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This study examined the contribution of phosphocreatine (PCr) and aerobic metabolism during repeated bouts of sprint exercise. Eight male subjects performed two cycle ergometer sprints separated by 4 min of recovery during two separate main trials. Sprint 1 lasted 30 s during both main trials, whereas sprint 2 lasted either 10 or 30 s. Muscle biopsies were obtained at rest, immediately after the first 30-s sprint, after 3.8 min of recovery, and after the second 10-and 30-s sprints. At the end of sprint 1, PCr was 16.9 ± 1.4% of the resting value, and muscle pH dropped to 6.69 ± 0.02. After 3.8 min of recovery, muscle pH remained unchanged (6.80 ± 0.03), but PCr was resynthesized to 78.7 ± 3.3% of the resting value. PCr during sprint 2 was almost completely utilized in the first 10 s and remained unchanged thereafter. High correlations were found between the percentage of PCr resynthesis and the percentage recovery of power output and pedaling speed during the initial 10 s of sprint 2 (r = 0.84, P < 0.05 and r = 0.91, P < 0.01). The anaerobic ATP turnover, as calculated from changes in ATP, PCr, and lactate, was 235 ± 9 mmol/kg dry muscle during the first sprint but was decreased to 139 ± 7 mmol/kg dry muscle during the second 30-s sprint, mainly as a result of a ~45% decrease in glycolysis. Despite this ~41% reduction in anaerobic energy, the total work done during the second 30-s sprint was reduced by only ~18%. This mismatch between anaerobic energy release and power output during sprint 2 was partly compensated for by an increased contribution of aerobic metabolism, as calculated from the increase in oxygen uptake during sprint 2 (2.68 ± 0.10 vs. 3.17 ± 0.13 l/min; sprint 1 vs. sprint 2; P < 0.01). These data suggest that aerobic metabolism provides a significant part (~49%) of the energy during the second sprint, whereas PCr availability is important for high power output during the initial 10 s.
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Contribution of phosphocreatine and aerobic metabolism
to energy supply during repeated sprint exercise
GREGORY C. BOGDANIS, MARY E. NEVILL,
LESLIE H. BOOBIS, AND HENRYK K. A. LAKOMY
Department of Physical Education, Sports Science, and Recreation Management,
Loughborough University, Loughborough, LEll 3TU; and Sunder-land District General Hospital,
Sunderland, SR4 7TP, United Kingdom
Bogdanis, Gregory C., Mary E. Nevill, Leslie H. Boo-
bis, and Henryk K. A. Lakomy. Contribution of phosphocre-
atine and aerobic metabolism to energy supply during re-
peated sprint exercise. J. Apple. Physiol. SO(3): 876-884,
1996.-This study examined the contribution of phosphocre-
atine (PCr) and aerobic metabolism during repeated bouts of
sprint exercise. Eight male subjects performed two cycle
ergometer sprints separated by 4 min of recovery during two
separate main trials. Sprint 1 lasted 30 s during both main
trials, whereas sprint 2 lasted either 10 or 30 s. Muscle
biopsies were obtained at rest, immediately after the first
30-s sprint, after 3.8 min of recovery, and after the second lo-
and 30-s sprints. At the end of sprint 1, PCr was 16.9 t: 1.4%
of the resting value, and muscle pH dropped to 6.69 5 0.02.
After 3.8 min of recovery, muscle pH remained unchanged
(6.80 t 0.03), but PCr was resynthesized to 78.7 t 3.3% of
the resting value. PCr during sprint 2 was almost completely
utilized in the first 10 s and remained unchanged thereafter.
