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Laboratory of Exercise Physiology, Faculty of Health and Sports Science, Fukuoka University, Fukuoka 814-0133; Department of Community Health Science, Saga Medical School, Saga 849-8501; and Laboratory of Biochemistry of Exercise and Nutrition, Institute of Health and Sport Sciences, University of Tsukuba, Tsukuba, Ibaraki 305, Japan
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The effect of a
single bout of mild exercise on glucose effectiveness
(SG) and insulin sensitivity
(SI) was studied in six young
male subjects by using a minimal model. An intravenous glucose tolerance test was performed under two conditions as follows: 1) 25 min after a bout of exercise
on a cycle ergometer at the lactate threshold level for 60 min (Ex) and
2) without any prior exercise (Con).
Leg blood flow (LBF) was also measured by strain-gauge plethysmography
simultaneously with blood sampling.
SI did not significantly change
after exercise (18.1 ± 1.5 vs. 17.7 ± 1.9 × 10
5 min/pM), whereas
SG significantly increased (0.016 ± 0.002 vs. 0.025 ± 0.002 min
1,
P < 0.01). The increased blood flow
after exercise remained high during the time period for measurement of
the glucose disappearance constant and may be a determinant of
SG. The incremental lactate area
under the curve until insulin loading was also significantly higher in
Ex than in Con (2.6 ± 0.9 vs. 3.5 ± 1.5 mM/min,
P < 0.05). These results suggest
that increased SG after mild
exercise may be due, at least in part, to increased LBF and lactate
production under a hyperglycemic state.
insulin sensitivity; minimal model; mild exercise
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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GLUCOSE EFFECTIVENESS (SG), which is analyzed by the minimal model technique, is defined as the effect of glucose per se to normalize its own concentration at basal insulin concentration and is a major determinant of glucose tolerance as well as insulin sensitivity (SI) (7). A recent report on the minimal model suggested that decreased SG might be associated with the development of non-insulin-dependent diabetes mellitus (NIDDM) rather than decreased SI (35). Therefore, increasing SG may be very important because preservation of SG might serve to prevent the development of NIDDM.
Acute exercise is well known to transiently enhance SI in untrained subjects with or without diabetes (20, 30). As far as we know, three studies have studied SG after a single bout of exercise (11, 19, 32); however, the findings are not consistent. Pestell et al. (32) observed no change in SI and SG 2 h after a strenuous ultramarathon run. We have recently reported no change in SG 11 h after mild, hard, and exhaustive exercise (19). On the other hand, Brun et al. (11) reported that SG and SI showed a marked increase 25 min after short-term exercise at 85% of maximal heart rate by using a reduced-sample protocol. A possible explanation for the discrepancies among these results may be the great variability among the exercise intensity, duration, and the time of the intravenous glucose tolerance test (IVGTT) or different methodologies.
Glucose uptake in the postexercise state may be influenced by the time of the IVGTT, because Ivy et al. (21) showed that glucose uptake immediately postexercise caused a 300% increase in the rate of glycogen storage above basal levels during the first 2 h of recovery and a 180% greater rate of storage above basal than in the second 2 h of recovery. If the time of the IVGTT was set more immediately after exercise, even more mild-intensity exercise, such as at the lactate threshold level (LT), would be expected to improve glucose uptake, because several reports have suggested that low-intensity exercise as well as high-intensity exercise improves glucose tolerance (9, 10, 41). We therefore designed this study to determine whether LT-intensity exercise improves SG immediately postexercise.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects.
Six male subjects participated in the present study after giving their
informed consent. Subjects had no family history of diabetes or
hypertension and were not insulin resistant on the basis of homeostasis
model assessment (29). The mean homeostasis model assessment value was
0.81 ± 0.04 (range, 0.74-0.95). The subjects' characteristics
are summarized in Table 1. Body composition was measured
by hydrostatic weighing, corrected for residual lung volume (15). The
subjects were instructed to abstain from strenuous exercise until the
end of the experiment.
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Preliminary testing.
Maximal oxygen consumption
(
O2 max) was
determined on an electrically braked cycle ergometer by using an
incremental exercise protocol; after the subjects cycled at a steady
work rate of 10 W for 4 min, the work rate continued and increased
gradually by 20 W every 4 min until the subject was unable to continue.
