among sampling times were assessed by Student’s t test for unpaired and paired samples, respectively, with a Bonferroni correction for multiple comparisons. VO, values were analyzed as excess postexercise VO, by subtracting resting levels before analysis. Comparisons between the 50 and 70% V02max recoveries were not altered when the analysis was performed on total rather than excess vo2 values. Results are expressed as means t SD. P < 0.05 was accepted as the level of significance for the analyses of variance and as the alpha level from which Bonferroni corrections were made for multiple comparisons. RESULTS
Physical characteristics of the subjects. The physical characteristics of the subjects in each group are presented in Table 1. The trained individuals were significantly lighter in weight (P < 0.05) and had smaller skinfold measurements (P < 0.01) than the untrained individuals. No significant difference in age or height was observed between the two groups. The mean Vozmax of the trained group was substantially higher (P < 0.01) than that of the untrained group. Rest. No significant difference was observed in RMR between the 2 days of testing. The data were highly reproducible, with no individual’s mean resting Vo2 varying by >O.Ol l/min on the two occasions. The trained group had significantly lower resting vo2 values (l/min) than the untrained, but this was largely related to the difference in body weight, and the difference was not significant when Vo2 was expressed as milliliters per kilogram per minute, (2.92 t 0.11 and 3.06 t 0.10, respectively). The resting R values of the trained (0.85 t 0.01) and untrained (0.84 t 0.01) groups were not significantly different, indicating that both groups were metabolizing approximately equal amounts of fat and carbohydrates in the resting state. The mean value for each group did not vary, and individual values were all within 0.01 on the two test days. Exercise. For the 30 min of exercise, the trained group worked at a mean Vo2 of 51.1 t 0.9 and 71.03 t 1.95%
. vo 2maxy and the untrained
group worked at 53.02 t 1.9 and 72.56 t 0.79% vo2max (no significant difference between groups). Because of the higher Vo2 max of the trained subjects, their mean work rate, and hence their VO, values were significantly higher (P < 0.01) than those of the untrained subjects during each exercise period (trained at 70% Vo2 max2.21 t 0.07 l/min, untrained at 70% VO, max 1.28 t 0.10 l/min, trained at 50% vo2max 1.59 t 0.06 11min, untrained at 50% V02max 0.94 t 0.09 Urnin). During the 50% irO, maxexercise bout, the trained subjects worked at 85 t 15 W, whereas during the 70% . vo 2max work bout they exercised at 115 t 15 W. The untrained group worked at 45 t 10 and 80 t 10 W, which elicited an Oo, equivalent to -50 and 70% VO, max, respectively. The R values during exercise were significantly higher at 70% V02max than at 50%. The trained subjects had significantly lower R values at both exercise intensities (P < 0.01; trained at 70% vo2 max0.95 t O.O$ untrained at 70% 60, max0.98 t O.Ol.,trained at 50% Vo2max 0.92 t 0.01, untrained at 50% Vo2max 0.94 t 0.01). Postexercise. The time course of postexercise VO, is shown in Figs. 1 (trained) and 2 (untrained). VO, at every sample period in the postexercise phase was significantly elevated (P < 0.01) above the pretest resting level after the two exercise intensities in both the trained (Fig. 1) and the untrained (Fig. 2) groups. At the end of 3 h of recovery, mean 60, was still elevated by 105 (untrained) and 135% (trained) after 50% Vo2max and by 53 (untrained) and 82% (trained) after 70% VO, max. In the last 2 h, the mean decline was only 0.04 (untrained) to 0.06 (trained) and 0.02 (untrained and trained) l/min in each case. From the first sample, lo-15 min into recovery, the VO, after work at 50% V02max remained significantly higher at every time period than after work at 70% . vo 2 maxfor both groups and each of the 10 individual subjects. The mean difference throughout was 104 t 18 ml/ min. The high reproducibility of the data can be seen from the low intersubject variability and the consistency of the values throughout the last 2 h of sampling in both groups.
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1716
EXERCISE
INTENSITY
2.0 i
30
0.70:
0
,‘ 30
60
90
,.,.,.,.I 60
120
90
120
150
180
.
.
150
180
POSTEXERCISE
\jo2
for . 105 min after 50% VO, maxand for 60 min after 70% vo 2 ma?* Estzmated fat metabolism. Because fat metabolism seemed. to be one of the few possible explanations of a higher VO, and lower R after 50% than after 70% VO, max, fat metabolism was calculated based on the tentative assumption that R approximated the true respiratory quotient (see DISCUSSION). Estimates of resting fat metabolism were consistent on the 2 days for each group: 51 t 4 (untrained) and 43 t 3 mg/min (trained). Individual values were all within 7 mg/min on the two test days. Estimates of fat metabolism during exercise suggested that untrained subjects metabolized approximately twice as much fat at 50% (102 t 19 mg/min) as at 70% TO, max (53 t 20 mg/min). The trained subjects appeared to metabolize -26% more fat at 50% (225 t 13 mg/min) than at70% V02max (178 t 24 mg/min). The trained subjects seemingly metabolized more than twice as much fat in absolute terms as the untrained subjects at 50% Vo2 max and more than three times as much at 70% VO, maxduring
2.5
0
AND
1.4 1
A L E
1.0
9
f
+ + -
50% 70% REST
0.8 -e + -
0.6
.2.
50% 70% REST
0.4 0.2
0
30
60
90
TIME
120
150
180
0.0: 0
.
30,
.
60,
(mln)
.
,
.
,
.
,
.
,
90
120
150
180
90
120
150
180
’ p < 0.01 50% vs 70% $02 max + p < 0.01 50% \jO2 max vs rest x p < 0.01 70% 002 max vs rest FIG. 1. Postexercise O2 uptake (~oJ, respiratory exchange ratio (R), and fat oxidation (FAT) after 30 min of exercise at 50% and 75% 00 2maxin trained subjects (n = 5).
After both exercise intensities, the trained group had a significantly higher iTo, than the untrained group, and VO, remained higher throughout the postexercise period, although a post hoc analysis of the individual samples showed only the first samples at lo-15 min to be significantly different. Pairwise comparisons across recovery time showed that, after exercise at 50% VO, m8X,significant falls in 60, occurred between samples in both trained and untrained subjects until 105 min. After exercise at 70% VO, max, significant falls occurred in both groups for only 60 min, even though the VO, values during the exercise were considerably higher than at 50% Vo2 m8X. R was significantly lower after 50% VO, m8Xthan after 70% v02max at every time point for both groups of subjects (Figs. 1 and 2). In the trained group, R fell below the resting level within the 1st h. In the untrained subjects, R reached the resting level within 1 h after 50% Vo2 maxbut not until 150 min after 70% VO, max. R followed a pattern similar to VO, in that it fell significantly between samples
30
0
60
. l . .
