Exercise metabolism at different time intervals after a meal

Exercise metabolism at different time intervals after a meal

SCOTT J. MONTAIN, MAR1 K. HOPPER, ANDREW R. COGGAN, AND EDWARD F. COYLE Human Performance Laboratory, Department of Kinesiology and Health, The University of Texas at Austin, Austin, Texas 78712

MONTAIN, SCOTT J., MARI K. HOPPER, ANDREW R. COG- GAN, AND EDWARD F. COYLE. Exercise metabolism at different time intervals after a meal. J. Appl. Physiol. 70(2): 882-888, 1991.-To determine how long a meal will affect the metabolic response to exercise, nine endurance-trained and nine un- traine$ subjects cycled for 30 min at 70% of peak 0, consumption (Vo,,, ) 2,4,6,8, and 12 h after eating 2 g carbohydrate/ kg body wt. In addition, each subject completed 30 min of cy- cling 4 h after the meal at an intensity that elicited a respiratory exchange ratio (RER) of 0.94-0.95. During exercise after 2 and 4 h of fasting, carbohydrate oxidation was elevated l3-15% compared with the response to exercise after an 8- and 12-h fast (P < 0.01). The increase in blood glycerol concentration during exercise (30 to 0 min) was linearly related to the length of fasting (r = 0.99; P < 0.01). In all subjects, plasma glucose concentration declined 17-21% during exercise after 2 h of fasting (P < 0.01). Plasma glucose concentration also declined (1525%) during exercise in the trained subjects after 4 and 6 h of fasting (P < 0.05) but did not change in the untrained subjects. However, the decline in plasma glucose concentration was similar (14%) in the two groups when the exercise intensity was increased in the trained subjects (i.e., 78 * 1% VO, pealr) and decreased in the untrained subjects (i.e., 65 k 3% Vozpeak) to elicit a similar RER. The results of this study demonstrate that at least 6 h of fasting are necessary after consuming a 500- to 600-kcal carbohydrate meal before carbohydrate oxidation and plasma glucose homeostasis during exercise at 70% vozpeak are similar to values after an 8- to 12-h fast. The progressive increase in blood glycerol accumulation during exercise as fasting increased from 2 to 12 h suggests that adipose tissue lipolysis increases in direct proportion to the length of fasting (i.e., 2-12 h). Finally, the magnitude of decline in plasma glucose concentration after a preexercise meal is dependent on the relative exercise intensity.

glucose; insulin; glucose uptake; hypoglycemia; lipolysis

SUBSTRATE UTILIZATION during exercise is influenced by the state of physical training, the intensity of exercise, and the amount of carbohydrate consumed during the days before exercise (15-17). In addition, it is well docu- mented that ingestion of carbohydrate 30-60 min before exercise, compared with an overnight fast, elevates carbohydrate oxidation and produces a decline in blood glucose concentration during the early minutes of exercise (1, 2, 4, 6, 12). The greater reliance on carbohydrate for energy during exercise after a preexercise carbohydrate meal may be due to factors regulating glucose oxidation, free fatty acid oxidation, or both. To date, no study has systematically determined the length of fasting neces-

sary to avoid elevated carbohydrate oxidation and a decline in blood glucose concentration during exercise after a preexercise carbohydrate meal. Furthermore, no study has determined what effect the length of fasting has on lipolysis and plasma free fatty acid concentration during exercise after a preexercise carbohydrate meal. A more complete understanding of the effect of a preexercise meal on metabolism is necessary to interpret exercise metabolism studies that have used different lengths of fasting before experimental treatments.

We recently reported that carbohydrate ingestion 4 h before exercise, compared with a 16-h fast, results in elevated carbohydrate oxidation, a reduction in blood glucose, and blunted lipolysis during exercise (7). Exercise metabolism was altered despite the fact that plasma insulin concentration, although elevated for 2 h after the meal, had returned to fasting basal levels during the 2-h period before exercise. These observations indicate that longer than 4 h of fasting are necessary before exercise metabolism will return to values found after an overnight fast (i.e., 12-16 h).

