Am. J. Physiol. Endocrinol. Metab.
278: E65–E75, 2000.
Effect of carbohydrate ingestion on glycogen resynthesis
in human liver and skeletal muscle, measured by 13C MRS
ANNA CASEY,1 ROB MANN,2 KATIE BANISTER,2 JOHN FOX,1 PETER G. MORRIS,2
IAN A. MACDONALD,1 AND PAUL L. GREENHAFF1
1School of Biomedical Sciences, University of Nottingham Medical School,
Nottingham NG7 2UH; and 2Department of Physics, Magnetic Resonance
Centre, University of Nottingham, Nottingham NG7 2RD, United Kingdom
Casey, Anna, Rob Mann, Katie Banister, John Fox,
Peter G. Morris, Ian A. Macdonald, and Paul L. Green-
haff. Effect of carbohydrate ingestion on glycogen resynthesis
in human liver and skeletal muscle, measured by 13C MRS.
Am. J. Physiol. Endocrinol. Metab. 278: E65–E75, 2000.—
This study investigated the effect of carbohydrate (CHO)
ingestion on postexercise glycogen resynthesis, measured
simultaneously in liver and muscle (n 5 6) by 13C magnetic
resonance spectroscopy, and subsequent exercise capacity
(n 5 10). Subjects cycled at 70% maximal oxygen uptake for
83 6 8 min on six separate occasions. At the end of exercise,
subjects ingested 1 g/kg body mass (BM) glucose, sucrose, or
placebo (control). Resynthesis of glycogen over a 4-h period
after treatment ingestion was measured on the first three
occasions, and subsequent exercise capacity was measured on
occasions four through six. No glycogen was resynthesized
during the control trial. Liver glycogen resynthesis was
evident after glucose (13 6 8 g) and sucrose (25 6 5 g)
ingestion, both of which were different from control (P ,
0.01). No significant differences in muscle glycogen resynthe-
sis were found among trials. A relationship between the CHO
load (g) and change in liver glycogen content (g) was evident
after 30, 90, 150, and 210 min of recovery (r 5 0.59–0.79, P ,
0.05). Furthermore, a modest relationship existed between
change in liver glycogen content (g) and subsequent exercise
capacity (r 5 0.53, P , 0.05). However, no significant differ-
ence in mean exercise time was found (control: 35 6 5,
glucose: 40 6 5, and sucrose: 46 6 6 min). Therefore, 1 g/kg
BM glucose or sucrose is sufficient to initiate postexercise
liver glycogen resynthesis, which contributes to subsequent
exercise capacity, but not muscle glycogen resynthesis.
13Cmagnetic resonance spectroscopy; magnetic resonance
imaging; submaximal exercise
GLYCOGEN IS THE PRIMARY FUEL supporting ATP homeo-
stasis during moderate-to-intense exercise (21). The
depletion of muscle glycogen observed during pro-
longed submaximal exercise is consequently associated
with an accelerated rate of adenine nucleotide loss (7)
and muscle fatigue (2). Resynthesis of glycogen during
the recovery period after exercise is therefore impor-
tant to the recovery of endurance exercise capacity.
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http://www.ajpendo.org 0193-1849/00 $5.00 Copyright r 2000 the American Physiological Society
Postexercise glycogen resynthesis in rodent liver and
skeletal muscle is well documented (8, 14, 16). Like-
wise, changes in human skeletal muscle glycogen con-
centration during prolonged exercise and recovery are
relatively well documented, both in whole muscle (2, 12)
and in muscle fiber subtypes (10), due largely to
widespread use of needle biopsy procedures. In the
absence of exogenous carbohydrate (CHO), there is
little change in human muscle glycogen concentration
after exercise-induced glycogen depletion (20). After
CHO ingestion, restoration of human muscle glycogen
concentration is typically complete within 24 h (2, 10),
but the optimal type of CHO, in terms of both glycogen
resynthesis and restoration of exercise capacity, re-
mains unclear.
Previous studies have shown that ingestion of CHO
with a high glycemic index (GI) is more effective in
promoting muscle glycogen resynthesis than ingestion
of lower GI CHO (9, 29, 45). Although relatively high,
sucrose has a lower GI than glucose, and glucose
ingestion might therefore be expected to promote greater
muscle glycogen resynthesis than sucrose. However,
due to its fructose content, sucrose may preferentially
restore liver, rather than muscle glycogen stores after
exercise, as predicted from the data of Nilsson and
Hultman (36) obtained in resting subjects. This may
alter the extent to which exercise capacity is restored,
by mediating blood glucose availability. Previous stud-
ies have demonstrated that fatigue during prolonged
exercise at 70% maximal oxygen uptake (V̇O2max) is pre-
ceded by a decline in the rate of CHO oxidation and that
fatigue can be delayed by maintaining a high rate of
CHO oxidation via oral glucose ingestion (13). The
authors demonstrated that highly trained subjects
administered glucose were able to exercise for longer
than when fasting, without any further reduction in
muscle glycogen. They suggested that toward the end of
exercise, oxidation of CHO was maintained as a result
of glucose ingestion, which was sufficient to offset the
reduction in muscle glycogen oxidation that occurred as
a result of glycogen depletion, enabling exercise to
continue. The lowering of blood glucose, and subse-
quent reduction in muscle glucose uptake and oxida-
tion, seen during the final stages of exercise without
CHO ingestion, was suggested to be a major cause of
fatigue. Recent tracer studies have confirmed this
suggestion that CHO oxidation is maintained by an
E65
E66 LIVER AND MUSCLE GLYCOGEN METABOLISM
increase in blood glucose oxidation and have shown
total glucose oxidation to be greater under hyperglyce-
mic (49) compared with euglycemic (48) conditions.
Together these studies suggest that any differences
between glucose and sucrose in terms of postexercise
liver glycogen resynthesis, and therefore blood glucose
availability, may have important consequences for sub-
sequent exercise capacity. To date, no studies have
investigated the relative merits of glucose and sucrose
administration, during recovery from exercise, in terms
of subsequent endurance exercise capacity.
Relatively little data are available describing in vivo
human liver glycogen homeostasis, because liver biop-
sies are not considered appropriate for research pur-
poses (18) and are generally excluded in normal sub-
jects. Over the last 15 years, information about human
liver glycogen homeostasis has been provided almost
exclusively by magnetic resonance spectroscopy (MRS).
However, even with the advent of MRS, very little data
have been gathered from normal subjects. The majority
of information has been obtained from patient popula-
tions, primarily to study the pathophysiology of glucose
homeostasis (11, 24, 33, 46). Existing data from normal
subjects has focused predominantly on responses to
feeding and fasting in the resting state (37–39, 43), and
the nature of liver glycogen homeostasis during exer-
cise and recovery remains unclear.