0
30
60
90
TIME
p < 0.01 + p < 0.01 x p < 0.01 l
50% 50%
120
150
180
(mln)
vs 70%
VO2
max
VO2 max vs rest 70% VO2 max vs rest
FIG. 2. Postexercise vo2, R, and fat oxidation after 30 min of exercise at 50% and 75% 2maxin untrained subjects (n = 5). VO
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EXERCISE
INTENSITY
the 30-min exercise bout. At 70% Vo2 max,the untrained subjects appeared to be metabolizing almost exclusively carbohydrate for their exercise needs. Estimates of recovery fatty acid oxidation showed significantly elevated levels of fat metabolism throughout the 3 h of the measurement period in both tests (P < 0.01). The estimated fat metabolism was significantly greater at every sample after 50% VoZmax than after 70% vo, max (Figs. 1 and 2) for both groups. At the end of 3 h, estimated fat metabolism after 50% V02max was still 56% higher (133 t 9 mg/min) than after 70% . vo 2max(85 t 7 mg/min) in untrained subjects and 45% higher (147 t 4 vs. 101 t 6 mg/min) in trained subjects. Trained subjects still appeared to be metabolizing 10 and 18% more fat than untrained subjects after 50 and 70% . vo 2 maxy respectively. DISCUSSION
Previous studies equating exercise intensity and varying duration or equating total work and varying intensity and duration (10, 11) have suggested that duration of exercise was more important than intensity in determining the extent of the elevation of metabolism after aerobic exercise. The present study has shown, in young women, that intensity of exercise is also an important factor in the long-term elevation of VO, after exercise. With duration held constant at 30 min, cycle ergometer exercise at 50% VO 2maxproduced consistently higher 60, values after the first 10 min of recovery than at 70% . vo 2max.The situation was the same for all 10 subjects, both trained and untrained, and at every sample period for every subject for a total of 50 data points. The variability of the measures was extremely low at rest, during exercise, and in recovery, indicating that random experimental error was minimal. Within each training group, intersubject variability was also very low. Although a third control condition without exercise was omitted for practical reasons, other studies have found little or no change in resting metabolism of postabsorptive subjects during a similar 4-h period (6, 27, 33). Where changes have been found (35), they have been of considerably lower magnitude than the postexercise elevations found in this study. In comparisons of the two exercise intensities, each subject acted as her own control, and there is no indication that minor variations in the very consistent resting VO, values could have had any substantial part in explaining the findings. The evidence appeared incontrovertible. These findings are not explained by the previously held views on the mechanisms postulated for the postexercise VO,, i.e., creatine phosphate replenishment, lactic acid removal, glycogen resynthesis, and the effects of increased core and muscle temperature (17), because these mechanisms would increasingly come into play as the intensity level of exercise increases. However, in the past decade research has shown that these factors may not be the only determinants of postexercise VO, because of the following: lactic acid has been shown to be an unlikely cause of the increased metabolism observed several hours after exercise cessation; increased temperatures return to resting levels before RMR has been reached
AND
POSTEXERCISE
Tjoz
1717
(11); creatine phosphate replenishment may only represent a small amount of the total postexercise 0, cost (20); and, because of the slow process of the resynthesis of muscle glycogen (23), it is questionable whether this mechanism can be used entirely to explain the elevation in postexercise VO,. It is possible, therefore, that although these mechanisms may be predominant early in the recovery phase and still remain active during the slow component of recovery, an additional mechanism must assume greater importance in the long-term postexercise VO,. One of the few possible explanations for increased VO, after lower exercise intensity is the metabolism of fat, a mechanism suggested recently by other authors (3, 27). The respiratory quotient has commonly been taken to indicate the proportion of fat and carbohydrate metabolized under steady-state conditions. The use of R as an estimate of the nonprotein respiratory quotient is not without risk because a change in the acidity of the blood, a relative hyperventilation, or a change in dissolved CO, levels in the tissues might cause R to be different from the respiratory quotient and invalidate its use as a measure of substrate metabolism. However, the exercise intensities chosen in this study have been shown to cause little lactate production (12,2l, 30). CO, output, because of changes in buffering of acids or hyperventilation, would most likely occur in the untrained subjects working at 70% VO, max. In this case, the difference in R between 50 and 70% Tjo, maxin the present study was 0.04 (untrained) and 0.03 (trained) at the end of exercise and 0.03 after 3 h of recovery for both groups, indicating that the untrained group had little, if any, greater such effect than the trained group. The duration of the exercise task (30 min) was such that a sustained hyperventilation would have been improbable. This was reinforced by the absence of any increase in CO, uptake observed during the last 20 min of the exercise tests. Furthermore, the shape of the recovery curve of R was similar for both exercise intensities and both groups. Any effect of acidity or hyperventilation would be expected to occur in the samples at the end of exercise and lo-15 min into recovery, resulting in a more steeply sloping curve after 70% . vo 2max.No such effect was apparent. R values were consistently lower after exercise at 50% Vo2max and went below the preexercise resting level sooner, suggesting that fat metabolism was the major energy source after the lower exercise intensity. Estimation of the absolute fat metabolism supported the view that more fat was metabolized after 50% than after 70% VO, max.The alternative that R was consistently reduced by a net uptake of CO, in the tissues seems unlikely over a 3-h period. The results from the present study once again confirm the view that postexercise metabolism may be elevated for several hours, depending on the duration and intensity of the exercise being performed. There is a long and somewhat neglected history of similar findings (6,13-15, 20,22,27,28,34). All these studies support the view that the elevation of metabolism after exercise extends beyond the replenishment of creatine phosphate and 0, stores, removal of lactate, and Q10effects. Much of the confusion and conflict apparently existing in the literature on 0, debt is related to differences in
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1718
EXERCISE
INTENSITY
