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Aerobic and anaerobic exercise capacities of elite middle-distance runners

after two weeks of training at moderate altitude

Article in Scandinavian Journal of Medicine and Science in Sports · January 2007

DOI: 10.1111/j.1600-0838.1991.tb00297.x

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 Aerobic and anaerobic exercise capacities of
elite middle-distance runners after two
weeks of training at moderate altitude
Svedenhag J, Saltin B, Johansson C, Kaijser L. Aerobic and anaerobtc J. Svedenhagl, B. Saltin3,
exercise capacities of elite middle-distance runners after two weeks of G. Johanssonz, L. Kaijserl
I training at moderate altitude. Departments of
lCllnical Physiology and
Scand J Med Sci Sports I99I: I:205-214. 20rthopedics, Huddinge University Hospital,
I 3Department of Physiology lll, Karolinska lnstitute,
ì

The effect of short-term altitude training on sea-level physiological char- Stockholm, Sweden
acteristics in elite runners was investigated. Seven middle-distance run-
ners (6 men, 1 woman) belonging to the Swedish national team (mean
age 23 years) spent 2 weeks of training at 2000 m above sea level in
Kenya. Tieadmill tests were performed before and 6 and 12 d after the
altitude sojourn. Six other runners (4 men, 2 women) had a correspond-
ing training sojourn at sea level in Portugal (control group). Two of the
runners (1 man, 1 woman) in the Kenya group were omitted from the
study because of gastroenteritis. The maximal oxygen uptake (Vor*u"i
pretravel: Kenya grotp 212 and control group 188 ml'kg 075 ' min-r),
maximal treadmill time and oxygen cost of running were unchanged in
both groups. The maximal oxygen deficit increased in all subjects after
the Kenya sojourn (mean 19+6"/"). Heart rates during running at spec-
ified submaximal running velocities were lower post-altitude (Kenya
group), but tended to be higher after sea-level training (control group).
Maximal heart rate was unchanged in both groups. Perceived exertion
(Borg) during submaximal running was lower post-altitude. Submaximal
Key words: maximal oxygen uptake; maximal
and maximal blood lactate and plasma catecholamine concentrations
oxygen deficit; running economy; heart rate;
were not altered in any of the groups. Post-exhaustive plasma ammonia
blood lactate; blood ammonia; perceived exertion
levels were decreased 72 d after altitude descent in the Kenya group.
catecholamines
The results suggest an unchanged aerobic capacity in elite middle-dis-
tance runners after short-term training at moderate altitude. However, a Dr. Jan Svedenhag, M,D., Ph,D., Department of
Clinical Physiology, Huddinge University Hospital,
change in the circulatory regulation during submaximal exercise was
I observed. Furthermore, anaerobic capacity improved but this bore no
S-141 86 Huddinge, Sweden

clear relation to lactate or ammonia metabolism. Accepted for publication October 21, 1991

It is generally accepted that training during an
extended altitude sojourn will improve perform-
ance at altitude. It is less clear whether training at
altitude is superior to sea-level training with regard
to performance at sea level (11).Tþrrados et al.
(8) found that, when bicycle training was executed
with the same power at simulated altitude in a
hypobaric chamber and at sea-level pressure, the
improvement in working capacity together with
the increase in activity of mitochondrial enzymes
was greater after the simulated altitude training.
However, conditions may be different at actual
altitude. Because of the reduced oxygen pressure,
training intensity must be reduced compared with
that at sea level. A cardiovascular adaptation takes
place, including, for example, reduced maximal
heart rate. If the altitude sojourn is long enough
and the altitude high enough, blood hemoglobin
concentration will also increase (9). Recent find-
ings also suggest an anaerobic adaptation to alti-
tude as judged by post-altitude increases in maxi-
mal oxygen deficit and muscle buffer capacity in
athletes (7). Thus, the present study was undertak-
en to evaluate what effects on sea-level exercise
capacities could be achieved by a training sojourn
at moderate altitude.
Material and methods
Subjects
Thirteen elite runners participated in the study; 7
belonged to the Swedish national team and the
other 6 were just below this level. All were racing
at middle distances, but 2 of the runners were
preferably aiming for 5000 m. Tþn of the runners

