Journal of Physiology (2002), 542.2, pp.

403412
The Physiological Society 2002

DOI: 10.1113/jphysiol.2002.018135
www.jphysiol.org

Journal of Physiology

Myocardial and skeletal muscle glucose uptake during

exercise in humans
Jukka Kemppainen *, Toshihiko Fujimoto*, Kari K. Kalliokoski *, Tapio Viljanen*, Pirjo Nuutila*
and Juhani Knuuti *
* Turku PET Centre, University of Turku, PO Box 52, 20521 Turku, Finland, Department of Medicine, University of Turku, Turku, Finland
and Department of Medicine and Science in Sports and Exercise, Graduate School of Medicine, University of Tohoku, Sendai, Japan

The purpose of this study was to investigate the effects of exercise on myocardial glucose uptake and
whether the pattern of glucose uptake is the same as in skeletal muscle. Glucose uptake was
measured using positron emission tomography (PET) and 2-[18F]fluoro-2-deoxy-D-glucose
([18F]FDG). Twelve healthy men were studied during rest, while 14 subjects were studied after
35 min of bicycle exercise corresponding to 30, 55 and 75 % of maximal oxygen consumption (O2,max)
on three separate days. [18F]FDG was injected 10 min after the start of exercise and exercise
continued for a further 25 min. Myocardial and skeletal muscle PET scanning was commenced
directly after the completion of the exercise bout. As compared to the resting state, exercise doubled
myocardial glucose uptake at the 30 % (P = 0.056) and 55 % intensity levels (P < 0.05), while at the
75 % intensity level glucose uptake was reduced significantly compared to the lower exercise
intensities. There was no significant difference between the highest intensity level and the resting
state (P = 0.18). At rest and during low-intensity exercise, myocardial glucose uptake was inversely
associated with circulating levels of free fatty acids. However, during higher exercise intensities
when plasma lactate concentrations increased significantly, this association disappeared. In
contrast to myocardial responses, skeletal muscle glucose uptake rose in parallel with exercise
intensity from rest to 30 % and then 55 % O2,max (P < 0.001) and tended to increase further at the
intensity of 75 % O2,max (P = 0.065). In conclusion, these results demonstrate that myocardial glucose
uptake is increased during mild- and moderate-intensity exercise, but is decreased during highintensity exercise. This finding suggests that the increased myocardial energy that is needed during
high-intensity exercise is supplied by substrates other than glucose.
(Received 1 February 2002; accepted after revision 19 April 2002)
Corresponding author J. Knuuti: Turku PET Centre, PO Box 52, 20521 Turku, Finland. Email: juhani.knuuti@tyks.fi

Limited data are available regarding the influence of

different physiological exercise intensities on myocardial
glucose uptake. It is not currently clear whether myocardial
glucose uptake increases with increasing exercise intensity,
as is seen in skeletal muscle (Kjaer et al. 1986). Gertz et al.
(1988) reported that myocardial glucose uptake increased
twofold during supine bicycle exercise performed at 40 %
of maximal oxygen consumption (J,max), but they were
unable to measure glucose uptake during high-intensity
exercise due to methodological limitations. In the study of
Camici et al. (1989), cardiac pacing increased myocardial
glucose uptake in parallel with the increase in heart rate.
However, cardiac pacing does not induce the same metabolic
response that is obtained during physiological exercise.
The heart has a greater oxygen consumption both at rest
and during exercise compared to skeletal muscle (Rowell,
1986). The greater demand for oxidative metabolism in
the heart is compensated for by a greater mitochondrial
volume and oxidative enzyme capacity, along with a greater

activity of cardiac-type lactate dehydrogenase (Jansson &

Sylven, 1986). Therefore, myocardial fuel preference
during exercise may be different to that of skeletal muscle
at different exercise intensities.
With regard to the difference in the oxidative capabilities
of heart and skeletal muscle and lack of quantified myocardial glucose uptake data during aerobic and anaerobic
exercise, it is physiologically relevant to study and compare
myocardial and skeletal muscle glucose uptake during
exercise of different intensities. The purpose of this study
was to investigate the effect of exercise on myocardial
glucose uptake and whether this glucose uptake pattern is
similar in skeletal muscle. Therefore, myocardial and
skeletal muscle glucose uptake was measured at rest and
after low-, moderate- and high-intensity bicycle exercise using
positron emission tomography (PET) and 2-[18F]fluoro2-deoxy-D-glucose ([18F]FDG). This approach allows a
direct assessment of myocardial and skeletal muscle
metabolism without interference from other tissues and

