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Physical Education School, Endocrinology Unit, and Heart Institute, University of São Paulo 05508-900; and Brigadeiro Hospital, São Paulo 01401-901, Brazil
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
FOOTNOTES
REFERENCES
ABSTRACT 
Ramires, P. R., C. L. M. Forjaz, C. M. C. Strunz, M. E. R. Silva, J. Diament, W. Nicolau, B. Liberman, and C. E. Negrão. Oral glucose ingestion increases endurance capacity in normal and
diabetic (type I) humans. J. Appl.
Physiol. 83(2): 608-614, 1997.
The effects of an
oral glucose administration (1 g/kg) 30 min before exercise on
endurance capacity and metabolic responses were studied in 21 type I
diabetic patients [insulin-dependent diabetes mellitus
(IDDM)] and 23 normal controls (Con). Cycle ergometer exercise (55-60% of maximal
O2 uptake) was performed until
exhaustion. Glucose administration significantly increased endurance
capacity in Con (112 ± 7 vs. 125 ± 6 min,
P < 0.05) but only in IDDM patients
whose blood glucose decreased during exercise (70.8 ± 8.2 vs. 82.8 ± 9.4 min, P < 0.05).
Hyperglycemia was normalized at 15 min of exercise in Con (7.4 ± 0.2 vs. 4.8 ± 0.2 mM) but not in IDDM patients (12.4 ± 0.7 vs.
15.6 ± 0.9 mM). In Con, insulin and C-peptide levels were
normalized during exercise. Glucose administration decreased growth
hormone levels in both groups. In conclusion, oral glucose ingestion 30 min before exercise increases endurance capacity in Con and in some
IDDM patients. In IDDM patients, in contrast with Con, exercise to exhaustion attenuates hyperglycemia but does not bring blood glucose levels to preglucose levels.
exercise; substrates; hormones; insulin-dependent diabetes mellitus
INTRODUCTION THE METABOLIC EFFECT of preexercise glucose
administration has been studied in healthy subjects. Despite the
described negative effects of glucose-induced hyperinsulinemia and
depressed free fatty acids (FFA) levels during high-intensity exercise
on endurance capacity (11, 13, 16), some investigators have reported that glucose load before exercise does not affect exercise time to
exhaustion in healthy subjects (10, 14). Indeed, glucose represents an
exogenous energy source in subsequent prolonged exercise (1) and
improves exercise tolerance (12). However, the effect of
glucose load before prolonged exercise to exhaustion on
substrate-hormonal response and on endurance capacity in patients with
insulin-dependent diabetes mellitus (IDDM) has not been described.
Despite abnormal substrate utilization during exercise in diabetic
patients (5, 18, 26, 31, 33, 34), both the hyperglycemia, provoked by
glucose administration, and the enhancement in muscle blood flow,
caused by the increase and distribution of cardiac output during
exercise, may favor muscle glucose uptake and oxidation and,
consequently, improve endurance capacity in these patients. In a recent
study (25), we observed that dynamic leg exercise tolerance was
significantly lower in IDDM patients with no insulin administration 12 h before exercise compared with healthy subjects. Nonetheless, we found
that prolonged moderate-intensity exercise significantly decreased
blood glucose in IDDM patients.
Physiological changes that take place in healthy subjects before and at
the onset of exercise after glucose administration may not
be promptly operative in IDDM patients and may explain some metabolic
differences between healthy and IDDM subjects. Therefore, increased
understanding of the effect of glucose administration on
substrate-hormonal response and endurance capacity in young IDDM
patients has clinical implications and should be studied.
We hypothesized that preexercise glucose administration would improve
muscle glucose uptake and oxidation, reduce muscle glycogen utilization
during exercise, and, consequently, increase endurance capacity in
normal controls and in well-controlled IDDM patients.
In the present study, we investigated the effect of oral glucose
ingestion 30 min before moderate cycle exercise to exhaustion on the
metabolic and hormonal responses, as well as on endurance capacity, in
normal controls and IDDM patients from whom insulin was withheld 12 h
before exercise.
METHODS
Table 1.
