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1 Research Institute for Sport
and Exercise Sciences, We studied the
effects of maintained hyperglycemia (12 mmol/l) on endurance exercise
to determine the hormonal and metabolic responses, the maximal rate of
glucose infusion (i.e., utilization), and the effects on muscle
glycogen stores. Eight men undertook two trials during which they
exercised on a cycle ergometer at an intensity of ~70% peak
O2 uptake for 120 min. In the
first trial (trial A), subjects had
their blood glucose concentration clamped at 12 mmol/l 30 min before exercise and throughout exercise. The same rate and volume
of infusion of saline as had occurred for trial
A were used in a placebo trial (trial
B). Maintained hyperglycemia resulted in
significantly lowered plasma concentrations of nonesterified fatty
acid, glycerol, 3-hydroxybutyrate, epinephrine, norepinephrine, and
growth hormone (P < 0.001) during
exercise, whereas concentrations of plasma insulin were significantly
elevated (P < 0.001). Calculations
of the rates of total carbohydrate oxidation showed that
trial A resulted in significantly
higher values when compared with trial
B (P < 0.01) and
that the maximal rates of glucose infusion varied between 1.33 and 2.78 g/min at 100-120 min. Muscle glycogen concentrations were
significantly depleted (P < 0.01)
after both trials (trial A, 170.3 µmol/g dry wt decrease; trial B, 206 µmol/g dry wt decrease), although this apparent difference may be
accounted for by storage of 22.6 g glucose during the 30-min prime
infusion. The results from this study confirm that maintained hyperglycemia attenuates the hormonal response and promotes
carbohydrate oxidation and utilization and that muscle glycogen may not
be spared.
glucose utilization; carbohydrate oxidation; fat oxidation; muscle
glycogen; glucose clamp technique
PROLONGED, INTENSE EXERCISE causes an increase in
plasma concentrations of catecholamines, glucagon, and growth hormone
(GH), and a concomitant reduction in insulin (17). These changes favor the release of fatty acids from triglyceride stores and their subsequent use as an energy source. Carbohydrate ingestion before or
during exercise, on the other hand, attenuates this response (9, 17).
Infusion of glucose in exercising subjects to maintain hyperglycemia
elevates plasma insulin; this leads to a high rate of carbohydrate
oxidation and a decrease in plasma nonesterified fatty acids (NEFA) and
fat oxidation (4, 15). Elevation of blood glucose above 11 mmol/l with
the use of glucose infusion significantly attenuates the catecholamine
response to prolonged exercise (18). To date, no investigation has
reported a complete hormonal and metabolite response to maintained
hyperglycemia during exercise, especially when hyperglycemia exists
before the onset of exercise. Such a scenario is of particular interest
with respect to the influence displayed by hyperinsulinemia, especially
the relationship between catecholamines and insulin.
The rate of glucose uptake by muscle depends on both exercise and
circulating insulin concentrations (6, 16). The hyperglycemic glucose
clamp technique is used to estimate the rates of glucose uptake and/or
disposal by tissues, where the glucose infusion rate represents glucose
uptake and/or disposal (6). Two studies have reported that the maximal
rate of glucose infusion during prolonged exercise at 70% maximal
O2 uptake
( The present investigation examined the effects of elevation of plasma
glucose before exercise and of maintenance of hyperglycemia throughout
120 min of exercise, not only on the hormonal and metabolic responses
but also on determination of the maximal rates of glucose infusion
(i.e., rate of glucose utilization) and on the effect on muscle glycogen.
Subjects.
Eight healthy, well-trained men (7 club-level cyclists and 1 club-level
cross-country runner) gave their informed consent in accordance with
the procedures approved by the Ethics Committees of the Royal Liverpool
Hospital and of Liverpool John Moores University. The age, body mass,
and peak O2 intake
( Experimental design.
To determine
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O2 max) is
2.6 g/min (4, 15). Despite these high levels of glucose uptake by
muscle during exercise, maintenance of hyperglycemia at 10 mmol/l did
not spare muscle glycogen (4). On the other hand, muscle glycogen was
spared if one leg was exercised and glucose was infused at a rate of 3 g/min; this led to a blood glucose concentration of 21 mmol/l
(2).
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O2 peak) were (mean ± SD) 37.4 ± 11.6 yr, 68.9 ± 6.7 kg, and 3,994 ± 540 ml/min, respectively.