205
Svedenhag et al
were men; 3 were women. The study was approved
by the Ethics Committee of the Karolinska In-
stitute, Stockholm.
Design
The 7 belonging to the Swedish national team (6
men, 1 woman) were selected for the altitude
training group. The other 6 served as a control
group. After an initial treadmill test at sea level (in
Sweden), the altitude group travelled to Kenya
and spent 2 weeks of training at2000 m above sea
level. The control group was training at sea level in
Portugal during this time. During these sojourns,
training was performed twice daily at normal train-
ing routines (with an adjusted intensity level in the
Kenya group, keeping the relative intensity the
same, and supervised by one of the authors). The
training periods for both groups were carried out
during first half of February in 1990.
After returning to Sweden, the Kenya group was
tested on 2 occasions,6 (range 5-6) and 12(11-13)
d after descent to sea level. The control group was
tested on one occasion, 5 (3-10) d after ending
their training camp. Upon return,2 of the runners
(1 man, 1 woman) in the Kenya group had devel-
oped gastroenteritis. Therefore, their post-altitude
treadmill tests were incomplete; these runners
were omitted from the final analysis.
Protocol
Submaximal and maximal treadmill tests were per-
formed. After a warm-up of about 5 min, the sub-
jects ran 4 min (2.8' uphill slope) at each of 3-4
different running speeds (12.0, 14.0,15.0 and 16.0
km.h-r for the men; 10.0, 12.0, 13.0 and 14.0
km'h-l for the women; no stop in between). Ox-
ygen uptake (Vo,) and heart rate were measured
continuously. During the last 30 s at each velocity,
3-ml blood samples for lactate and ammonia deter-
minations were drawn from a venous catheter in-
serted into an antecubital vein of the right arm. A
blood sample for catecholamine determination was
taken at the end of the third velocity. At the end of
each velocity the subject rated his or her perceived
exertion.
After exactly 10 min of rest, the maximal oxygen
uptake test was started. The subject ran at an
individually set running speed (15.5-19.5 km.h-1)
with an inclination of 2.8'. Expect for one of the
subjects, the speed was then futher elevated by
0.5-1 km.h-r after 4-5.5 min of running time (in-
dividually set), to keep exhaustion time within rea-
sonably close limits. For each subject the same
speed increase protocol was used in all tests. Blood
lacfate and ammonia samples were obtained at
206
30 s, 3.5 min and 5min, and a blood catecholamine
sample at 30 s after exhaustion.
Methods
Lung ventilation, O, uptake and CO2 production
were measured using an open-circuit system con-
nected on-line to a Copam PC-401 computer. Ex-
pired gas was sampled from a mixing chamber at
contant flow (Ametek R-1) and analyzed for O,
and CO2 with an Ametek oxygen (5-34/1, N-22M;
zirconia cell) and carbon dioxide (CD-34, P-618;
infrared detection) analyzer system. Lung ventila-
tion was measured on the inspiratory side by a flow
transducer with an impeller (KL Engineering CO,
K520). The sampling rate of 02 and CO2 was 140/s;
integrations with ventilation over 30 s periods were
made by the computer. The oxygen uptake during
the last L-1.5 min of each velocity (submax test)
and the peak 30-s Vs, during the maximal tesî
were used. To minimize the dependence of Ve" on
body weight during running, oxygen uptake is also
expressed as ml .kg-ozs.min-l, which better de-
scribes the effect of body weight than
ml.kg-1 .min-1 (10). Since there was no system-
atic difference and only 6 d between test 2A and
2B afTer the altitude sojourn (Kenya group), these
tests can be treated as duplicate determinations,
with a calculated coefficient of variation of 2.1'/.
for Vgr.u" .
The maximal oxygen deficit was determined as
the difference (area) between oxygen demand (ex-
trapolated from the submaximal running velocity-
V6, relationship) and the actual V6, meâsufement
at each 30 s period of the Vo,-u" test. Because
Vo,.o" had to be determined by-Douglas bags in 2
control subjects, a technical error at early max test
in another, and generally lesser number of sub-
maximal work loads, the maximal oxygen deficit
could not be safely calculated for the control
group. Electrocardiogram was registered contin-
uously on a Mingograph (Model 62, Siemens-
Elema). The mean of repeated heart rate measure-
ments during the last min at each velocity was
used. Perceived exertion was rated according to
theÇ20 degree RPE scale (11). Plasma adrenaline
and noradrenaline concentrations were deter-
mined by means of cation-exchange high-perform-
ance liquid chromatography with electrochemical
detection (12). Blood lactate was determined fluo-
rometrically by a standard enzymatic method.
Blood samples for determination of plasma NH,
were centrifuged immediately (within 90 s) and the
supernatant was stored on ice until analyzed
(within 45 min) by flow injection analysis (13).
Muscle biopsies were taken from m. gastrocnemius
 Altitude training in elite runners