Blood samples from the earlobe were obtained just before the end of each stage to determine the blood LT (5, 19). The blood lactate concentrations were plotted against the workload. The LT as the initial
break point for blood lactate was determined by visual inspection. The
average of the LT determined blindly by three experts was used for
exercise intensity.
Experimental design.
Subjects consumed a meal containing 57% carbohydrate, 15% protein,
and 28% fat calories at 6:00- 7:00 PM on the evening previous to
each IVGTT. A 12- to 13-h fast was imposed on the subjects. They stayed
at the laboratory one night before each IVGTT and woke at 7:00 AM. An
18-gauge catheter was placed in an antecubital vein in one arm for
blood sampling, and a similar catheter was placed in the opposite arm
for administration of intravenous solutions; patency of the catheters
was maintained with an infusion of saline (40-50 ml/h) throughout
the experiment. Leg blood flow (LBF) was measured for the resting state
three times before exercise. Subjects exercised on a cycle ergometer
for 60 min at LT intensity (45.4 ± 3.1% of
O2 max). Heart rate
and the rate of perceived exertion were recorded during exercise. Heart
rate during exercise was 115 ± 4, 119 ± 5, 121 ± 5, 122 ± 5, 127 ± 4, and 130 ± 5 beats/min at 10, 20, 30, 40, 50, and 60 min, respectively, and the subjects registered
their rate of perceived exertion as between "fairly light" and
"somewhat hard." The IVGTT was performed 25 min postexercise or
without any prior exercise. In brief, three baseline samples were taken
at 10, 15, and 20 min after exercise. At minute
25, glucose (300 mg/kg body wt) was administered
intravenously within 2 min, and subsequent blood samples were taken
from the contralateral antecubital vein at 28, 29, 30, 31, 33, 35, 37, 39, 41, 44, 47, 49, 51, 53, 55, 58, 61, 65, 75, 85, 95, 105, 125, 145,
165, 185, and 205 min. An additional infusion of insulin (Humalin,
Shionogi, Osaka, Japan) was administered (20 mU/kg) via the antecubital vein from 45 to 50 min. Two IVGTTs were scheduled in a randomized design and were separated by at least 1 wk.
LBF. The knee joint was bent slightly, and supporting pillows were placed under the thigh and Achilles tendon. A mercury rubber strain gauge (Vasculab, Medasonics) was wrapped around the calf at the level of the widest circumference. The relative change in the volume of the calf segment under the strain gauge was registered on a chart recorder and was used for calculations of plethysmographic blood flow according to the principle outlined by Whitney (39), including calibration. The occlusion cuff was placed around the thigh. The cuff pressure used was 50 mmHg. LBF was measured simultaneously with blood sampling during the IVGTT.
Analytic methods. Plasma glucose concentrations were measured in triplicate spectropotometrically with glucose oxidase (glucose B test, Wako Pure Chemical, Osaka, Japan). The measurement error of glucose was assumed to be "white," with a Gaussian value of zero mean and a coefficient of variation of 1.5%. Immunoreactive insulin was measured in duplicate by using a Phadeseph insulin radioimmunoassay kit (Shionogi, Osaka, Japan). Coefficients of variation were 4% for >180 pM insulin and 7% for <180 pM insulin. Blood lactate was measured by flow-injection analysis with the use of immobilized enzyme (lactic oxidase) columns with detection through chemiluminescence (Shimadzu CL-760, Kyoto, Japan) (34). The coefficient of variation of this assay was within 2% of the established standard lactate solutions (1.0-10.0 mmol/l).
Data analysis. The glucose disappearance constant (KG) value was calculated as the slope of the least squares regression line relating the natural logarithm of the glucose concentration to time from five samples drawn between 10 and 19 min. Endogenous plasma insulin responses were expressed as the area under the insulin curve during the first 10 min, calculated by using the trapezoidal method (14). The area under the lactate curve was determined by using the trapezoidal method for 20 min before the insulin injection or the period after the insulin injection.
SI and SG were estimated by the minimal model approach (6-8, 12, 35). In this analysis, fluctuations in circulating glucose levels over time are described by the following differential equations: dG(t)/dt =p1[G(t) Gb] X(t)G(t)
and
dX(t)/dt = p2X(t) + p3[I(t) Ib], where
G(t) is the plasma glucose
concentration, I(t) is the plasma
insulin concentration, and Gb and
Ib are baseline concentrations;
p1,
p2, and
p3 are model
parameters; and
X(t) represents the time course of the peripheral insulin effects (expressed as min1).
