Effect of feeding and fasting on excess postexercise oxygen consumption ROALD Department

BAHR

AND

OLE M. SEJERSTED

of Physiology,

National

Institute

of Occupational Health, N-0033 Oslo 1, Norway

BAHR,ROALD,ANDOLE M. SEJERSTED.Effectoffeeding and fasting on excess postexerciseoxygenconsumption.J. Appl. Physiol. 71(6): 2088-2093,1991.-This study wasundertaken to determine the effect of fasting on the magnitude and time course of the excesspostexercise 0, consumption (EPOC). Six lean untrained subjectswere studied in the fasted state for 7 h after a previous strenuous exercisebout (80 min at 75% of maximal O2uptake) and in a control experiment. The results were compared with identical control and exercise experiments where the subjectswere fed a 4.5MJ test meal after 2 h of rest. EPOC was calculated as the difference in 0, uptake between the corresponding control and exercise experiments. The total EPOC (O-7 h postexercise) was 20.9 t 4.5 (fasting) and 21.1 k 3.6 liters (food, NS). A significant prolongedEPOC component was observed in the fasted and in the fed state. The thermic effect of food (TEF) wascalculated from O2consumption and respiratory exchangeratio asthe difference in energy expenditure betweenthe corresponding food and fasting experiments. The total TEF (O-5 h postprandial) was 321 t 32.0 (control) and 280 t 37.7 kJ/5 h (exercise, NS). It is concluded that the prolonged component of EPOC is present in the fasting state. Furthermore, no major interaction effects between food intake and exercise on the postexercise O2consumption could be detected.

ences in opinion as to whether the interaction exists (10, 19, 20, 23, 27). It is clear that both the variability of EPOC and the precision of indirect calorimetry will set limits to how large an interaction will be detectable even with a large number of subjects. To reduce variation as much as possible, a paired design was chosen in which each subject participated in four experiments in random sequence, exercise experiments with and without food intake and resting experiments with and without food intake. Six lean untrained subjects were studied after a 4.5MJ test meal with or without a previous strenuous exercise bout, and the results were compared with identical fasting experiments. 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 about all procedures before written consent was obtained. Data from related studies on the same subjects have been published elsewhere (3,4)* Preexperimental procedures. Before the experiments dietary-induced thermogenesis;humans; oxygen uptake; resting metabolic rate; respiratory exchangeratio; thermic effect of started, all subjects were familiarized with bicycle exerfood cise at a constant pedaling rate and with breathing through the mouthpiece and the breathing valve used in all metabolic measurements. All testing and experimenAFTER A BOUT of strenuous exercise there is an increase tal exercise procedures were performed on a modified in resting 0, uptake that has been termed the excess Krogh cycle ergometer. About 2 wk before the experiments started, maximal O2 uptake was measured using postexercise 0, consumption (EPOC) (13). The EPOC decreases rapidly during the 1st h postexercise, but there criteria modified for the cycle ergometer from Taylor et is also a prolonged EPOC component that may persist al. (26). In this protocol the subjects performed 3-min for as much as 12 h (2, 18). This prolonged elevation of work bouts with lo-min resting periods and 19-W increresting 0, consumption has partly been connected to the ments in work load. These results were used to predict work loads corresponding to 75% of maximal 0, uptake cost of increased triglyceride-fatty acid substrate cycling in each subject. (1). It has also been suggested that the prolonged EPOC component is somehow related to food intake in the reExperimental protocol. Each subject participated in covery period after exercise, possibly by potentiating the four experiments, two exercise experiments (with and thermic effect of food (TEF) (2,18). This study was therewithout food) and two control experiments (with and without food). Experiments were separated by 2 wk, and fore designed to determine whether a prolonged EPOC component can be detected in the fasted state, when the sequence of the experiments was randomized. The there is no TEF and when the rate of glycogen synthesis subjects reported to the laboratory at 7:00 A.M. after an overnight fast. They were transported by car to avoid is low (6, 16, 17). The second purpose was to examine whether there is unnecessary physical activity before each experiment. any major interaction between food and exercise on the The subjects were told not to partake in any exercise for postexercise 0, consumption. There are many claims for 2 days before an experiment and not to make any a synergistic interaction of food and exercise on energy changes in their dietary or exercise habits. No tobacco or alcohol was allowed 24 h before each experiment. expenditure, but several recent reviews reveal differ2088

0161-7567/91 $1.50 Copyright 0 1991 the American Physiological Society

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FOOD INTAKE AND EXCESS POSTEXERCISE 0, CONSUMPTION

2089

TABLE 1. Physical characteristics and exercise data for all subjects Body Subj

No. 1

2 3 4 5 6

Mean t SE

Age, yr

Ht, cm

25 23 24 24 20 23

189 187 185 186 183 178

80 87 71 79 75 58

23t0.6

185U.4

75t3.7

W

kg

Fat,* %

Maximum 0, Uptake, ml. kg-‘. min”

12.5 15.6 9.4 10.2 11.1 8.2 11.2tl.l

Intensity, % of max

58.5 47.4 50.6 44.4 48.1 49.0

77 77 74 72 78 70

49.9t1.4

75H.3

* Estimated from skinfolds.