experimental design and methods. Most studies have restricted their interest to the first two of the three components of postexercise elevation of VO,. In these cases, the measurement of recovery VO, has generally been limited to short periods, often with exercise baselines, with the specific intention of eliminating the long-term elevation of metabolism. Pacy et al. (33) concluded that there was no prolonged thermogenic effect of moderate repeated aerobic exercise in weight-maintaining lean subjects. The lack of significance may have been due to the small sample size and the increased variance due to the mixed-gender sample and the range of exercise intensities. The exercise loads were reported to represent 3545% Tjo2 M8X,although no mention was made as to how this was determined. Gore and Withers (18) also found that in well-trained male subjects EPOC was of little physiological significance. It is possible that the observed differences in the two studies were either gender or experimental-design related. Although the 28-h measurement of RMR was performed by Gore and Withers (18) to account for circadian variations, the effect of increased thermogenesis on metabolic rate may have elevated the “resting” state and hence underestimated EPOC. The weight of accumulating evidence suggests that postexercise metabolism may be raised for several hours depending on the duration and intensity of exercise. Exercise of sufficiently short duration or low intensity may minimize the effect. In the present study, exercise for 30 min at 50% V02max produced a greater extended EPOC than after 70% Vogmax in both trained and untrained females. Trained individuals had significantly greater extended EPOCs than untrained. R values were lower after 50% TO, maxand in trained subjects, suggesting fat metabolism as a possible mechanism. Estimates of fat metabolism support this view both in this study and in two recent studies (6,27). Subsequent studies in this laboratory have also supported this hypothesis. When fat metabolism was stimulated by the ingestion of caffeine (9) or by dietary manipulation (8), the extended EPOC was higher than in control conditions. The precise mechanism for increased fat metabolism in recovery is not yet clear. Increased substrate cycling, as proposed by Newsholme (31, 32), is one possibility. The ATP production per mole of 0, is also less for fat than for carbohydrate metabolism. The conversion of fat to restore glycogen stores has also been considered but does not appear to be a major factor (6, 13). Barbee et al. (4), in their in situ muscle preparation in anesthetized ventilated dogs, showed that, after 10 min of stimulated isometric contractions, vo2 returned to resting level within 30 min. If this could be generalized to whole body human activity of 30 min, one could speculate that the long-term increase in metabolism may occur in tissues other than muscle. Because lipid oxidation rate has been shown to be largely independent of plasma free fatty acid levels (6, 25) but related to specific lipid stores (5) and individual long-chain fatty acid composition (24)) further elucidation of mechanisms and refinement of detail may require considerably more research. It is not yet clear what effect exercise at higher intensities for short durations may have on long-term elevation
AND
POSTEXERCISE
ire,
of metabolism. There is ample evidence that muscle and blood lactate levels are not closely coupled even to the second or slow component of EPOC in humans, other mammals, reptiles, or amphibians (17). If duration is adequate for muscle and core temperatures to rise to a sufficient level, then the Q10 effect may be substantial. The evidence is that both of these are relatively short-lived effects lasting only 1 or 2 h. If fat metabolism is the major factor, then there may be a parabolic relationship between exercise intensity and extended EPOC provided duration is adequate. Our data on young women, both trained and untrained, suggest that the peak may be at -50% voz max for 30 min of exercise, perhaps approximating the so-called ventilatory threshold. A recently published study has not found such a relationship in young males (18). The present results suggest that 30 min of moderate exercise may produce a distinct postexercise elevation of metabolism, possibly that of fat; this may be important in weight loss, particularly in middle-aged people, for whom high-intensity exercise may constitute an increased cardiac risk. Address tion, Univ. Canada. Received
for reprint requests: of Saskatchewan,
6 February
K. E. Chad, Saskatoon,
1990; accepted
in final
College of Physical EducaSaskatchewan S7N OWO,
form
16 November
1990.
REFERENCES 1. ADAMS, R. P., AND H. G. WELCH. Oxygen uptake acid-base status, and performance with varied inspired oxygen fractions. J. Appl. Physiol. 49: 863-868, 1980. 2. AMERICAN COLLEGE OF SPORTS. Guidelines for Exercise Testing and Prescription (3rd ed.). Philadelphia, PA: Lea & Febiger, 1986, p. 31-52. 3. BAHR, R., I. INGNES, 0. VAAGE, 0. M. SEJERSTED, AND E. NEWSHOLME. Effect of duration of exercise on excess postexercise 0, consumption. J. Appl. Physiol. 62: 485-490, 1987. 4. BARBEE, R. W., W. N. STAINSBY, AND S. J. CHIRTEL. Dynamics of 0,, CO,, lactate, and acid exchange during contractions and recovery. J. Appl. Physiol. 54: 1687-1692, 1983. 5. BARCLAY, J. K., AND W. N. STAINSBY. Intramuscular lipid store utilization by contracting dog skeletal muscle in situ. Am. J. Physiol. 223: 115-119, 1972. 6. BIELINSKI, R., Y. SCHUTZ, AND E. JEQUIER. Energy metabolism during the postexercise recovery in man. Am. J. Clin. Nutr. 42: 69-82, 1985. 7. BROOKS, G. A., K. J. HITTELMAN, J. A. FAULKNER, AND R. E. BEYER. Temperature, skeletal muscle mitochondrial functions, and oxygen debt. Am. J. Physiol. 22: 1053-1059, 1971. 9. CHAD, K. E., AND B. M. QUIGLEY. The effects of substrate utilization, manipulated by caffeine, on post-exercise oxygen consumption in untrained female subjects. Eur. J. Appl. Physiol. Occup. Physiol. 59: 48-54, 1989. 10. CHAD, K. E., AND H. A. WENGER. The effects of duration and intensity on the exercise and post-exercise metabolic rate. Au&. J. Sci. Med. Sport 17: 14-18, 1985. 11. CHAD, K. E., AND H. A. WENGER. The effect of exercise duration on the exercise and post-exercise oxygen consumption. Gun. J. Sport Sci. 13: 204-207, 1988. 12. COSTILL, D. L. Metabolic responses during distance running. J. Appl. Physiol. 28: 251-255, 1970. 13. COURTICE, F. C., AND C. G. DOUGLAS. The effects of prolonged muscular exercise on the metabolism of man. Proc. R. Sot. Land. Biol. 119: 381-439, 1936. 14. DEVRIES, H. A., AND D. E. GRAY. Aftereffects of exercise upon resting metabolic rate. Res. Q. 34: 314-321, 1963.
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EXERCISE 15. EDWARDS,
quirement
INTENSITY
H. T., A. THORNDIKE, AND D. B. DILL. The energy rein strenuous exercise. N. Engl. J. Med. 213: 532-535,
1935. 16. FREEDMAN-AKABAS, SUNYER. Lack of
S., E. COLT, H. R: KISSILOFF, AND F. X. PIsustained increase in VO, following exercise in fit and unfit subjects. Am. J. Clin. Nutr. 41: 545-549, 1985. 17. GAESSER, G. A., AND G. A. BROOKS. Metabolic bases of excess postexercise oxygen consumption: a review. Med. Sci. Sports Exercise
16: 29-43,1984. 18. GORE, C. J., AND
R. T. WITHERS. Effect of exercise intensity and duration on postexercise metabolism. J. Appl. Physiol. 68: 2362-
2368,199O. 19. HAGBERG,
J. M., J. P. MULLIN, AND F. J. NAGLE. Effect of work intensity and duration on recovery 0,. J. Appl. Physiol. 48: 540-
544, 1980. 20. HERMANSEN, L., M. GRANDMONTAGNE, IGNES. Postexercise elevation of resting
S. MAEHLUM, AND I. oxygen uptake: possible mechanisms and physiological significance. In: Physiological Chemistry of Training and Detraining. Basel: Karger, 1984, p. 119-129. 21. HERMANSEN, L., AND I. STENSVOLD. Production and removal of lactate during exercise in man. Acta Physiol. Stand. 86: 191-201,
1972. 22. HILL,
A. V., C. N. H. LONG, AND H. LUPTON. Muscular exercise, lactic acid and the supply and utilization of oxygen. Pt. IV-VI. Proc.