404

J. Kemppainen and others

Table 1. Characteristics of the subjects in the two

experimental groups (exercising and resting)

Journal of Physiology

Exercise
(n = 14)
Age (years)
Body mass (kg)
Height (cm)
BMI
J,max (ml kg_1 min_1)

30.4 6.2
79.1 12.2
181.2 4.9
24.1 2.8
49.6 9.7

Rest
(n = 12)
30.1 7.7
77.2 9.3
182.8 5.3
23.1 3.0
NA

BMI, body mass index; J,max, maximum oxygen consumption;

NA, not applicable.

without invasive cardiac catheterisation. Moreover, myocardial and skeletal muscle glucose uptake can be quantified
within any given regions of interest (ROIs) in vivo.

METHODS
Subjects
Twenty-six well-conditioned, apparently healthy men participated
in the study. The subject characteristics are presented in Table 1.
The subjects were not taking any medications and were healthy as
judged by their history, a physical examination and routine
laboratory tests. The purpose and potential risks of this study were
explained to the subjects and written informed consent to
participate was obtained from them. The study was performed
according to the Declaration of Helsinki and the joint Ethical
Committee for the Turku University Central hospital and the
University of Turku approved the study protocol.
Study design
The subjects were instructed to maintain a regular diet. They
fasted for at least 12 h before the study and any kind of strenuous
physical activity was prohibited for at least 1 day before the
experiment. Subjects were divided into two groups, resting and

J. Physiol. 542.2

exercising: 14 subjects participated in the exercise protocol and

12 subjects were studied only at rest. Each subject involved in the
exercise protocol was studied on three separate days within
3 weeks with a minimum of 2 days separating each study day. The
study design is illustrated in Fig. 1. Two catheters were inserted,
one in an antecubital forearm vein for injection of [18F]FDG, and
another in the opposite antecubital vein for sampling of
arterialised venous blood. Plasma glucose samples were drawn at
0, 10, 20, 35, 50 and 60 min after the start of exercise. Serum
insulin samples were drawn at 0, 35, 40, 50 and 60 min. The blood
samples for cortisol, free fatty acids (FFAs) and lactate were drawn
before and at the end of exercise, and after the heart PET scan.
Arterialised venous blood samples for measurement of plasma
radioactivity were obtained from the time of injection to the end
of scan as follows: 10 samples within the first 3 min, thereafter
samples at 4, 5, 7.5, 10, 20, 30, 40 and 50 min after the injection. At
the beginning of the study, transmission scans of the femoral and
thoracic regions were performed and the scanning areas were
carefully marked on the skin. Subjects cycled (828E Monark,
Sweden) on three separate days at workloads of 30, 55 or 75 %
J,max at a pedal cadence of 60 r.p.m. After 10 min of exercise,
[18F]FDG (156.2 2.8 MBq) was injected, and the exercise
continued thereafter for 25 min, giving a total exercise time of
35 min. PET imaging started immediately after the end of exercise. A
12 min static scan of the femoral region was performed, followed
by a 12 min static scan of the thoracic region. In the group studied
only at rest, skeletal muscle scans were performed on five subjects,
while seven subjects completed the whole study protocol. PET
scanning and blood sampling was carried out as in the exercise
group.
PET tracer, image acquisition and processing
[18F]FDG was synthesised with an automatic apparatus by a
modification of the method of Hamacher et al. (1986). The
specific radioactivity at the end of the synthesis of [18F]FDG was
~74 GBq mmol_1 and its radiochemical purity exceeded 98 %. An
eight-ring ECAT 931/08-tomograph (Siemens/CTI, Knoxvill, TN,
USA) with an axial resolution of 6.7 mm and an in-plane
resolution of 6.5 mm was used. All data were corrected for
deadtime, decay and measured photon attenuation. Static FDG
scans were reconstructed into a 128 w 128 matrix using the
median root prior (MRP) technique (Alenius & Ruotsalainen,
1997). The final in-plane resolution of the reconstructed images
was 8 mm.
Regions of interest
For determination of myocardial glucose uptake, ROIs were
drawn on four adjacent midventricular planes, with care taken to
avoid the myocardial borders. ROIs within the quadriceps femoris
(QF) were drawn on four adjacent planes in the middle of the QF
between the patella and the spina iliaca anterior superior on both
the left and right legs. The average value of these ROIs was used to
calculate glucose uptake. Example ROIs are presented in Fig. 2.