The major purpose of this investigation was to determine the length of fasting necessary after a preexercise meal before exercise metabolism can be considered similar to that observed after an overnight fast (i.e., 12 h). Another purpose was to better describe the conditions associated with a lowering of blood glucose during the early minutes of exercise initiated several hours after eating. We have found that both the state of training and the relative exercise intensity influence blood glucose homeostasis during exercise after a carbohydrate meal.

METHODS

Subjects. Nine male subjects who regularly performed endurance exercise and nine untrained male subjects par- ticipated in this study (Table 1). The experimental pro- cedures were explained to all subjects, and written in- formed consent was obtained. This study was approved by the Human Studies Committee at The University of Texas.

Experimental design. During the first laboratory visit each subject completed a continuous incremental protocol on the cycle ergometer (Monark model 870) for determination of the blood lactate threshold (8). After a brief rest, subjects then completed another incremental test on the cycle.ergometer for determination of peak 0, consumption (VO, peak ). On subsequent experimental days,

882 0161-7567/91 $1.50 Copyright 0 1991 the American Physiological Society

EXERCISE METABOLISM AND FASTING DURATION 883

TABLE 1. Physical characteristics of trained and untrained subjects

Variable

Body wt, kg %pmk

Trained Untrained

65.8+ 1.9* 77.3k1.9

l/min 4.27+0.05-f 3.69kO.16 ml. kg-’ . min-’ 65.&1.9* 47.81-2.0

V~Z at LT 3.31t0.15” 2.27t0.15 %VO, peak at LT 77.3&1.6* 64.5t3.1

Values are means & SE; n = S/group. LT, the blood lactate threshold. Significantly different from untrained: * P c 0.01; t P c 0.05.

the subjects reported to the laboratory 2,4,6,8, or 12 h after consuming a carbohydrate meal consisting of ba- gels, jelly, and orange juice (2 g/kg carbohydrate, 0.3 g/kg protein, and negligible fat). During these five trials the subjects exercised for 30 min at 70% 00, peak. During another trial, performed 4 h after the meal (4RER) the subjects exercised for 30 min at an intensity eliciting a respiratory exchange ratio (RER) of 0.94-0.95. Venous blood samples were obtained before and after 5,15, and 30 min of exercise. The order of the six trials was randomized for each subject and separated by a minimum of 24 h. The average time between trials was 24 h. The time of day of exercise was kept constant for all trials. Thus the post- prandial time before ingestion of the preexercise meal varied between trials. Subjects refrained from other aer- obic exercise during the experiment and were instructed to eat their normal diet. In addition, the resting plasma insulin and glucose responses to the meal were moni- tored during the 4-h period after eating and before the 4RER trial.

Determination of blood lactate threshold and peak 0, consumption. Lactate threshold (LT) was determined using a continuous incremental protocol. Each exercise stage lasted 5 min with work rates eliciting -50, 60, 70, and 80% Vo2 peak* Blood samples (1 ml) were drawn from a butterfly catheter inserted in an antecubital vein, placed in cold 8% perchloric acid, and subsequently as- sayed for lactate (14). 0, consumption (00,) was determined continuously during the test. LT was defined as the VO, when blood lactate concentration was 1 mM above baseline (8). This protocol has been previously shown to elicit similar results as a 10 min/stage discon- tinuous protocol (27; unpublished observations). .

vo 2 peak was determined using an incremental test on a cycle ergometer. The initial work load was set at 70% estimated 60, peak. After 4 min, the work load was increased incrementally every l-2 min until the subject could not continue. Vozpeak was defined as the highest 1-min value obtained during the test. Achievement of . vo 2 peak was assessed by leveling off of VO,, RER > 1.15, and attainment of predicted maximal heart rate.