High correlations were found between the percentage of PCr
resynthesis and the percentage recovery of power output and
pedaling speed during the initial 10 s of sprint 2 (r = 0.84,
P < 0.05 and r = 0.91, P < 0.01). The anaerobic ATP turn-
over, as calculated from changes in ATP, PCr, and lactate, was
235 ? 9 mmol/kg dry muscle during the first sprint but was
decreased to 139 t 7 mmol./kg dry muscle during the second
30-s sprint, mainly as a result of a -45% decrease in
glycolysis. Despite this -41% reduction in anaerobic energy,
the total work done during the second 30-s sprint was reduced
by only -18%. This mismatch between anaerobic energy
release and power output during sprint 2 was partly compen-
sated for by an increased contribution of aerobic metabolism,
as calculated from the increase in oxygen uptake during
sprint 2 (2.68 2 0.10 vs. 3.17 * 0.13 l/min; sprint 1 vs. sprint
2; P < 0.01). These data suggest that aerobic metabolism
provides a significant part (-49%) of the energy during the
second sprint, whereas PCr availability is important for high
power output during the initial 10 s.
sprinting; muscle fatigue; recovery; glycogenolysis; glycoly-
sis; muscle lactate; muscle pH; oxygen uptake
IN RECENT
YEARS, physiologists have used the model of
maximal dynamic exercise to further understanding of
the regulation of the metabolic pathways and to shed
light on the etiology of fatigue during high-intensity
exercise. After the introduction of the Wingate test (2),
it was possible to examine the metabolic responses to
sprinting while concurrently monitoring the power
output during the test. It is now well documented that
during a single 30-s cycle ergometer sprint 25-30% of
the ATP resynthesized from anaerobic metabolism
comes from phosphocreatine (PCr) breakdown, while
the major part (65-70%) comes from glycolysis (3, 32).
However, such studies examining a single sprint can
only make a limited contribution to understanding the
causes of fatigue and limitations of performance, as all
metabolic changes occur concurrently. More recently,
the model of intermittent exercise has become more
popular. This model has the advantage that, because of
the different rates of recovery of various muscle metabo-
lites, the metabolic status of the muscle can be changed
and the effect on performance in a subsequent sprint
can be examined (3, 7, 18, 27). With the use of this
model, some authors have shown a great reduction in
the rate of glycolysis in subsequent bouts of exercise
without a proportional decrease in power output (7,18,
27) and have suggested, although oxygen uptake
(vo2)
was not determined, that the decrease in energy supply
from anaerobic pathways may be partially compen-
sated by an increase in aerobic metabolism (18, 27).
Thus one of the purposes of the present study was to
examine whether
vo2
is increased in a second bout of
sprint exercise.
It has also been suggested that PCr resynthesis, and
thus PCr availability, is important for power output
recovery (7,11,25), but in most cases these suggestions
have been based on speculation and not on simulta-
neous measurements of muscle metabolites. In a recent
study (3), the time course of power output recovery in
the first few seconds of a second 30-s sprint was found
to occur in parallel with the resynthesis of PCr, despite
muscle pH remaining low throughout recovery. How-
ever, muscle metabolism during the second sprint was
not examined. Therefore, a second purpose of the
present study was to examine the relationship between
the metabolic status of the muscle before a second
sprint and the subsequent performance and changes in
muscle metabolites during that sprint.
Finally, although it is widely accepted by the sporting
community that a high maximum oxygen uptake
m
2nd
and d
en urance fitness (training status) are
important determinants of the ability to recover power
output after sprinting, there is little information to
support such beliefs in the physiology literature. A
further purpose of the present study was, therefore, to
examine the relationship between
Vo2,,,
endurance
fitness, and the recovery of power output during sprint-
ing.
In summary, the purpose of the present study was to
examine the changes in muscle metabolism and power
output when a bout of sprint exercise was repeated
after a short recovery interval to further understanding
of the regulation of the metabolic pathways, the etiol-
ogy of fatigue during sprinting, and the factors affect-
876 0161-7567/96 $5.00 Copyright o 1996 the American Physiological Society
ENERGY METABOLISM DURING REPEATED SPRINT EXERCISE
877
ing recovery from maximal exercise. Muscle metabo-
lism during sprint 2 was examined in more detail by
taking muscle biopsies after the first 10-s and at the
end of the second 30-s sprint. The study tests the
following hypotheses: I) that an increase in aerobic
metabolism partially compensates for the reduction in
energy supply from anaerobic pathways during sprint
2; 2) that PCr is completely utilized during the first
10 s
of sprint 2 and that the recovery of power output during
the first 10 s of the sprint 2 is related to the PCr
resynthesis after sprint 1; and 3) that the recovery of
power output in sprint 2 is related to
Vozrnax
and
endurance fitness.