X(t)
is increased by
p3 in proportion
to the change in plasma insulin above the basal level and decreases by
a first-order process proportional by
p2 to
X(t)
itself. Parameter
p1 represents the effect of glucose per se, at basal insulin, to normalize its own concentration in plasma independent of increased insulin. This parameter, known as SG, has been
verified through comparison with studies in which the insulin secretory
response in normal dogs was suppressed with somatostatin infusion (1)
or in which insulin-dependent diabetes mellitus patients received basal
insulin infusion during IVGTT (37).
SG is comprised of the following
two components: a non-insulin-dependent component and a basal insulin
component. The basal insulin component of
SG (BIE) can be calculated as the product of Ib and
SI: BIE = Ib × SI (24). Therefore, the
contribution of the non-insulin-dependent component
(SG at 0 insulin, GEZI) is the
difference between total SG and
BIE: GEZI = SG (Ib × SI) (24). The
p3-to-p2
ratio defines the SI index, which
represents the increase in the net glucose disappearance rate dependent
on a rise in insulin above basal. The
SI index has been validated by
comparison with a direct measure of
SI from glucose-clamp experiments in humans (4, 12). The minimal model program was written in Pascal
(Borland, Scotts Valley, CA) on a Macintosh IIcx (Apple Computer,
Cupertino, CA) as described previously (14, 35).
Statistics. Results are presented as means ± SE. Statistical comparison between control and exercise conditions was performed by Student's t-test. P < 0.05 was considered significant.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Neither basal plasma glucose nor plasma insulin concentrations before
IVGTT showed a significant difference between control and exercise
conditions (Table 2). The plasma glucose,
insulin, and lactate concentrations during IVGTT are illustrated in
Fig. 1. The plasma glucose concentration is
significantly lower in the exercise condition than in the control
condition at 26, 28, 30, 36, 40, and 50 min, respectively
(P < 0.05, Fig. 1). No significant difference in the plasma insulin concentration was observed between both conditions. The plasma lactate concentration gradually increased in both conditions after glucose loading. The incremental lactate area
under the curve before insulin injection was significantly higher in
the exercise condition than in the control condition (2.6 ± 0.9 vs.
3.5 ± 1.5 mM/min, P < 0.05)
but not after injection.
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KG was
significantly higher in the exercise condition than in the control
condition (Table 2). There was no significant difference in the
integrated area of plasma insulin between conditions (Table 2).
SI did not significantly change
after exercise (Table 2, Fig.
2).
SG is significantly higher after
exercise than in the control condition
(P < 0.05, Table 2, Fig. 2). LBF was
significantly higher in the exercise condition than in the control
condition (at 8, 14, and 16 min, P < 0.05, Fig. 3). During the corresponding time (10-19 min) for calculation of
KG, LBF in the
exercise condition was significantly higher than in the control
condition (P < 0.05, Fig.
4).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The major finding of the present study was that mild exercise at the LT leads to a marked increase in SG immediately postexercise. We have previously shown that endurance- or strength-trained athletes, respectively, have higher SG than do sedentary subjects (13, 36). In the present study, an increase in SG immediately after a single bout of mild exercise is similar to the level in trained subjects.
The five comparable studies on non-insulin-mediated glucose uptake (2, 11, 19, 28, 32) have reported inconsistent findings. Marin et al. (28) examined the effect of glycogen-depleting exercise on hyperglycemic clamp-derived glucose uptake in premenopausal women. In this study, non-insulin-mediated glucose uptake was not increased 24 h after exercise, but insulin-mediated glucose uptake was increased. We have recently reported that SG was not increased in sedentary subjects 11 h after three types of exercise (exercise at LT, exercise at 4-mM lactate level, or exhaustive exercise), whereas SI was increased only after exhaustive exercise (19). Pestell et al. (32) studied the effect of a strenuous ultramarathon run on glucose tolerance 2 h after exercise in highly trained subjects, but both SG and SI were not significantly increased. However, SG in the present study was increased 25 min after exercise, in agreement with the finding by Brun et al. (11). They found that SG was increased 25 min after exercise at 85% of maximum heart rate (11). Taken together, these findings indicate that the effect of a single bout of exercise on SG could rapidly decreased in a time-dependent way.