Blood sampling and analysis. A butterfly catheter was placed in an antecubital vein before exercise. Blood (5-8 ml) was obtained immediately before exercise and after 5,15, and 30 min of exercise. Blood (4 ml) was placed in tubes containing 0.20 ml of 82 mM EDTA. The tubes were centrifuged, and plasma was separated for measurement of plasma glucose concentration using a glucose analyzer (Yellow Springs Instruments model 23A) and plasma free fatty acid concentration (5 subj) (23). Blood

(3 ml) was placed in tubes containing 0.15 ml aprotinin. After centrifugation the plasma was separated for determination of plasma insulin concentration (Radioassay Systems Laboratories, Carson, CA) (13). Blood (0.5 ml) was placed in 1 ml of cold 8% perchloric acid, centrifuged, and analyzed for blood lactate concentration (14) and blood glycerol concentration (10).

Measurement of gas exchange. 60, and RER were determined at 5-10 and 22-28 min of each trial. The subjects breathed through a Daniel’s valve while inspired volume was measured using a dry gasmeter (Parkinson- Cowan CD4). Expired gases were sampled from a mixing chamber and analyzed for 0, (Applied Electrochemistry S3A) and CO, (Ametek CD-3A). Analog outputs from the instruments wpre directed to a laboratory computer for calculation of VO, and RER. The gas analyzers were cali- brated with gases previously analyzed by the micro- Scholander method (26). The dry gasmeter was cali- brated against a Tissot spirometer. Carbohydrate oxidation was calculated using the average vo2 and RER from each experimental trial.

Determination of heart rate and perceived exertion. Heart rate was recorded using a single-channel electro- cardiograph at 7 and 25 min of each trial. Rating of perceived exertion (RPE) was also recorded at 7 and 25 min (5).

Statistical analysis. Data for trained and untrained responses during exercise were analyzed using a two-way analysis of variance with repeated measures. Significant differences were located using Tukey’s post hoc analysis. Differences between the trained and untrained subjects were identified with an unpaired t test when appropriate. A significance level of P < 0.05 was chosen for all compar- isons. Data are presented as means t SE.

RESULTS

Plasma insulin and glucose concentration in response to meal. Plasma insulin concentration increased significantly above premeal values in both trained and untrained groups during the first 60 min after the meal (Ta- ble 2). However, the plasma insulin concentration re- mained elevated for a longer period of time in the untrained subjects compared with the trained subjects (P < 0.05). In both trained and untrained groups plasma glucose concentration rose significantly and peaked 30 min after the meal, after which it declined and stabilized at basal levels.

Cardiovascular and metabolic response to exercise. There were no differences due to length of fasting (i.e., 2, 4,6,8, or 12 h) for vo2, heart rate, perceived exertion, or blood lactate concentration during the trials performed at 7O%V0 2 eak for either the trained or untrained groups. However, tie trained subjects exercised at a 17% higher VO, (2.98 t 0.12 vs. 2.53 + 0.17 l/min; P < 0.05) and a lower blood lactate concentration (2.58 t 0.58 vs. 3.68 t 0.66 mM; P < 0.05) than the untrained subjects. The time of feeding produced similar responses for several vari- ables in both the trained anduntrained groups, and therefore the results of the two groups were pooled to increase statistical power.

Carbohydrate oxidation and RER. The rates of carbohydrate oxidation (g/min) were not different between the

884 EXERCISE METABOLISM AND FASTING DURATION

TABLE 2. Resting plasma insulin and glucose response to preexercise meal for trained and untrained subjects

Time, min

0 30 60 120 180 240

Trained 12.1tl.l Untrained 12.4t2.1

Trained 4.35kO.10 Untrained 4.4520.17

Plasma insulin concentration, pUlm1 50.6&6.4* 54.7k10.2' 29.8k3.4 64.1t8.7' 84.1t21.9’ 55.9+7.4*7

Plasma glucose concentration, mM 6.16t0.42' 4.66~0.30 3.92t0.16 5.81kO.25' 4.99t0.32 4.84kO.35.f