METHODS
Subjects. Eight male university students, aged 24 t 2 (SD)
yr, 177 ? 7 cm in height, and 79 t 10 kg in body mass,
volunteered to take part in this study. All subjects were
physically active (recreational athletes) and were informed in
writing about the purpose of the study, any known risks, and
the right to terminate participation at will. Each expressed
understanding by signing a statement of informed consent. A
medical history questionnaire was also completed in the
presence of the experimenter, and subjects with medical
problems were excluded. The protocol was approved by the
Ethical Committee of Loughborough University.
Equipment. A modified friction-loaded cycle ergometer
(Monark, model 864), interfaced with a microcomputer, was
used to attain high-frequency logging of the flywheel angular
velocity. The ergometer frame was mounted on a baseplate
and strengthened with metal struts to prevent bending of the
frame and handle bars. The instantaneous power generated
during the sprints was corrected for the changes in kinetic
energy of the flywheel (14), and results were averaged over
l-s intervals. By taking into account the work done in
accelerating the flywheel during the initial seconds of the
sprint, peak power was always reached before peak speed. A
restraining harness, passed around the subject’s waist and
fixed to a metal rail bolted on the floor behind the bicycle
frame, restricted exercise to the leg muscles during the
sprints. Toe clips were used with the subject’s feet strapped to
the pedals with strong tape.
Preliminary tests. During a preliminary visit, the
voarn,
of
each subject was determined by using a continuous incremen-
tal test on the Monark cycle ergometer. Subjects performed a
2-min warm-up at 60 W [60 revolutions/min (rpm)], and then
power output was increased by 30-60 W every 3 min until
exhaustion (N 11-14 min). Power output at
vo2max
was 303 2
13 W. Expired air was collected during the last 60 s of each
stage by using the Douglas bag technique. Samples of expired
air were analyzed for fractions of O2 and CO2 by using a
paramagnetic oxygen analyzer (Servomex-Sybron/Taylor,
model 570A) and a carbon dioxide analyzer (Lira infrared gas
analyzer, model 303), and the volume of expired air was
measured by a Harvard dry-gas meter. All gas volumes were
corrected to
STPD.
In a separate session, subjects performed five continuous
4-min stages of submaximal cycling at power outputs corre-
sponding to 61 _
+ 2 71 + 2, 80 2 2, 86 t 2, and 93 of: 2%
vo 2ma. Expired air’wascollected during the last minute of
each stage, and duplicate samples of arterialized capillary
blood (20 ul each) were taken from a prewarmed thumb
during the last 15 s of each stage for lactate (La) determina-
tion. From this test, the relative intensity
(%VOzmm)
corre-
sponding to a blood La concentration of 4 mmol/l (%4 mM)
was estimated for each subject by linear interpolation. This
value (%4 mM> was accepted as an indication of endurance
training status (endurance fitness), as the
%VO2mm
at a given
blood La concentration has been shown to increase with
tests were performed at the same time of day, 1 wk apart.
Subjects recorded their diet (with estimated portion sizes)
and refrained from intense physical exercise for 48 h before
the first main trial. They repeated this regimen in the 48 h
before test 2. A standardized warm-up consisting of 4 min of
pedaling at 60 W, followed by one bout of 30 s at 80 W and one
bout of 30 s at 100 W, preceded each test. This warm-up has
been previously shown to cause a minimal metabolic distur-
bance (4). Five minutes after the completion of the warm-up,
subjects performed two maximal cycle ergometer sprints,
separated by 4 min of passive recovery on the bicycle seat.
During one main trial, a 30-s sprint was followed by another
30-s sprint (30-30 main trial), and in the other main trial, a
30-s sprint was followed by a 10-s sprint (30-10 main trial;
Fig. 1). The resistive load was 75 N*kN body wt-l (average
load: 59 t 3 N), and each sprint started from a rolling start of
-70 rpm. Strong verbal encouragement was given during
each sprint.