The urinary bladder was emptied, body weight was measured, and a thermistor (type DU3S, Ellas Instruments, Copenhagen, Denmark) was inserted lo-15 cm into the rectum. Then the subjects rested in bed until the exercise period started. On two separate days the subjects exercised at a constant pedaling rate of 75 rpm for 80 min at 75% of maximal 0, uptake (Table 1). They were allowed a 5-min rest period once every 20th min. After exercise the subjects rested in bed for 7 h. Two control experiments without exercise were also performed and the conditions were identical to the resting period of the exercise experiments. The start of exercise was adjusted so that the recovery period always started at 9:30 A.M. After exercise the subjects rested in bed until 4:30 P.M. but were not allowed to sleep during this period. In one of the exercise experiments (food exercise) and one of the control experiments (food control) the subjects were given a meal consisting of bread (3 g/kg body wt), jam (2 g/kg body wt), and skim milk (0.5 liters). The average caloric content per meal was 4.5 MJ (5% fat, 81% carbohydrate, 14% protein). The meal was taken 2 h after exercise. All meals were completed within 30 min. In the other exercise (fasting exercise) and control experiment (fasting control) the subjects fasted for the entire recovery period. Measurements. In each experiment the fasting baseline O2 uptake was measured for 15 min in the morning before exercise after 30 min of bed rest. The fasting baseline measurement of 0, uptake was repeated on nine separate occasions for each subject, and the coefficient of variation was ~6%. During exercise 0, uptake was measured from 15 to 18,35 to 38,55 to 58, and 75 to 78 min. Postexercise 0, uptake was measured continuously for the 1st h and thereafter for the last 15 min of every hour for the next 7 h. In the control experiments O2 uptake was measured for 15 min of every hour for the entire experiment. Rectal temperature was recorded continuously during the whole experimental period. The subjects breathed through a mouthpiece, and expired air was collected in Douglas bags. 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; COZ, 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 standard temperature and pressure dry.

EPOC was calculated as the time integral of the difference in O2 uptake between the exercise and control experiments for the postexercise period. Total energy expenditure (EE), which includes the contribution made by protein oxidation, was calculated from 0, uptake (VOW, ml/min) and respiratory exchange ratio (R) according to the formula (12) EE = ire, (15.480 + 5.550 R) TEF was calculated as the time integral of the difference in energy expenditure between the postprandial and fasted state for the time period after the meal. The rate of fatty acid (FA) oxidation was estimated as described in detail previously (l), assuming that the rate of nitrogen excretion was 7.8 mg/min. This average value was taken from the measured values determined in a similar study on recovery from exercise from our laboratory, where it was shown that there is no change in the rate of nitrogen excretion after exercise compared with a control experiment (1). A 20% error in this assumed value (which exceeds the total range of values in the previous study) would have had no significant effect on the estimated rate of FA oxidation. In estimating the rate of FA oxidation it was assumed that dioleoylpalmitoyl-glycerol (33,976 kJ/mol) represents triglycerides from human fat stores. Statistical methods. The results are presented as means t SE. The experiment was divided into three intervals for statistical analysis. The first interval (-2 to 2 h) consists of the observations during rest before the meal. The second interval lasts from the end of the exercise period until the end of the experiment (O-7 h), and this interval provides information on the effects of exercise on recovery metabolism. The data obtained in the third interval (2-7 h postexercise, O-5 h postprandially) provides information on the effects of food intake and the prolonged EPOC component. The data obtained in the different time intervals were compared using analysis of variance for repeated measures with two withinsubject factors: food or exercise, and time. Significant main effects were then followed by paired comparisons using t tests. Calculated EPOC, TEF, and FA oxidation (time integrals) were compared using a paired t test. Rejection level was chosen as P 5 0.05. l

RESULTS 0, uptake. In the control experiments

uptake was 238 t 14 (fasting control)

l

the value for 0, and 248 t 14 ml/

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2090

FOOD INTAKE I

400

1

I

I 0

‘z‘ .E L E u

360

-

320

I

I

0

Fasting

e

Food

R

AND EXCESS

I

I

q n

control

control

1

Fasting Food

I exercise

exercise

1

POSTEXERCISE

1

-

2 %

280

O2 CONSUMPTION

n

2 w u z

300

:0 z g

200

.-E f Fr

0

0

Control

ESl

Exercise

m

Exercise

- control

100

3 I

g

240 200

l-J

’ -2

FIG.

1.

I 0

s u 2 Time

,

1 4

1

I 6

I

T

I

n.s.

t

-100

* n.s.

n.s.

n.s.