R. Sot. Lond. B Biol. 97: 84-138, 1924. 23. HULTMAN, E., AND J. BERGSTROM. Muscle
glycogen synthesis in relation to diet studied in normal subjects. Acta Physiol. Stand.
109: 109-117, 1967. 24. JONES, P. J. H., P.
B. PENCHARZ, AND M. T. CLANDININ. Whole body oxidation of dietary fatty acids: implications for energy utilization. Am. J. Clin. Nutr. 42: 769-777, 1985. 25. KRZENTOWSKI, G., F. PIRNAY, A. S. LUYCKX, N. PALLIKARAKIS, M. LACROIX, F. MOSORA, AND P. J. LEF~BVRE. Metabolic adaptations in post-exercise metabolism. CLin. Physiol. Oxf. 2: 277-288, 1982. 26. LEMON,
P. W. R., AND F. J. NAGLE. Effects of exercise on protein and amino acid metabolism. Med. Sci. Sports Exercise 13: 141-149,
1981. 27. MAEHLUM,
AND POSTEXERCISE
S., M. GRANDMONTAGNE,
E. A. NEWSHOLME,
AND
Vo,
1719
0. M. SEJERSTED. Magnitude and duration of excess postexercise oxygen consumption in healthy young subjects. Metabolism 35: 28.
425-429,1986. MARGARIA,
R., H. T. EDWARDS, AND D. B. DILL. The possible mechanisms of contracting and paying the oxygen debt and the role of lactic acid in muscular contraction. Am. J. Physiol. 106:
689-715,1933. 29. MILLWARD, D. J., C. T. M. DAVIES, D. HALLIDAY, S. L. WOLMAN, D. MATTHEWS, AND M. RENNIE. Effect of exercise on protein metabolism in humans as explored with stable isotopes. Federation Proc. 41: 2686-2691, 1982. 30. NAGLE, F., D. ROBINHOLD, E. HOWLEY, J. DANIELS, D. BAPTISTA, AND K. STOEDEFALKE. Lactic acid accumulation during running at submaximal aerobic demands. Med. Sci. Sports 2: 182-186,197O. 31. NEWSHOLME, E. A. Substrate cycles: their metabolic, energetic and thermic consequences in man. Biochem. Sot. Symp. 43: 183-205, 1978. 32. NEWSHOLME, E. A. The glucose/fatty acid cycle and physical exhaustion. In: Human Muscle Fatigue: Physiological Mechanisms. London: Pitman, 1981, p. 89-101. (Ciba Found. Symp. 82) 33. PACY, P. J., N. BARTON, J. D. WEBSTER, AND J. S. GARROW. The
energy cost of aerobic exercise in fed and fasted normal subjects. Am. J. Clin. Nutr. 42: 764-768, 1985. 34. PASSMORE, R., AND R. E. JOHNSON.
Some metabolic changes following prolonged moderate exercise. Metabolism 9: 452-456, 1960. 35. REILLY, T., AND G. A. BROOKS. Investigation of circadian rhythms in metabolic responses to exercise. Ergonomics 25: 1093-1107, 1982. 36. SCHNEIDER,
E. G., in aerobic work. J. 37. STAINSBY, W. N., deficit, steady level
S. ROBINSON, AND J. L. NEWTON. Oxygen debt Appl. Physiol. 25: 58-62, 1968. AND J. K. BARCLAY. Exercise metabolism: O2 O2 uptake and 0, uptake for recovery. Med. Sci. Sports 2: 177-181, 1970. 38. TELFORD, R., D. TUMULTY, AND G. DAMM. Skinfold measurements in well-performed Australian athletes. Sports Sci. Med. Q. 14: 471-476, 1984. 39. THODEN, J. S., J. D. MACDOUGALL, AND B. A. WILSON. Testing aerobic power. In: Physiological Testing of the Elite Athlete, edited by D. MacDougall, H. A. Wenger, and H. J. Green. Ithaca, NY: Mouvement Publications, 1982, p. 39-54.