Physical and functional characteristics of IDDM patients and normal
controls
Diabetic (n = 21)
Control
(n = 23)
Age, yr
23 ± 1.0
23 ± 0.5
Weight, kg
66 ± 1.9
68 ± 1.6
Height, cm
172 ± 1.6
176 ± 1.3
Body mass index, kg/m2
22 ± 0.5
22 ± 0.4
Maximal heart rate,
beats/min
187 ± 3
187 ± 2
Maximal systolic
blood pressure, mmHg
201 ± 5
194 ± 4
Maximal workload, W
196 ± 8
208 ± 5
O2 max,
ml · kg
1 · min1
39 ± 1.2
40 ± 0.8
Values are means ± SE; n, no. of subjects. IDDM,
insulin-dependent diabetes mellitus;
VO2 max, maximal O2 uptake.
O2 max) were
determined at the maximal workload achieved during a maximal exercise
test on an electrically braked cycle ergometer (Standart Lannoy
Ergometer, Godart-Statham, Bilthoven, Holland) with 50-W
increments every 3 min until the subjects reached exhaustion (Table
1).
Exercise tolerance protocol.
All subjects were studied in the morning after an overnight fast (12 h), and insulin was withheld 12 h before the test in the IDDM patients.
The studies were carried out on 2 different days, with 7 days
intervening. All subjects performed two bouts of moderate leg exercise
to exhaustion (55-60% of
O2 max) on an
electrically braked cycle ergometer. Oral glucose (Dextrosol, 1 g/kg)
or placebo (saccharine) solutions were randomly administered in a
double-blind fashion 30 min before exercise. In the normal control
group, 13 subjects performed exercise with placebo first and 10 with
glucose first. In the IDDM group, 10 patients took placebo first and 11 took glucose first.
Ninety minutes before exercise (
90 min), a catheter for blood
sampling was placed in the forearm vein of subjects resting in supine
position. As shown in Fig. 1, blood samples
were obtained at preingestion fasting (30 min); at postingestion
resting (0 min); at 15, 30, and 60 min of exercise; and at exhaustion.
Exhaustion was defined as the time when the subject could no longer
maintain 60 revolutions/min pedaling for 10 s. Heart rate, blood
pressure, and expired air samples were obtained simultaneously with
blood samples.
, Glucose or placebo ingestion; *,
blood samples; EX, exercise to exhaustion.
The mean exercise workload performed during exercise tolerance test was 95 ± 3 and 99 ± 2 W for the IDDM patients and normal controls, respectively, and corresponded to 58 ± 2 and 57 ± 2% of the
O2 max.
Cardiovascular and respiratory analyses.
Samples of expired air collected in meteorological balloons during the
exercise tolerance protocol were analyzed for
O2 and CO2 fractions by Scholander
microtechnique (29) (Godart-Statham). Minute ventilation was measured
by Tissot spirometer (Godart-Statham) and rates of oxygen consumption
(O2) and carbon dioxide
output (CO2) were
calculated from these data. The respiratory exchange ratio (RER) was
calculated as
O2/CO2.
Heart rate was continuously monitored by electrocardiogram (model
7830A; Hewlett-Packard, Waltham, MA), and blood pressure was measured
by a sphygmomanometer (model 980; Oftec, São Paulo, Brazil).
Biochemical analyses.
Colorimetric microdetermination was used to analyze serum FFA levels
(24). Commercial enzymatic kits were used for serum glucose (Glicose;
Abbott, São Paulo, Brazil) and plasma lactate (Monotest Lactato;
Merck, Rio de Janeiro, Brazil) analyses. Commercial radioimmunoassay
kits were used for plasma glucagon (Radioassay System, Anaheim, CA),
serum cortisol (Clinical Assay), C peptide (Serono, Milano, Italy), human growth hormone (GH; Pharmacia
Diagnostic, Uppsala, Sweden), and insulin (Pharmacia
Diagnostic). Intra-assay and interassay variation
coefficients for hormone analyses were, respectively, 10 and 8% for
glucagon, 3.5 and 6.0% for cortisol, 6.2 and 14.8% for C
peptide, 4.3 and 7.5% for GH, and 3.6 and 7.5% for insulin.
Statistical analysis.
Data were subject to three-way analysis of variance (ANOVA) with
repeated measures (Bio-Medical Data Processing, 1985, University of California, Los Angeles, CA). A Pearson correlation
coefficient analysis was used to verify the relationship between the
endurance capacity and the change (
) of glucose levels
during exercise within the IDDM patients. Scheffé's post hoc
test was used to locate significant differences.
