Journal of Sports Sciences, 1998, 16, S77 S84

Physiological and metabolic responses to increasing

work rates: Relevance for exercise prescription
S.C. D EN NIS and T.D. N OAKES*
M RC/U CT B ioenergetics of E xercise Research U nit, Sports Science Institute of South Africa, PO B ox 115,
New lands 7725, South A fr ica

Interest in rises in oxygen consum ption (V O 2) with increasing exercise intensity largely originate from the work
of Hill and colleagues in the 1920s. Their studies led to a belief that cardiac output and V O 2 `plateau at
increasing work rates and that muscle hypoxia leads to fatigue. Hence, it was assum ed that the prim ary bene t of
exercise training is to increase muscle oxidative capacity and that the greatest bene t of training would occur at
work rates around the `anaerobic threshold . In this paper, we question whether working m uscles become
hypoxic at high work rates. Rather than being a threshold response to hypoxia, we propose that plasm a lactate
accum ulation and curvilinear rises in ventilation at high work rates are both independent consequences of
the acceleration of carbohydrate metabolism with increasing exercise intensity. Evidence is also presented to
suggest that athletic performances are not exclusively related to muscle oxidative capacity. Once an athlete
has adapted to prolonged, `aerobic training, intervals of `anaerobic , high-intensity exercise further improve
performance without additional increases in muscle mitochondrial density or alterations in m etabolism . Until
the m echanisms underlying the latter improvem ents in performance are understood, it is diY cult to advise
athletes on how best to prepare for com petition.

K eywords : exercise training, heart rate, lactate, m aximal oxygen uptake, performance.

Introduction to assum e that the prim ary bene t of exercise training is

In m ost endurance-training program m es, athletes
rst increase their exercise volum e and then raise their
exercise intensity. Once an athlete has fully adapted
to prolonged `aerobic training, m ost coaches and
physiologists consider that intervals of high-intensity
`anaerobic exercise produce the greatest im provem ents
in perform ance.
The classi cation of exercise as either `aerobic
or `anaerobic originates from the work of H ill and his
colleagues (Hill and L upton, 1923; Hill et al., 1924a,b,
c; H ill, 1925). Hill believed that oxygen consum ption
(V O 2 ) reaches a `plateau at increasing work rates and
that exercising skeletal m uscle becom es `anaerobic
towards exh austion. Subsequently, others proposed
that m uscle hypoxia stim ulates the onset of lactate
production at the so-called `anaerobic threshold and
that the resultant `lactic acidosis above that work rate
leads to fatigue. Against this background, it was natural
* Author to whom all correspondence should be addressed.
to increase the oxidative capacity of the working m uscles
and that the greatest bene t of training is likely to occur
at work rates around the `anaerobic threshold . In this
paper, we consider the conventional m arkers of m uscle
hypoxia in progressive ram p exercise tests to exhaustion
and exam ine their value in advising athletes on their
training intensities.
C ardiovascular changes with increasing
exercise intensity
A useful indicator of an athlete s training intensity
is provided by the linear rise in heart rate with in-
creasing V O 2 (Fig. 1). In progressively intense exercise,
~ 300% rises in heart rate and ~ 60% im provem ents
in stroke volum e increase cardiac output by ~ 500%
(M itchell and Raven, 1994). Even with the suggestion
of a plateau in the im provem ents in stroke volum e,
cardiac output increases as a linear function of work
rate, even towards exhaustion. At the sam e tim e, rises in