Table 1, Physical characteristics of the Kenya (K) and control (c) runners (pre{ravel test)

Subject Sex Age Stature Body mass Vo,,", Type 1 Best Best
(years) (m) (ks) l%l distance performance
(l'min-1) (ml'kg-ozs't'n-1) (ml'kg-1'min-1) (m) {min: s)

K1 (JD) M 25 .91 77.0 5.80 223 75.3 80 5000 13:21

K2 (ME) M 24 .76 65,0 4.33 189 66,6 57 800 1:47
K3 (MT) M 19 .78 65.0 4.86 212 14,8 55 1 500 3:42
K4 (MEx) M 31 .77 64,2 5.00 220 77,9 77 5000 13:45
K5 (PN) M ¿7 .i8 62.0 4.77 216 76.9 81 3000 8:32
steeplechase

Mean 24.8 '1,80 66.6 4.95 212 74.3 70

c1 (MA) F 19 1.72 51.2 2,97 155 58.0 56 800 2:08

c2 (AP) M 23 1.75 63.0 4.96 222 78.7 56 1 500 3:45
c3 (AK) F 20 1.65 51.3 3.30 172 64.3 1 500 4:12
c4 {KT) M 20 1.78 68,5 4.79 201 ô9,9 45 800 1:47
c5 (TJ) M 19 1.77 65,5 4.24 184 64,7 48 800 1:47
c6 (MEk) M 21 1,79 64.5 4.49 19t 69.6 49 1 500 3:5'1

Mean 20.3 1.74 60.7 4.12 188 67.5 51

Biopsies from m. gastrocnemius. Best performance notation from the preceding orfollowing summer seasons.

during local anesthesia with the Bergström needle Results

technique; details are given separately (26).
Physical characteristics

Age, stature, body mass, maximal oxygen uptake

Statistics
For comparisons of test occasions (within a group;
for example, test 1,, 2A and 2B in the Kenya
group), two-way analysis of variance (ANOVA)
was used (the second way being submaximal run-
ning velocities or the different sampling times after
max). For comparisons of test occasions with sin-
gle variables, one-way ANOVA was applied. The
relationship of Ve, (l.min-1) to the heart rate of
each subject for each occasion was analyzed by
linear regression. The data are presented as means
+ SE.
(Vo,.u*i pretravel test), percentage type I fibres,
best running distance and best performance of the
runners are shown in Täble 1. The body mass was
unchanged in both groups during the course of the
study (66.8 + 2.7 and 66.6 + 2.7 kg in the Kenya
group at test occasion 2A and 28, respectively;
and 60.5 + 3.2kg in the control group at test 2).
The hemoglobin (Hb) concentration (initially 145
g.l-t) was unchanged in the Kenya group (Tä-
bleZ). In the control group, Hb was found to
increase slightly (P<0.05).

Table 2. Hemoglobin concentration (Hb), aerobic running capacity and heart rate, ventilation and respiratory exchange ratio (RER) at peak exercise intensity
before and after training sojourns in the 2 groups

Kenya group (n=5) Control group (n=6)

2A 28 2

Hb (g.l-r) 14513 148!2 14613 137!4 144r3

Max running time (s) 285!17 288!12 2t0t23 321 r18 320r 1 6
Vo, to Vo, -.r-t (%) 79.0r2.3 78.8r2,3 78.51 1.9 86.i13.7 86.1r2.8
Vor ru'Vor.ur-1 (%) 85.312.5 85,6t2,2 84.9r2.0 91.613.1 91.7!2.4
1) 187!2
Max heart rate (beats.min 1 8814 18814 1 8613 189r2
r,
Max ventilation (l .min STPD) 13218 127!S 128r9 114!7 10916

Max RER 1.1310.01 1.1410.01 1.1410.01 1.13t0.02 1.1410.03

Valuesaremeans*SE.ForV6r,o'Vo'u,-t{Verat14km'h lino/ootYsr-u*) andVor,u'Vo,u"-t,n=4inthecontrol group.