P < 0.05 was accepted as being statistically significant. Data are presented as means ± SE.
RESULTS
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0.58, P < 0.05) between endurance capacity (in min) and glucose levels
(exhaustion levels minus resting levels, in mM) during exercise was
observed. These data showed that, in fact, there were two subgroups of
IDDM patients: 1)
patients whose glucose levels decreased during exercise to exhaustion
(n = 12) and
2) patients whose glucose levels did
not decrease during exercise to exhaustion
(n = 7). Further ANOVA between these
two subgroups of IDDM patients (Table 3)
showed that preexercise glucose ingestion significantly increased
endurance capacity by 16.9% (P < 0.05) in the diabetic patients whose glucose levels decresed during
exercise to exhaustion and did not significantly change endurance
capacity [3.89%, not significant (NS)] in the diabetic
patients whose glucose levels did not decrease during exercise.
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O2 max)] on
respiratory exchange ratio (RER) at rest and during exercise to
exhaustion in insulin-dependent diabetes mellitus (IDDM) patients with
insulin withheld 12 h before exercise and in normal controls. Data are
means ± SE. P < 0.05:
* vs. control group, 
vs. placebo, 
vs.
30 min, § vs. 0 min, # vs. 15 min of
exercise, and & vs. 60 min
of exercise.
Substrates. Glucose levels were significantly higher in the IDDM patients compared with the normal controls at preglucose fasting (8.3 ± 0.7 vs. 5.1 ± 0.1 mM, respectively) and throughout the exercise (Fig. 3). Exercise to exhaustion after placebo caused no significant change in glycemia in the normal controls, but it provoked a significant decrease in glycemia (from 8.3 ± 0.7 to 6.4 ± 0.8 mM) in the IDDM patients compared with fasting values. Glucose administration significantly increased resting glycemia in both IDDM patients (from 8.3 ± 0.7 to 12.4 ± 0.7 mM) and in normal controls (from 5.1 ± 0.1 to 7.4 ± 0.2 mM). In the normal controls, glycemia had returned to fasting levels at 15 min of exercise and was maintained at a steady state until exhaustion. However, in the IDDM patients, glycemia was higher during all exercise periods compared with placebo trial. Although glycemia significantly decreased after 60 min of exercise, it was still significantly higher at exhaustion compared with fasting levels (12.1 ± 1.1 vs. 8.3 ± 0.7 mM, respectively).
O2 max) on glucose, lactate, and free fatty acid (FFA) concentrations at rest and during
exercise to exhaustion in IDDM patients with insulin withheld 12 h
before exercise and in normal controls. Data are means ± SE.
P < 0.05: * vs. control group,
vs. placebo, vs. 30 min, § vs. 0 min,
# vs. 15 min of exercise,
and & vs. 60 min of
exercise.
Fasting lactate levels and exercise-induced enhancement of lactate levels at 15 and 30 min of exercise were not significantly different between the two groups studied (Fig. 3). In the normal controls, lactate levels significantly decreased from 2.5 ± 0.2 mM at 30 min of exercise to 1.9 ± 0.1 mM at exhaustion. In the IDDM patients, lactate levels did not decrease at exhaustion and were significantly higher than in normal controls (2.8 ± 0.2 vs. 1.9 ± 0.1 mM, respectively). During all experimental procedures, glucose administration did not significantly change lactate levels in either the IDDM patients or the normal controls. Fasting serum FFA levels were similar between the two groups studied (Fig. 3). In the normal controls, glucose administration compared with placebo trial significantly decreased FFA levels at rest (0.30 ± 0.02 vs. 0.19 ± 0.02 meq/l), at 15 min of exercise (0.35 ± 0.04 vs. 0.11 ± 0.01 meq/l), at 30 min of exercise (0.43 ± 0.04 vs. 0.13 ± 0.01 meq/l), and at 60 min of exercise (0.59 ± 0.05 vs. 0.21 ± 0.02 meq/l). Although FFA levels in the normal controls significantly increased at exhaustion when compared with 60 min of exercise (from 0.21 ± 0.02 to 0.90 ± 0.11 meq/l), these levels were still significantly lower than those in the placebo trial (1.18 ± 0.11 meq/l). In the IDDM patients, glucose administration did not significantly change FFA levels either at rest or during all exercise periods. After glucose administration, FFA levels were significantly higher at exhaustion compared with fasting (0.50 ± 0.06 vs. 0.29 ± 0.04 meq/l, respectively), but these levels were not significantly different from placebo. Indeed, in the glucose trial, FFA levels at exhaustion were significantly lower in the IDDM patients compared with normal controls (0.50 ± 0.06 vs. 0.90 ± 0.11 meq/l, respectively). Hormones. Serum insulin levels were analyzed only in the normal controls (Fig. 4). Glucose administration significantly increased insulin levels at rest (from 10 ± 0.0 to 68 ± 8.2 µU/ml). A 15-min period of exercise significantly decreased insulin levels (to 21 ± 1.7 µU/ml) compared with postglucose resting levels (68 ± 8.2 µU/ml), but these levels were still higher than placebo levels (11 ± 1.1 µU/ml). At exhaustion, insulin levels had returned to fasting and placebo levels.