To date, no studies have used interleaved 13C liver
and muscle spectra to quantify changes in human liver
and muscle glycogen content with exercise and during
recovery. No studies have related postexercise liver and
muscle glycogen resynthesis to subsequent endurance
exercise capacity. Furthermore, the relative merits of
glucose and sucrose, in terms of the effect of liver and
muscle glycogen resynthesis on subsequent exercise
capacity, are unknown.
We hypothesize that postexercise administration of
glucose and sucrose will have a differential effect on
liver glycogen resynthesis, which may have important
consequences for the restoration of exercise capacity.
Therefore, the first aim of this study was to quantify
changes in human liver and muscle glycogen content
during 1) exercise and 2) the recovery period after CHO
administration. A second aim was to compare the
effects of glucose and sucrose ingestion on 1) postexer-
cise liver and muscle glycogen resynthesis and 2)
subsequent endurance exercise capacity.
METHODS
Subjects. Ten healthy males gave their written consent to
take part in the present study, which was approved by the
University of Nottingham Medical School Ethical Committee.
All subjects were well trained (5–7 days/wk on a regular
basis), and all competed in various sports at a good club or
international level. Trained subjects were chosen to avoid a
training effect from repeated exercise trials. Age, weight,
body mass (BM) index, V̇O2 max, and normal daily energy
intake were 25 6 2 yr, 76.1 6 1.8 kg, 23.7 6 0.6 kg/m2, 4.01 6
0.17 l/min, and 12.6 6 0.8 MJ/day, respectively (means 6 SE).
Before beginning the study, all subjects participated in a
routine medical examination.
Experimental protocol. Preliminary measurements made
on all subjects during the first five visits established their
V̇O2 max, normal dietary composition, and endurance exercise
capacity, as detailed below. The next series of trials (visits
6–8) used endurance exercise to deplete tissue glycogen levels
and examined the effect of CHO ingestion on postexercise
liver and muscle glycogen resynthesis. The final series of
trials (visits 9–11) depleted glycogen levels and administered
CHO in a similar fashion. On these occasions, measurements
of glycogen resynthesis were omitted; however, endurance
exercise capacity was measured at the end of the recovery
period. In addition, during visits 9–11, blood and expired air
samples were collected throughout both exercise periods and
recovery. It is not feasible to combine protocols for measure-
ment of liver and muscle glycogen with those for blood and
gas sampling for instrumentation reasons (4).
On the first visit to the laboratory, subjects were thor-
oughly familiarized with all procedures involved in the study.
On the second visit, V̇O2 max was determined for all subjects
with a discontinuous, incremental exercise test to exhaustion
on an electrically braked cycle ergometer (Lode N.V. Instru-
menten, Groningen, Holland). This was verified on a third
visit, separated from the second by a minimum of 3 days.
To promote similar liver and muscle glycogen concentra-
tions before each of the subsequent trials, both diet and
training were controlled for 3 days beforehand. Initially
subjects weighed and recorded their normal diet for 3 days.
CHO, fat, and protein intake, represented as a percentage of
total daily energy intake, were 48 6 2, 36 6 2, and 16 6 1%,
respectively (means 6 SE). An identical (weighed) diet was
prescribed for 3 days before all subsequent trials, ensuring
the same CHO and total energy intake on each occasion for an
individual subject. In addition, subjects were instructed to
maintain the same pattern of training throughout each of
these 3-day periods and to exclude any strenuous training for
24 h before each trial.
Subjects reported back to the laboratory after an overnight
fast on eight further occasions, having been instructed, in
addition to dietary and training requirements, to abstain
from alcohol intake for 24 h before each trial and from caffeine
intake on the day of each trial. On the fourth visit, subjects
cycled to volitional exhaustion at 70% V̇O2 max. Exercise time-
to-exhaustion was used as a measurement of endurance
exercise capacity and was verified by the repetition of the
protocol on a separate occasion.
On the following six occasions (visits 6–11), subjects cycled
at 70% V̇O2max for a fixed period (exercise time-to-exhaustion 2
10 min; bout 1), to deplete tissue glycogen levels by a similar
amount on each occasion. Subjects were administered 3 ml/kg
BM of plain water every 15 min during exercise, split into two
drinks, and any deficits in nude BM after exercise were
immediately restored with plain water. Immediately after
exercise, subjects were administered a single bolus of 1 g/kg
BM CHO in the form of 18.5% (wt/vol) glucose, 18.5% (wt/vol)
sucrose, or an equivalent volume of placebo (control). CHO
ingestion was followed by a 4-h recovery period. A crossover
design was adopted, with subjects receiving all three treat-
ments on separate occasions, in a double-blind fashion. These
trials were separated by a minimum of 2 wk.
On visits 6–8, liver and muscle glycogen was measured in
six subjects before and after exercise and during the 4-h
recovery period after CHO ingestion. Glycogen measure-
ments (mmol/l) were made by natural abundance 13C MRS.
Liver and muscle volume (liters) was measured immediately
after each liver and muscle spectrum acquisition, respectively,
with multislice magnetic resonance imaging (MRI). This
 LIVER AND MUSCLE GLYCOGEN METABOLISM
enabled calculation of total glycogen content in millimoles
and therefore in grams. Liver spectra and volume measure-
ments were obtained within the first 30 min after CHO
ingestion and hourly thereafter. A typical sequence of spectra
is shown in Fig. 1. Muscle spectra and volume measurements
were obtained from 30–60 min and hourly thereafter.
During visits 9–11, 10 subjects completed an identical
pattern of exercise and CHO ingestion. On these occasions,
arterialized-venous blood samples were obtained at rest in
the fasting state, every 15 min during exercise, and at hourly
intervals during the 4-h recovery period. Expired gas samples
were obtained at rest, every 15 min during exercise, and at
30-min intervals during the recovery period. For the last 25
min of recovery, subjects were allowed to be mobile and to
perform gentle stretching exercises in preparation for the
second bout of exercise. At the end of the recovery period,
endurance capacity was measured in 10 subjects. Subjects
cycled at 70% V̇O2 max to volitional exhaustion (bout 2), and the
exercise time was recorded. Water was given during exercise
as before. As before, trials were separated by a minimum of
2 wk.