The following performance parameters were obtained for
each sprint: peak power output (PPO); pedaling speed at
which peak power output was attained (Spppg >; maximum
pedaling speed (Spm,); mean power output for the first 10 s
(MPOlo), the last 20 s (MPOL2& and the whole sprint
(MPO&; and the percent decline from peak to end power
output (fatigue index; FI). The mean pedaling speed during
the above time intervals was also calculated (Splo, SpL20,
Sp&. Expired air samples were collected in Douglas bags
during each sprint. The test-retest reliability for
v02
measure-
ments during sprinting was determined in separate experi-
ments. For a 30-s sprint, test 1 vs. test 2
q02
values were
2.53 t 0.28 vs. 2.59 t 0.29 l/min [not significant (NS) n = 191,
and the correlation coefficient r was 0.94 (SE of estimate: 0.12
l/min). For a 10-s sprint, test 1 vs. test 2
VOW
values were
1.64 ? 0.20 vs. 1.69 ? 0.19 l/min (NS; n = 7), and the r was
0.96 (SE of estimate: 0.15 Vmin).
Muscle samples. On arrival at the laboratory, subjects
rested on a couch for 30 min while small incisions were made
through the skin and fascia over the vastus lateralis muscle
(in both main trials, two incisions were made in the same leg
-3 cm apart; in one of the two main trials, another incision
was made in the other leg) under local anesthesia (1% plain
lidocaine). All postexercise biopsies were taken with the
subject sitting on the cycle ergometer (Fig. 1). The biopsy leg
(left or right), the choice of the two or three sampling points in
each main trial (from rest, after sprint 1, 3.8 t 0.01 min into
recovery, after the 10-s sprint 2, and after the 30-s sprint 2),
and the main trial order (30-30 main trial or 30-10 main trial)
were randomized in a balanced design, so that biopsies before
and immediately after each sprint were taken from the same
leg. Thus, over two main trials, a total of five biopsies were
taken from each subject through different incisions in the
skin. Muscle samples were plunged directly into liquid nitro-
gen in the needle and were kept in liquid nitrogen until they
were freeze dried (within 24 h of sampling).
Analytical methods. The freeze-dried samples were dis-
sected free of connective tissue and blood and homogenized.
The muscle powder was then divided in two parts. One part of
878
ENERGY METABOLISM DURING REPEATED SPRINT EXERCISE
H- 30 s maximal sprint
a- 10 s maximal sprint
4
muscle biopsy
turnover by the duration of the sprint (e.g., 10 or 30 s). No
correction has been made for anaerobically produced ATP as a
result of Pyr oxidation or for La efflux during the sprint.
ATP turnover = 2( -AATP) - APCr
+ 1.5ALa + 1.5APyr (1)
WARM-UP
I I# I I I
1 I
5 min
1 2 3 4
min
where 2 active phosphates are cleaved per ATP utilized and
1.5 mmol ATP is produced for every millimole of La and Pyr.
Glycogenolytic and glycolytic rates during each sprint
(mmol glucosyl units
l
kg-l dry muscle
l
s-l) were calculated
from accumulation of glycolytic metabolites
glycogenolysis = (AG-1-P + AG-6-P
+ AF-6-P) + 0.5(ALa + APyr) (2)
WARM-UP
1 I# I
I I
glycolysis = 0.5(ALa + APyr) (3)
The underestimation in the above calculations, due to La
efflux, is thought to be small because of the short duration of
t
I I
1 2 3 4 the exercise bouts and the slow kinetics for the release of La
5 min min
(time constant 30 min for repeated 30-s bouts of isokinetic
t tft
cycling; see Ref. 16).
The concentration of Pi in the muscle after the sprints and
during recovery was calculated from changes in ATP, PCr, and
Schematic representation of experimental design. A total of 5
hexose monophosphates (G-l-P, G-6-P, and F-6-P)
Fig. 1.
muscle biopsies were obtained from each subject during the 2
conditions.