Figure 1. Study design

The arrow indicates 2-[18F]fluoro-2-deoxy-D-glucose ([18F]FDG)
injection 10 min after the beginning of exercise. Before and
immediately after exercise, transmission and emission scans were
obtained from the thoracic and femoral regions, respectively.
Exercise duration was 35 min and the total study time was
120 min. PET, positron emission tomography; J,max, maximal
oxygen consumption.

Calculation of regional glucose uptake

Quantification of glucose uptake was based on the method
developed by Sokoloff et al. (1977). The rate of glucose uptake
(rGU) is obtained by multiplying the fractional rate of tracer
uptake (Ki) by the plasma glucose concentration ([Glc]p) divided
by a lumped constant term (LC): rGU = ([Glc]p/LC) w Ki. The LC
accounts for differences in the transport and phosphorylation of
[18F]FDG and glucose. An LC value of 1.2 was used for skeletal
muscle (Kelley et al. 1999; Peltoniemi et al. 2000) and 1.0 was used
for the myocardium (Ng et al. 1998). Since the PET scans were

Journal of Physiology

J. Physiol. 542.2

Myocardial glucose uptake during exercise

performed after exercise, we applied a simplified graphical

analysis on the data. The Ki was calculated as Cm/Cp : (Cp)/Cp,
where Cm is either myocardial or skeletal muscle radioactivity, Cp
is plasma radioactivity concentration, and Cp is the integral of
plasma radioactivity concentration from the time of injection to
the end of the respective scan. Since the plasma radioactivity is
very low 25 min after tracer injection and exercise, the period
between the end of exercise and the start of the scan has a minor
effect on myocardial and skeletal muscle tissue tracer counts.
Thus, the measured Ki reflects the situation during exercise.
J,max measurement
J,max was determined for each subject using a continuous
incremental cycle ergometer protocol and gas exchange analysis
(Model 800S, Ergoline, Mijnhardt, The Netherlands). Individual
aerobic and anaerobic thresholds were determined by lactate
measurements during the test. Workloads for the PET studies
were individually chosen to be 30, 55 and 75 % J,max.
Other measurements
Heart rate was monitored during the exercise using a heart rate
monitor (Vantage XL, Polar Electro, Finland). Plasma glucose was
determined by a glucose oxidase method (GM7 Analyser, Analox
Instruments, Hammersmith, London, UK). Plasma lactate was
determined by enzymatic analysis (Marbach & Weil, 1967).
Serum free insulin concentrations were measured using a doubleantibody radioimmunoassay (Pharmacia Insulin RIA kit, Pharmacia,
Uppsala, Sweden) after precipitation with polyethylene glycol.
Serum FFAs were determined with an enzymatic colorimetric
method (Nefa C test, Wako Chemicals, Neuss, Germany), and
serum cortisol concentrations by radioimmunoassay (Cortisol
[125I] Radioimmunoassay; Orion Diagnostica, Espoo, Finland).
Statistics
Statistical analysis was performed with the SAS statistical program
package (SAS Institute, Cary, NC, USA ) and Microsoft Excel 97. A
two-tailed Students unpaired t test was used to determine
whether there was a difference in myocardial or skeletal muscle
glucose uptake between the group studied only at rest and the
exercise group. An ANOVA followed by Tukeys Studentised

