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Physiological responses to maximal intensity intermittent exercise

Article  in  European Journal of Applied Physiology and Occupational Physiology · February 1992

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Eur J Appl Physiol (1992) 65:144-149
Physiological responses to maximal intensity intermittent exercise
1 1 2 1
P. D . Balsom , J . Y . Seger , B. Sjödin , and B. Ekblom
1
Karolinska Institute, Department of Physiology I I I , Box 5626, S-11486 Stockholm, Sweden
2
National Defence Research Establishment, Stockholm, Sweden
Accepted March 26, 1992
Summary. Physiological responses to repeated bouts of
short duration maximal-intensity exercise were evalu-
ated. Seven male subjects performed three exercise pro-
tocols, on separate days, with either 15 (S ), 30 (S ) or 15
40 (S ) m sprints repeated every 30 s. Plasma hypoxan-
40
thine ( H X ) and uric acid (UA), and blood lactate con-
centrations were evaluated pre- and postexercise. Oxy-
gen uptake was measured immediately after the last
sprint i n each protocol. Sprint times were recorded to
analyse changes i n performance over the trials. Mean
plasma concentrations of H X and U A increased during
S and S f P < 0 . 0 5 ) , H X increasing f r o m 2.9 (SEM
30 40
1.0) and 4.1 (SEM 0.9), to 25.4 (SEM 7.8) and 42.7
- 1
(SEM 7.5) n m o l - 1 , and U A f r o m 372.8 (SEM 19) and
382.8 (SEM 26), to 458.7 (SEM 40) and 534.6 (SEM 37)
-1
u . m o l - 1 , respectively. Postexercise blood lactate con-
centrations were higher than pretest values in all three
protocols (P<0.05), increasing to 6.8 (SEM 1.5), 13.9
(SEM 1.7) and 16.8 (SEM 1.1) m m o l - l in S , S and- 1
S , respectively. There was no significant difference be-
40
tween oxygen uptake immediately after S [3.2 (SEM
1
0.1) 1-min" ] and S [3.3 (SEM 0.4) 1 - m i n ] , but a
40
-1
lower value [2.6 (SEM 0.1) 1 - m i n ] was found after S
(P<0.05). The time of the last sprint [2.63 (SEM'0.04)
s] i n Sis was not significantly different f r o m that of the
first [2.62 (SEM 0.02) s]. However, in S o and S o sprint
3 4
times increased f r o m 4.46 (SEM 0.04) and 5.61 (SEM
0.07) s (first) to 4.66 (SEM 0.05) and 6.19 (SEM 0.09) s
(last), respectively (P<0.05). These data showed that
with a fixed 30-s intervening rest period, physiological
and performance responses to repeated sprints were
markedly influenced by sprint distance. While 15-m-
sprints could be repeated every 30 s without decreases i n
performance, 40-m sprint times increased after the third
sprint (P<0.05) and this exercise pattern was associated
with a net loss to the adenine nucleotide pool.
Key words: Hypoxanthine - Uric acid - Blood lactate -
Maximal intensity intermittent exercise - Performance
Correspondence to: P. D. Balsom
European
Applied
Journal of
Physiology
and Occupationa! Physiology
© Springer-Verlag 1992
Introduction
The physiology of maximal intensity intermittent exer-
30 cise is extremely diverse as patterns of time relation-
ships between work and recovery periods have no de-
fined limits. Earlier studies, describing physiological re-
sponses to dynamic high intensity intermittent exercise,
have standardised exercise intensity by using either a se-
iected power output on a cycle ergometer (Saltin et al.
1976; Essen 1978) or a given speed and gradient on a
motorised treadmill (Christensen et al. 1960; Åstrand et
al. 1960; Margaria et al. 1969). More recently, there has
been a growing interest in the physiology of multiple
sprint sports, e.g. soccer or hockey, where exercise peri-
ods are characterised by maximal intensity short sprints
with higher energy demands (Williams 1990). Physiolog-
ical responses to this type of exercise pattern have been
previously described for repeated 6-s exercise periods by
15 30
Williams and co-workers on a cycle ergometer (Wootton
and Williams 1983) and on a nonmotorised treadmill
30 (Holmyard et al. 1988; Brooks et al. 1990). However,
-1
responses to shorter periods of maximal intensity sprint
15 exercise have not been evaluated.
The high rate of energy expenditure during sprinting
has been found to result in a net loss o f the adenine nu-
cleotide pool via adenosine 5 '-monophosphate ( A M P )
deamination (Hellsten-Westing et al. 1991). During in-
tensive exercise when the rate of adenosine 5 '-triphos-
phate (ATP) turnover exceeds the rate of adenosine 5-
diphosphate (ADP) rephosphorylation adenylate kinase
catalyses the reaction of 2ADPs to form A T P and A M P
thus reducing the accumulation of A D P in muscle.
While adenine nucleotide degradation facilitates the
continuation o f contractile activity during intensive
exercise (Sahlin and Broberg 1990) it has been proposed
that decreases i n muscle A T P concentration in the cell
could increase the production of superoxide radicals
which can cause damage to skeletal muscle (Sjödin et al.
1990).
Previous studies have used postexercise changes i n
plasma concentrations of the purines hypoxanthine and
uric acid to evaluate the effect of exercise intensity on