O2 max) on insulin, C peptide, and glucagon concentrations at rest and during
exercise to exhaustion in IDDM patients with insulin withheld 12 h
before exercise and in normal controls. Data are means ± SE.
P < 0.05: * vs. control group,
vs. placebo, vs. 30 min,
§ vs. 0 min,
# vs. 15 min of exercise,
and & vs. 60 min of
exercise.
Serum C peptide was significantly lower in the IDDM patients compared with normal controls at fasting (0.2 ± 0.04 vs. 1.3 ± 0.05 ng/ml, respectively) and during all exercise periods (Fig. 4). Neither glucose administration nor exercise had any effect on C-peptide levels in the IDDM patients. As expected, glucose administration significantly increased C-peptide levels (to 4.0 ± 0.30 ng/ml) in the resting state in the normal controls. During exercise, C-peptide levels gradually decreased, and at exhaustion they returned to placebo levels. Plasma glucagon levels were significantly higher in the IDDM patients compared with normal controls at fasting (264 ± 38 vs. 115 ± 15 pg/ml) and during all exercise periods (Fig. 4). In the normal controls, glucagon levels significantly increased (to 171 ± 14 pg/ml) at exhaustion compared with fasting, and glucose administration did not change glucagon levels during exercise. In the IDDM patients, glucagon levels were significantly higher during all experiments in the glucose trial, and the exercise-induced enhancement of glucagon levels was similar in both glucose and placebo trials. Fasting serum cortisol levels were similar between the two groups studied (Fig. 5). Cortisol levels significantly increased at exhaustion compared with fasting in both the IDDM patients (19 ± 1.7 vs. 13 ± 1.1 µg/dl, respectively) and normal controls (20 ± 1.7 vs. 12 ± 1.0 µg/dl, respectively). Glucose administration had no significant effect in the exercise-induced enhancement of cortisol in both groups.
O2 max) on cortisol and
growth hormone (GH) concentrations at rest and during exercise to
exhaustion in IDDM patients with insulin withheld 12 h before exercise
and in normal controls. Data are means ± SE.
P < 0.05: * vs. control group,
vs. placebo, vs. 30 min,
§ vs. 0 min, and
# vs. 15 min of
exercise.
Fasting serum GH levels were not significantly different between the two groups studied (Fig. 5). A 30-min period of exercise significantly increased GH levels in both the IDDM patients (from 3 ± 0.6 to 8 ± 1.7 ng/ml) and normal controls (from 2 ± 0.5 to 12 ± 3.0 ng/ml). Glucose administration significantly inhibited the exercise-induced enhancement of GH levels when compared with placebo, and these levels were significantly lower in the IDDM patients compared with the normal controls at 60 min of exercise (13 ± 2.3 vs. 20 ± 4.6 ng/ml, respectively) and at exhaustion (12 ± 2.2 vs. 22 ± 4.5 ng/ml, respectively).
DISCUSSION
There are three main findings of the present investigation. 1) Preexercise glucose administration significantly increases endurance capacity in normal controls. 2) Preexercise glucose administration significantly increases endurance capacity in a subgroup of IDDM patients whose blood glucose levels decrease during exercise. 3) Cycle ergometer exercise for 15 min normalizes glycemia levels after glucose load in normal controls but not in IDDM patients, whose blood glucose levels are still increased at exhaustion.