405

range test was used to compare the effect of different exercise

intensities. Non-linear regression analysis was used between
myocardial glucose uptake and FFA levels because it described the
relationship better, as documented previously (Nuutila et al.
1994). This analysis method was also used between myocardial
glucose uptake and plasma lactate concentrations. Calculations of
non-linear correlations were performed with Microsoft Excel 97.
R2 values were produced by exponential least-square fit. Critical
r values for P < 0.05 were obtained from statistical tables. The
results are expressed as means S.D.

RESULTS
Exercise parameters
The mean J,max in the exercise group was 49.6 9.7 ml
kg_1 min_1 and the maximal heart rate during the J,max test
was 190 9 beats min_1. The average exercise intensities at
30, 55 and 75% J,max were 91 24, 167 38 and 226 35 W,
respectively. Heart rates at the end of exercise at these three
intensities were 104 8, 149 16 and 177 10 beats min_1,
respectively. There were significant differences in both the
absolute values of exercise intensities and heart rates at
each exercise intensity level (P < 0.001).

Metabolic parameters
The concentration of plasma glucose and serum insulin
did not change during or after the exercise at 30 or 55 %
J,max. Plasma glucose started to increase slightly towards
the end of the 75 % J,max exercise period and was
significantly higher at the end of the exercise, remaining
slightly elevated for the subsequent 20 min (Fig. 3A).
Concomitantly, serum insulin concentration doubled
5 min after the end of exercise at the highest exercise
intensity as compared to pre-exercise values (Fig. 3B).
Compared to basal values, plasma lactate concentrations
did not increase significantly at the lowest exercise

Figure 2. Myocardial and femoral PET images at rest, and during exercise at 30, 55 and 75 %
J,max
The images are scaled to the fixed uptake level. Examples of regions of interest (ROIs) are presented on
myocardium and skeletal muscle.

J. Kemppainen and others

J. Physiol. 542.2

Journal of Physiology

406

Figure 3. Plasma glucose (A), serum insulin (B),

plasma lactate (C ), serum free fatty acid (FFA; D),
serum cortisol (E), and average plasma
radioactivity concentrations (F ) from the start of
the exercise period to the end of the PET scan
during three different exercise intensities
In AF, data relating to the three exercise intensities
imposed (30, 55 and 75 % J,max) are indicated by , 0 and
9, respectively. The resting state timeactivity curve is
presented in F (&). Values are expressed as means S.D. The
number of subjects who took part in the exercise studies was
14, while 7 were tested while resting. * P < 0.05 vs. baseline;
P < 0.05 and P < 0.01 vs. 30 % intensity, and P < 0.01
vs. 55 % intensity.

Journal of Physiology

J. Physiol. 542.2

Myocardial glucose uptake during exercise

intensity, but increased by a factor of 3.6 and 9.4 at

intensity levels of 55 and 75 % J,max, respectively (Fig. 3C).
Changes in serum FFA concentrations were minor. Serum
FFA concentrations increased significantly compared with
baseline values at the end of the lowest-intensity exercise
bout (Fig. 3D), while they remained unchanged at the
other two exercise intensity levels. Serum cortisol
remained unchanged during low-intensity exercise, but
was significantly increased during the higher exercise
intensities (Fig. 3E).

Circulating tracer concentrations

As shown in Fig. 3F, after injection of [18F]FDG, plasma
radioactivity increased immediately but then started to
decrease rapidly within a few minutes, and was very low
25 min after the tracer injection and exercise. The
availability of the tracer (the area under the timeactivity
curves; AUC) calculated from the plasma timeactivity
curves was significantly larger in the resting subjects, but
was similar between the different exercise intensity levels
(data not shown). The AUC between the end of exercise
and the start of the cardiac imaging was approximately
21 % of the total AUC. In addition, the variability of the
AUC during this period between the different exercise
intensities was less than 2 % of the total AUC.