adenine nucleotide degradation during a single bout of
exercise (Ketai et al. 1987; Hellsten-Westing et al. 1991).
Although hypoxanthine accumulates in the muscle it has
been shown that it can diffuse through cell membranes
and ultimately into the blood stream (Sjödin et al.
1990). In the current study, we measured postexercise
concentrations of hypoxanthine and uric acid following
repeated short sprints to evaluate whether adenine nu-
cleotide degradation occurred during repeated sprints
with distances similar to those observed i n the multiple
sprint sports.
The aim of this study was to describe physiological
responses to repeated short sprints and to evaluate how
these responses and performance were influenced by
changes in sprint distance.
Methods
Subjects
Seven moderately to well-trained highly motivated male physical
education students participated as subjects in this study. The mean
age (range), body mass and maximal oxygen uptake ( F 0 J of 2 n
the group was 27.7 (21-36) years, 77.4 (SEM 2.4) kg, and 4.86
- 1
(SEM 0.13) l - m i n , respectively. The experimental design of the
study was approved by the Ethics Committee of the Karolinska
Institute. Test procedures were explained to the subjects prior to
them giving their informed consent to participate.
Procedures
The subjects performed three intermittent exercise protocols, on
separate days, consisting of a series of repeated sprints, with a 30-s
rest period between each sprint. In each test protocol the total
sprint distance was 600 m performed as either 40 x 15 m (S ),
20 x 30 m (S ) or 15 x 40 m (S ). A l l sprints were on an indoor
30 40
tårtan running track, from a standing start and the subjects were
instructed to complete each sprint in the shortest possible time.
The protocol order was randomised, and at least 5 days were al-
lowed between each test session. A standardised 20-min warm-up,
of continuous submaximal cycling, stretching exercises and short
bursts of acceleration on the track preceded each test. The sub-
jects were familiarised with this form of exercise before complet-
ing the first test protocol.
The sprint direction alternated for each sprint, i.e. the finish-
ing position of one sprint became the start of the next. During the
periods between sprints, the subjects rested passively at the start
line of the next sprint.
Sprint times. Sprint times were measured in one direction (i.e. for
the first sprint and then every other sprint) using electronic photo-
cells connected to a HEGO 3000 timer (HEGO Systems A B ,
Stockholm, Sweden) and were recorded with an accuracy of
0.001 s. In S and S an intermediate photo-cell was placed at
30 40
15 m to give a split time for the first 15 m (0-15 m). In an attempt
to standardise the part of the body which broke the photo-cell
light beam the first photo-cell was positioned 50 cm from the
ground and the cell at 15 and 40 m was positioned at head height
for each subject.
Hypoxanthine and uric acid. Venous blood, for the measurement
of plasma hypoxanthine and uric acid concentrations, was drawn
from a superficial vein in the forearm using venous puncture with
heparinised vacutainer tubes. Samples were collected after the
warm-up, and 15 and 60 min after the last sprint to measure peak
145
hypoxanthine and uric concentrations, respectively (Hellsten
Westing et al. 1989). The blood was immediately chilled and cen-
trifuged within 15 min of collection. Plasma was stored at —20° C
before being analysed using high performance liquid chromato-
graphy (HPLC) (Waters Association Inc. Milford, Mass., USA)
with a modified method described by Wung and Howell (1980).
Blood lactate. Whole blood lactate concentrations were measured
enzymatically using an YSI 23L lactate analyser (Yellow Springs
Instruments, Ohio, USA) from finger tip blood. Samples (25 pl)
were taken after the warm-up, during seiected rest periods be-
tween trials (see Fig. 3), and also 2 and 4 min after the last sprint,
to measure peak postexercise concentrations. The blood was hae-
molysed in a buffer solution of 1:2 dilution containing triton,
stored at less than 4° C and analysed within 24 h.
Oxygen uptake. Oxygen uptake was measured immediately after
the last sprint using the conventional Douglas bag method. A 20-s
collection time was used to evaluate the contribution of aerobic
metabolism to recovery processes during this type of exercise. The
expired gases were analysed for oxygen and carbon dioxide frac-
tions using Servomex 570A (Crowborough, Sussex, England) and
a Beckman LB-2 (Beckman Instruments Inc., Fullerton, USA) gas
v
analysers, respectively. The k 0 x was also measured using Dou-
2ma
glas bags and was determined using an incremental exercise proto-
col to exhaustion, on a motorised treadmill.
Test reliability
The performance reliability of this type of exercise was studied
with three subjects performing one each of the three exercise pro-
tocols, on two occasions. For each subject, the 15 sprint times for
each test were summed and these two means were compared using
a Studenfs Mest. No significant difference (P>0.05), between the
two means, was found for any of the three subjects.
Statistics
15
To analyse the effect of preceding exercise on subsequent per-
formance, the first sprint time in each protocol was used as a ba-
seline measure of performance. Subsequent sprint times were then
compared for significant differences from the baseline time, using
an analysis of variance (ANOVA) with dependent groups. Pre-
and posthypoxanthine and uric acid concentrations were com-
pared using a Studenfs Mest for paired samples. The level of sig-
nificance used to reject the null hypothesis was P<0.05.
Results
Sprint times
Sprint times are illustrated in Fig. 1. I n Si the time of5
the last sprint [2.62 (SEM 0.02) s] was not significantly
different f r o m the first sprint [2.63 (SEM 0.04) s]. How-
ever, in S and S sprint times increased significantly
30 40
f r o m 4.46 (SEM 0.04) and 5.61 (SEM 0.07) s, to 4.66
(SEM 0.05) and 6.19 (SEM 0.09) s, respectively. The
mean sprint times for S , S and S , were 2.62, 4.58
15 30 40
and 5.94 s, respectively. The 0-15 m times of the first
sprint i n S [2.63 (SEM 0.04) s], S [2.61 (SEM 0.02) s]
15 30
and S [2.58 (SEM 0.03) s], were not significantly dif-
40
ferent confirming that base line performance was repro-
ducible on different days.
146