All treatments were supplied by SmithKline Beecham. The
solutions were supplied in identical containers, labeled with a
code, which was released by SmithKline Beecham after
completion of the study. All solutions were identical in
appearance. The placebo consisted of a sugar-free solution
bearing as close a resemblance as possible to the taste of the
glucose and sucrose solutions. This allowed double-blind
trials to be undertaken. Glucose and sucrose were chosen
because they are the constituents of most commercially
available preparations. Ingestion of 1 g/kg BM CHO was
chosen to approximate the CHO intake associated with a
palatable fluid volume, such as a standard can of drink (330
ml), standardized for BM. Previous studies from this labora-
tory have investigated the effects of large quantities of CHO
on postexercise liver and muscle glycogen resynthesis (35).
MRS-MRI. All MRS data were acquired on an in-house
built dual-channel spectrometer, with a 1-m bore, 3.0 tesla (T)
whole body magnet (Oxford Magnet Technology, Oxford, UK).
Dual carbon and proton surface coil transmit-receive probes
were built for the liver and muscle. The 13C coils were both
circular single-turn designs, with diameters of 12 and 9 cm
E67
for the liver and muscle, respectively. The proton coils were
both 16 3 16 cm parallel loop butterfly designs. They were
used for localized shimming of the static magnetic field to
optimize its homogeneity and for proton decoupling. Position-
ing of surface coils over the anterolateral aspect of the
quadriceps and the liver was initially established for indi-
vidual subjects with MRI (see below). When subjects were
positioned in the 3.0-T spectrometer, data were acquired with
a simple pulse-acquire (decouple) sequence, with the excita-
tion pulse flip angle determined by Ernst angle consider-
ations. Repetition times were 171 and 114 ms for liver and
muscle acquisitions, respectively. The flip angle at the 13C coil
centers was 220°, which minimized spectral contamination
from superficial adipose tissue and, for the liver spectra, from
abdominal muscle. Broad-band proton decoupling was ap-
plied for the duration of each 27-ms sampling period. Without
decoupling, the 13C resonance is sensitive to the spin orienta-
tions of attached protons and the signal is split into a doublet
with a relatively low signal-to-noise ratio. A Waltz-8 decou-
pling sequence was used, resulting in a peak transmitted
power of 30 W; the acquisition period and repetition times for
liver and muscle ensured mean power deposition remained
within specific absorption rate limits of 8 and 12 W/kg,
respectively. Proton decoupling had the effect of doubling the
signal-to-noise ratio of the 13C glycogen signal. In addition,
proton-decoupled 13C spectra were summed over 15 min to
further improve the signal-to-noise ratio. Each spectrum
consisted of 5,200 and 7,800 acquisitions for the liver and
muscle, respectively. No adjustments to the spectrometer
were made between measurements, except for retuning the
13C surface coil and reshimming the static magnetic field
immediately before data acquisition. The signal of interest
arises from the C-1 position of glycogen at 100.5 particles/min
(relative to tetramethylsilane 5 0). Resonances from other
glycogen carbons (C-2 to C-6) are obscured by the lipid peaks.
The spectra were line broadened with a filter matched to the
C-1 glycogen line width, baseline flattened, and integrated
(8NMR 1; New Methods Research, New York, NY). The
coefficient of variation, calculated for repeated analysis of a
single spectrum, was 3.80% (n 5 15). The lipid peak at 30
particles/min (-CH2-) was used as an internal standard,
which did not vary by more than 6% over the course of the
Fig. 1. Typical sequence of proton de-
coupled, natural abundance 13C spectra
obtained by magnetic resonance spec-
troscopy (MRS) at 3.0 T (5,200 scans).
Resonance arises from the C-1 position
of glycogen at 100.5 particles/minute
(ppm) (relative to tetramethylsilane 5
0). Sequence shows time course of hu-
man liver glycogen resynthesis during
exercise and recovery. Spectra were ob-
tained before and after prolonged sub-
maximal exercise at 70% maximal oxy-
gen uptake (V̇O2 max), within the first 30
min after carbohydrate (CHO) inges-
tion (1 g/kg body mass) and then hourly
during the remainder of recovery. Coef-
ficient of variation, calculated for re-
peated analysis of a single spectrum,
was 3.80% (n 5 15).
E68 LIVER AND MUSCLE GLYCOGEN METABOLISM
study. The C1 signal was quantified by comparison with
spectra from a glycogen phantom (200 mmol/l oyster glycogen
and 150 mmol/l KCl; total volume 2 liters).
Initial positioning of the surface coils and measurements of
liver and muscle volume were accomplished with multislice
echo-planar imaging. This technique provides detailed ana-
tomical images based on proton density, by noninvasive and
nonradioactive means (34). Echo-planar imaging was per-
formed on an in-house spectrometer, with a 1-m bore, 0.5-T
whole body magnet (Oxford Magnet Technology). The optimal
positions for the carbon-proton coils over the liver and
quadriceps femoris were established with water-filled Eppen-
dorf tubes as coil markers. Measurements of total liver and
quadriceps femoris volume were coupled to each of the liver
and quadriceps femoris spectroscopy measurements, respec-
tively. Each image was acquired in 130 ms, with the MBEST8
(Modulus Blipped, Echo-Planar, single-pulse technique) imag-
ing sequence with a readout gradient switching rate of 0.5
kHz. An ultra-fast multislice sequence was employed, taking
,3 s to acquire 10 transverse slices. Slice width was 10 mm,
with an in-plane resolution of 3 mm. Usually, six sequential
sets of 10 slices were required to define muscle volume from
the bladder to the knee. Analysis of muscle volume began at
the urethra and ended before the quadriceps femoris tapered
to distal insertion points. Three sequential sets of 10 slices
were usually required to define liver volume from the supe-
rior to the inferior aspect. When liver images were obtained,
subjects were instructed to hold their breath at the same
point during the outward phase of the breathing cycle during
each 3-s acquisition period. Together with the short acquisi-
tion time, this removes the motion artefact arising from
respiration associated with conventional MRI (6). The total
number of slices used for analysis differed between subjects
due to anatomical differences but numbered ,20 slices for the
liver and 25 slices for the muscle. The same number of slices
was analyzed on each occasion for a given subject. Liver and
muscle volumes were calculated with the stereology method
within the ANALYZE image analysis program (Biomedical
Imaging Resource, Mayo Foundation, Rochester, Minnesota).
This method reduced the subjective element of manual trac-
ing. The coefficient of variation, calculated for repeated
analysis of a single image, was 1.9% (n 5 15) for both liver
and muscle.
Blood sampling and analysis. Blood was collected into
fluoride oxalate for immediate determination of whole blood
glucose concentration (Yellow Springs Instruments, Farnbor-
ough, UK). A second sample was collected into a plain tube,
from which a 100-µl sample was immediately deproteinized
in 1 ml 10% perchloric acid, centrifuged, and stored at 220°C
for lactate analysis (30) at a later date. A further sample was
collected into lithium heparin, mixed, and centrifuged. The
plasma was divided between a tube containing EGTA-
glutathione, which was stored at 280°C for future plasma
catecholamine analysis (31), and a plain tube, which was
snap-frozen in liquid nitrogen and stored at 280°C for plasma
ammonia analysis (15) within 24 h.