0264 0414 /98 1998 E & FN Spon

S78
150
(ml)
SV
100
200
(beats min 1)
150
HR
100
20
(l min 1)
15
CO
10
5 time when he ran at increasing speeds around a track. Rises in
0 1 2 3 4 redrawn from the analysis of Hill and Lupton s (1923) nd-
. ings by Noakes (1988).
VO2 (l min 1 )
F igure 1 Rises in cardiovascular variables with increasing
V O 2. Stroke volume (SV), heart rate (HR) and cardiac output
(CO) data were taken from M itchell and Raven (1994).
sym pathetic neuronal activity progressively restrict the
ow of blood to less active tissues and further im prove
the supply of oxygen to the working m uscles (M itchell
and Raven, 1994).
O xygen consumption with increasing exercise
intensity
D espite the large rise in the supply of oxygen to the
working m uscles at high work rates, som e believe that
increases in cardiac output are not suY cient to m eet the
m axim um dem ands of the working m uscles for oxygen.
An oxygen-lim itation in m axim al exercise was rst pro-
posed by Hill and Lupton (1923). They m easured the
V O 2 of H ill every 30 s w hen he ran at speeds of 10.9,
12.1 and 16 km h - 1 for 3 4 m in around an 85-m circular
grass track (Fig. 2). Because H ill fatigued at a running
speed of 16 km h - 1 , he assum ed that he had developed
an increasing `oxygen-debt and that his real V O 2 at
16 km h - 1 would therefore have been higher than the
m easured values. H owever, Hill and Lupton s (1923)
data did not indicate that Hill had reached `som e
critical speed above w hich the m axim um oxygen
intake is inadequate (Hill et al., 1924a). N oakes (1988)
later showed that H ill s V O 2 values rose linearly
w ith increasing running speed, with no evidence of a
`plateau (Fig. 2).
O thers have also found it diY cult to identify a
`plateau in V O 2 during progressive ram p exercise tests
Dennis and Noakes
km h 1
16.0
3 12.1
VO 2 (l min 1)
10.9
2 4
(l min 1)
VO2
2
.
1 0
0 5 10 15
Speed (km h 1)
0 1 2 3 4
Running time (min)
F igure 2 Rises in the oxygen consumption of A.V. Hill over
V O 2 over tim e at the three indicated running speeds were
to exhaustion (C um m ing and Borysyk, 1972; N oakes,
1988; D ennis et al., 1992; How ley et al., 1995; M acRae
et al., 1995b; Arm strong et al., 1996). O ne possible
explanation for a com m on failure to detect a `plateau
in V O 2 is that breath-to-b reath di erences in tidal
volum es introduce too m uch variability into V O 2
m easurem ents over inter vals of less than 30 60 s
(M yers et al., 1990). W ithin a sam pling period of
30 60 s, a reduction in the slope of the rise in V O 2
towards zero could be obscured by previous increases
in V O 2 at that work rate.
A `plateau in V O 2 m ight also be obscured by the 1 2
m in lag between rises in work rates and increases in
steady-state V O 2 values (Fig. 2). M easurem ents of V O 2
cannot elim inate the possibility that working m uscles
becom e hypoxic towards exhaustion. However, it is
diY cult to see why 1 2 m in of hypoxia should cause
term ination of exercise either before or so soon after
a putative `plateau in V O 2, as is usually described.
E ither working m uscles do not becom e hypoxic or
hypoxia does not further activate oxygen-independent
glycogenolysis in progressive exercise to exhaustion. A
full activation of oxygen-independent glycogenolysis in
a 20 30 s sprint generates ~ 500 m m ol of ATP before
m etabolite-induced m echanical arrest slows contractile
activity (Spreit et al., 1987). Adding ~ 500 m m ol of AT P
to the ~ 1200 m m ol m in - 1 calculated turnover of AT P
at a m axim um oxygen consum ption (V O 2 m ax) of,
say, 4.5 l m in - 1 should allow the athlete to continue
exercising to a work rate equivalent to 1.9 l m in - 1 of O 2
above the rate of oxygen consum ption at the `plateau .
Since no-one has described such a prolonged
`plateau in V O 2 , it is doubtful that oxygen dem and
Exercise physiology and athletic training
exceeds oxygen supply in exhaustive exercise. Instead, it
is m ore likely that an inhibition of cross-bridge cycling
by a shift in the cytosolic H + + H PO 42- H 2PO 4- equi-
librium to the right and, m aybe, a slowing of action
potential conduction by an extracellular accum ulation
of K + in the T -tubules, lim its the dem and of the m uscles
for energy before AT P concentrations fall to critically
low levels. An adequate supply of AT P is essential