6.5 r

3.0 [•

2.5 Fig. 1. Sprint times (mean and SEM, n = 7) for Si 5

120 200 280 360 440 ( • ) , S (V), and S ( • ) • S , S , S40, sprints over
30 40 15 30

Accumulated distance (m) 15, 30 and 40 m, respectively

Hypoxanthine and uric acid concentrations

5 5 0 \-
Plasma concentrations of hypoxanthine and uric acid
are illustrated i n Fig. 2. There was no significant differ-
ence between pretest plasma concentrations of hypoxan-
thine, or uric acid, in S , S and S . Postexercise,15 30 40

plasma concentrations of both hypoxanthine and uric

acid were significantly higher than pretest values i n S 30

and S . I n S , although the mean postexercise plasma

40 15
1
hypoxanthine [7.7 (SEM 1.8) u.mol-1" ] and uric acid
1
[383.1 (SEM 9.39) u.mol-1" ] concentrations were ele-
vated with respect to corresponding pre-exercise values
1
[3.3 (SEM 0.8) pimol-r and 346.2 (SEM 17.9)
p,mol T ~ ' ] the difference was not significant due to int-
er-subject variation. I n S postexercise hypoxanthine
40

and uric acid concentrations [42.7 (SEM 7.5) and 534.6

1
(SEM 37) p - m o M " ] e higher (P<0.05) than in S
w e r 30
1
(25.4 and 458.7 p-mol-r ).

Blood lactate

Blood lactate concentrations are illustrated i n Fig. 3.

There was no significant difference in the pretest con-
centrations f o r S [2.4 (SEM 0.2)], S [2.8 (SEM 0.3)]
15 30
- 1
and S [2.9 (SEM 0.2) mmol T ] . I n all three exercise
40

protocols postexercise concentrations were significantly

higher than pretest values.