18.7t2.2 15.021.7 48.Ok 13.8t 19.5k4.4

4.04t0.23 4.24k0.16 4.24k0.37 3.98kO.20

Values are means t SE n = 9 for trained and n = 7 for untrained. * Significantly greater than 0 min, P < 0.05. t Significantly greater than trained subjects, P < 0.05.

trained and untrained subjects, since the trained subjects had a higher Vo2 and lower RER (P < 0.05) during exercise compared with the untrained subjects. When both groups were combined, carbohydrate oxidation was similar during exercise initiated 8 and 12 h after the carbohydrate meal (2.33-2.34 g/min). In contrast, carbohydrate oxidation was significantly higher during exercise after 2 and 4 h of fasting (-15 and d3%, respectively) compared with 8 or 12 h of fasting (Fig. 1; P < 0.01). Carbohy- drate oxidation during exercise after 6 h of fasting was intermediate to and not significantly different from 2-4 and 8-12 h of fasting (P > 0.05).

Plasma insulin concentration. Plasma insulin concentration was elevated before exercise in both groups when fasted 2 h (P < 0.01; Table 3). There were no other differences in plasma insulin concentration either before or after 30 min of exercise when comparing all trials. The preexercise plasma insulin concentration after 2 h of fasting was 84% higher in the untrained group compared with the trained group (P < 0.05). There were no other differences in plasma insulin concentration between the two groups.

Blood glycerol and plasma free fatty acid concentration. Preexercise blood glycerol concentration was similar for both groups when fasted 2,4, 6, 8, and 12 h. Blood glycerol concentration rose with time in all trials, becoming significantly greater than resting concentrations by 30 min of exercise (P < 0.01). The magnitude of the increase

3.00

4 6 8 12

Length of Fast (h) FIG. 1. Relationship between carbohydrate (CHO) oxidation and

length of fast for all subjects. Values are means k SE. *Significantly greater than 8- and 12-h values (P < 0.01).

in blood glycerol concentration during exercise was directly related to the length of the fast (r = 0.99; P < 0.01). The change in blood glycerol (30 to 0 min) concentration was significantly lower after 2, 4, or 6 h of fasting compared with 12 h (Fig. 2; P < 0.05). In addition, the change in blood glycerol concentration was significantly lower during exercise after 2 h of fasting compared with 8 h (P < 0.05).

Plasma free fatty acid concentration (FFA) at rest and during exercise was also related to the length of fasting. The mean plasma FFA concentrations (i.e., mean t SE of 0,15, and 30 min) during each trial were 114 t 16,210 k 37,339 t 27,528 t 44, and 489 k 45 PM after 2,4,6,8, and 12 h of fasting, respectively. The mean plasma FFA concentration after 2 and 4 h of fasting was significantly lower than after 8 and 12 h (P < 0.05). In addition, the mean plasma FFA concentration after 2 h of fasting was lower than after 6 h (P < 0.05). There was an inverse relationship between the mean plasma FFA concentration and carbohydrate oxidation during exercise (Fig. 3).

PZasma glucose concentration. The length of fasting af- fected plasma glucose homeostasis during exercise (Fig. 4). Plasma glucose concentration was maintained during 30 min of exercise after 8 and 12 h of fasting. In contrast, plasma glucose concentration declined 17-21% during the first 15 min of exercise when subjects were fasted 2 h (P < 0.01). Plasma glucose concentration also declined (15-25%) during exercise in trained subjects when fasted 4 and 6 h (P < O.Ol), whereas the plasma glucose concentration did not decline during exercise in the untrained subjects. When the change in plasma glucose concentration during exercise (i.e., 15-min resting value) was calculated for each trial, the trained subjects had a signifi-

TABLE 3. SUmmay Of phna i?ZSdi?t COncentratiOn

for fasted trained and untrained subjects

Trained Untrained Length of

Fast, h 0 min 30 min 0 min 30 min

2 24.4t3.8" 11.1kl.l 44.9s3.3' 14.8k1.9 4 11.9t1.2 9.2kO.9 18.1k3.5 13.5-tl.9 6 14.5t3.0 10.2t1.3 13.1kO.9 10.9t0.6 8 9.8kO.9 8.6tl.l lO.lt0.9 10.6kl.O

12 10.7~1.0 9.321.8 11.7kl.O 8.7t0.8

Values are means t SE; n = 9 for trained and n = 8 for untrained. Plasma insulin concentrations were determined before (0 min) and after 30 min of exercise after subjects had fasted for different time intervals before exercise. * Significantly different from all other times, P < 0.01.