for the continued detachm ent of the myosin heads from
the actin lam ents and a prevention of `rigor (Noakes,
1997).
Plasm a lactate accum ulation with increasing
exercise intensity
Another hypothesis originating from Hill and L upton s
(1923) belief that exercising m uscles develop an
`oxygen-debt , is that delivery of oxygen to the exer-
cising skeletal m uscles becom es inadequate not only
at V O 2 m ax, but also at lower work rates. Proponents of
the `anaerobic (lactate) threshold concept argue that:
(1) m uscle hypoxia accelerates lactate production at
work rates above the `threshold , and (2) a respiratory
com pensation for `lactic acidosis leads to curvilinear
rises in ventilation (V E ) with increasing carbon dioxide
expiration (V CO 2 ) during progressive exercise
(Wasserm an and M cIlroy, 1964; Wasserm an et al.,
1973, 1990; W hipp et al., 1984):
hypoxia
% glycolysis is taken into consideration, and the sum s
glycogen lactate - + H +
H + + H CO 3- H 2O + C O 2
respiratory com pensation
for `lactic acidosis
One concern w ith the `anaerobic (lactate) threshold
hypothesis is in the estim ated contribution to energy
production that would be derived from a sudden
acceleration of oxygen-independent glycogenolysis
above the `threshold . From (1) the typical ~ 2 m m ol l- 1
m in - 1 rises in lactate concentration towards the end of
progressive exercise, (2) the presum ed ~ 7-litre non-
steady-state lactate distribution volum e (M acRae et al.,
1992, 1995a,b) and (3) the AT P form ation : lactate
production ratio of 1.5, we calculated that a `threshold
increase in oxygen-independent glycogenolysis would
accelerate AT P synthesis by only ~ 2 7 1.5 m m ol
S79
m in - 1 . An additional production of ~ 20 m m ol ATP
m in - 1 from oxygen-independent glycogenolysis would
have a m inim al e ect on the calculated 800 1200 m m ol
m in - 1 turnover of AT P via oxidative phosphorylation
at V O 2 values of 3.0 4.5 l m in - 1 . Such sm all (1 2% )
contributions to energy production from `sudden
increases in oxygen-independent glycogenolysis m ay
explain w hy the putative developm ent of hypoxia at the
`threshold is not associated with any lag in the rises in
V O 2 (Noakes, 1988; D ennis et al., 1992).
It is also unlikely that the rises in plasm a lactate
concentrations at the `anaerobic threshold are due to
a sudden onset of oxygen-independent glycogenolysis.
Brooks (1985, 1986a,b) and M acRae et al. (1992,
1995a,b) found that plasm a lactate concentrations
depend on the relative rates of lactate appearance (R a )
and disappearance (R d ). Even at work rates well below
the `threshold , there were progressive increases in
lactate R a values that were largely m atched by corre-
sponding increases in lactate R d values (Fig. 3). Plasm a
lactate accum ulated only when exponential increases
in lactate R a values gradually exceeded exponential
increases in lactate R d values. C ur vilinear rises in plasm a
lactate concentrations and lactate R a and R d values
were not associated with any slowing of the linear
rises in V O 2 w ith increasing work rates, but they were
paralleled by an exponential acceleration of carbo-
hydrate oxidation (Fig. 3).
Continuous exp onential rises in carbohydrate oxi-
dation at increasing work rates probably exp lain both
the accum ulation of plasm a lactate and the respiratory
com pensation for m etabolic acidosis during progressive
exercise. W hen ATP synthesis by oxygen-independent
of the likely electrical charges of the reactants and
products are com pared, it is found that the conversion
of glucose or glycogen to lactate does not produce a net
gain of H + ions (G evers, 1977; D ennis et al., 1991;
M acRae and D ennis, 1995):
glycolysis + M g AD P - + P i2 - M gAT P 2- + lactate -
glycolysis + M gA D P - + P i2 - + N AD +
pyruvate - + M gAT P 2- + N AD H + H +
H + ions only arise when pyruvate is delivered to the
m itochondria for oxidation, but those H + ions cannot
accum ulate. E ither the N AD H + H + is used in the
reduction of pyruvate to lactate or it enters the m ito-
chondria via the m alate-aspartate shuttle. Unless the
N AD H + H + produced in the cytoplasm is oxidized
in the m itochondria, the m etabolism of pyruvate does
not proceed. A stoichiom etric oxidation of pyruvate
and N AD H results from a split in the T CA cycle into
two pathways. T he rst pathway is from acetyl CoA
S80 Dennis and Noakes