S15 S30 S40

Oxygen uptake
Fig. 2. Plasma hypoxanthine {below) and uric acid (above) con-
centrations (mean and SEM, n = l) for pre (@) and post ( \ ) test
Oxygen uptake measured directly after the last trial in
(mean and SEM, « = 7; • post greater than pre, P<0.05) - 1
S [3.2 (SEM 0.2) l - m i n ] and S [3.3 (SEM 0.4)
30 40
1
1-min" ; P > 0 . 0 5 ] , was higher (P<0.05) than that mea-
-1
sured after S [2.6 (SEM 0.1) 1 - m i n ] .
15

18
j ~ 16
oj 12
o
tj
5 10
T>
O
o
m 8
2
PRE 40 120 200 280 360 440 520
0 15
Accumulated distance (m)
Discussion
The data f r o m this study show how physiological and
performance responses to repeated sprints with 30-s rest
periods are markedly affected by sprint distance.
A significant decrease i n performance, i.e. increase in
sprint time (Fig. 1), with the repeated 40-m sprints was
found after only three sprints. This was comparable to
the performance characteristics reported during re-
peated 6-s bouts of maximal intensity exercise, with 30-s
recovery periods on a nonmotorised treadmill (Hol-
myard et al. 1988; Brooks et al. 1990) and a cycle er-
gometer (Wootton and Williams 1983). I t can be con-
cluded that 30-s recovery periods are not sufficient to
sustain performance during repeated 6-s bouts of maxi-
mal intensity exercise. This is in contrast to the findings
of earlier studies evaluating responses to high intensity
intermittent exercise. Margaria et al. (1969) concluded
that repeated 10-s bouts of "very strenuous" exercise
with a fixed speed and gradient on a motorised treadmill
could be repeated every 30-s indefinitely without fati-
gue. This highlights the consequences of the higher ener-
gy demands of maximal sprinting where a set distance is
covered in as short a time as possible.
The high energy demand o f the repeated 30 and 40-m
sprints performed i n the current study was reflected by
the elevated postexercise plasma concentrations of hy-
poxanthine and uric acid. The formation of these pu-
rines during exercise was indicative of a net degradation
of A T P in the muscle. Furthermore, the production of
uric acid was evidence of a loss of the total adenine nu-
cleotide pool. Under normal conditions the rapid re-
phosphorylation of A D P via creatine phosphate (CP)
minimises intracellular increases in A D P (Cain and Dav-
ies 1962) and reduces adenine nucleotide degradation.
However, during high råtes of energy turnover A D P ac-
cumulates in the muscle when the rate of A T P hydroly-
sis exceeds the rate of A D P rephosphorylation. To
maintain a high intracellular A T P : A D P ratio, adenylate
147
l 1
Fig. 3. Blood lactate concentrations (mean
2 4 and SEM, « = 7) for S ( • ) , S (V) and S
30 40
P o s t - t e s t (min) (T). For definitions see Fig. 1
kinase catalyses a reaction where 2ADPs combine to
f o r m A T P and A M P . The subsequent deamination o f
A M P to inosine monophosphate is important to allow
A T P resynthesis via the adenylate kinase reaction to
continue. The adenylate kinase system has also been re-
cognised as an important link i n the proposed creatine-
CP energy shuttle (Bessman 1985). Although it is d i f f i -
cult to quantify A T P resynthesis via the adenylate k i -
nase reaction, the importance o f this pathway during
short duration high intensity exercise has been reported
by Thorstensson et al. (1975) who found an increase in
the activity of adenylate kinase following 8 weeks of
training with repeated 5-s sprints.
Although CP concentration was not directly mea-
sured i n this study the finding that there was no signifi-
cant increase in plasma hypoxanthine concentration dur-
ing the repeated 15-m sprints would suggest that the CP-
creatine phosphokinase system was able to buffer energy
demands during each exercise period and that there was
an adequate resynthesis of CP during the subsequent re-
covery periods. This was supported by the performance
characteristics of S where there were no significant in-
]5
creases in sprint times over the trials. During intermit-
tent exercise with longer exercise periods, Harris et al.
(1977) have suggested that intracellular acidosis could
reduce the concentration to which CP could effectively
be restored during rest periods. This may explain in part
the decreases i n performance seen in S 3 0 and S 4 0 .
Hypoxanthine is a substrate f o r the enzyme xanthine
dehydrogenase which catalyses the production of uric
f r o m hypoxanthine. In a previous study (Hellsten-West-
ing et al. 1989) the metabolic time curves for hypoxan-
thine and uric acid were shown to follow each other with
a 20-min delay of uric acid in relation to hypoxanthine.
Our results (Fig. 2) agree with the finding of that study
showing that uric acid production and thus xanthine de-
hydrogenase activity was clearly associated with the
availability of hypoxanthine. While adenine nucleotides
may be salvaged f r o m hypoxanthine in a reaction cata-
148
lysed by hypoxanthine-phosphoribosyltransferase, uric
acid is produced in an irreversible reaction resulting in a
net loss to the total adenine nucleotide pool.
With the repeated 40-m sprints performed in the cur-
rent study the increase in plasma uric acid concentration
- 1
was 152 u m o l T . With an estimated blood volume of
5.51, an active muscle mass of 15 kg and a resting A T P
l
concentration of 25 mmol-kg x~ (dry mass), assuming
that all the uric acid was produced in the muscle, we have
calculated the net loss to the total adenine nucleotide pool
to be in the region of 1 % . Although the acute effects of
such a relatively small net loss would not appear to be too
harmful, the de novo resynthesis of adenine nucleotides
has been shown to be relatively slow. Thus, frequently
repeated sessions of high-intensity exercise could lead to