Statistical analysis. All MRS data in the glucose and
sucrose trials refer to six subjects. One subject was unable to
complete all three visits; hence, MRS data in the control trial
refers to 5 subjects. Changes in liver and muscle glycogen
content pre- and postexercise were examined with Students
t-test for paired data. Differences in glycogen resynthesis
during recovery were examined with two-way repeated-
measures ANOVA (SuperANOVA) with condition (control,
glucose, and sucrose) and time (sampling points) as indepen-
dent variables.
Measurements of endurance capacity, blood metabolites,
and CHO oxidation refer to all 10 subjects. Reporting of blood
metabolite data and CHO oxidation (g/min) data during the
second bout of exercise is restricted to the first 15 min of
exercise to ensure equal subject numbers, because exercise
time-to-exhaustion differed between subjects. Differences in
resting, pretreatment, and peak blood metabolite concentra-
tions were examined with one-way ANOVA, with condition as
the independent variable. Differences between resting and
peak blood metabolite concentrations were examined with
Student’s t-test for paired data. Differences in total CHO
oxidation (g) during exercise and recovery, and differences in
exercise time-to-exhaustion, blood metabolite accumulation,
and CHO oxidation rate (g/min) during the initial 15 min of
exercise bout 2, were examined by one-way ANOVA, with
condition as the independent variable. Differences in blood
glucose, serum insulin, and blood lactate concentration, and
respiratory exchange rate values during the recovery period
were examined with two-way repeated-measures ANOVA,
with condition and time as independent variables.
The Duncan New Multiple Range test for comparing mean
values was used as a post hoc test when significant interac-
tions were detected. Relationships between 1) the CHO load
and change in (D) tissue glycogen and 2) Dtissue glycogen and
subsequent exercise duration were examined by computing a
correlation coefficient (r) with a linear fit and a second order
polynomial fit, respectively (Statview). Statistical signifi-
cance was accepted at the 5% level (P , 0.05). Values are
presented in the text and in Tables 1–3 and Figures 1–5 as
means 6 SE.
RESULTS
Performance. During bout 1, subjects cycled for 83 6
8 min on each occasion to deplete liver and muscle
glycogen stores. After the recovery period, exercise
time-to-volitional fatigue during bout 2 appeared to be
longer after CHO administration, but no significant
differences among trials were found (control: 35 6 5,
glucose: 40 6 5, and sucrose: 46 6 6 min).
CHO oxidation. As expected, total CHO oxidation
during exercise bout 1 did not vary among trials
[control: 152.5 6 15.5; glucose: 155.1 6 18.4; and
sucrose: 160.9 6 22.5 g, nonsignificant (NS)]. Treat-
ments were administered after exercise. During the
recovery period after treatment ingestion, total CHO
oxidation was significantly elevated above control lev-
els (2.8 6 2.0 g) in both the glucose (16.4 6 4.1 g, P ,
0.05) and sucrose (18.4 6 5.7 g, P , 0.05) trials.
Respiratory exchange ratio values during recovery are
given in Table 1. After 15 min of exercise in bout 2, CHO
oxidation had risen to 2.1 6 0.2 and 2.1 6 0.3 g/min in
the glucose and sucrose trials, respectively, both of
which were significantly different from control (1.2 6
0.3 g/min; P , 0.05). Total CHO oxidation in bout 2
(which also reflects exercise duration) was higher in the
sucrose trial (102.3 6 18.7 g; P , 0.01) but not
significantly higher in the glucose trial (67.0 6 7.8 g),
when compared with control (38.8 6 7.5 g). No signifi-
cant differences in CHO oxidation were found between
the glucose and sucrose trials.
Blood metabolites. Fasting blood glucose was 4.6 6
0.1, 4.4 6 0.1, and 4.4 6 0.1 mmol/l in the control,
glucose, and sucrose trials, respectively (NS). At rest
 LIVER AND MUSCLE GLYCOGEN METABOLISM E69

Table 1. Blood glucose, serum insulin, blood blood lactate concentration increased from a resting
lactate, and RER level of 1.3 6 0.2 mmol/l (all trials, n 5 30), to a peak of
5.9 6 0.5 mmol/l (n 5 30, P , 0.001) within 15 min
PE R1 R2 R3 during exercise bout 1. Values during recovery are
Blood glucose given in Table 1. Lactate concentrations before and
Control 4.1 6 0.1 4.6 6 0.5 4.2 6 0.1 3.9 6 0.1 after 15 min of exercise bout 2 were no different among
Glucose 3.8 6 0.1 6.6 6 0.6* 4.7 6 0.2 3.7 6 0.2 trials (control: 1.2 6 0.2 and 3.5 6 0.7, glucose: 1.5 6 0.3
Sucrose 3.7 6 0.2 5.6 6 0.4‡ 4.1 6 0.1† 3.7 6 0.1
Serum insulin and 3.4 6 0.7, sucrose: 1.4 6 0.4 and 3.4 6 0.5 mmol/l,
Control 8.3 6 2.3 17.6 6 4.2 20.8 6 8.7 12.4 6 6.5 respectively; NS). Resting epinephrine and norepineph-
Glucose 14.5 6 6.7 86.8 6 31.5 31.3 6 8.1 22.1 6 8.8 rine were 0.29 6 0.04 and 1.19 6 0.13 nmol/l (n 5 30),
Sucrose 16.0 6 7.1 57.5 6 22.3 20.5 6 9.1 15.6 6 6.1 rising to 5.09 6 1.25 nmol/l (n 5 30, P 5 0.001) and
Blood lactate
Control 1.5 6 0.3 1.3 6 0.3 1.4 6 0.3 1.2 6 0.2
14.06 6 1.16 nmol/l (n 5 30, P , 0.001) during exercise
Glucose 1.9 6 0.4 1.6 6 0.3 1.6 6 0.2 1.5 6 0.3 bout 1, respectively. Before and after 15 min of exercise
Sucrose 2.1 6 0.3 2.8 6 0.4 1.3 6 0.3 1.4 6 0.4 bout 2, there was no difference among trials in epineph-
RER rine (control: 0.59 6 0.21 and 2.42 6 0.63, glucose:
Control 0.71 6 0.02 0.70 6 0.02 0.74 6 0.02 0.72 6 0.02
Glucose 0.72 6 0.02 0.83 6 0.03† 0.84 6 0.03† 0.78 6 0.02
0.92 6 0.41 and 4.63 6 1.42, sucrose: 0.34 6 0.12 and
Sucrose 0.71 6 0.02 0.85 6 0.03† 0.78 6 0.02 0.74 6 0.02 3.29 6 1.73 nmol/l, respectively; NS) or norepinephrine
(control: 1.06 6 0.23 and 13.96 6 2.40, glucose: 3.67 6
Values are means 6 SE. V̇O2 max , maximal oxygen uptake. Blood
glucose (mmol/l), serum insulin (mU/l), blood lactate (mmol/l), and
1.82 and 12.96 6 4.01, sucrose: 1.01 6 0.21 and 10.37 6
respiratory exchange ratio (RER) measured postexercise (PE; 83-min 1.63 mmol/l, respectively; NS) concentration.