Figure 4. Myocardial (A) and quadriceps

femoris muscle (B) glucose uptake during
rest and exercise (30, 55 and 75 % J,max)
Glucose uptake is shown per unit of mass. Values
are expressed as means S.D. The number of
subjects who took part in the exercise study was 14,
while the number of subjects tested while resting
was 7 in A and 12 in B. * P < 0.01 compared with
30 and 55 % J,max intensity; **P < 0.01 compared
with 30 % J,max intensity.

407

Myocardial glucose uptake

Myocardial glucose uptake did not increase in a linear
manner with increasing exercise intensity. Compared to
the resting state, exercise doubled myocardial glucose
uptake at 30 % (P = 0.056) and 55 % J,max (P < 0.05,
Fig. 4A). At the highest exercise intensity, glucose uptake
decreased significantly as compared to both the 30 % and
55 % intensity levels (P < 0.05), but remained somewhat
higher as compared to the resting state. However, the
difference between the highest exercise intensity and the
resting state was not statistically significant (P = 0.18).
Serum FFA concentration at the end of exercise and
myocardial glucose uptake correlated inversely at rest
(Fig. 5A) and during low-intensity exercise (Fig. 5B).
However, during moderate- and high-intensity exercise
(Fig. 5C and D), no significant association between serum
FFA and myocardial glucose uptake was found. Plasma
lactate concentration at the end of exercise was significantly
associated with myocardial glucose uptake only during the
55 % intensity level (r = _0.56, P < 0.05, Fig. 6C), but not
any more when the outlier point was removed (r = _0.26,
P = not significant). Serum insulin concentrations were not
significantly associated with myocardial glucose uptake
(data not shown).

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J. Kemppainen and others

Journal of Physiology

Skeletal muscle glucose uptake

QF glucose uptake paralleled the increase in exercise
intensity from rest to 30 % and then 55 % J,max (P < 0.001;
Fig. 4B). Glucose uptake tended to increase further at the
intensity of 75 % J,max (P = 0.065). There was no correlation
between skeletal muscle glucose uptake and plasma lactate,
serum FFA or insulin either at rest or during the three
different exercise intensities (data not shown). Example
myocardial and skeletal muscle PET images with ROIs are
shown in Fig. 2.

DISCUSSION
The purpose of this study was to investigate the effect of
exercise on myocardial glucose uptake and whether this
glucose uptake pattern is similar in skeletal muscle. We
found that in contrast to skeletal muscle, myocardial
glucose uptake did not increase linearly with increasing
exercise intensity. During low- and moderate-intensity
exercise, myocardial glucose uptake doubled as compared
to the resting state, but during the highest intensity it was
lower than during the other exercise levels. This indicates
that during high-intensity exercise the increased myocardial
energy requirements are provided by substrates other than
glucose. At rest and during low-intensity exercise, myo-

J. Physiol. 542.2

cardial glucose uptake correlated inversely with circulating

levels of FFAs, indicating that the glucoseFFA cycle
operates under these conditions. However, during higher
exercise intensities, this association disappeared. In contrast
to the myocardial responses, skeletal muscle glucose
uptake rose in parallel with exercise intensity, a result that
is in accordance with those of previous studies (Kjaer et al.
1986; Kristiansen et al. 2000; van Loon et al. 2001).
There is a paucity of data in the literature regarding
myocardial glucose uptake during exercise. There are only
two previous studies in which myocardial glucose uptake
was quantified during exercise or myocardial stress (Gertz
et al. 1988; Camici et al. 1989). Gertz et al. (1988) found in
a dual-carbon-labelled isotope study that myocardial
glucose uptake doubled during exercise at 40 % J,max
compared to the resting state, which is concordant with
the results of the present study. According to our results,
increasing the exercise intensity (to 55 % J,max) did not
further enhance glucose uptake. Interestingly, high-intensity
exercise (75 % J,max) led to a significant decrease in myocardial glucose uptake when lactate levels increased almost
10-fold. In contrast, in a study by Camici et al. (1989),
cardiac pacing evoked no increase in lactate levels, while
myocardial glucose uptake increased in parallel with heart