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E. CHAD
AND
BRIAN
M. QUIGLEY
of Human Movement Studies, University of Queensland, Brisbane, Queensland 4607, Australia
CHAD,KARENE., ANDBRIANM. QUIGLEY.Exerciseintensity: effect on postexercise O2 uptake in trained and untrained women. J. Appl. Physiol. 70(4): 1713-1719, 1991.-Despite many reports of long-lasting elevation of metabolismafter exercise,little is known regardingthe effects of exerciseintensity and duration on this phenomenon.This study examined the effect of a constant duration (30 min) of cycle ergometer exercise at varied intensity levels [50 and 70% of maximal -0, co.nsumption (vo2,,)] on 3-h recovery of oxygen uptake (VO,). VO, and respiratory exchange ratios were measuredby open-circuit spirometry in five trained female cyclists (age25 t I..7 yr) and five untrained females(age27 k 0.8 yr). PostexerciseVO, measured at intervals for 3 h after exercise was greater (P < 0.01) after exercise at 50% V02- in trained (0.40 t 0.01 Urnin) and untrained subjects(0.39 k 0.01 l/min) than after 70% VO,,, in trained (0.31 t 0.02 l/min) and untrained subjects(0.29 t 0.02 Urnin). The lower respiratory exchange ratio values (P < 0.01) after 50% Oo,, in trained (0.78 & 0,Ol) and untrained subjects (0.80t 0.01) comparedwith 70% VO,,, in trained (0.81 t 0.01) and untrained subjects (0.83 t 0.01) suggestthat an increasein fat metabolism may be implicated in the long-term elevation of metabolism after exercise. This was supported by the greater estimated fatty acid oxidation (P < 0.05) after 50% % maxin trained (147 * 4 mg/min) and untrained subjects (133 t 9 mg/min) comparedwith 70%VO, mBx in trained (101 t 6 mg/min) and untrained subjects (85 t 7 mg/min). metabolism;metabolic rate; postexercise recovery; oxygen uptake; oxygen debt; respiratory exchange ratio; energy cost
theenergycostofexercise is generally assessed from the 0, uptake (VO,) during the activity, with the well-documented elevation of metabolism during recovery, variously referred to as 0, debt (22), recovery 0, (37), or, more recently, excess postexercise 0, consumption (EPOC) (17) ignored. Hill et al. (22) and Margaria et al. (28) found increased resting metabolism for several hours after exercise but considered the long-term effect to be something other than the recovery process and eliminated it from their recovery 0, measurements. Research on 0, debt since then has concentrated on the two phases described by Margaria et al. (28) as the rapid alactacid phase and the slower lactacid phase, which was purportedly due to the removal of lactic acid and resynthesis of glycogen. Other authors have since ascribed at least part of the EPOC to the increase in rate of chemical reaction for each 10°C increase in temperature (QJ effect of elevated body temperatures (7, 19). None of these studies, however, has considered the long-term elevation of metabolism reIN~EIGHTREDUCTIONPROGRAMS
ferred to by Hill et al. (22) and confirmed by many other authors (3, 6, 13-15, 20, 27, 34). Little is known about the factors associated with the prolonged elevation of metabolism after exercise. In the past, studies have found that resting metabolic rate (RMR) was restored within 1 h after 3-2q min of exercise at 3045% of maximal 0, consumption (VO, ,,) (33,36), after 40 min of exercise at ventilatory threshold (16), or after exercise to exhaustion at 90% VO, mw (1). However, other investigators (3, 6, 20, 27) have shown that metabolic rate after l-3 h of exercise at 50-75% Vozmax was still significantly elevated above rest 5-12 h after completion of exercise. It would appear from these studies that if exercise duration is too short (even with high intensity) or intensity is too low, no long-lasting calorigenie effect of exercise is observed. Moderate exercise maintained for a sufficient period of time may be more successful in elevating postexercise metabolic rate hours after exercise cessation (11). Chad and Wenger (10, 11) found that when exercise intensity or total work was equated, elevation of postexercise metabolism was related to exercise duration. Core temperatures returned to resting levels within 2 h, whereas Vo2 remained elevated for 2-8 h. Since then a recent study has been published indicating that, in untrained males, 3-h recovery of VO, was positively related to both duration and intensity of exercise (18). The effect of exercise intensity, independent of duration, on the extended EPOC has not been studied in women. This study investigated the effect of constant duration and varying intensity (and thereby total work) on the postexercise metabolic rate. The effects of 30 min of cycling at 50 and 70% Vogrnax on 3-h recovery of VO, were determined. Exercise intensity and duration were chosen as typical of recommendations for aerobic conditioning (2). Because training status influences the intensity of exercise that can be maintained for a given duration, trained female cyclists and untrained females were compared. METHODS Subjects. Five trained female cyclists (age 25.2 t 1.72 yr) and five untrained females (age 27.2 t 0.75 yr) volunteered to participate in the study. The cyclists averaged at least 300 km/wk, and the untrained individuals did no formal exercise. All subjects were eumenorrheic and were not in the menstrual phase of the female cycle during the time of the experiment. Before participation, all subjects
0161-7567/91 $1.50 Copyright 0 1991 the American Physiological Society
1713
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1714
EXERCISE
INTENSITY
completed an informed voluntary consent form and a medical history questionnaire. The procedures were approved by the Human Experimentation Ethical Review Committee of the University of Queensland. Experimental protocol. One week before the 1st day of testing, height and skinfold measurements were taken. Seven skinfold sites (triceps, subscapular, suprailiac, umbilical, biceps, thigh, and medial midcalf) were measured to the nearest 0.1 mm with Harpenden calipers, with the sum of the seven being recorded for each subject (38). The weight of each subject was measured on a beam scale and recorded to the nearest 0.1 kg before commencement of each testing session. Before the testing, the subjects were also familiarized with cycle ergometer exercise at a constant pedaling rate while breathing through a mouthpiece and valve that were to be used in all metabolic measurements. All subjects performed a stepwise incremental test (39) to measure VO, max. The VO, maxtest, performed on a Monark cycle ergometer, consisted of a 5-min warm-up at 100 (trained) or 50 W (untrained), after which time the load was increased by 25 W every 2 min. Pedaling speed was constant at 90 and 60 revolutions/min (trained and untrained, respectively) (39). Verbal encouragement was given to each subject to attain maximal values. Attainment of VO 2maxwas based on the following criteria: 1) a plateau or change of l.OO. Pulmonary ventilation, VO, and CO, output were measured an< recorded during the last minute of every 2-min stage. VO, was then plotted against power output to determine the work rates at 50 and 70% Vo2max for each subject. This estimation was confirmed by measurement of vo2 at that power output during a lo-min pretest conducted 2 days later. One week after the confirmation of test work rates, each subject was tested at approximately the same time of day for two trials scheduled 1 wk apart. The protocols for the 2 days of testing were identical with the exception of . the exercise intensity (1 at 50% 00, m8Xand 1 at 70% vo 2max ) 7 with duration held constant at 30 min. Once they reported to the laboratory (after a 12-h fast), the subjects consumed no food or beverage, with the exception of water, until the test was completed. All subjects were requested to maintain a mixed diet 1 wk before and throughout the experiment. This was confirmed from dietary records. RMR was determined by taking the mean of six 5-min VO, measurements, which were sampled over a continuous period of 30 min to ensure stability of the baseline. The subjects sat quietly on a chair for 1 h before this measurement. They were allowed to read, write, or watch television during this rest period. After RMR was established each day, the subject exercised at either 50 or 70% . vo 2maxfor 30 min. The order of the treatments was counterbalanced. After exercise, subjects returned to the sitting position to read, write, or watch television as in the preexercise phase for a period of 3 h. Subjects were dressed in shorts and T-shirts and wore running shoes throughout the test. The laboratory was air conditioned and held at a constant temperature of 22 t 0.5OC.