O2 peak,
each subject first underwent a test on an electrically braked cycle
ergometer, using a continuous incremental test to volitional
exhaustion. During subsequent visits to the laboratory (after an
overnight fast), subjects exercised for 120 min at an intensity
corresponding to 70%
O2 peak while under a
condition of maintained hyperglycemia by using glucose infusion
(trial A) or saline infusion
(trial B). The glucose-infusion trial took place first, because the rate of saline infusion needed to
match that for glucose infusion. Subjects had similar dietary intakes
and refrained from strenuous exercise for 48 h before each trial.
O2 peak. During the
prime infusion and throughout the exercise bout, plasma glucose
concentration was maintained at close to 12 mmol/l by variation of the
rate of infusion every 5 min, according to the arterialized plasma glucose concentration, and measured by using an Analox GM7 analyzer (Analox Instruments, London, UK). Changes in infusion rate were calculated by using a Sharp MZ-80B computer.
30 min), after the
prime infusion (0 min), and every 20 min during the exercise. The blood
was centrifuged at 3,000 rpm and then was divided into aliquots. Plasma
was stored at 20°C before later analysis for lactate, NEFA,
glycerol, 3-hydroxybutyrate (3-OHB), cortisol, insulin and GH. Plasma
samples for the determination of catecholamines were stored at
70°C, while blood for glucagon assays was collected in
syringes containing Trasylol.
An on-line gas-analysis system (PK Morgan) was used for the
determination of O2 and
respiratory exchange ratio over a 5-min period before the prime
infusion, in the last 5 min of the prime infusion, and at
15, 30, 60, 90, and 120 min of exercise. These values were subsequently
used for the calculation of carbohydrate and fat oxidation rates.
Immediately after the exercise bout, subjects were requested to lie
supine while the infusion rate was slowly decreased, so as to prevent
rebound hypoglycemia. Furthermore, a muscle biopsy sample was taken
from the anterior quadriceps by using a conchotome, after
administration of a local anesthetic and after an incision of the skin
and muscle fascia. This process occurred within 5 min of the completion
of exercise. The muscle sample was placed in a sterile Eppendorf tube
before being plunged into liquid nitrogen. The sample was then stored
at 70°C until it was analyzed later for glycogen content. To
minimize trauma, we did not take a resting muscle sample on the same
day as the exercise; rather, the sample was taken at the same time of
day 3 wk after the second trial. Subjects conformed to
their previous eating and exercise patterns for the 48-h period before
the sample was taken.
Subjects repeated the same procedure 3 wk after the first trial, but
they received a 0.9% saline infusion instead of the dextrose. The rate
of infusion of the saline was identical to that for the glucose-infusion trial, so that the total volume given in both trials
was identical.
Analyses. Plasma NEFA values were determined by an enzymatic spectrophotometric method, while a portion of the plasma was deproteinized with perchloric acid (7% wt/vol) before assay for lactate, glycerol, and 3-OHB by using enzymatic methods. All these analyses were performed on a Cobas-Bio centrifugal analyzer (Roche Products, Welwyn Garden City, Herts, UK). Plasma insulin was determined by using RIA with an insulin RIA kit (IM.78, Amersham International, Amersham, UK), and plasma glucagon was determined by using an 125I-glucagon RIA kit (IDS, Bournemouth, UK). Both plasma GH and cortisol were assayed by using in-house RIA methods; the former was accomplished with reagents supplied by the Supra Regional Assay Laboratory (Royal Infirmary, Edinburgh, UK), and the 125I-label was supplied by NETRIA (St. Bartholomew's Hospital, London, UK), and the latter was accomplished by reagents supplied by Bioanalysis (Cardiff, UK). The two in-house assays showed a bias of <10% on the National External Quality Assessment Scheme. Plasma epinephrine and norepinephrine concentrations were analyzed by using high-performance liquid chromatography with electrochemical detection via an in-house method (Department of Clinical Chemistry, Royal Liverpool University Hospital, Liverpool, UK).
Freeze-dried muscle biopsy samples were prepared and analyzed for glycogen concentration according to the method of Edwards et al. (8).Statistics. ANOVA with repeated measures was used to determine whether there were any significant differences between the trials and the time points for the plasma metabolites and hormones. Significant F values were followed up by using a Tukey post hoc test. The carbohydrate oxidation rates were subjected to the determination of the area under the curve before a t-test was applied. The rate of glucose utilization was analyzed by employing a one-way ANOVA to determine whether significant differences accrued with time. Paired t-tests were performed on the muscle glycogen concentrations. Significance was accepted at P < 0.05.