250 At low rates of carbohydrate oxidation, H + ions from

( mol min 1 kg 1) Ra glycolytic AT P turnover are taken into the m itochondria
200 Rd together with pyruvate - ions. However, as rates of
turnover
Lactate

carbohydrate m etabolism are further accelerated to

150
sustain higher exercise intensities, H + and pyruvate -
100 ions accum ulate in the cytosol and progressively dis-
place the lactate dehydrogenase and lactate translocase
50
equilibria towards lactate form ation and H + + lactate -
6
co-eZ ux. Thus, m uscles generate lactate w henever
(mmol l 1)
Plasma
lactate

carbohydrate utilization is increased to provide energy

4
for high-intensity exercise, irrespective of the presence
or absence of hypoxia:
2
3
Carbohydrate

glycolytic ATP
(g min 1)
oxidation

turnover
2

acidosis

3
H+
+
(l min 1)

pyruvate - + N AD H + H + lactate - in + N AD +
VO 2

2
--------- --------- --------- --------- ------ - - - - - - - - - - - - -
.

1 lactate - out
60 140 220 300
Work rate (W)
F igure 3 Plasm a lactate turnover and accumulation with the
acceleration of carbohydrate oxidation and V O 2 at increasing
work rates. These data are from the studies of M acRae et al.
(1992, 1995a,b) on previously sedentary subjects after a 9-
week cycling endurance-training programm e. Exercise tests
were started at a work rate of 60 W and increased by 40 W
every 6 min. R a and R d are rates of lactate appearance and
disappearance, respectively.
to 2-oxoglutarate, w hich leaves the m itochondria in
exchange for m alate to participate in the m alate-
aspartate shuttle. T he second pathway starts w ith 2-
oxoglutarate regenerated from the shuttle and ends
at oxaloacetate. Since a continued m etabolism of
pyruvate depends on the provision of oxaloacetate,
this m echanism ensures that any increase in pyruvate
oxidation has to be m atched by a corresponding ac-
celeration of cytosolic N AD H + H + reoxidation.
Instead, H + ions arise from the turnover of glyco-
lytically produced AT P. Unlike in the turnover of
AT P via oxidative phosphorylation or creatine phos-
phate breakdown, H + ions released by AT P hydrolysis
are not re-consum ed when the ATP is re-synthesized by
glyco(geno)lysis:
glyco(geno)lysis + M g AD P - + P i 2- M gAT P 2 - + lactate -
--------- --------- --------- -----
+
H+
A `dum ping of fuel in the form of lactate to clear
H + ions from the m uscles at high work rates, however,
need not necessarily coincide w ith the curvilinear rises
in V E above the `threshold . Exp onential rises in V E w ith
increasing V O 2 are not entirely due to a bu ering of
H + ions by the H + + H CO 3 - H 2O + C O 2 equilibrium .
U pward deviations from linearity in rises in V E w ith
increasing V O 2 also results from greater rises in V CO 2
than in V O 2, as the percent contribution to energy
production from carbohydrate oxidation is accelerated
at increasing work rates. M acRae et al. (1995b) showed
that lower steady-state V E versus V O 2 curves after 9
weeks of endurance training were m ore closely linked
to a decreased reliance on carbohydrate oxidation
(C HO OX ) than to an attenuated rise in blood lactate
concentrations w ith increasing exercise intensity after
training (Fig. 4). Both before and after training,
steady-state l m in - 1 V E values rose as a linear V E =
18 ? C HO OX + 14 function of g m in - 1 rates of C HO OX ,
despite a m arked shift to the right in the `arterialized
venous blood lactate concentrations versus CH O OX
curves.
Poole and G aesser (1985) also showed that 8 weeks
of training at 50, 70 or 105% of V O 2 m ax dissociated
lactate and ventilation `thresholds . W hereas lactate
`thresholds were consistently increased by ~ 35% ,
V E `thresholds were increased by 19, 28 and 46% ,
respectively. T hey speculated that these discrepancies
H+ m ay have been due to rises in V E being under both
Exercise physiology and athletic training
Pre-training
6 conversion of glycogen to lactate in exercising m uscles
Plasma lactate
(mmol l 1)
4 Post-training
2
Pre- and post-training
75
Ventilation
(l min 1)
50
y = 18x +14
r = 0.99
25
0 1 2 3
Carbohydrate oxidation (g min )
1 via the m alate-aspartate shuttle. Less pyruvate - + H +
F igure 4 E ects of endurance training on rises in plasma
lactate concentration and ventilation volum es with increasing
carbohydrate oxidation. Plasma lactate concentrations and
ventilation volumes before and after 9 weeks of endurance