AND
POSTEXERCISE
ire,
All ventilatory measurements were made by standard open-circuit spirometry. For at least 5 min before sampling, subjects wore noseclips and breathed through a Hans Rudolph low-resistance low-dead-space valve (model 2700) that was connected to a mixing chamber via lightweight tubing. The volume of air inspired during measurement periods was measured by a turbine ventilometer (Morgan Mark 2). Volume of expired air was calculated from this measurement by use of the Haldane transformation. All volumes were corrected to STPD. Morgan CO, (infrared type 901 MK2) and 0, (paramagnetic model OA 500D) analyzers were used for measurement of respiratory gases. Calibration of the gas analyzers by use of certified gravimetric calibration gas and the ventilometer was conducted before and after the preexercise phase, 15 min after exercise, and, thereafter, immediately before each postexercise measurement. The Monark cycle ergometer was calibrated before each exercise bout. Heart rate was recorded from chest electrodes by a Rigel cardiac monitor (model 302). Five-minute ventilatory measurements were taken during the rest (preexercise) and exercise periods. In the postexercise phase, a 5-min ventilatory sample was taken from 10 to 15 min and, thereafter, every 40-45 min for the next 3 h, which was selected as the predetermined recovery period because of fasting and time constraints. To seek an explanation for the unexpected results, R values were subsequently used to estimate the proportional contribution from fat and carbohydrate in total energy yield. Absolute fat metabolism was also estimated. Because the work performed was predominantly aerobic, the proportions of 0, consumed in the oxidation of fatty acids and carbohydrate were calculated with a nonprotein R assumed and by use of the accepted values for fatty acid (R = 0.70) and carbohydrate (R = 1.00): %fatty acid = (1 - R)/0.3 X 100% and %carbohydrate = (R - 0.7)/0.3 X 100%. By use of palmitic acid as a typical fatty acid, yielding an R = 0.7, the absolute quantity of fatty acid oxidized may be calculated from the equation palmitic acid + 130 phosphate + 130 ADP + 23 0, + 16 CO, + 146 H,O + 130 ATP. Oxidation of 1 mol of fatty acid requires 23 mol of 0, or (23 X 22.4) liters because 1 mol of a gas occupies 22.4 liters (STPD). One liter of O,, therefore, accounts for the oxidation of 1000/(23 X 22.4) liters or 1.94 mmol of fatty acid. Millimoles of fatty acid are converted to milligrams by multiplying by the gram molecular weight, in this case 256, yielding ~500 mg fatty acid/l 0, consumed in the oxidation of fatty acid. Data analysis. The physical characteristics of the trained and untrained subjects were compared by Student’s t test for unpaired samples. For resting and exercise VO, and R values differences between means of six 5-min samples were analyzed across fitness group (trained vs. untrained) and test day (50% v02max vs. 70% vo 2max)by a two-way analysis of variance with repeated measures on test day. Postexercise comparisons were made by three-way analysis of variance across fitness level, exercise intensity, and time into recovery (15, 60, 105, 150, and 180 min), with repeated measures on exercise intensity and time. Differences between trained and untrained groups, between exercise intensities at each individual sampling
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EXERCISE
1. Physical characteristics
TABLE Subj
No.
INTENSITY
AND
POSTEXERCISE
1715
ire,
of untrained and trained subjects
Age, yr
Ht, m
28 28 26 27 27
1.73 1.52 1.54 1.67 1.64
59.0 59.5 60.0 67.5 62.5
124.0 130.4 145.3 186.3 152.7
1.73 1.74 1.80 1.96 1.60
27.2kO.75
1.62kO.08
61.7k3.14
147.9t21.65
1.77kO.12
1.70 1.65 1.72 1.73 1.64
54.0 60.0
80.5 107.0
2.95
7 8 9 70
24 23 28 25 26
59.0
92.0
2.98
57.0 55.5
85.0 98.3
3.10 3.31
Mean -t SD
25.2k1.72
1.69kO.04
57.1t2.20
W
kg
Sum of Skinfolds,
mm
VO
2mex, l/min
Untrained
Mean + SD
Trained
92.68k9.33
3.21
3.11-to.13
n = 10 women.
time in recovery, and among sampling times were assessed by Student’s t test for unpaired and paired samples, respectively, with a Bonferroni correction for multiple comparisons. VO, values were analyzed as excess postexercise VO, by subtracting resting levels before analysis. Comparisons between the 50 and 70% V02max recoveries were not altered when the analysis was performed on total rather than excess vo2 values. Results are expressed as means t SD. P < 0.05 was accepted as the level of significance for the analyses of variance and as the alpha level from which Bonferroni corrections were made for multiple comparisons. RESULTS
Physical characteristics of the subjects. The physical characteristics of the subjects in each group are presented in Table 1. The trained individuals were significantly lighter in weight (P < 0.05) and had smaller skinfold measurements (P < 0.01) than the untrained individuals. No significant difference in age or height was observed between the two groups. The mean Vozmax of the trained group was substantially higher (P < 0.01) than that of the untrained group. Rest. No significant difference was observed in RMR between the 2 days of testing. The data were highly reproducible, with no individual’s mean resting Vo2 varying by >O.Ol l/min on the two occasions. The trained group had significantly lower resting vo2 values (l/min) than the untrained, but this was largely related to the difference in body weight, and the difference was not significant when Vo2 was expressed as milliliters per kilogram per minute, (2.92 t 0.11 and 3.06 t 0.10, respectively). The resting R values of the trained (0.85 t 0.01) and untrained (0.84 t 0.01) groups were not significantly different, indicating that both groups were metabolizing approximately equal amounts of fat and carbohydrates in the resting state. The mean value for each group did not vary, and individual values were all within 0.01 on the two test days. Exercise. For the 30 min of exercise, the trained group worked at a mean Vo2 of 51.1 t 0.9 and 71.03 t 1.95%
. vo 2maxy and the untrained
group worked at 53.02 t 1.9 and 72.56 t 0.79% vo2max (no significant difference between groups). Because of the higher Vo2 max of the trained subjects, their mean work rate, and hence their VO, values were significantly higher (P < 0.01) than those of the untrained subjects during each exercise period (trained at 70% Vo2 max2.21 t 0.07 l/min, untrained at 70% VO, max 1.28 t 0.10 l/min, trained at 50% vo2max 1.59 t 0.06 11min, untrained at 50% V02max 0.94 t 0.09 Urnin). During the 50% irO, maxexercise bout, the trained subjects worked at 85 t 15 W, whereas during the 70% . vo 2max work bout they exercised at 115 t 15 W. The untrained group worked at 45 t 10 and 80 t 10 W, which elicited an Oo, equivalent to -50 and 70% VO, max, respectively. The R values during exercise were significantly higher at 70% V02max than at 50%. The trained subjects had significantly lower R values at both exercise intensities (P < 0.01; trained at 70% vo2 max0.95 t O.O$ untrained at 70% 60, max0.98 t O.Ol.,trained at 50% Vo2max 0.92 t 0.01, untrained at 50% Vo2max 0.94 t 0.01). Postexercise. The time course of postexercise VO, is shown in Figs. 1 (trained) and 2 (untrained). VO, at every sample period in the postexercise phase was significantly elevated (P < 0.01) above the pretest resting level after the two exercise intensities in both the trained (Fig. 1) and the untrained (Fig. 2) groups. At the end of 3 h of recovery, mean 60, was still elevated by 105 (untrained) and 135% (trained) after 50% Vo2max and by 53 (untrained) and 82% (trained) after 70% VO, max. In the last 2 h, the mean decline was only 0.04 (untrained) to 0.06 (trained) and 0.02 (untrained and trained) l/min in each case. From the first sample, lo-15 min into recovery, the VO, after work at 50% V02max remained significantly higher at every time period than after work at 70% . vo 2 maxfor both groups and each of the 10 individual subjects. The mean difference throughout was 104 t 18 ml/ min. The high reproducibility of the data can be seen from the low intersubject variability and the consistency of the values throughout the last 2 h of sampling in both groups.