Figure 5. Association between myocardial glucose uptake and serum FFA concentration at
rest (A), and while exercising at 30 % (B), 55 % (C) and 75 % J,max (D)

J. Physiol. 542.2

Myocardial glucose uptake during exercise

Journal of Physiology

rate. Because lactate is one of the main energy substrates

utilised during exercise and its concentration may increase
over 10 times during strenuous exercise (Kjaer et al. 1986),
the dynamics of myocardial glucose uptake during cardiac
pacing does not represent physiological conditions.
FFAs play an important role in determining the rate of
myocardial glucose uptake through the glucose-fatty acid
cycle both at rest (Wisneski et al. 1985, 1990; Nuutila et al.
1992) and during prolonged low- to moderate-intensity
exercise (Wahlqvist et al. 1973), but this seems to be
unlikely during high-intensity exercise. In our study,
myocardial glucose uptake was inversely associated with
the circulating levels of FFAs at rest and during lowintensity exercise, which is concordant with the findings
by Wahlqvist et al. (1973). However, this negative relationship was not seen during exercise at higher intensities
(55 and 75 % J,max) in our study. Bertrand et al. (1977)
hypothesised that glucose and lactate would compensate
for the decrease in FFA availability as an energy source
during exercise. Evidence from animal studies suggests
that an enhanced supply of lactate could effectively inhibit
cardiac fatty acid oxidation (Spitzer, 1974; Drake et al.
1980; Bielefeld et al. 1985) by inhibiting the activity of
carnityl acyl CoA transferase in the cardiac myocyte
(Bielefeld et al. 1985).

409

Since serum FFA concentration changes were minor

during exercise, increased lactate availability and uptake
could provide an explanation as to why myocardial
glucose uptake was not further increased at the highest
exercise intensity. It has been shown that myocardial
lactate extraction is related to arterial lactate levels at rest
(Gertz et al. 1980) and during submaximal exercise
(Carlsten et al. 1961; Krasnow et al. 1962). It has been
suggested that lactate could account for up to 65 % of the
substrate for myocardial oxidative metabolism during
exercise (Keul, 1971; Bertrand et al. 1977). Takala et al.
(1983) showed in a study using rats that myocardial
glucose uptake was decreased during 20 min of swimming
exercise when lactate levels increased sevenfold, suggesting
that inhibition of myocardial glucose uptake during
exercise is due to an increased availability of other
substrates for oxidative metabolism.
An enhanced availability of lactate due to increased
exercise intensity provides an alternative energy source for
the myocardium, therefore diminishing the demand for
glucose. This may serve as a cardioprotective mechanism
during ischaemic stress as well as during conditions of
increased cardiac work, since lactate has been shown to
divert glucose from glycolysis to glycogen synthesis, causing
accumulation of glycogen in myocardial cells (Depre et al.

Figure 6. Association between myocardial glucose uptake and plasma lactate concentration
at rest (A), and while exercising at 30 % (B), 55 % (C ) and 75 % J,max (D)

Journal of Physiology

410

J. Kemppainen and others

1993, 1998). The lack of inverse association with serum

lactate and myocardial glucose uptake during highintensity exercise might be due to the inability of PET and
[18F]FDG to measure separately the amount of glucose
entering oxidative and non-oxidative metabolism. Using
[18F]FDG it is possible to measure glucose uptake, but not
to obtain direct information of its later fate. Nevertheless,
it may be hypothesised that by increasing the exercise
intensity and lactate availability the proportion of glucose
entering glycolysis will diminish, whereas the proportion
entering glycogen synthesis increases (Depre et al. 1993).
In contrast to the myocardial responses, skeletal muscle
glucose uptake rose in parallel with exercise intensity in the
present study, suggesting that skeletal muscle is more
dependent upon a continuous glucose supply during highintensity exercise. At rest and during low- to moderateintensity exercise, lipids predominate as the preferred
energy source. When exercise intensity increases, a shift in
substrate utilisation towards carbohydrates occurs (Brooks
& Mercier, 1994; Friedlander et al. 1997).