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Blood metabolites.
Glucose infusion maintained plasma glucose concentrations at ~12
mmol/l, whereas saline infusion resulted in a relatively constant value
of 5 mmol/l (Fig. 1). Plasma glucose in the
exercise period ranged from 11.5 ± 1.0 to 12.6 ± 0.6 mmol/l for
the glucose infusion; this reflects the stability of the clamp
procedure. Hypoglycemia was not displayed by any of the subjects with
saline infusion, where plasma glucose concentrations at 100 and 120 min were 5.1 ± 0.4 and 4.7 ± 0.7 mmol/l, respectively. ANOVA found a significant difference between trials
(P < 0.01). Differences were also
apparent with time (P < 0.01),
although this was mainly because of the changes in concentration from
resting values to values after the prime infusion of glucose
(P < 0.01).
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Plasma hormones.
Elevated plasma insulin concentrations resulting from glucose infusion
were apparent (Fig. 3). Mean values
increased from 7.0 ± 2.5 mU/l at rest to 25.9 ± 6.3 mU/l after
the prime infusion. During subsequent exercise by the subjects, the
insulin concentrations became elevated up to 60 min (33.7 ± 15.9 mU/l) before falling to 20.9 ± 6.1 mU/l at 120 min. During exercise
under conditions of saline infusion, a typical response to exercise
occurred, with a decrease in insulin levels from 7.2 ± 2.4 mU/l at
the start to 3.3 ± 0.5 mU/l at 120 min. ANOVA revealed a
significant difference between the trials
(P < 0.01).
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Oxidation rates.
Calculations of the rate of whole body carbohydrate and fat oxidation
from the O2 and RER data are
displayed in Figs. 5 and
6. The mean area under the curve,
followed by a paired t-test, revealed
a significantly higher carbohydrate oxidation rate
(P < 0.01) for glucose infusion than
for saline infusion (320.8 ± 56.3 vs. 229.7 ± 46.1 g/120 min, respectively). The rate of carbohydrate oxidation during
exercise did not vary significantly with time for glucose infusion
(P > 0.05) but decreased
significantly for saline infusion (P < 0.01).
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Glucose infusion.
The rate of glucose infusion, as measured from the glucose-clamp
procedure, increased significantly during exercise
(P < 0.01). Figure
7 shows that this increase occurred up to
80-100 min before a plateau was established. At this stage, the
mean value of 1.8 g/min represents a 61% increase from the start of
the exercise period. When expressed as a percentage of the mean total
carbohydrate oxidation rate, the mean glucose utilization rate (i.e.,
the rate of glucose infusion) was 40.8, 53.7, 57.2, 68.9, and 68.3% at 15, 30, 60, 90, and 120 min, respectively.
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Muscle glycogen. Muscle glycogen concentrations were significantly lower at the end of both trials, as a result of the exercise, when compared with a resting value taken on a subsequent occasion (P < 0.01). The resting concentration was 308.5 ± 64.8 µmol/g dry wt, whereas the postexercise values were 138.2 ± 33.3 and 102.5 ± 27.5 µmol/g dry wt after conditions of glucose or saline infusion, respectively. Differences between the trials were also significant (P < 0.01).
Glucose storage during rest.
The mean total glucose infused was 29.2 ± 7.7 g over the 30-min
priming period when subjects were resting. The total carbohydrate oxidized during this 30-min period, calculated from the respiratory measures at 30 min and 0 min, was 6.6 ± 1.3 g.
The difference between the glucose infused and that oxidized is assumed
to result in storage of glucose. A value of 22.6 g was estimated to be
stored during this period.
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Hyperglycemia was maintained with little variation throughout the exercise period; this emphasizes the suitability of the clamp procedure to circumstances other than rest. This finding is in agreement with two other studies in which the glucose clamp has been used during exercise (4, 15), although those studies maintained hyperglycemia at 10 mmol/l. Because little variation occurred in the present investigation, the rate of glucose infusion appears to be reliable as a measure of whole body glucose utilization.