0.08

0.06

0.02 . I , . , . . . 1

0 2 4 6 8 10 12

Length of Fast (h)

FIG. 2. Relationship between the change (delta) in blood glycerol concentration during 30 min of exercise (i.e., 3O- to 0-min concentration) and length of fast for all subjects. Values are means t SE.

cantly greater fall in plasma glucose concentration than the untrained subjects when fasted 4 and 6 h (Fig. 5). None of the subjects displayed symptoms of hypoglycemia, and perceived exertion was not different when plasma glucose concentration declined during exercise.

Plasma glucose concentration during exercise at similar RER. The average RER during exercise was 0.94 t 0.01 and 0.95 t 0.01 in the trained and untrained groups, respectively, when the power output was adjusted to elicit a VO, associated with the onset of blood lactate accumulation (i.e., LT) during exercise. For the trained subjects this required increasing the power output to a work load that would elicit 78 t 1% of vo2 peak # In contrast, the untrained subject’s power output was lowered to 65 t 3% Of 7jo2 peak l

When the trained and untrained groups exercised at a similar RER during exercise, both groups had an equiva- lent decline (14%; P < 0.01) in plasma glucose concentration after 15 min of exercise (Fig. 6). Thus increasing the power output in the trained (78% VO, peak) and decreasing the power output in the untrained (65% vogpeak) group eliminated the difference between the two groups in their ability to maintain plasma glucose homeostasis during exercise after 4 h of fasting.

DISCUSSION

The present study was designed to systematically in- vestigate the effects of various lengths of fasting after a carbohydrate meal on carbohydrate oxidation, indexes of lipolysis, and plasma glucose homeostasis during moder- ately intense exercise. We found that 1) at least 6 h of fasting are necessary for carbohydrate oxidation to return to values similar to an S- to 12-h fast, 2) carbohydrate oxidation was inversely related to the plasma free fatty acid concentration, 3) the change in blood glycerol concentration during exercise was directly related to the length of the fast, 4) plasma glucose concentration declined during exercise at 70% Vogpeak when trained subjects fasted 2, 4, or 6 h and when untrained subjects fasted 2 h, and 5) the decline in plasma glucose concentration was exercise-intensity dependent inasmuch as plasma glucose concentration declined 14% in both the trained and untrained groups when the power output was

adjusted to elicit a similar RER during exercise 4 h after the carbohydrate meal.

The increase in carbohydrate oxidation above overnight fasting levels (i.e., S-12 h) during exercise after a preexercise meal may be from increased muscle glycogenolysis as a result of elevated muscle glycogen stores or from increased muscle glucose uptake and oxidation during exercise. In the present study, muscle glycogen concentration was not measured. However, it is unlikely that differences in muscle glycogen concentration were responsible for the elevation in carbohydrate oxidation after 2 and 4 h of fasting compared with 8-12 h. The subjects’ diet and activity were similar during the 24 h preceeding each trial, unlike our previous study (7), and only the length of fasting was different between trials. In addition, Knapik et al. (20) have reported no difference in muscle glycogen concentration with different lengths of fasting. It is therefore more likely that elevations in carbohydrate oxidation during exercise after 2-4 h of fasting were due to elevated muscle glucose uptake (2). Insulin secretion in response to a meal has the potential to increase carbohydrate oxidation by increasing muscle glucose uptake and/or reducing lipolysis. Our finding of a decline in plasma glucose concentration during exercise after 2 and 4 h of fasting agrees with the hypothesis that the preexercise meal may have elevated muscle glucose uptake and oxidation during exercise.