cycling at 70% V̇O2 max ) and hourly for 3 h (R1–R3) after subsequent Liver volume and liver glycogen. Liver volume (liters)
ingestion of 1 g/kg body mass glucose (n 5 6), sucrose (n 5 6), or an and liver glycogen concentration (mmol/l) at rest, after
equivalent volume of placebo (control; n 5 5). Mean values were exercise, and during recovery are shown in Table 2.
significantly different from control: * P , 0.05, † P # 0.01; and
glucose: ‡ P , 0.05. Rates of liver glycogen resynthesis are shown as concen-
tration per unit time in Table 3.
Liver volume was lower during the recovery period
after exercise bout 1, and immediately before ingestion after exercise compared with resting values and ap-
of the drinks, blood glucose was 4.1 6 0.1, 3.8 6 0.1, and peared to fall further in the absence of exogenous CHO
3.7 6 0.2 mmol/l in the control, glucose, and sucrose (control; Table 2). This may be partly a consequence of a
trials, respectively (NS). As expected, 60 min after fall in liver glycogen concentration, which followed a
subjects ingested the drinks, blood glucose was higher similar pattern. CHO administration appeared to ar-
in the glucose (P , 0.01) and sucrose (P , 0.05) trials rest the decline in both liver glycogen concentration
compared with control (Table 1). A significant difference and liver volume (Table 2). However, a significant
was also found between the glucose and sucrose trials correlation between liver glycogen concentration and
(P , 0.05). Glucose concentrations fell to a similar level liver volume was not found in either the control,
after 180 min of recovery (NS between trials; Table 1), glucose, or sucrose trials.
and declined even further after 15 min of exercise bout Liver glycogen content (g) declined during exercise
2 (3.6 6 0.2, 3.4 6 0.1, and 3.4 6 0.1 mmol/l in the by 54 6 4 (P , 0.01), 56 6 6 (P , 0.05), and 58 6 6%
control, glucose, and sucrose trials, respectively; NS ). (P , 0.05) in the control, glucose, and sucrose trials,
It was common for values to fall below 3.0 mmol/l at the respectively. The decline was of the same magnitude in
end of exercise, and values as low as 2.5 mmol/l were all trials (NS). The time course of liver glycogen deple-
recorded in some individuals. Serum insulin concentra- tion and resynthesis is shown in Fig. 2, top. ANOVA
tions during the recovery period are given in Table 1. demonstrated a significant difference among trials in
Resting concentrations of plasma ammonia were Dliver glycogen content during recovery (P , 0.05;
73 6 4 , 69 6 6, and 62 6 4 µmol/l in the control, Fig. 3). It is evident from Fig. 3 that there was no
glucose, and sucrose trials, respectively (NS). No differ- glycogen resynthesis in the control trial after 30 min
ence in peak plasma ammonia concentration was found (219 6 12 g), 90 min (211 6 14 g), 150 min (219 6
during exercise bout 1 (156 6 16, 143 6 9, and 164 6 16 12 g), or 210 min (215 6 16 g) of recovery. However,
µmol/l; NS in the control, glucose, and sucrose trials, glycogen resynthesis was evident in both the glucose
respectively) or exercise bout 2 (183 6 20, 159 6 17, and and sucrose trials (Fig. 3). The change in liver glycogen
189 6 20 µmol/l; NS in the control, glucose, and sucrose from postexercise values after glucose ingestion was
trials, respectively). There was a tendency for the significantly different from control after 30 min (12 6
change in plasma ammonia concentration during the 8 g, P , 0.01), 90 min (9 6 5 g, P 5 0.01), 150 min (17 6
initial 15 min of exercise bout 2 to be lower after CHO 7 g, P , 0.01), and 210 min (13 6 8 g, P , 0.01) of
administration, but the difference among means did recovery. Similarly, the change in liver glycogen after
not reach significance (102 6 14, 65 6 8, and 85 6 11 sucrose ingestion was significantly different from con-
µmol/l in the control, glucose, and sucrose trials, respec- trol after 30 min (6 6 6 g, P , 0.01), 90 min (10 6 8 g,
tively; P 5 0.069). P 5 0.01), 150 min (18 6 4 g, P , 0.01), and 210 min
There was no difference in the blood lactate or (25 6 5 g, P , 0.01) of recovery. No differences in liver
plasma catecholamine response to exercise and recov- glycogen resynthesis were found between the glucose
ery among trials. To give an indication of the response, and sucrose trials.
E70 LIVER AND MUSCLE GLYCOGEN METABOLISM

Table 2. Liver volume, liver glycogen concentration, muscle volume, and muscle glycogen concentration
Rest PE R1 R2 R3 R4

Liver
C volume 1.87 6 0.10 1.80 6 0.09 1.75 6 0.10 1.72 6 0.12a 1.69 6 0.14 1.63 6 0.15a
C glycogen 375 6 61 191 6 52b 130 6 12b 155 6 11a 135 6 16b 151 6 18a
G volume 1.89 6 0.14 1.82 6 0.14 1.76 6 0.14b 1.79 6 0.10 1.74 6 0.11b 1.77 6 0.13b
G glycogen 397 6 84 177 6 43a 213 6 44a 211 6 49a,c 242 6 51c 228 6 49
S volume 1.85 6 0.17 1.71 6 0.13a 1.65 6 0.16b 1.68 6 0.19b 1.67 6 0.14a 1.67 6 0.13a
S glycogen 387 6 194 141 6 64 161 6 55 178 6 50 206 6 82c 233 6 77d,e
Muscle
C volume 4.86 6 0.27 5.17 6 0.43 5.05 6 0.40 5.10 6 0.45 4.98 6 0.42 5.04 6 0.42
C glycogen 166 6 35 70 6 18b 58 6 7a 69 6 10a,e 64 6 3a 68 6 8a
G volume 5.06 6 0.26 5.07 6 0.25 5.03 6 0.27 4.99 6 0.24 4.95 6 0.28 4.99 6 0.29
G glycogen 153 6 39 60 6 12a 100 6 46b 85 6 36b 93 6 38b 92 6 38b
S volume 4.83 6 0.23 5.01 6 0.21 5.03 6 0.25 4.92 6 0.23 4.99 6 0.17 5.05 6 0.20
S glycogen 159 6 31 55 6 13b 60 6 8a 72 6 13a,d 72 6 8a 80 6 10a
Values are means 6 SE. Liver volume (liters), liver glycogen concentration (mmol/l), muscle volume (liters), and muscle glycogen
concentration (mmol/l) measured pre- (rest) and postexercise at 70% V̇O2 max and hourly for 4 h (R1–R4) after subsequent ingestion of 1 g/kg
body mass glucose (G; n 5 6), sucrose (S; n 5 6), or an equivalent volume of placebo [control (C); n 5 5]. Mean values were significantly different
from rest: a P , 0.05, b P # 0.01; PE: c P , 0.05, d P # 0.01; R1: e P , 0.05.