Pi = 2.9 + [2(-AATP) - APCr
- (AG-1-P + AG-6-P + AF-6-P)]/3 (4)
the powder was extracted with 0.5 mol/l HC104, and the
extract was neutralized with 2.1 mol./l KHCOS (10). PCr,
creatine (Cr), ATP, free glucose, glucose l-phosphate (G-l-P),
glucose 6-phosphate (G-6-P), fructose 6-phosphate (F-6-P),
pyruvate (Pyr), and La were assayed enzymatically by fluoro-
metric analysis (17). Glycogen was determined both on the
neutralized extract (acid-soluble glycogen fraction) and on
the muscle pellet left after the extraction procedure by prior
HCl hydrolysis (acid-insoluble glycogen fraction). Muscle
metabolite contents (except La and glucose) were adjusted to
the individual mean total Cr content (PCr+Cr; range of
corrections O-11%). Because the sum PCr+Cr should not
change during exercise, this acts as an internal reference to
account for errors in muscle metabolite concentrations aris-
ing from the variable inclusion in the muscle samples of any
remaining connective tissue, fat, or blood (10). All muscle
metabolite concentrations are expressed as millimoles per
kilogram dry muscle.
Muscle pH was determined on the second part of the
freeze-dried muscle powder after homogenization at 4°C with
a solution containing 145 mmol/l KCl, 10 mmol/l NaCl, and 5
mmol/l iodoacetic acid (23). The dilution ratio used was 100 ul
of homogenizing solution per milligram dry muscle. Homoge-
nates were equilibrated to 37°C for 5 min, and the pH was
measured by using a MI-410 microelectrode (Microelectrode)
connected to a radiometer acid-base analyzer (Radiometer
PHM73).
Venous blood samples, taken from a cannula placed in an
antecubital vein, were deproteinized in 2.5% perchloric acid
and assayed for La by using an enzymatic and fluorometric
method (17).
Cakzdations. Anaerobic ATP turnover (mmol/kg dry muscle)
was calculated from the values of ATP, PCr, La, and Pyr
before and immediately after each sprint, by using Eq 1
below. The mean anaerobic ATP turnover rate (mmolkg dry
muscle-l
l
s-l) was obtained by dividing the anaerobic-ATP
where 2.9 is resting value from Chasiotis (6); 3 is 3 liters of
intracellular water per kilogram dry muscle; and Pi concentra-
tion is expressed in millimoles per liter of muscle water.
StatisticaL analysis. One-way (for muscle metabolites-
factor: sampling point) or two-way analyses of variance (for
performance variables) for repeated measures on both factors
(sprint number and condition) were used where appropriate
for statistical analysis (Statistica Mac). Where significant F
ratios were found (P < O.OS), the means were compared
by using a Tukey’s post hoc test. Relationships between
variables were examined by calculating the product
moment correlation coefficient r. Results are presented as
means -+ SE.
RESULTS
Power output.
The power output
profiles during
sprint I and sprint 2 are shown in Fig. 2. In both
sprints, peak power was reached 2 s after the start of
the
sprint,
whereas Sp,,, was attained at 3.9 t 0.2 s for
sprint 1 and at 4.0 - + 0 3 s for sprint 2. Reproducibility .
of PPO and MPO was checked by comparing mean
values and calculating the correlation coefficients be-
tween the two main trials (sprint I in the first main
trial vs. sprint 1 in the second main trial: PPO r = 0.99,
MPOlo r = 0.99, MPOsO r = 1.0; NS between sprints.
Sprint 2: PPO r = 0.93, MPOlo r = 0.96; NS between
sprints). For example, PPO and MPO values (MPO&
during sprint 1 were 17.5 -+ 1.2 and 9.2 t 0.3 W/kg in
the 30-30 main trial and 17.6 t 1.1 and 9.2 t 0.3 W/kg
in the 30-10 main trial, respectively. Therefore, the
mean values of the two main trials are presented for
each sprint.