Limitations of the study

Except for insulin and cortisol, other hormonal factors
were not measured in the present study. Therefore, we
cannot exclude the influence of other factors such as
growth hormone or cathecolamines on glucose uptake.
However, myocardial glucose extraction has not been
significantly related to arterial insulin, growth hormone or
glucocorticoid concentrations during exercise (Wahlqvist
et al. 1973). Observed responses in myocardial and skeletal
muscle glucose uptake may be partly related to hormonal
changes. In the present study, cortisol levels increased in
parallel with exercise intensity. However, neither insulin
nor cortisol concentrations were correlated with myocardial glucose uptake levels during exercise (data not
shown). During exercise at the highest intensity, plasma
glucose increased slightly, but the average glucose value
remained euglycaemic.
Currently, PET scanning during dynamic exercise is
technically problematic. Therefore, the injection of
[18F]FDG, as utilised in the present study, was performed
during exercise, which was then continued for an
additional 25 min, and scanning was performed directly
after the exercise. Despite this, the measured glucose
uptake values reflect the actual glucose uptake during
exercise. After phosphorylation, the glucose analogue
([18F]FDG) is trapped inside the muscle cell where further
metabolism is prevented due to its chemical characteristics.
This metabolic state of phosphorylated [18F]FDG is
preserved for approximately 2 h after injection (Gallagher
et al. 1977). Plasma radioactivity peaked shortly after
[18F]FDG injection, and then decreased quickly during
exercise (Fig. 3F). In addition to the tissue glucose uptake,
the total uptake of tracer into the tissues is dependent upon

J. Physiol. 542.2

the availability of the tracer, specifically the AUC for the

timeactivity relationship. The AUC between the end of
exercise and the start of the cardiac imaging was only a
fraction of the total AUC, and the variability of AUC
during this period between the different exercise
intensities was very small (< 2 % of the total AUC).
Furthermore, taking into account that during this period
tissue glucose uptake is presumably lower than during
exercise, the contribution of the post-exercise period of
12 min to the results of the present study is insignificant.
Moreover, our results obtained at the 30 and 55 % J,max
intensity levels are in accordance with a study conducted
by Gertz et al. (1988), although they used a different
approach.
As mentioned earlier, [18F]FDG enables us to quantify
tissue glucose uptake but provides no information about
the fate of glucose in the cell. Thus, we were unable to
measure the amount of glucose entering oxidative and
non-oxidative metabolism. The affinity of [18F]FDG and
glucose for glucose transporters and hexokinase are not
necessarily always identical. These differences are corrected
by using a correction factor, the LC. In experimental
animal studies of anoxia, the physiological range of flow,
insulin, glucose and external work did not effect LC (Ratib
et al. 1982; Marshall et al. 1983; Huang et al. 1987;
Krivokapich et al. 1987). In contrast, in some studies
changes in the sensitivity of LC to supraphysiological
amounts of lactate (40 mM: Hariharan et al. 1995), insulin
and glucose (Ng et al. 1991) were documented. All of these
studies were performed with isolated heart preparations
under non-physiological or in vitro conditions. Currently,
there is only one study in humans where the myocardial
LC was tested, and it was shown to be stable under basal
and insulin-stimulated conditions (Ng et al. 1998).
In order to limit the radioactive dosage, two groups of
volunteers were studied; one at rest and the other directly
after exercise.
In conclusion, the results of the present study demonstrate
that exercise increases myocardial glucose uptake, but that
this increase does not parallel exercise intensity, in contrast
to the situation in skeletal muscle. These findings suggest
that the increased myocardial energy that is needed during
high-intensity exercise is supplied by substrates other than
glucose.

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Acknowledgements
The authors thank the entire staff of the PET Centre and Jukka
Kapanen, Paavo Nurmi Center, for J,max determinations. This
work was supported by grants from the Novo Nordisk
foundation, the Finnish Foundation for Cardiovascular Research,
the Turku University Foundation and the University Hospital of
Turku.