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1716
EXERCISE
INTENSITY
2.0 i
30
0.70:
0
,‘ 30
60
90
,.,.,.,.I 60
120
90
120
150
180
.
.
150
180
POSTEXERCISE
\jo2
for . 105 min after 50% VO, maxand for 60 min after 70% vo 2 ma?* Estzmated fat metabolism. Because fat metabolism seemed. to be one of the few possible explanations of a higher VO, and lower R after 50% than after 70% VO, max, fat metabolism was calculated based on the tentative assumption that R approximated the true respiratory quotient (see DISCUSSION). Estimates of resting fat metabolism were consistent on the 2 days for each group: 51 t 4 (untrained) and 43 t 3 mg/min (trained). Individual values were all within 7 mg/min on the two test days. Estimates of fat metabolism during exercise suggested that untrained subjects metabolized approximately twice as much fat at 50% (102 t 19 mg/min) as at 70% TO, max (53 t 20 mg/min). The trained subjects appeared to metabolize -26% more fat at 50% (225 t 13 mg/min) than at70% V02max (178 t 24 mg/min). The trained subjects seemingly metabolized more than twice as much fat in absolute terms as the untrained subjects at 50% Vo2 max and more than three times as much at 70% VO, maxduring
2.5
0
AND
1.4 1
A L E
1.0
9
f
+ + -
50% 70% REST
0.8 -e + -
0.6
.2.
50% 70% REST
0.4 0.2
0
30
60
90
TIME
120
150
180
0.0: 0
.
30,
.
60,
(mln)
.
,
.
,
.
,
.
,
90
120
150
180
90
120
150
180
’ p < 0.01 50% vs 70% $02 max + p < 0.01 50% \jO2 max vs rest x p < 0.01 70% 002 max vs rest FIG. 1. Postexercise O2 uptake (~oJ, respiratory exchange ratio (R), and fat oxidation (FAT) after 30 min of exercise at 50% and 75% 00 2maxin trained subjects (n = 5).
After both exercise intensities, the trained group had a significantly higher iTo, than the untrained group, and VO, remained higher throughout the postexercise period, although a post hoc analysis of the individual samples showed only the first samples at lo-15 min to be significantly different. Pairwise comparisons across recovery time showed that, after exercise at 50% VO, m8X,significant falls in 60, occurred between samples in both trained and untrained subjects until 105 min. After exercise at 70% VO, max, significant falls occurred in both groups for only 60 min, even though the VO, values during the exercise were considerably higher than at 50% Vo2 m8X. R was significantly lower after 50% VO, m8Xthan after 70% v02max at every time point for both groups of subjects (Figs. 1 and 2). In the trained group, R fell below the resting level within the 1st h. In the untrained subjects, R reached the resting level within 1 h after 50% Vo2 maxbut not until 150 min after 70% VO, max. R followed a pattern similar to VO, in that it fell significantly between samples
30
0
60
. l . .
0
30
60
90
TIME
p < 0.01 + p < 0.01 x p < 0.01 l
50% 50%
120
150
180
(mln)
vs 70%
VO2
max
VO2 max vs rest 70% VO2 max vs rest
FIG. 2. Postexercise vo2, R, and fat oxidation after 30 min of exercise at 50% and 75% 2maxin untrained subjects (n = 5). VO
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EXERCISE
INTENSITY
the 30-min exercise bout. At 70% Vo2 max,the untrained subjects appeared to be metabolizing almost exclusively carbohydrate for their exercise needs. Estimates of recovery fatty acid oxidation showed significantly elevated levels of fat metabolism throughout the 3 h of the measurement period in both tests (P < 0.01). The estimated fat metabolism was significantly greater at every sample after 50% VoZmax than after 70% vo, max (Figs. 1 and 2) for both groups. At the end of 3 h, estimated fat metabolism after 50% V02max was still 56% higher (133 t 9 mg/min) than after 70% . vo 2max(85 t 7 mg/min) in untrained subjects and 45% higher (147 t 4 vs. 101 t 6 mg/min) in trained subjects. Trained subjects still appeared to be metabolizing 10 and 18% more fat than untrained subjects after 50 and 70% . vo 2 maxy respectively. DISCUSSION
Previous studies equating exercise intensity and varying duration or equating total work and varying intensity and duration (10, 11) have suggested that duration of exercise was more important than intensity in determining the extent of the elevation of metabolism after aerobic exercise. The present study has shown, in young women, that intensity of exercise is also an important factor in the long-term elevation of VO, after exercise. With duration held constant at 30 min, cycle ergometer exercise at 50% VO 2maxproduced consistently higher 60, values after the first 10 min of recovery than at 70% . vo 2max.The situation was the same for all 10 subjects, both trained and untrained, and at every sample period for every subject for a total of 50 data points. The variability of the measures was extremely low at rest, during exercise, and in recovery, indicating that random experimental error was minimal. Within each training group, intersubject variability was also very low. Although a third control condition without exercise was omitted for practical reasons, other studies have found little or no change in resting metabolism of postabsorptive subjects during a similar 4-h period (6, 27, 33). Where changes have been found (35), they have been of considerably lower magnitude than the postexercise elevations found in this study. In comparisons of the two exercise intensities, each subject acted as her own control, and there is no indication that minor variations in the very consistent resting VO, values could have had any substantial part in explaining the findings. The evidence appeared incontrovertible. These findings are not explained by the previously held views on the mechanisms postulated for the postexercise VO,, i.e., creatine phosphate replenishment, lactic acid removal, glycogen resynthesis, and the effects of increased core and muscle temperature (17), because these mechanisms would increasingly come into play as the intensity level of exercise increases. However, in the past decade research has shown that these factors may not be the only determinants of postexercise VO, because of the following: lactic acid has been shown to be an unlikely cause of the increased metabolism observed several hours after exercise cessation; increased temperatures return to resting levels before RMR has been reached
AND
POSTEXERCISE
Tjoz
1717