Glucose administration increased C-peptide levels only in the normal controls, showing that our IDDM patients were, in fact, in the diabetic state. Furthermore, withholding of insulin 12 h before exercise excluded a hyperinsulinemic state before and during exercise in diabetic patients. Indeed, the glycosylated hemoglobin levels <12%, the absence of ketosis, the similarity of FFA and GH levels at resting state, and the similarity of cortisol and GH responses during exercise between IDDM patients and normal controls demonstrated that our IDDM patients were well controlled and had a normal counterregulatory response to moderate exercise (3).
We hypothesized that preexercise glucose administration, by improving muscle glucose uptake and oxidation and also by reducing muscle glycogen utilization during exercise, would increase endurance capacity in normal controls and in well-controlled IDDM patients. Actually, preexercise glucose administration did increase endurance capacity in normal controls and in IDDM patients. However, the increase in endurance capacity was only observed in IDDM patients whose glucose levels decreased during exercise.
Some investigators (11, 13, 16) have reported a negative effect of
hyperinsulinemia after glucose loading 30-45 min before
high-intensity prolonged exercise in healthy subjects because hyperinsulinemia provokes early hypoglycemia, increases
muscle glycogen utilization, and reduces endurance performance. On the contrary, and in agreement with other investigators (10, 12, 14), our
results did not show any hypoglycemic state during all the exercise
periods in normal controls. Moreover, endurance capacity was increased
by 11.2% in normal controls. Chryssanthopoulos et al. (10) showed that
glucose load 30 min before intense running exercise (70% of
O2 max) did not reduce
endurance performance in recreational runners. Devlin et al. (12) found
that ingestion of a mixed macronutrient snack (43 g glucose, 9 g fat,
and 3 g protein) significantly increased plasma glucose and insulin
concentrations before exercise but did not reduce endurance performance
or increase muscle glycogen depletion during high-intensity cycle
exercise (70% of
O2 max) in untrained
healthy humans.
Increased FFA levels, decreased lactate levels, and decreased RER values as exercise was prolonged to exhaustion are indicative of decreased muscle glycolysis (27) and increased hepatic lactate uptake (2, 34). These metabolic adaptations that take place at the latter stage of prolonged exercise in the present study show a shift from carbohydrate to lipid metabolism as muscle energy supply and may explain, in part, the benefit of preexercise glucose administration on endurance capacity in healthy humans performing a moderate-intensity dynamic exercise.
It has been suggested that exogenous carbohydrate load during
prolonged cycle exercise (70% of
O2 max) increases
work capacity by attenuating the muscle glycogen-depletion rate and
reversing the decrease in hexose monophosphate and tricarboxylic acid
cycle intermediates in skeletal muscle supplied with blood glucose in the latter stage of exercise (30). Indeed, by increasing muscle glucose
uptake and oxidation (1, 17), the described synergistic effect of
higher glucose and insulin levels at the onset of exercise seems to
compensate for the decreased FFA oxidation during exercise in normal
controls.
The increased endurance capacity after glucose ingestion in the IDDM patients whose blood glucose levels decreased during exercise has physiological implications. First, this longer period of exercise requires an increase of 7,500 ml in oxygen consumption or an increase of 37.3 kcal in caloric expenditure in IDDM patients. Second, this additional increase in metabolic rate is provided, at least in part, by blood glucose metabolism, because blood glucose levels were reduced in those IDDM patients who showed a significant increase in endurance capacity.
The present study does not clarify the mechanisms underlying the increase in endurance capacity in IDDM patients after preexercise glucose administration. Nonetheless, the physiological adaptations that take place during exercise give us some insights into this issue. The enhancement of cardiac output and, consequently, the increased muscle blood flow may favor muscle glucose uptake during exercise. Indeed, the increase in glucose mass action on the muscle membrane, in concert with a more sensitive receptor, may improve muscle glucose uptake during prolonged exercise even in IDDM patients.
Interestingly, however, endurance capacity did not increase in all diabetic patients studied. In fact, our data showed that there are two subgroups of IDDM patients: 1) those in whom preexercise glucose ingestion significantly increased endurance capacity and 2) those in whom preexercise glucose ingestion did not increase endurance capacity. The different responses to exercise between these two groups is not clear, but it is a very interesting topic for future studies.