A relationship was found between the CHO load (g) toward an increase in muscle glycogen was observed
and Dliver glycogen content (g) after 30 min (r 5 0.63; during the recovery period after CHO ingestion, but no
P , 0.05), 90 min (r 5 0.59; P , 0.05), 150 min (r 5 0.79; significant differences were found among trials.
P , 0.01), and 210 min (r 5 0.70; P , 0.01) of recovery. A No relationship was found between the CHO load (g)
weak but statistically significant relationship was evi- and Dmuscle glycogen content (g) during recovery (r 5
dent between Dliver glycogen content (g) after 240 min 0.06–0.39; NS). Furthermore, no relationship was evi-
of recovery and time-to-exhaustion during exercise dent between Dmuscle glycogen content (g) after 240-
bout 2 (n 5 15; Fig. 4). min recovery and time-to-exhaustion during exercise
Muscle volume and muscle glycogen. Muscle volume bout 2 (r 5 0.44; NS). However, a relationship was
(liters) and muscle glycogen concentration (mmol/l) at found between the CHO load (g) and the sum of Dliver
rest, after exercise, and during recovery are shown in and muscle glycogen resynthesis (g) after 60 min (r 5
Table 2. Rates of muscle glycogen resynthesis are 0.64; P , 0.05), 180 min (r 5 0.65; P , 0.01), and 240
shown as concentration per unit time in Table 3. min (r 5 0.62; P , 0.05) of recovery. A weak but
Muscle volume was unchanged after 83 min of cy- statistically significant relationship was evident be-
cling exercise at 70% V̇O2 max and subsequent ingestion tween the sum of Dliver and Dmuscle glycogen content
of placebo or 1 g/kg body mass glucose or sucrose. (g) after 240 min of recovery and time-to-exhaustion
Muscle glycogen content (g) declined by 56 6 5 (P , during exercise bout 2 (n 5 15; Fig. 5).
0.01), 58 6 7 (P , 0.05), and 61 6 6% (P 5 0.01) in the The mean CHO load was 76 g in both glucose and
control, glucose, and sucrose trials, respectively. The sucrose trials. Assuming equal glycogen resynthesis in
decline was of the same magnitude in all trials (NS). both legs, the calculated increase in total CHO disposal
The time course of muscle glycogen depletion and during the 4-h recovery period after glucose and su-
resynthesis is shown in Fig. 2, bottom. No glycogen crose ingestion ([CHO oxidation 2 control CHO oxida-
resynthesis was evident in the control trial. A trend tion] 1 [Dliver glycogen resynthesis 0–210 min 2
Dcontrol liver glycogen resynthesis 0–210 min] 1
Table 3. Rates of liver and muscle glycogen resynthesis [Dmuscle glycogen resynthesis 0–240 min 2 Dcontrol
muscle glycogen resynthesis 0–240 min, 32]) was 64
R1 R2 R3 R4 and 82 g, respectively (NS between trials).
Liver
Control 261 6 42 25 6 9 220 6 14 16 6 18 DISCUSSION
Glucose 36 6 20 22 6 25 31 6 24 214 6 8
Sucrose 20 6 13* 17 6 10 28 6 34 27 6 17 This is the first investigation of simultaneous changes
Muscle in human liver and skeletal muscle glycogen content,
Control 212 6 21 10 6 15 25 6 9 4 6 11 corrected for tissue volume, during exercise and recov-
Glucose 40 6 39 215 6 11 866 21 6 4 ery. It is also the first occasion postexercise resynthesis
Sucrose 569 11 6 7 068 869
of liver and muscle glycogen has been related to subse-
Values are means 6 SE. Rates of liver and muscle glycogen quent endurance exercise capacity.
resynthesis (mmol · l21 · h21 ) measured hourly for 4 h (R1–R4) after 83 MRS allows direct, noninvasive, and repeated mea-
min of exercise at 70% V̇O2 max and subsequent ingestion of 1 g/kg body
mass glucose (n 5 6), sucrose (n 5 6), or an equivalent volume of
surement of liver and muscle glycogen stores (18, 35,
placebo (control, n 5 5). Mean values were significantly different from 37). Despite its large molecular size, glycogen is 100%
control: * P , 0.05. visible with MRS (18, 40, 41). The first natural abun-
 LIVER AND MUSCLE GLYCOGEN METABOLISM
Fig. 2. Human liver (top) and skeletal muscle (bottom) glycogen
content (g) before and after 83-min cycling exercise at 70% V̇O2 max
and during recovery after ingestion of 1 g/kg body mass glucose or
sucrose or an equivalent volume of placebo (control; n 5 6). Glycogen
measurements (mmol/l) were made by natural abundance 13C MRS.
C-1 signal was quantified by comparison to spectra from a glycogen
phantom (200 mmol/l oyster glycogen and 150 mmol/l KCl; total vol
2 liters). Lipid peak at 30 ppm (-CH2-) was used as an internal
standard. Liver and muscle volume (liters) was measured immedi-
ately after acquisition of each liver and muscle spectrum, respec-
tively. This enabled calculation of total glycogen content in millimoles
and therefore in grams. Liver spectra and volume measurements
were obtained within the first 30 min after CHO ingestion and then
hourly. Muscle spectra and volume measurements were obtained
from 30–60 min and then hourly.
dance 13C glycogen signals from human liver and
muscle were obtained in the mid-1980s (26), but these
measurements lacked the sensitivity to monitor physi-
ological changes. Subsequent pilot investigations, with
a higher field strength, successfully monitored changes
in muscle glycogen during exercise and recovery (1).