(11); creatine phosphate replenishment may only represent a small amount of the total postexercise 0, cost (20); and, because of the slow process of the resynthesis of muscle glycogen (23), it is questionable whether this mechanism can be used entirely to explain the elevation in postexercise VO,. It is possible, therefore, that although these mechanisms may be predominant early in the recovery phase and still remain active during the slow component of recovery, an additional mechanism must assume greater importance in the long-term postexercise VO,. One of the few possible explanations for increased VO, after lower exercise intensity is the metabolism of fat, a mechanism suggested recently by other authors (3, 27). The respiratory quotient has commonly been taken to indicate the proportion of fat and carbohydrate metabolized under steady-state conditions. The use of R as an estimate of the nonprotein respiratory quotient is not without risk because a change in the acidity of the blood, a relative hyperventilation, or a change in dissolved CO, levels in the tissues might cause R to be different from the respiratory quotient and invalidate its use as a measure of substrate metabolism. However, the exercise intensities chosen in this study have been shown to cause little lactate production (12,2l, 30). CO, output, because of changes in buffering of acids or hyperventilation, would most likely occur in the untrained subjects working at 70% VO, max. In this case, the difference in R between 50 and 70% Tjo, maxin the present study was 0.04 (untrained) and 0.03 (trained) at the end of exercise and 0.03 after 3 h of recovery for both groups, indicating that the untrained group had little, if any, greater such effect than the trained group. The duration of the exercise task (30 min) was such that a sustained hyperventilation would have been improbable. This was reinforced by the absence of any increase in CO, uptake observed during the last 20 min of the exercise tests. Furthermore, the shape of the recovery curve of R was similar for both exercise intensities and both groups. Any effect of acidity or hyperventilation would be expected to occur in the samples at the end of exercise and lo-15 min into recovery, resulting in a more steeply sloping curve after 70% . vo 2max.No such effect was apparent. R values were consistently lower after exercise at 50% Vo2max and went below the preexercise resting level sooner, suggesting that fat metabolism was the major energy source after the lower exercise intensity. Estimation of the absolute fat metabolism supported the view that more fat was metabolized after 50% than after 70% VO, max.The alternative that R was consistently reduced by a net uptake of CO, in the tissues seems unlikely over a 3-h period. The results from the present study once again confirm the view that postexercise metabolism may be elevated for several hours, depending on the duration and intensity of the exercise being performed. There is a long and somewhat neglected history of similar findings (6,13-15, 20,22,27,28,34). All these studies support the view that the elevation of metabolism after exercise extends beyond the replenishment of creatine phosphate and 0, stores, removal of lactate, and Q10effects. Much of the confusion and conflict apparently existing in the literature on 0, debt is related to differences in
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1718
EXERCISE
INTENSITY
experimental design and methods. Most studies have restricted their interest to the first two of the three components of postexercise elevation of VO,. In these cases, the measurement of recovery VO, has generally been limited to short periods, often with exercise baselines, with the specific intention of eliminating the long-term elevation of metabolism. Pacy et al. (33) concluded that there was no prolonged thermogenic effect of moderate repeated aerobic exercise in weight-maintaining lean subjects. The lack of significance may have been due to the small sample size and the increased variance due to the mixed-gender sample and the range of exercise intensities. The exercise loads were reported to represent 3545% Tjo2 M8X,although no mention was made as to how this was determined. Gore and Withers (18) also found that in well-trained male subjects EPOC was of little physiological significance. It is possible that the observed differences in the two studies were either gender or experimental-design related. Although the 28-h measurement of RMR was performed by Gore and Withers (18) to account for circadian variations, the effect of increased thermogenesis on metabolic rate may have elevated the “resting” state and hence underestimated EPOC. The weight of accumulating evidence suggests that postexercise metabolism may be raised for several hours depending on the duration and intensity of exercise. Exercise of sufficiently short duration or low intensity may minimize the effect. In the present study, exercise for 30 min at 50% V02max produced a greater extended EPOC than after 70% Vogmax in both trained and untrained females. Trained individuals had significantly greater extended EPOCs than untrained. R values were lower after 50% TO, maxand in trained subjects, suggesting fat metabolism as a possible mechanism. Estimates of fat metabolism support this view both in this study and in two recent studies (6,27). Subsequent studies in this laboratory have also supported this hypothesis. When fat metabolism was stimulated by the ingestion of caffeine (9) or by dietary manipulation (8), the extended EPOC was higher than in control conditions. The precise mechanism for increased fat metabolism in recovery is not yet clear. Increased substrate cycling, as proposed by Newsholme (31, 32), is one possibility. The ATP production per mole of 0, is also less for fat than for carbohydrate metabolism. The conversion of fat to restore glycogen stores has also been considered but does not appear to be a major factor (6, 13). Barbee et al. (4), in their in situ muscle preparation in anesthetized ventilated dogs, showed that, after 10 min of stimulated isometric contractions, vo2 returned to resting level within 30 min. If this could be generalized to whole body human activity of 30 min, one could speculate that the long-term increase in metabolism may occur in tissues other than muscle. Because lipid oxidation rate has been shown to be largely independent of plasma free fatty acid levels (6, 25) but related to specific lipid stores (5) and individual long-chain fatty acid composition (24)) further elucidation of mechanisms and refinement of detail may require considerably more research. It is not yet clear what effect exercise at higher intensities for short durations may have on long-term elevation
AND
POSTEXERCISE
ire,
of metabolism. There is ample evidence that muscle and blood lactate levels are not closely coupled even to the second or slow component of EPOC in humans, other mammals, reptiles, or amphibians (17). If duration is adequate for muscle and core temperatures to rise to a sufficient level, then the Q10 effect may be substantial. The evidence is that both of these are relatively short-lived effects lasting only 1 or 2 h. If fat metabolism is the major factor, then there may be a parabolic relationship between exercise intensity and extended EPOC provided duration is adequate. Our data on young women, both trained and untrained, suggest that the peak may be at -50% voz max for 30 min of exercise, perhaps approximating the so-called ventilatory threshold. A recently published study has not found such a relationship in young males (18). The present results suggest that 30 min of moderate exercise may produce a distinct postexercise elevation of metabolism, possibly that of fat; this may be important in weight loss, particularly in middle-aged people, for whom high-intensity exercise may constitute an increased cardiac risk. Address tion, Univ. Canada. Received
for reprint requests: of Saskatchewan,
6 February
K. E. Chad, Saskatoon,
1990; accepted
in final
College of Physical EducaSaskatchewan S7N OWO,
form
16 November
1990.
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EXERCISE 15. EDWARDS,
quirement
INTENSITY
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