The hyperinsulinemia as a consequence of glucose infusion was expected, whereas the decrease after 60 min of exercise was similar to that observed previously (4) and was probably caused by the elevation in epinephrine that occurs during exercise. After 60 min of exercise, the plasma epinephrine concentration was 0.55 nmol/l, an increase of 50% above resting levels. Because insulin began to decrease after this time point, it is possible to speculate that a threshold exists at which insulin is inhibited by epinephrine. This is supported by findings that the insulin response to glucose infusion at rest in healthy subjects results in a continuous elevation of plasma insulin, whereas the epinephrine concentration did not rise to >0.38 nmol/l (13). The response with saline infusion was similar to that normally observed during exercise, i.e., a gradual decline in insulin concentration caused by the sympathoadrenal inhibition of the beta cells of the pancreas via an increase in epinephrine levels (3).
Maintained hyperglycemia had a pronounced attenuating effect on the plasma glucagon concentration. This is an expected response to hyperglycemia, probably caused by a direct effect of glucose on the pancreatic alpha cells rather than mediated by epinephrine, and the response illustrates the antagonistic roles of insulin and glucagon. The effect of a diminished glucagon concentration can be realized in a lowered splanchnic glucose output from glycogenolysis and gluconeogenesis. Therefore the infusion rate of glucose probably represents the total glucose uptake by tissues during exercise, because none is likely to accrue from the splanchnic beds.
The epinephrine response during saline infusion is typical of that to
prolonged severe exercise, in which impulses from the motor centers in
the brain and from exercising muscle elicit a work rate-dependent
increase in sympathoadrenal activity. The increases in catecholamines
in turn depress insulin secretion by 
-receptor-mediated mechanisms
(11). The diminished epinephrine levels under glucose infusion are
caused by the availability of glucose in the ventromedial and
ventrolateral cells of the hypothalamus which reduce sympathetic
activity (9). The results of norepinephrine concentration in our study
support previous findings of an increase during exercise, and further
corroborate those findings that elevated plasma glucose concentrations
attenuate the normal response to exercise.
At the onset of exercise, impulses from motor centers in the brain and
from active muscles elicit an increase in sympathoadrenal activity and
in the release of some pituitary hormones. Among these are increases in
circulating levels of GH and ACTH. The latter leads to an increase in
cortisol. Clearly, the results from the saline infusion
in this study support the view that prolonged exercise elevates plasma
GH and cortisol. Intensity and duration of exercise are the important
factors governing secretion of these hormones (19). The fact that
hyperglycemia suppresses GH has been demonstrated previously (14) and
is probably a result of reduced activation of -receptors by
the cells of the hypothalamic ventromedial nuclei that are
glucoreceptors. With saline infusion, the data for cortisol show an
extended latent period (i.e., 80 min) compared with that for GH. Other
authors (5, 12) have shown that cortisol is elevated after exercise,
particularly if the exercise is prolonged. The 16% decrease in plasma
cortisol concentration, as a result of the prime infusion of glucose
and the subsequent reduction during exercise, gives credence to the view that glucose-sensitive receptors can modulate the cortisol response. A high-fat diet enhances the secretion of cortisol, whereas a
high-carbohydrate diet attenuates this response (10). Nevertheless,
plasma cortisol concentration may become elevated, despite an increase
in blood glucose levels.
Elevated concentrations of insulin, together with diminished levels of catecholamines, cortisol, and GH that result from glucose infusion, favored a depression in plasma NEFA and 3-OHB throughout the exercise period. Insulin inhibits lipolysis and promotes lipogenesis, so any increase in glycerol noted during exercise demonstrates the occurrence of lipolysis, whereas continued depression of NEFA is suggestive of re-esterification. The prime glucose infusion significantly reduced concentrations of both glycerol and NEFA; this denotes impaired lipolysis. At no stage during exercise was the NEFA concentration elevated above the preexercise resting levels.
Saline infusion was accompanied by no significant change in NEFA, glycerol, or 3-OHB levels in plasma as a consequence of the prime infusion. Exercise, however, produced a significant increase in concentrations of these metabolites caused by enhanced hormonally stimulated lipolysis.
A notable effect of hyperglycemia was that total carbohydrate oxidation was maintained at a rate >2.5 g/min for the duration of the exercise. This is in contrast to a progressive reduction in carbohydrate oxidation to 1.5 g/min during saline infusion. The results compare favorably with those of Coyle et al. (4), but the values for carbohydrate oxidation during glucose infusion are somewhat lower than the 3.6 g/min observed by Hawley et al. (15). The maintenance of elevated carbohydrate oxidation with hyperglycemia and the decline during saline infusion meant that the difference between trials in relation to carbohydrate oxidation became progressively greater. At 120 min of exercise, the rate of carbohydrate oxidation was ~40% higher with glucose infusion compared with saline infusion.