However, postexercise refeeding was not controlled, 13C
signals were not quantified, and no measurements of
liver glycogen or restoration of exercise capacity were
made.
Jue et al. (27) employed interleaved measurements of
human liver and muscle glycogen to study responses to
a mixed meal after a 30-h fast (n 5 1). However, only
E71
limited data are currently available from interleaved
measurements of human liver and muscle glycogen
during exercise and recovery (35).
In the present study, a consistent decline in liver and
muscle glycogen content (,55–60%) was found after
83 min of exercise at 70% V̇O2 max. These results support
previous observations of a decline in both liver and
muscle glycogen after prolonged exhaustive exercise in
humans (2, 22). Liver glycogen content increased dur-
ing the recovery period after CHO ingestion, and these
changes were significantly greater throughout recovery
when compared with the control trial (Fig. 3). In the
absence of exogenous CHO, hepatic glycogenolysis is
the principal means of maintaining euglycemia during
exercise, and the rate of glycogenolysis is directly
related to the hepatic glycogen content (47). Figure 3
demonstrates that both glucose and sucrose ingestion
increased liver glycogen stores, thereby increasing the
potential for substrate delivery to skeletal muscle
during a subsequent bout of exercise.
It has been suggested that the ability to perform
prolonged submaximal exercise becomes increasingly
dependent on blood glucose availability as exercise
progresses, particularly in well-trained subjects (13).
The authors demonstrated that as muscle glycogen
stores were reduced, oxidation of CHO from alternative
sources was increased to meet the energy demands of
contraction. It was also shown that fatigue could be
delayed by maintaining a high rate of CHO oxidation
via oral glucose ingestion. Interestingly, later studies
have indicated that the magnitude of the increase in
contribution of blood glucose to total energy production
during exercise is primarily a function of glucose avail-
ability (48, 49). Together these studies suggest that
blood glucose availability, whether supplied from exog-
enous CHO or liver glycogenolysis, is important to
endurance exercise capacity. It also suggests that differ-
ences between glucose and sucrose in terms of postexer-
cise liver glycogen resynthesis could have important
consequences for subsequent exercise capacity.
The results of the present study provide support for
the importance of blood glucose availability to postexer-
cise glycogen resynthesis, and, in some degree, to
subsequent exercise capacity. After the initial bout of
glycogen-depleting exercise in the present study, no
evidence of liver or muscle glycogen resynthesis was
found in the control trial, in which no CHO was given.
Liver glycogen resynthesis was evident during the
recovery interval after CHO ingestion. Given that the
Michaelis-Menten constant (Km) of glucokinase is in the
order of 8 mmol/l and blood glucose concentration was
still ,6 mmol/l 1 h after CHO ingestion, it is likely that,
as expected, the direct pathway probably contributed to
a significant proportion of glycogen resynthesis. The
importance of glucose availability is illustrated by the
significant relationship found between the CHO load
and Dliver glycogen content throughout recovery (r 5
0.59–0.79, P , 0.05). Of course, this represents only net
glycogen synthesis, and no account has been taken of
liver glycogen turnover, which has been shown to
proceed under conditions of net glycogen synthesis in
E72 LIVER AND MUSCLE GLYCOGEN METABOLISM
Fig. 3. Change in liver glycogen content (g) after
exercise-induced glycogen depletion and subsequent
ingestion of 1 g/kg body mass glucose or sucrose
(n 5 6) or an equivalent volume of placebo (control;
n 5 5). Change in glycogen content in the glucose
and sucrose trials was significantly different from
control throughout recovery (P # 0.01). No differ-
ences were found between glucose and sucrose trials.
humans (32). Furthermore, a modest but significant
relationship was evident between Dliver glycogen con-
tent at the end of the recovery period and subsequent
exercise time-to-exhaustion (r 5 0.53, P , 0.05). Based
on animal studies, Terjung et al. (44) postulated that
when both liver and muscle glycogen stores are de-
pleted during exercise, repletion of liver glycogen might
be the rate-limiting factor in the capacity for prolonged
strenuous exercise. The present results indicate that,
after a small CHO load in humans, subsequent endur-
ance capacity may be dependent to some degree on a
liver-mediated increase in muscle glucose delivery.
No differences in liver or muscle glycogen resynthesis
or subsequent endurance exercise capacity were found
when comparing responses to 1 g/kg BM glucose or
sucrose ingestion. This is somewhat surprising given
sucrose contains equimolar fractions of glucose and
Fig. 4. Relationship between Dliver glycogen content (g) after 240
min of recovery and subsequent exercise time-to-exhaustion (r 5
0.53, P , 0.05). Exercise commenced 240 min after exercise-induced
glycogen depletion and subsequent ingestion of 1 g/kg body mass
glucose or sucrose or an equivalent volume of placebo (control).
fructose, which are metabolized predominantly by
muscle and liver, respectively (3, 50). Although the
GLUT-5 transporter isoform is expressed in human
skeletal muscle (23), the affinity of hexokinase for
fructose is very low, and, in the absence of the enzyme
fructokinase, phosphorylation of fructose will be very
slow in comparison with glucose. It appears that skel-
etal muscle can only utilize significant quantities of
fructose after conversion to glucose in the liver. Fructo-
kinase is present in liver, where it has a low Km, and,
consequently, a high affinity for fructose. On the basis
of this, sucrose might have been expected to preferen-
tially restore liver, rather than muscle, glycogen stores
after exercise. The finding that it did not may be related
to the small quantity of CHO given, an increase in
insulin sensitivity as a result of the exercise, or an
increase in liver glycogen turnover in the sucrose trial.
Fig. 5. Relationship between the sum of Dliver and Dmuscle glycogen
content (g) after 240 min recovery and subsequent exercise time-to-
exhaustion (r 5 0.55, P , 0.05). Exercise commenced 240 min after
exercise-induced glycogen depletion and subsequent ingestion of 1
g/kg body mass glucose or sucrose or an equivalent volume of placebo
(control).