207
 Kenya 1: 4.95+-0.24
Svedenhag et al. Kenya 2A: 4.94+-0.25
Kenya 2B: 4.92+-0.23
Maximal oxygen uptake (l.min-l) Maximal oxygen deficit (l)
Control 1: 4.12+-0.33
5 Control 2: 4.13+-0.32
5

3
4

0
Kenya group Control group
Flg. 1. Maximal oxygen uptake (V6, -,., l.min 1) before and 3
after 2 weeks of altitude training in the Kenya group and
corresponding sea-level training in the control group. 2A and
2B refers to tests 6 and 12 d after descent in the Kenya group.
Values are means + SE. 0
TT 1
ï TtoTæT
Kenya group
Maximal oxygen uptake Fig. 2. Maximal oxygen deficit (l) before and after 2 weeks of
altitude training in the Kenya group. 2A and2B refers to tests
Pretravel Vo,.u* was 4.95 + 0.24l.min-1 in the 6 and 12 d after descent (see Methods and Results).
Kenya group and 4.I2 + 0.33 l.min-1 in the con-
trol group (the 4 male control runners: 4.62 + 0.16 ml.kg-1 .min-1. Likewise, the fractional utiliza-
l.min-r). Neither altitude training in the Kenya tion of Vo,.u" when running at 14 and 15 km . h-1,
group nor sea-level training in the control group (i.e. aerobic running capacity; Vo,,o.Vo..,"-t,
altered vo,,u*. expressed as I'min-1 (Fig. 1), Vo,,s . Vo,.u*-t) was unaltered in both groutris, the
ml 'kg-''min-r or ml .kg-ozs.min-r. latter being 84.9 - 85.6% and 91.6 - 91.7% in the
Kenya and control group, respectively (Table 2).
The mean calculated (i.e., extrapolated) oxygen
Maximal running time
cost of running at the initial speed of the Kenya
Time to exhaustion in the Ve,.u" test (pretravel K:
285 s, C: 321 s; Thble 2) did not significantly Oxygen uptake (ml.kg-0.7s .m¡n-1)
change in either group.
190
Maximal oxygen deficit
Control group
The initial maximal oxygen deficit in the Kenya 170
group was 4.30liters and it increased in all subjects
Kenya group
at the first test (2A) after the altitude sojourn
(mean 19+6%). Six days later (test 28) it had Kenya 1 at 15 km/h: 180+-3
150 Kenya 2A at 15 km/h: 180+-3
increased further in 1, subject (MT), was un- 1
Kenya 2B at 15 km/h: 179+-3
changed in another (JD), and had decreased in the 2A
28
Control at 15 km/h: 185+-5
other 3 subjects. The overall response (test 1 to Control at 12 km/h: 145+-3
2B) (Fig. 2) was not significant with ANOVA 130 Kenya 1 at 12 km/h: 137+-1.5
(P:0.13), although the ¡-test between test 1 and Kenya 2A at 12 km/h: 136+-1.5
Kenya 2B at 12 km/h: 135+-2
2A was (t:4.08, P<0.05). Expressed per kgO75, 0
the corresponding values were 186+13, 218+7 and 01213141516
203+lZ ml . kg-o 7s, respectively. Running velocity
(km.h-r)
Fig. 3. Modified running economy (ml .kg 0.7smin-I, see
Oxygen cost of running
Methods) at different running velocities before and after 2
The oxygen cost of running at treadmill velocities weeks of altitude training in the Kenya group and correspond-
ing sea-level training in the control group. 2A and 28 refers to
of 12.0,14.0, 15.0 and (for the Kenya group) 16.0 tests 6 and 12 d alter descent in the Kenya group (n:5).
km'h-1 were unchanged in both groups, both Control group 12 km'h-1, n=6;74-15 km.h 1, n:4. Values
when expressed as ml.kg-O75.min-1 (Fig.3) and are means * SE. Kenya 1 at 14 km/h: 169+-3
Kenya 1 at 16 km/h: 191+-3.5 Kenya 2A at 14 km/h: 168+-3
208 Kenya 2B at 14 km/h: 165+-3
Kenya 2A at 16 km/h: 189.7+-3
Kenya 2B at 16 km/h: 190+-3 Control at 14 km\h: 172+-3
 Altitude training in elite runners
Respiratory exchange ratio Heart rate (beats'min-r)
1.t 190