In parallel with the widening in the rate of carbohydrate oxidation
between trials, the rate of glucose infused (glucose utilization) increased steadily, from 1.1 g/min at the start of exercise to 1.8 g/min after 80-100 min and then remained at that level. This increase in the rate of glucose utilization during exercise was 40%.
Since the rate of glucose uptake by muscle is mediated by GLUT-4
transporters, it is suggested that a combination of exercise, hyperglycemia, and hyperinsulinemia resulted in the maximal rate of
uptake being 1.8 g/min. Although this value is lower than the rate of
2.6 g/min presented by other authors (4, 15), the fact that our
subjects were, on average, older and had a lower O2 peak (and thereby
exercised at a lower absolute exercise intensity) may account for the
discrepancies. Indeed, two of the younger and fitter cyclists in our
group produced peak glucose utilization rates of 2.57 and 2.78 g/min
between 100 and 120 min, whereas two of our older cyclists produced
peak values of only 1.33 and 1.51 g/min. Further investigations are
warranted on the effects of age and exercise intensity on the rate of
glucose utilization.
The differences between the rate of total carbohydrate oxidation and the rate of glucose utilization suggest that, despite hyperglycemia, exercising muscles use their own endogenous glycogen stores. This is supported by our findings of a significant depletion of muscle glycogen after glucose infusion. If we assume that the resting muscle glycogen concentration obtained on the subsequent visit reflects normal values, then the decrease in muscle glycogen after the glucose- and saline-infusion trials is 170.3 and 206 µmol/g dry wt, respectively. Interpretation of these findings needs to be treated with caution, because the resting muscle glycogen value was achieved on a separate day from the postexercise value, albeit at the same time of day and after similar patterns of nutrition and activity over the previous 48 h. Furthermore, the 30-min prime infusion of glucose would most likely have resulted in elevated levels of muscle glycogen before exercise in that trial compared with saline infusion. We calculated a glucose storage of 22.6 g during the prime infusion. It is possible to speculate that the difference in postexercise muscle glycogen may be accounted for by elevated preexercise levels after glucose infusion, and, therefore, muscle glycogen was not spared. Indeed, this speculation is supported by the results of a study that established that the contribution of muscle glycogen to the total energy provision varied between 80 and 41% under conditions of maintained hyperglycemia, whereas under euglycemia the contribution varied between 50 and 21% (15). Clearly, hyperglycemia favors carbohydrate oxidation, and that includes use of muscle glycogen.
Previous studies on glucose infusion during exercise have demonstrated muscle glycogen sparing (2) or no sparing (4). Bergstrom and Hultman (2) infused glucose into men at a rate of ~3 g/min iv during 1 h of one-legged exercise. They found that, as a result of an average blood glucose concentration of 21 mmol/l, muscle glycogen concentration was reduced compared with that of the controls. The fact that only one leg was exercised and that supraphysiological doses of glucose were infused could have resulted in this finding. More recently, Coyle et al. (4) elevated blood glucose to 10 mM in humans and maintained that level during 2 h of exercise. No muscle glycogen sparing was observed.
In summary, the results from this study confirm that maintained
hyperglycemia promotes factors that enhance carbohydrate oxidation and
utilization. The maximal rates of glucose utilization by tissue during
endurance exercise at 70%
O2 peak varied between
2.78 g/min for fitter, young subjects to 1.33 g/min for the less fit, older subjects, although the relationship between age or exercise intensity with the rate of glucose utilization needs further
investigation. Finally, whether muscle glycogen is spared under
conditions of maintained hyperglycemia remains a matter of conjecture,
although we suggest that it is not spared.
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ACKNOWLEDGEMENTS |
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We greatly appreciate the help of Dr. Keith Frayn with the hyperglycemic clamp procedure, Dr. John Coakley with the muscle biopsy sampling, Prof. Malcolm Jackson with the muscle glycogen assays, and Dr. Les Hipkin with the hormonal assays.
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FOOTNOTES |
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Address for reprint requests and other correspondence: D. P. M. MacLaren, Research Institute for Sport & Exercise Sciences, Liverpool John Moores Univ., Trueman Bldg., Webster St., Liverpool L3 2ET, UK (E-mail: d.p.maclaren{at}livjm.ac.uk).
Received 23 October 1997; accepted in final form 10 March 1999.
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