Araujo-Vilar et al. (2) have demonstrated that there was a significant
45% increase in SG during
exercise at 50% of
O2 max, which is
similar to the exercise intensity of our study. Our
findings show similar increases in
SG even after exercise compared
with their study. The increased SG
is due to either the increased glucose disposal in tissue or an
augmented effect to suppress hepatic glucose production. Possible
residual effects of the exercise that may cause increased
SG are increased blood flow or
increased glucose transporter in the plasma membrane.
Hespel et al. (18) showed that glucose uptake in muscle is stimulated by increased blood flow in the absence of insulin. In this study, we found that increased blood flow in skeletal muscle, a major site of glucose disposal, remains significantly elevated until the corresponding time to determine KG that is significantly correlated to SG (25). Thus we speculated that the increased blood flow, which enhances glucose delivery to peripheral tissue, may contribute to the increased SG. In addition to the increase in blood flow, our results show an increase in the integrated blood lactate area during the same period, suggesting that a significant component of SG can be derived from the metabolism of glucose to lactate (38).
Goodyear et al. (16) reported that 30 min after exercise both the number of plasma membrane glucose transporters and glucose transport activity remain elevated (1.6- and 1.8-fold above baseline, respectively), even though glycogen concentrations had returned to baseline concentrations. This may also contribute to the increased SG. In addition, the effect of exercise on hepatic glucose production may be a reason for the change in SG. Further study is needed to clarify these topics by using the stable-labeled, minimal model approach.
It is well known that a single bout of exercise causes an increase in
SI (19, 28, 30). Brun et al. (11)
also demonstrated that SI as well
as SG were significantly increased
immediately after exercise at 85% of maximum heart rate (70-80%
of O2 max, as predicted
by age). In contrast to these studies, we observed no significant
increase in SI immediately after
mild exercise at LT intensity (45.4 ± 3.1% of
O2 max) for 60 min. The
reasons for this discrepancy remain obscure, but the differences in
exercise intensity may contribute to the contradictory results. The
factor responsible for the increase in
SI could be an increase in
capillary insulin transport and/or an increase in insulin action at the target cell (7). Yang et al. (40) have shown that transcapillary insulin transport is a rate-limiting step for insulin action on its
target tissues. Insulin as well as exercise can directly induce an
increase in LBF in humans (3, 23). However, as shown in Fig. 3, LBF
under both conditions did not change significantly after the glucose
and insulin boluses, which elevate the plasma insulin levels. The
results suggest that blood flow is elevated only by the effect of
exercise. Furthermore, blood flow enhancement through exercise lasts
until 25 min after the glucose bolus. Increased blood flow in the
KG-determined
period may have contributed less to
SI, because
SI does not correlate with
KG (25). LBF
during exercise has been shown to be positively correlated with
exercise intensity (23). Thus we speculate that the blood flow might have remained higher longer in the study of Brun et al. (11) than in
the present study, resulting in increased
SI.
An alternative explanation for this discrepancy could be related to glucose transporter concentration, because insulin-stimulated glucose transport has been found to be proportional to glucose transporter GLUT-4 protein concentration (17). Recent evidence has shown an increase in GLUT-4 protein expression immediately after a single but prolonged strenuous-exercise bout in an animal study (22). Thus it is possible that the exercise in this study may not have increased the GLUT-4 protein concentration, because the exercise intensity was not high enough.
In conclusion, the present study suggests that the mild exercise at LT intensity could be one of the physiological conditions that improves SG with no alterations in SI, indicating acute improvement in glucose tolerance. Our results may lead to effective exercise therapy not only for hypertension (26, 27) and hyperlipidemia (31, 33) but also for patients with glucose intolerance.
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ACKNOWLEDGEMENTS |
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The present study was supported by grants from the Ministry of Education, Science and Culture of Japan and the Central Research Institute of Fukuoka University.
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FOOTNOTES |
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The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Address for reprint requests and other correspondence: H. Tanaka, Laboratory of Exercise Physiology, Faculty of Health and Sports Science, Fukuoka Univ., Fukuoka 814-0133, Japan (E-mail: htanaka{at}fukuoka-u.ac.jp).
Received 9 October 1998; accepted in final form 17 August 1999.
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DISCUSSION
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