Control group Control group

1.0 + 170
1-1--
i b==== Kenya group
2
1
& a group
+
29 1

0.9 150
2A
I 28

0.8 130

0 0
o 12 13 14 1s 16 0 12 13 14 1s 16
Running velocity Running velocity
(km.h-1) (km.h-1)
Frg. 4. Respiratory exchange ratio(RER) at different running Flg. 5. Heart rate at different running velocities before and
velocities before and after 2 weeks of altitude training in the after 2-week altitude training in the Kenya group and corre-
Kenya group and corresponding sea-level training in the con- sponding sea level training in the control group. For 2A,2B
trol group. For 2A,28 and dotted line, see legend to Fig. 3. *
and dotted line, see legend to Fig. 3. P<0.05 and
** P<0.01,
* P<0.05, effect of sea-level training. A tendency (P<0.10) to
effect of training sojourn (ANOVA). Values are means t SE.
RER increase at low running velocities in the Kenya group.
Values are means + SE.

Heart rate

group max treadmill test was 5.15+0.16, In the Kenya group, the overall heart rate during
|
5 .29 + 0.21, and 5. 25 + 0 .22 |' min- at test 1., 2A and submaximal treadmill running was lower
2B, respectively (NS). (ANOVA, P<0.01) at the post- as compared with
the pre-altitude tests. This change was most clearly
seen at the last test (12 d after descent; Fig. 5) (24:
Respiratory exchange ratio (RER)
4.0+2.5, 4.0+L.7 and -2.811.8;28: 1.2+3.8,
RER during submaximal exercise increased after
the sea level training period in the control group Perceived exertion (Borg)
(12-15 km'h-1: +0.016 to 0.030, P<0.05; Fig. a).
17
A tendency to an increase was also noted at lower
running velocities in the Kenya group (ZB t2-1'5
km.h-1: +0.015 to 0.042, interaction term
p:0.06). RER at maximal exercise did not change 14 Control group
in either group (Table 2).
**
Ventilation 11 2
1 k:1
V Kenya group
Submaximal and maximal (Täble 2) ventilation
2A
(STPD) did not change with altitude or sea-level '1

training inthe2 groups. The ventilatory equivalent 28

(V, ' Vo,-1) tended (P:0.08) to be higher at the

last test in the Kenya group, being 19.3+0.8 (test
I),19.3+0.7 (24) and 20.5+0.7 (28) at L4 km'h-l 0
and 20.8+0.9, 20.4+0.9 and 21.4+0.8 at 15 0 12 13 14 15 16

km'h-1; control group 20.1+0.8 (1), 20.1+0,3 (2) Running velocity

Ikm.h-r)
and 21.9+I.2,22.4+0.9 for the corresponding ve-
locities. Fig. 6. General rated perceived exertion (Borg's 6-20 scale) at
different running velocities before and after 2 weeks of altitude
training in the Kenya group and corresponding sea-level train-
ing in the control group. 2A, 28 and dotted line, see legend to
Fig. 3. ** P<0.01, effect of altitude sojourn (ANOVA). Val-
ues are means + SE.

14 Scand J Med Sci Sports 209

 Kenya 1 at 16 km/h: 5.9+-1.3
Kenya 2A at 16 km/h: 5.7+-1.3
Kenya 2B at 16 km/h: 5.7+-1.3
Svedenhag et al.
Blood lactate (mmol.l-1)
10
Control at 15 km/h: 7+-1.8
Control at 14 km/h: 3.95+-0.9
I Control at 12 km/h: 2.5+-0.7
Kenya 1 at 15 km/h: 3.2+-1.1
Kenya 2A at 15 km/h: 3.0+-1.1
Kenya 1 at 12 km/h: 1.8+-0.4
Kenya 2B at 15 km/h: 3.1+-1.1
Kenya 2A at 12 km/h: 1.8+-0.4
Kenya 2B at 12 km/h: 1.8+-0.4 Blood ammonia/lactate conc. ('10-3)
40
Kênya group

30 2A

b 1

28
2A 29

Control group 20 1

4
Control group
2
T 1

/ttttteaaa
2 10
Kenya group

0 0
0 12 13 14 15 16 0 12 13 14 15 16
Kenya 1 at 14 km/h: 2+-0.3 Running velocity Running velocity
Kenya 2A at 14 km/h: 1.9+-0.3 (km.h-1) (km.h-r)
Kenya 2B at 14 km/h: 1.98+-0.3
Fig. 7. Blood lactate concentrations (mmol .l 1) at different Flg. 8. Plasma ammonia/blood lactate concentration ratio
running velocities before and after 2 weeks of altitude training ('10-3) at different running velocities before and after 2 weeks
in the Kenya group and corresponding sea-level training in the of altitude training in the Kenya group and corresponding
control group. For 2A ,28 and dotted line, see legend to Fig. 3. sealevel training in the control group. For 2A,28 and dotted
Values are means + SE. line, see legend to Fig. 3. Values are means -F SE.