 LIVER AND MUSCLE GLYCOGEN METABOLISM
In a previous study from this laboratory, Moriarty et
al.(35) investigated the effects of glucose and sucrose
ingestion on postexercise liver and muscle glycogen
resynthesis alone. Tissue glycogen was represented as
a percentage of the lipid peak. Muscle glycogen levels
were shown to fall during exercise and to increase
during recovery, but no changes in liver glycogen levels
were found. Furthermore, no differences in liver or
muscle glycogen resynthesis were found after glucose
or sucrose ingestion. However, nutrient intake was not
controlled before exercise, positioning of the 13C liver
and muscle probes did not have the benefit of imaging
techniques, and, perhaps as a consequence of this,
inter- and intra-individual resting muscle and liver
glycogen levels were highly variable. Proton decoupling
was not used, resulting in a signal-to-noise ratio that
was approximately one-half of that obtained in the
present study. In addition, no attempt was made to
quantify the glycogen signal. On the basis of the results
of the present study, it appears methodological prob-
lems may account for failure of the authors to demon-
strate a decline in liver glycogen during exercise or
resynthesis of liver glycogen during recovery.
It is possible that administration of a relatively large
CHO bolus (177 g) by Moriarty et al. was sufficient to
mask a difference between glucose and sucrose uptake
and disposal by liver and muscle. The present study
demonstrates, however, that a differential response
does not exist after a smaller CHO load. This is
supported, in the case of muscle glycogen resynthesis,
by Blom et al. (5), who compared feedings of 0.7 g/kg
BM glucose and sucrose given at 2-h intervals during a
6-h recovery period after exercise-induced glycogen
depletion. With this relatively small intake, no differ-
ence in the average rate of muscle glycogen resynthesis
was found between the two conditions (5.8 6 1.0 and
6.2 6 0.5 mmol · kg wet wt21 · h21, respectively). Van
den Bergh et al. (45) found a significantly higher rate of
postexercise muscle glycogen resynthesis when re-
peated ingestion of 80 g of glucose (total 320 g) was
compared with a similar regimen of fructose ingestion
over an 8-h period. Furthermore, Burke et al. (9)
measured muscle glycogen concentration 24 h after
exercise, during which time subjects consumed 10 g/kg
BM CHO (690 g) of either high or low GI foods. They
demonstrated a clear advantage of high GI CHO sources
compared with low GI sources in terms of short-term
muscle glycogen resynthesis. Differences between these
studies may have been a function of the type or
quantity of the CHO load and/or recovery time, but they
do suggest a high CHO load does not preclude the
ability to measure differences between glucose- and
sucrose-mediated glycogen resynthesis. Neither Burke
et al. nor Blom et al. (5) performed measurements of
liver glycogen resynthesis or assessed the effects of
these different types of CHO on restoration of exercise
capacity.
Significant changes in muscle glycogen content after
CHO ingestion were not demonstrated. This is surpris-
ing given previous studies have demonstrated that
short-term skeletal muscle glycogen resynthesis after
E73
exercise-induced glycogen depletion is linearly related
to the exogenous CHO load; albeit, CHO ingestion was
relatively high (12 g/kg BM; Ref. 42). Consequently,
this finding may be due to administration of a relatively
small CHO load, a proportion of which was extracted by
the liver (,30%) before being made available to the
relatively large mass of skeletal muscle. The relation-
ship between CHO load and muscle glycogen resynthe-
sis and the relationship of muscle glycogen availability
to endurance exercise performance is well established
in humans (20, 28). A possible dilution effect in the
present study is supported by the absence of a relation-
ship between the CHO load and Dmuscle glycogen
content during recovery or between Dmuscle glycogen
content and subsequent exercise performance. A rela-
tionship between the sum of glycogen synthesis in the
liver and muscle and these variables would suggest a
pattern of resynthesis, which, although undetectable in
muscle alone, was similar to that in the liver. Accord-
ingly, the CHO load was significantly correlated with
the sum of Dliver and Dmuscle glycogen content during
recovery (r 5 0.62–0.65, P , 0.05). A modest but
significant relationship was evident between the sum of
Dliver and Dmuscle glycogen content at the end of the
recovery period and subsequent exercise time-to-
exhaustion (r 5 0.55, P , 0.05).
The absence of a significant change in muscle glyco-
gen, together with the inability to detect differences
between glucose- and sucrose-mediated liver or muscle
glycogen resynthesis, also appears to be due to the
large interindividual variation in glycogen measure-
ments. The relatively small interindividual variation in
the control trial suggests that this represented a physi-
ological variation in rates of CHO disposal rather than
variation resulting from instrumentation. A number of
factors may account for this variation. One factor may
be interindividual variations in muscle composition.
The rate of postexercise glycogen resynthesis, deter-
mined with biochemical analysis, has been shown to be
25% higher in human type I muscle fibers when com-
pared with type II fibers during the initial 3 h of
recovery (10). This is probably related to fiber-type
variations in the rate of muscle glucose uptake. In this
respect, it has been shown that muscles composed
predominantly of type I fibers have a greater plasma
membrane glucose transporter number (17), and more
specifically, the highest content of the GLUT-4 glucose
transporter isoform (25). A second factor may be the
glucose load. As discussed earlier, glucose availability
to the muscle will be higher after glucose than fructose
ingestion.Variation in glycogen resynthesis, arising
from fiber-type differences in glucose uptake and dis-
posal, might therefore be expected to be greater after
glucose ingestion.
Plasma ammonia accumulation during the initial
period of exercise bout 2 tended to be lower after CHO
administration, suggesting improved maintenance of
the ATP-to-ADP ratio. This would be expected to trans-
late into reduced rates of fatigue, but differences in
exercise time-to-exhaustion did not reach significance.
E74 LIVER AND MUSCLE GLYCOGEN METABOLISM
From a methodological point of view, this study
demonstrates for the first time that significant changes
in liver volume occur with this experimental paradigm.
These changes in volume may confound analysis of
changes in liver glycogen concentration during pro-
longed exercise and recovery. Accordingly, coupling of
tissue glycogen measurements to tissue volume mea-
surements, enabling calculation of liver glycogen con-
tent (g), provides a more accurate means to investigate
changes in liver glycogen under these conditions.
In conclusion, this study has demonstrated that 1
g/kg BM glucose or sucrose is sufficient to initiate
postexercise liver glycogen resynthesis. A weak but
statistically significant correlation between postexer-
cise liver glycogen resynthesis and subsequent exercise
capacity was demonstrated, but no difference in mean
exercise time was found after placebo, glucose, or
sucrose ingestion. The role of liver glycogen homeosta-
sis during exercise and recovery has been previously
underestimated. It is not possible to detect significant
changes in postexercise muscle glycogen content after
administration of relatively small amounts of CHO.
We are grateful to SmithKline Beecham for supporting this
research.
New address for A. Casey: Centre for Human Sciences, DERA,
Farnborough, Hants GU14 6TD, UK.
Address for reprint requests and other correspondence: P. Green-
haff, School of Biomedical Sciences, University of Nottingham Medi-
cal School, Nottingham NG7 2UH, UK.
Received 13 October 1998; accepted in final form 7 September 1999.
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