In the normal controls, hyperglycemia was normalized after a short 15-min exercise period. On the other hand, in the IDDM patients, blood glucose levels significantly decreased only at latter stages of exercise, and this reduction was not sufficient to bring blood glucose levels to preglucose-ingestion levels. In IDDM patients, the related exercise effects of increasing leg glucose uptake (34) and decreasing glycemia (25) seem to be quite limited compared with the effects in healthy subjects, and, according to our data, differ even among between well-controlled IDDM patients. The limited muscle blood flow (21), the decreased pyruvate dehydrogenase activity (4, 6, 15, 20, 22) and the increased lactate dehydrogenase activity in diabetic subjects (28) may have predisposed our IDDM patients to a greater anaerobic metabolism (increased lactate production) and, consequently, early fatigue. Despite the augmented hepatic gluconeogenesis rate in diabetic subjects (32), the lower endurance capacity observed in the IDDM patients may have limited the hepatic lactate uptake during exercise. Indeed, the absence of decreasing lactate levels in the IDDM patients as exercise continued to exhaustion suggests that in these patients muscle glycogen represents an important energy supply for exercising muscle during all exercise periods.
In agreement with previous studies (1, 7, 10, 11, 13, 14, 16, 19), preexercise glucose load in normal controls significantly reduced FFA levels at rest and during all exercise periods. Taken together, the hyperglycemia and hyperinsulinemia in the early stages of exercise and the lowered GH but not cortisol levels during all exercise periods could suggest that glucose, insulin, and GH levels would play a role in the FFA mobilization during exercise. In the IDDM patients, however, glucose load provoked hyperglycemia and decrease in GH levels but no change in FFA levels during exercise. Therefore, we conclude that, in fact, insulin is the major inhibitory factor of FFA mobilization during exercise in humans.
The exercise-induced enhancement of glucagon levels found in the present study in both groups studied might be catecholamine mediated, because neither IDDM patients nor normal controls showed any hypoglycemic state during all exercise periods. In IDDM patients, the rise in glucose levels in the glucose trial did not suppress glucagon release during exercise but, in contrast, elicited a paradoxical increase in this hormone, as previously reported by other investigators (9). The greater glucagon response in the IDDM patients was probably due to a loss of the restraining influence of insulin on glucagon secretion. In normal controls, despite the fact that glucose load caused significant increases in glucose and insulin levels, no restraining of glucagon levels during exercise was observed. It seems that in normal controls the neurotransmitted signals during exercise may overcome the glucose and insulin effect on glucagon release during exercise.
Although we have not measured free insulin concentration in the IDDM patients, both the absence of an abrupt blood glucose reduction in the early stage of exercise with placebo and the increased blood glucose during up to 60 min of exercise in the glucose trial confirm that our IDDM patients were not in a hyperinsulinemic state during the experimental procedures.
The motivation for exercise up to exhaustion could be different between the 2 experimental days. The experimental conditions under glucose or placebo administration were well controlled (see METHODS). During prolonged exercise, pedaling was continuously monitored by the same investigator (P. R. Ramires). Indeed, the subjects were asked to perform the exercise as long as they could, and the exhaustion state was only accepted when they pointed to number 10 on Borg's scale (8) and could no longer maintain pedaling at 60 revolutions/min for 10 s.
In conclusion, oral glucose ingestion 30 min before exercise improves
endurance capacity in young normal controls and in a subgroup of
well-controlled IDDM patients whose glucose levels decrease during
exercise. Despite the fact that cycle ergometer exercise performed to
exhaustion (55-60% of
O2 max) attenuates hyperglycemia provoked by glucose administration in young IDDM patients
with no insulin administration for 12 h, it fails to normalize serum
glucose levels in these patients.
ACKNOWLEDGEMENTS
The authors are grateful to Dr. Holly R. Middlekauff for critical review of this manuscript.
FOOTNOTES
Address for reprint requests: P. R. Ramires, Univ. of Wisconsin, Madison, School of Education, Dept. of Kinesiology, Rm. 1149, Gym. Unit II, 2000 Observatory Dr., Madison, WI 53706-1189 (E-mail: ramires{at}gandalf.physed.wisc.edu).
Received 21 June 1996; accepted in final form 4 April 1997.
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