-5.4+2,2 and -5.2+2.5 beats.min-1 at 12,14 and haustion in the max test were very similar and were
15 km.h-1, respectively). The heart rate-Vo, rela- also almost completely unchanged in both groups
tionships showed similar slopes (25.9 - 27.4 during the course of the study (around 11.8 and
beats.l-1) but the intercept tended to be lower 13.4 mmol .l-1 in the Kenya and control group,
post-altitud e (l: 65.7 + 12.0, 2A: 59.4+ 10.0, 2B: respectively).
56.6+7.5 beats .min-1, NS). The calculated heart
rates at Vo, 3.0 l.min-r (around 140
beats.min-1), and 4.0 I'min-1 (around 167
beats.min-l) were slightly (2A: -3.8, -2.9; 2B:
4.6, -3.1 beats.min-1, respectively) lower post-
altitude (NS). In the control group, tendencies to
increased heart rates were found after the sea-level Plasma ammonia "max" (¡rmol.l-l)
training. For the 4 control runners that were tested
at 12, 14 and 15 km.h-r (i.e. the male runners), 180
this increase was significant (P<0.05). The maxi- Kenya group
mal heart rate was unchanged in both groups (Th-
ble 2). 140
Control group
2
Perceived exertion
100 **
At higher treadmill velocities, the Kenya group
had lower ratings of perceived exertion after ys
before the altitude sojourn (28 vs 11Ç16 km . h-1: 60
4.9+0.4, -1.0+0.4, -1.4+0.5; interaction term
P<0.01;Fig. 6). No significant change was seen in
the control group. 0
012345
Time after exhaustion
Plasma lactate (minl

The plasma lactate concentrations at the different
submaximal running velocities were unchanged in
both the Kenya and the control group (Fig. 7). The
blood lactate levels 0.5, 3.5 and 5.0 min after ex-
Frg. 9. Plasma ammonia levels (¡rmol'l 1) at 30 s, 3.5 min and
5 min after treadmill test exhaustion at the different test occa-
sions in the 2 groups. 2A and 28 refers to tests 6 and 12 d after
descent in the Kenya group. ** P<0.01, effect of altitude
sojourn (ANOVA). Values are means + SE.