an accumulated loss of adenine nucleotides. Preliminary
findings f r o m our laboratory have shown decreases of
around 10%-20% in resting adenine nucleotides follow-
ing high-intensity intermittent training. A secondary con-
sideration of uric acid production is the activity of xan-
thine dehydrogenase, which through biochemical mecha-
nisms may be converted to its oxidase f o r m resulting in a
markedly increased rate of oxygen free radical produc-
tion which could lead to a loss of cell viability and even
cell necrosis (Sjödin et al. 1990).
Previous studies (Margaria et al. 1969; Christensen et
al. 1960) describing the physiological response to high
intensity intermittent exercise, with similar time relation-
ships between exercise and rest periods as used in the
current study, have reported only small increases in
blood lactate concentration. Thus, the high mean blood
lactate concentration measured during S
40
1 1
(16.8 m m o l T " , range 14.1-22.8 m m o l T " ) must re-
flect the extra energy demand of the exercise periods in
the current study. This again illustrates the diversity of
high intensity intermittent exercise and clearly shows
how physiological responses are markedly affected by
the intensity of the exercise during exercise periods.
The peak postexercise blood lactate concentration for
the repeated 2.5-s bouts of exercise (S ) was 15
_ 1
6 . 8 m m o l T . It can be seen f r o m Fig. 3 that an in-
crease in blood lactate was evident even after the second
sprint, suggesting that anaerobic glycolysis contributed
to energy production during each 15-m sprint. This
agrees with findings of Hultman and Sjöholm (1983)
who have reported that with an electrically stimulated
maximal isometric contraction anaerobic glycolysis was
activated within the first second. I n dynamic exercise,
during a 6-s bout of maximal intensity exercise Boobis
(1987) has reported that anaerobic glycolysis contributed
around 50% of the total energy production. Thus, in
humans, it would appear that the anaerobic glycolytic
pathway contributes to energy production concomitant-
ly with CP breakdown f r o m the very beginning of exer-
cise. With intermittent exercise there exists a possibility
that anaerobic glycolysis could also be active and contri-
bute to A T P resynthesis during the rest periods. Wilkie
(1981) has shown that in vitro, CP could be resynthe-
sised under anaerobic conditions with a resultant in-
crease in lactic acid but in vivo this finding has yet to be
confirmed.
In conclusion, the data presented in this study
showed how physiological and performance responses to
repeated sprints with a standardised intervening recove-
ry period was influenced by sprint distance. It is clear
that these responses differed markedly f r o m those pre-
viously reported for high intensity intermittent exercise
using exercise intensities of a similar duration but with
controlled power outputs. The finding that 15-m sprints
could be repeated every 30 s with low metabolic stress
and without significant decreases in performance would
suggest that with this exercise pattern the muscle could
recover sufficiently between bouts so that contractile ac-
tivity was not impaired. This has practical applications
for training or participation in a multiple sprint sport.
With a longer sprint distance of 30 or 40 m , correspond-
ing to exercise periods of about 4.5 and 6 s, respectively,
decreases in performance over the trials and a net loss to
the adenine nucleotide pool were found indicating high
metabolic stress. I t would appear that, with the longer
sprint distances, 30 s was not enough time for the mus-
cle to recover f r o m the increased energy demands. L i m -
iting factors at the metabolic level need to be addressed
in future studies.
Acknowledgements. The authors wish to acknowledge Elisabeth
Malm, Ailo Mikiver and Maarja Mikiver for their skillful techni-
cal assistance.
References
Åstrand I , Åstrand PO, Christensen E H , Hedman R (1960) Inter-
mittent muscular work. Acta Physiol Scand 48:448-453
Bessman SP (1985) The creatine-creatine phosphate energy shut-
tle. Annu Rev Biochem 54:831-862
Boobis L H (1987) Metabolic aspects of fatigue during sprinting.
In: Macleod D, Maughan RJ, Nimmo M , Reilly T, Williams C
(eds) Exercise: benefits, limitations and adaptions. Spon, Lon-
don, pp 116-140
Brooks S, Nevill M E , Meleagros L , Lakomy H K A , Hall GM,
Bloom SR, Williams C (1990) The hormonal response to repe-
titive brief maximal exercise in humans. Eur J Appl Physiol
60:144-148
Cain DF, Davies RE (1962) Breakdown of adenosine triphosphate
during a single contraction of working muscle. Biochem Bio-
phys Res Commun 8:361-366
Christensen E H , Hedman R, Saltin B (1960) Intermittent and con-
tinuous running. Acta Physiol Scand 50:269-286
Essen B (1978) Studies on the regulation of metabolism in human
skeletal muscle using intermittent exercise as an experimental
model. Acta Physiol Scand [Suppl] 454:1-32
Harris RC, Sahlin K, Hultman E (1977) Phosphagen and lactate
contents of m. quadriceps femoris of man after exercise. J
Appl Physiol 43 :852-857
Hellsten-Westing Y, Ekblom B, Sjödin B (1989) The metabolic re-
lationship between hypoxanthine and uric acid in man follow-
ing maximal short distance running. Acta Physiol Scand
137:341-345
Hellsten-Westing Y, Sollevi A, Sjödin B (1991) Plasma accumula-
tion of hypoxanthine, uric acid and creatine kinase following
exhausting runs of different durations in man. Eur J Appl
Physiol 62:380-384
Holmyard DJ, Cheetham M E , Lakomy H K A , Williams C (1988)
Effect of recovery duration on performance during multiple
treadmill sprints. In: Reilly T, Lees A, Davids K, Murphy WJ
(eds) Science and football. Spon, London, pp 134-142