The elevated carbohydrate oxidation after 2 and 4 h of fasting was associated with a decreased plasma free fatty acid concentration (Fig. 3). The inverse relationship between carbohydrate oxidation and the plasma free fatty acid concentration when carbohydrate is fed at different time intervals before exercise suggests that the plasma free fatty acid concentration may be an important factor influencing muscle glucose uptake and carbohydrate oxidation during exercise. Rennie and Holloszy (24) have demonstrated in experiments with rat hindlimb perfu- sion that elevations in plasma free fatty acid concentration reduce skeletal muscle glucose uptake at rest and during muscle contraction. Whether the presently observed reduction in circulating plasma free fatty acid concentration in response to the preexercise meal was responsible for the elevation in carbohydrate oxidation 2

E 5 2.7

2.9

u

s

l s 2.5

i

:: 0 2.3 I 0

2.1

1

.

.

I

.

I , , I , . I .

0 100 200 300 400 500 60 0

FFA Concentration (PM) FIG. 3. Relationship between carbohydrate (CHO) oxidation and

plasma free fatty acid (FFA) concentration during exercise with different lengths of fasting for 5 subjects. Values are means + SE.


5.0

n z E 4.5

10 20 30

Time (min)

1 3.0 f m 1 I I I I 4

0 10 20 30

Time (min)

and 4 h after the meal cannot be directly determined from our data.

Glycerol accumulation in blood is reflective of adipose tissue lipolysis (30, 31). Therefore our observation that the change in blood glycerol concentration during exercise was linearly related to the length of fasting (Fig. 2) suggests that the effect of the preexercise carbohydrate meal on decreasing adipose tissue lipolysis is progres- sively diminished with time. To our knowledge, this is the first study to determine the relationship between elevations in plasma glycerol concentration during exercise and the length of fasting. Studies using a perfused isolated fat cell system have previously demonstrated that insulin can have a persistent inhibitory effect on epineph- rine-stimulated lipolysis (3, 28). Our results are also in agreement with studies that have reported greater increases in blood glycerol concentration during exercise after prolonged fasting (16-120 h) compared with 2-12 h of fasting (7,9,11,20). Interestingly, the assumed elevation of lipolysis (30) when the length of fast increased from 6 to 12 h had little effect on fat or carbohydrate oxidation. This observation emphasizes that the rate of lipolysis is not the only factor regulating plasma free

2h

4h 6h 8h

12h

FIG. 4. Influence of length of fasting before exercise and plasma glucose concentration during 30 min of exercise at 70% VO,- in trained (A) and untrained (B) subjects. Values are means t SE. *Significantly different from 8- and 12-h values (P < 0.05). tSignificantly less than 8-h values (P < 0.05).

~1 2h I 4h v 6h v 8h 1~ 12h

fatty acid concentration or fat oxidation (Figs. 2 and 3) and that other factors such as free fatty acid reesterifica- tion should be considered.

Both the trained and untrained subjects developed a relative hypoglycemia during exercise after 2 h of fasting. However, the trained subjects also had a decrease in plasma glucose concentration during exercise when fasted 4 and 6 h, whereas the untrained subjects maintained plasma glucose homeostasis during exercise after 4 and 6 h of fasting (Fig. 5). Because plasma glucose concentration reflects the balance between glucose output by the liver and glucose uptake by tissues, the fall in plasma glucose concentration during exercise after the preexercise meal was due to a reduction in glucose ap- pearance, increased glucose uptake by muscle, or both. Ahlborg and Felig (2) have previously demonstrated that a preexercise glucose meal can blunt liver glucose output and increase muscle glucose uptake during exercise at 30% of maximal 0, consumption (VO, ,,,).