2-3h

3-4h

4-5h

(h)

h

l-2h

Postprandial

min (food control, NS vs. fasting control) in the morning, and there were no differences in 0, consumption between the food and fasting control experiments in the time period before the meal (-2 to 2 h; Fzo4 , = 0.51, NS; Fig. 1). In the exercise experiments, O2 uptake increased to 2.79 t 0.21 (fasting exercise) and 2.86 t 0.19 l/min (food exercise, NS vs. fasting exercise) at the end of the 80-min work periods. After exercise 0, uptake fell sharply, but postexercise 0, uptake was higher than control values in both the food and fasting exercise experiments (O-7 h; food exercise vs. food control: &, 10 = 71.2, P < 0.0005; fasting exercise vs. fasting control: &@,1o = 86.7, P < 0.0005; Fig. 1). There was a significant increase in 0, uptake after meals to a peak value of 308 t 13 (food control, P < 0.001 vs. fasting control) and to 343 t 17 ml/min (food exercise, P < 0.001 vs. fasting exercise; Fig. 1). In the time period after meals, 0, uptake remained higher than in the fasting experiments for the whole observation period (2-7 h; food exercise vs. fasting exercise: Fzo 4 = 7.32, P < 0.0025; food control vs. fasting control: F,,; 9 = 6.41, P < 0.0025). EPOC and TEF. The total O2 consumption over the 7-h recovery period after exercise and for the corresponding time period of the control experiments is shown in Table 2. EPOC amounted to ~21 liters over the 7-h period whether or not food was given. The time course of accumulated EPOC is shown in Fig. 2. Postexercise 0, consumption was significantly higher than in the resting condition throughout the periods before (O-2 h) and after the meal (2-7 h). Hence, the prolonged component of EPOC (2-7 h) amounted to 11.8 t 3.5 liters in the fasted state and 10.4 t 2.5 liters in the fed state. TEF amounted to -13 liters (corresponding to -300

time

I

period

Thermic effect of food in 6 postprandial 6). Bars, SE. FIG.

n.s. 1 1 Sum 0-Sh

L O-1

Time plot of mean 0, uptake (n = 6). Bars, SE,

1

n.s.

2.

time periods (n =

kJ) in both the exercise and control conditions. The time course of TEF is shown in Fig. 3. Because EPOC was of similar magnitude whether the subjects were rested or had exercised, TEF was also not different between the food and fasting experiments (Table 2). Table 2 shows that no interaction between food and exercise could be detected. However, the design of the study does not allow us to conclude that such an interaction does not exist. Considering the SE of 3.9 liters, the test power (1 - ,6) falls below 0.8 at an interaction of -9.5 liters. We therefore conclude that both major effects, EPOC and TEF, are not significantly changed by the interventions. Increased TEF cannot account for EPOC but, on the other hand, we cannot exclude the possibility that it contributes because the design only allowed detection of major interaction effects. R. R increased from 0.78 + 0.02 (mean morning value in the control experiments) to 0.90 t 0.02 at the end of the exercise periods (Fig. 4). After exercise R fell sharply below the level of the control experiments, and there was a significant reduction in R in the postexercise interval in the food and fasting experiments (O-7 h; food exercise vs. food control: FSo1o= 5.84, P < 0.0005; fasting exercise vs. fasting control: &o 1o = 5.32, P < 0.0005) (Fig. 4). However, we detected ho effect on R in response to meals compared with the corresponding fasting experiments

2. Total O2consumption (O-7 h) during rest and recovery after exercise in the four experimental conditions

TABLE

Exercise

Control

Difference

With food

(EPOC)

No food

l

-a

O-0 1

Food Fasting Difference (TEF)

136.7t5.7

115.6,t4.8

21.lt3.6*

123.4t5.5

102.6t,5.7

20.9t4.5”

13.2t2.6*

13.0t1.9*

0.2+3.9t

Values are means + SE in liters; n = 6. EPOC, excess postexercise 0, consumption; TEF, thermic effect of food. * P c 0.05; t NS.

I

I

1

0

2 Recovery

I

4 time

I

I

I

I

6 (h)

FIG. 3. Time plot of accumulated excess postexercise O2 uptake (n = 6). Bars, SE.

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FOOD INTAKE

*

-2

0

Food

FIG.

4.

n

control

2 Time

AND EXCESS

4

Food

POSTEXERCISE

exercise

6

(h)

Time plot of mean respiratory exchange ratio (R; n = 6).

Bars, SE.

(2-7 h; food control vs. fasting control: Fgo4 = 2.05, P = 0.13; food exercise vs. fasting exercise: F,,‘,, = 2.84, P =

0.052).

Rate of FA oxidation. The rate of FA oxidation (2-7 h postexercise) was 45 t 5.9 mmol/5 h in the food control experiments and increased after exercise to 92 t 8.1 mmol& h (food exercise) (P < 0.01). In the fasting control experiments the rate of FA oxidation (2-7 h postexercise) was 88 t 7.1 mmol/5 h, and it increased to 114 + 6.5 mmol/5 h after exercise (fasting exercise); (P

Effect of feeding and fasting on excess postexercise oxygen consumption.

This study was undertaken to determine the effect of fasting on the magnitude and time course of the excess postexercise O2 consumption (EPOC). Six le...
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