Hultman E, Sjöholm H (1983) Substrate availability. In: Knuttgen
HG, Vogel JA, Poortmans J (eds) Biochemistry of exercise.
Human Kinetics, Champaign, 111., pp 63-75
Ketai L H , Simon R H , Kreit JW, Grum CM (1987) Plasma hy-
poxanthine and exercise. A m Rev Respir Dis 136:98-101
Margaria R, Oliva RD, D i Prampero PE, Cerretelli P (1969) Ener-
gy utilization in intermittent exercise of supramaximal intensi-
ty. J Appl Physiol 26:752-756
Sahlin K, Broberg S (1990) Adenine nucleotide depletion in hu-
man muscle during exercise: causality and significance of A M P
deamination. Int J Sports Med 11 [Suppl 2J: S62-S67
Saltin B, Essen B, Pedersen K (1976) Intermittent exercise: its
physiology and some practical implications. In: Jokl E (ed)
Medicine sport, vol 9. Advances in exercise physiology. Kar-
ger, Basel, pp 23-51
Sjödin B, Hellsten Westing Y, Apple F (1990) Biochemical mecha-
nisms for oxygen free radical formation during exercise. Sports
Med 10:236-254
View publication stats
149
Thorstensson A , Sjödin B, Karlsson J (1975) Enzyme activities
and muscle strength after sprint training in man. Acta Physiol
Scand 94:313-318
Wilkie D (1981) Shortage of chemical fuel as a cause of fatigue:
studies by nuclear magnetic resonance and bicycle ergometry.
In: Human muscle fatigue: physiological mechanisms. Ciba
Foundation symposium 82. Pitman Medical, London, pp 102-
119
Williams C (1990) Metabolic aspects of exercise. In: Reilly T, Si-
chir N , Snell P, Williams C (eds) Physiology of sports. Spon,
London, pp 3-39
Wooton SA, Williams C (1983) The influence of recovery dura-
tion on repeated maximal sprints. In: Knuttgen HG, Vogel JA,
Poortmans J (eds) Biochemistry of exercise. Human Kinetics,
Champaign, 111., pp 269-273
Wung WE, Howell SB (1980) Simultaneous liquid chromatogra-
phy of 5-fluorouracil, uridine, hypoxanthine, xanthine, uric
acid, allopurinol and oxipurinol in plasma. Clin Chem
26:1704-1708