training are from the studies of MacRae et al. (1995b),
described in the legend to Fig. 3. While training m arkedly
slowed the rises in plasm a lactate concentrations with increas-
ing carbohydrate oxidation (P < 0.01), it had no e ect on
ventilation at equivalent rates of carbohydrate oxidation.
m etabolic and neurogenic control. T hus, factors
other than an `excess pC O 2 derived from a HC O 3-
bu ering of `lactic acid m ay explain how blood lactate
concentration and ventilation `thresholds can be
dissociated in patients with M cArdle s disease, who
lack glycogen phosphorylase activity (H agberg et al.,
1982), and in subjects who are carbohydrate-depleted
(Hugh es et al., 1982; H eigenhauser et al., 1983). W here-
as curvilinear rises in V E with increasing exercise
intensity are closely linked to the acceleration of V C O 2
from carbohydrate oxidation, blood lactate accum u-
lation is only indirectly related to the rates of carbo-
hydrate m etabolism .
Both H urley et al. (1984) and M acRae et al. (1995b)
found that blood lactate concentrations were lower
at equivalent rates of carbohydrate oxidation after
training than before training. T he studies of M acRae
et al. (1992, 1995a) suggested that decreased blood
lactate concentrations after endurance training were due
to reductions in lactate R a , rather than to im provem ents
in lactate R d , at given rates of carbohydrate oxidation
(data not shown). Part of the reduction in lactate R a at
com parable rates of carbohydrate oxidation could have
been due to a decreased catecholam ine release during
subm axim al exercise after training (W inder et al., 1979).
S81
Less b-adrenergic stim ulation m ay have reduced the
(Richter et al., 1982).
Lactate R a values at equivalent rates of carbohydrate
oxidation could also have been decreased by the
increased oxidative capacity of endurance-trained
m uscles (H olloszy, 1967; D avies et al., 1981). M ore
m itochondria im prove the sensitivity of respiratory
control (Dudley et al., 1987). W ith lower AD P con-
centrations required for any given rate of oxidative
phosphorylation, the activation of glycogenolysis by the
displacements of the creatine kinase and adenylate
kinase equilibria m ay have been m ore closely m atched
to the dem ands of the m itochondria for pyruvate - + H +.
An increased m itochondrial content of endurance-
trained m uscles could also have reduced the cytosolic
N AD H + H + concentrations required for given rates
of reducing equivalent transport into the m itochondria
accum ulation and/or lower cytosolic N AD H + H + con-
centrations would have lim ited the displacements of the
lactate dehydrogenase and lactate translocase equilibria
towards lactate form ation and eZ ux at high rates of
carbohydrate oxidation.
Putative indices of muscle hypoxia as
predictors of perform ance
Although `aerobic , endurance training m ay be of
bene t in raising the m itochondrial content of the active
skeletal m uscles, it is doubtful whether further
im provem ents in perform ances with subsequent
`anaerobic , high-intensity, inter val training are due to
additional increases in m uscle oxidative capacity. We
found that high-intensity, interval training signi cantly
im proved the 40-km cycling speeds of 20 already well-
trained endurance cyclists (Lindsay et al., 1996; H awley
et al., 1997; Westgarth-Taylor et al., 1997) without any
change in either their m uscle m itochondrial oxidative
capacity (Weston et al., 1997) or their utilization of
carbohydrate at equivalent relative exercise intensities
(Westgarth-Taylor et al., 1997). Instead, high-intensity,
inter val training im proved both the absolute and the
relative work rates of the cyclists during the rides
(Fig. 5).
F urther evidence to suggest that exercise perform -
ance m ay not be exclusively related to m uscle oxidative
capacity also com es from m easurem ents of plasm a
lactate concentrations and V O 2 m ax values in progres-
sive exercise tests to exhaustion. W hile plasm a lactate
concentrations at subm axim al work rates (Farrell et al.,
1979; Tanaka and M atsura, 1984; H eck et al., 1985;
Jacobs, 1986; Coyle et al., 1988, 1991) and V O 2 m ax
values at fatigue (Foster, 1983; H awley and N oakes,
S82 Dennis and Noakes

contestants is that they are obtained from linear exercise

ram ps involving xed work rates. M any athletes do not
exercise at a constant work rate. Palm er et al. (1994)
Work rate (W)