210

Table 3. Plasma catecholamine concentrations at submaximal and maximal running before and aftertraining sojourns in the 2 groups
Kenya group
2A
Third velocity:
Noradrenaline (nmol. l-1) 25.813.6 25.9!2,4
Adrenaline (nmol .l-t) 3.2310.53 2.53r0.49
Vo, -"- test:
Ñoradrenaline {nmol. l-1) 81.9r6.6 90.3r9.7
Adrenaline (nmol .l 1) 17.5!4.8 23.416.6
Values are means + SE.
Plasma ammonia
The plasma ammonia concentrations and the am-
monia/lactate ratio at the different submaximal
running velocities tended to be higher post- vs
prealtitude in the Kenya group (most notably at
test 2A ; ratio 12-1.6 km . h-1 : + 53, 19, 21 and I4"/",
NS) (Fig. 8). In the control group, these concen-
trations were unchanged. For maximal exercise in
the Kenya group, plasma ammonia levels 0.5, 3.5
and 5 min after exhaustion were significantly
(P<0.01) lower at test 28 than at test 1 and 2A(28
vs I: -28+9, -26+7 and -23+1,07o, respectively;
Fig. 9). For the control group, a tendency of a
decrease was noted after the corresponding sea-
level training period (NS).
Catecholamines
During the course of the study, the noradrenaline
and adrenaline responses at the end of the third
running velocity (of each individual) and at 30 s
after exhaustion (V6, *u" test) showed relatively
large intraindividual differences. However, no sys-
tematic or significant alterations within or between
groups were found (Table 3).
Discussion
We studied the effect of short-term altitude train-
ing on exercise capacity in highly trained elite mid-
dle-distance runners of national to international
caliber. For successful performance, this category
of runner may benefit from even small enhance-
ments in aerobic and anaerobic running capacity.
In seeking these performance improvements (such
as before major competitions), many athletes have
tried altitude training, even though it is still not
clearly known what effects that really can be antici-
pated.
The runners were studied during the off-season
winter period when their training programs are at a
high and even level and can be controlled. Even
l4*
Altitude training in elite runners
Control group
28 2
23,011 .6 33.1r5.8 3\,2!5.7
2.28r0.59 4.22!0.73 3,6510,83
72.9!6.2 92.4t10.2 74.5!4.1
14.915.4 25.6r6.0 1ô.614.1
so, most of the runners planned to participate in
one or two indoor races (including the national and
European championships), and high-intensity
workouts were therefore included in their training
programs,
Aerobic aspects
The altitude training did not influence sea-level
Vo,.u*. In some earlier studies with well-trained
subjects, both increased (4, 5, 14) and an un-
changed (I-3,6,7) postaltitude V6,*u* have been
reported. Comparing these studies (including the
present one), no consistent differences (such as
actual altitude or duration of training sojourn) are
seen between studies reporting increased or un-
changed Vo,.u*. The only major exceptions may
be the 10-week alternated sea-level and altitude
regimen performed by Daniels & Oldridge (4) and
the 4-week 2500 m living, 1300 m training regimen
reported by Levine et al. (14). Thus, if long-term
and/or discontinuous regimens are excluded, alti-
tude training may not raise Vo,.u, in already well-
trained individuals.
In spite of unaltered aerobic power, the exercise
heart rates were slightly lower after the altitude
sojourn in the Kenya group. In contrast, heart
rates during submaximal running were rather
higher in the control group after the training so-
journ; the latter therefore supports a true differ-
ence between the groups. With exposure to a
reduced 02 pressure (at high altitude or in a hypo-
baric chamber), several cardiovascular adjust-
ments are seen. After the initial acclimatization
phase (with an increased cardiac output), most of
the studies at (or simulating) moderate to high
altitude and at submaximal loads have shown an
unaltered cardiac output, reduced stroke volume
(possibly coupled to smaller plasma volume and
venous return), unchanged cardiac contractility
and an increased heart rate (15-18).
With this in mind and the unaltered exercise
catecholamines, the reduction in submaximal heart
211
Svedenhag et al.
rates (with unchanged oxygen uptakes and thus
elevated oxygen pulse) in the post-altitude tests
(Kenya group) could indicate an altered circula-
tory regulation by the autonomic nervous system
during submaximal running. For example, atrial
B-adrenoceptor responsiveness could be reduced,
since it has been shown elsewhere that both acute
and chronic hypoxia lower the heart rate response
to infused isoprenaline in human subjects (19). A
post-altitude increase in ventricular and/or vascu-
lar adrenoceptor responsiveness is another alterna-
tive. An increase in exercise stroke volume medi-
ated by an expanded plasma volume on retufn to
sea level seems less likely, however, in view of the
unchanged hemoglobin concentration in the Ke-
nya group after their altitude training sojourn.
Further, altitude sojourns are known to increase
pulmonary vascular resistance (20). As a conse-
quence, right ventricular hypertrophy is known to
develop in most mammals (including humans) liv-
ing at high altitude (21,). A thrilling alternative
explanation of our lower submaximal heart rates
could then also be an altitude-induced increase in
right ventricular performance leading to raised left
ventricular preload and, thereby, stroke volume.
Regarding maximal exercise, earlier studies
have shown Vo,.u* (acute effect) and also maxi-
malt heart rate (after a couple of days) to be lower
at altitude (I9,2225).In the present study, both
these variables were unchanged in the postaltitude
test. Furthermore, blood lactate levels were also
unaltered after the altitude sojourn (first test after
6 d). Thus, at least after the reacclimatization pe-
riod, no effect of the altitude training were seen in
these regards. Furthermore, the lowered perceived
exertion seen at higher submaximal running veloc-
ities was unrelated to ventilation, lactate or ammo-
nia (see also below).
The present findings of unaltered sea-level
Vo, -u* are in agreement with most previous alti-
tude training studies (2,6,7) but seem to diverge
from a recent study of one-legged training at simu-
lated altitude in a hypobaric chamber. In that
study (8), the simulated altitude and sea-level legs
trained at the same absolute work load and the
simulated altitude-trained leg showed greater im-
provements in several variables, including working
capacity. However, if the subject is training with
larger muscle groups (for example, in running),
the absolute load will most often be lower at alti-
tude because of the reduced Vo,.o*, and this can
probably account for the differences seen.
212
Anaerobic aspects
In the first post-altitude test, maximal oxygen def-
icit had increased in all of the Kenya group. This is
in line with an enhanced muscle-buffering capacity
of the same group at that time (26). Similar find-
ings, i.e., increased oxygen deficit and muscle-
buffering capacity after altitude training, have re-
cently also been reported for skiers (7). Such an
effect on buffering capacity may be the result of
high muscle lactate and H* concentrations during
exercise, which probably prevail during acute ex-
posure and early acclimatization to altitude. Fur-
thermore, a compensated respiratory alkalosis
may, at least initially, lead to decreased blood- and
probably also muscle-butÏering capacity with a
larger fall in pH per mmol H+ release, which has
been suggested (27) to inhibit phosphofructoki-
nase activity. An increased buffering capacity
could thus be an adaptive mechanism compensat-
ing for such pH decrements. Furthermore, effects
of this adaptation seem to persist for at least 1
week after return to sea level.
It may seem contradictory that maximal tread-
mill time 6 d after the altitude training sojourn in
the present study did not improve (compared with
pre-altitude), whereas oxygen maximal deficit in-
creased and Vq,,nu" was unchanged. This could be
due to a somewhat (NS) raised oxygen cost of
running at maximal test treadmill speed after the
altitude sojourn (determined by extrapolation of
submaximal data). Such a tendency at high but not
moderate running velocities may be explained by
lower training velocities at altitude compensatory
to the decreased barometric pressure.
A 13-d altitude acclimatization to 4300 m has
been reported to attenuate plasma ammonia levels
during submaximal exercise (28). This was, in
turn, postulated to lower the glycolytic flux by less
activation of phosphofructokinase (PFK), thereby
explaining an altered substrate utilization at alti-
tude, i.e. sparing of glycogen and increased ox-
idation of FFA (28, 29) (see also above). A re-
duced PFK activity by training at low barometric
pressure has also been reported (30). Further-
more, the perception of fatigue has been suggested
to follow an plasma ammonia decrement (28). The
reason for a lower exercise ammonia level after
altitude acclimatization is not known, but may in-
volve steps before inosine monophosphate (IMP)
formation, since muscle IMP during maximal exer-
cise is also lowered at altitude (31).
In the present study, ammonia levels after max
test were significantly decreased 1,2 d after the
altitude descent. This finding was unexpected and
is not readily explainable. It could be due to a late
effect of altitude training on the total ammonia
production capacity or on ammonia elimination.