The exercise intensity may be responsible for the different ability of the trained and untrained subjects to maintain euglycemia during exercise 4-6 h after ingest- ing the carbohydrate meal. During the first 15 min of


exercise at 70% VO 2 peak, initiated after 4 h of fasting, the trained subjects displayed a 25% reduction in plasma glucose concentration compared with only a 7% decline in the untrained subjects (Fig. 5). However, exercise at 70% VO2 peak aPP eared more metabolically stressful as re- flected by a significantly higher RER and blood lactate concentration for the untrained subjects than the trained subjects. When the power output was lowered to 65% . vo 2 peak 9 the untrained subjects also displayed a reduction in, plasma glucose concentration (i.e., 14%; Fig. 6). Thus the greater relative exercise stress for the untrained subjects at 70% v02peak may account for their better maintenance of plasma glucose concentration, probably due to more appropriate liver glucose output. It is unlikely that increased muscle glucose uptake was responsible for the decline in plasma glucose concentration when power output was decreased from 70 to 65% VO, peak in the untrained subjects, as glucose uptake decreases with decreased work rate (19, 25, 29).

The trained subjects demonstrated a similar relationship to that found in the untrained subjects between the relative exercise intensity and the magnitude of the decline in glucose concentration. When the trained subjects exercised at 70% of their VO, peak9 plasma glucose concentration declined 25% during the first 15 min of exercise (Fig. 5). However, when the exercise intensity was increased to 78% VO, peak) the plasma glucose concentration declined only 14% (Fig. 6). Thus the development of a relative hypoglycemia appears to be dependent on the intensity of exercise.

Not all investigators have reported a fall in plasma glucose concentration during the early minutes of exercise begun 3-4 h after a preexercise meal (l&21,22). One explanation for the divergent findings may be the carbohydrate content of the preexercise meal. In this investigation, subjects were fed 500-600 kcal of carbohydrate. In contrast, in the studies finding no change in plasma glucose homeostasis the subjects were fed 240-400 kcal of carbohydrate (18, 21, 22). A second explanation may be the relative exercise intensity. The study of Levine et al. (22) had subjects with Vo2,, values similar to those of our untrained subjects exercise for 30 min at 75%

0.5

Trained [7 Untrained

.

2h 4h 6h 8h 12h FIG. 5. Comparison of trained and untrained subjects regarding

change in plasma glucose concentration during O-15 min of exercise with different lengths of fasting before exercise. Values are means t SE. *Significant delta plasma glucose concentration (P < 0.05). tDif- ferent from untrained (P < 0.05).

T . - Tfained

n

sv Untrained

Time (min) FIG. 6. Plasma glucose responses in trained and untrained subjects

during 30 min of exercise at 78 and 65% VO, peak, respectively. Trials were conducted 4 h after meal. Values are means k SE. *Significantly less than preexercise glucose concentration (P < 0.01).

. vo 2 max. Thus the relatively high exercise intensity in the study of Levine et al. (22) may have prevented a decline in plasma glucose concentration during exercise.

In summary, our results demonstrate that at least 6 h of fasting are necessary after the consumption of a 5OO- to 600-kcal carbohydrate meal before carbohydrate oxidation and plasma glucose homeostasis during exercise at 70% VO 2 peak will be similar to an overnight fast (i.e., 12 h). Associated with the increase in carbohydrate oxidation and decline in plasma glucose concentration during exercise was a low plasma free fatty acid concentration. In addition, we found progressive increases in blood glycerol accumulation during exercise as the length of the fast increased from 2 to 12 h, suggesting that adipose tissue lipolysis during exercise responds directly and pro- portionately to the length of fast (i.e., 2-12 h). Finally, the magnitude of the decline in plasma glucose concentration during exercise was dependent on the relative exercise intensity.

We appreciate the technical assistance of John Beltz, Marc Hamil- ton, Cristine Heaps, Jose Gonzalez Alonso, and Jeff Horowitz.

This study was supported in part by the Louise Spence Griffeth Fellowship to the University of Texas at Austin.

Address for reprint requests: E. F. Coyle, Dept. of Kinesiology and Health, Belmont 222, The University of Texas at Austin, Austin, TX 78712.

Received 17 January 1990; accepted in final form 19 September 1990.

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Exercise metabolism at different time intervals after a meal