400 P < 0.0001 showed that elite cyclists racing in a pack random ly vary
their work rates from around 50% to alm ost 100% of
350
peak sustained power output, independently of the
course terrain.
300
Perform ances in races involving rapid increases
250 and decreases in work rates m ay be in uenced m ore
by an athlete s ability to recover from pulses of high-
100 intensity exercise than by their ability to sustain a
certain power output. We recently found that the
P < 0.05 rankings of seven, good club, provincial and national
Peak power (%)

level m ale cyclists in an 80-km m ass-sta rt road race were

80 predicted better by their recover y heart rates than by
their peak power outputs (Fig. 6) or plasm a lactate con-
centrations during progressive exercise (unpublished
obser vations).
60

0 20 40 60
P ractical im plications
Time (min)
F igure 5 E ects of high-intensity, interval training on simu- Since exercise perform ances are not exclusively related
lated 40-km cycling time-trial performances. Absolute and to the oxidative capacity of the working m uscles, other
relative work rates during sim ulated 40-km cycling tim e-trials
determ inants of athletic ability have to be considered. In
before (s ) and after ( d ) high-intensity, interval training
particular, it is im portant to understand how high-
(HIT) are from the studies of Lindsay et al. (1996). They
showed that six HIT sessions of six to nine 5-min rides at 80%
intensity, interval training im proves exercise perform -
of peak sustained power output, with 1-min recovery periods ances and why heart rate recoveries are m ore rapid in
between rides, improved the 40-km cycling times of already
well-trained endurance cyclists by ~ 2 m in.

1992) indicate w hether athletes are recreational, r = 0.72

(W kg 1)

com petitive or elite, they are less reliable predictors of 6 P < 0.05
W peak

endurance perform ance in athletes with sim ilar abilities.

Am ong com parable athletes, V O 2 m ax values can be
dissociated from perform ances (Pollock, 1977; D aniels 5
et al., 1978; Scrim geour et al., 1986), and m axim um
steady-state plasm a lactate concentrations can vary
10
from 2 to 8 m m ol l- 1 (Stegm ann and K inderm ann,
(D % of peak min 1)

1982).
Heart rate

O ne possible exp lanation for the poor predictive 20 r = 0.93

value of V O 2 m ax and lactate m easurem ents am ong P < 0.005
m ore hom ogeneous groups of athletes is that som e
30
individuals m ay be able to continue endurance exercise
above their so-called `anaerobic threshold . As
Stegm ann and Kinderm ann (1982) showed, certain 1 2 3 4 5 6 7
athletes are able to m aintain exercise even when their
Subject
plasm a lactate concentrations exceed the supposedly
`critical value of 4 m m ol l - 1 (Kinderm ann et al., 1979; F igure 6 Prediction of m ass-start road cycle racing per-
H eck et al., 1985). form ances. Peak sustained power outputs (W p e a k ) and falls in
Another possible reason for the lim ited usefulness of heart rate in the rst minute after stopping exercise were cor-
lactate and V O 2 peak m easurem ents in distinguishing related to the cyclists rankings from 1 to 7 in an 80-km m ass-
between the racing perform ances of reasonably m atched start road race by Kubukeli et al. (unpublished observations).
Exercise physiology and athletic training
better athletes than in poorer athletes. Heart rate
recoveries could possibly be used by athletes to m onitor
the bene ts of their high-intensity, interval training
prior to com petition. W hereas laborator y exercise tests
to exhaustion interfere w ith training, recovery heart
rates could be m onitored after each session of
high-intensity, inter val training. Such m easurem ents
would be facilitated by the athlete already having
to wear a hear t rate m onitor to adjust the intensity of
his or her exercise inter vals. U nlike plasm a lactate
determ inations, heart rate m easurem ents provide a
reliable indication of an individual s relative exercise
intensity.
Acknowledgem ents
T he studies reported here were funded by the M edical
Research Council of South Africa, the N ellie Atkinson
and Harry C rossley Sta Research F unds of the
U niversity of Cape Town, the Liberty Life Insurance
Com pany, the Founding D onors of the Sports Science
Institute of South Africa, Brom or Foods Inc., the Potato
G rowers Association of South Africa and Polar Electro
O y, Kem pele, F inland.
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