The reason for such a late effect at maximal but
not submaximal exercise could, as compared with
the results of Young et al. (28), be related to the
lower altitude used in the present study (2000 us
4300 m). There could also be a more short-lasting
overriding effect of sea-level return on exercise
ammonia levels, as judged by the tendency of in-
creased plasma ammonia concentrations at sub-
maximal exercise after altitude descent in the Ke-
nya group. Since a smaller tendency of a decrease
in post-exhaustive ammonia also was seen in the
control group, the training load (related to resting
periods) could have influenced the results some-
what, irrespective of the altitude.
Submaximal blood lactates at the same absolute
load increased during acute exposure to altitude
(32) and decreased towards sea-level values after
acclimatization. In contrast, maximal lactate is
roughly unchanged rÌuring acute altitude exposure
but decreases after acclimafization, especially at
higher altitudes (27, 28, 33, 34). Any effect of
altitude on lactate production in the Kenya group,
however, seems to have reversed after the altitude
descent, as maxirnal blood lactate levels were com-
pletely unchanged in the post- vs pre-altitude tests.
In summary, these results suggest an unchanged
aerobic capacity in elite middle-distance runners
after short-term training at moderate altitude.
However, a change in the circulatory regulation
during submaximal exercise was observed. Fur-
thermore, anaerobic capacity improved but this
bore no clear relation to lactate or ammonia me-
tabolism.
Acknowledgements
We thank Gittan Jonas and Eva-Lena Olausson for skillful
technical assistance and Eva Brimark for expert secretarial
help. The cooperation of Anders Gärderud of the Swedish
Track and Field Association is also gratefully acknowledged.
The study was supported by grants from IBM, Sweden.
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