B
18
25
I
$12
B
-9
3
4
o 6
&I
3
ENERGY METABOLISM DURING REPEATED SPRINT EXERCISE
879
ii
io io io
b I I d
0 10 20 30
TIME (s)
Fig. 2. Power output profiles (average for n = 8 subjects) for sprint 1
(A) and sprint 2 (B). Boxes represent mean power output for 1st 10 s
and last 20 s of each sprint.
None of the power output indexes had returned to the
control (sprint 1) values after the 4 min of passive
recovery (P < 0.01). The MPO during the second 30-s
sprint (MPO& was 7.6 - + 0 3 W/kg, which corresponded .
to 82 t 2% of the MPOsO generated during sprint 1.
PPO during sprint 2 was 14.4 t 0.8 W/kg (82 -+ 2% of
sprint I), whereas NIpo10 and MPOLBO were 84 t 2 and
_ 81 t 2% of the corresponding sprint 1 values, respec-
tively (Fig. 2). As can be seen in Fig. 2, -45% of the total
work during the sprint was generated in the first 10 s,
and this percent remained the same for both sprint 1
and sprint 2. The FI was also the same for sprint 1 and
sprint 2 (62 - + 3 vs 62 + 1%, NS). The pedaling speed
parameters for both sprints are shown in Table 1.
The subjects with a higher PPO during sprint I had a
higher FI during that sprint (r = 0.87; P < 0.01) and a
lower endurance fitness, as expressed by the
%Vozmax
Table 1. SP,,~,
SPPPO,
SPIO,
SPL.20, and &m
for sprint 1 and sprint 2
SPIWiX SPPPO SPlO
SPLZO SP30
Sprint 1 17057 15625 154+5 11123 12524
Sprint 2* 14955 138+4 132t3 9024 10453
% of sprint 1 8823 8922 8622 8122 8352
Values are means t SE, n = 8 subjects. Sp,,,, maximum pedaling
speed; Spppo, speed at which peak power output was attained; Spio,
Sp~zo, and Spso, mean pedaling speed during 1st 10 s, last 20 s, and
30 s, respectively. Sp values in rpm. *All sprint 2 parameters
significantly different from sprint 1, P < 0.01.
corresponding to a blood La concentration of 4 mmol/l
(%4 mM; r = -0.89; P < 0.01). Furthermore, signifi-
cant negative correlations (r = -0.77 to -0.81, P < 0.05
to P < 0.01) were found between power output during
sprint 1 (PPO and MPOlo) and the recovery of power
(the power output during sprint 2 expressed as a
percentage of the power output during sprint 1) and
pedaling speed during sprint 2 (%MPOlo, %Sp&. Fi-
nally, recovery of the above power and pedaling speed
indexes during sprint 2 was correlated with %4 mM
(r = 0.75-0.94; P < 0.05 to P < 0.01).
Muscle metabolites. The muscle metabolite concentra-
tions at rest, immediately after sprint 1, 12 t 0.6 s
before sprint 2, and after the second lo- and 30-s
sprints are shown in Table 2. Total Cr was -118
mmol/kg dry muscle and was similar at all sampling
points. The decrease in muscle glycogen during sprint 1
was -99 mmol glucosyl units/kg dry muscle, compared
with only 57 mmol glucosyl units/kg dry muscle during
sprint 2. The soluble portion of glycogen represented
20-24% of the total at all sampling points. The major
part (97%) of the decrease in glycogen during sprint 1
could be accounted for by the accumulation of the
measured glycolytic intermediates, Pyr, and La, whereas
only 75% of the decrease in glycogen could be accounted
for during sprint 2. The -5% increase in muscle
glycogen during the 3.8 min between sprints was not
statistically significant. The rate of glycogenolysis and
glycolysis during sprint 2 was decreased by -56% and
-45%, respectively, compared with sprint 1. The ratio
of glycogenolysis to glycolysis was 1.74 t 0.06 in the
first 30-s sprint and 1.41 t 0.09 and 1.38 t 0.07,
respectively, during the first 10-s and the whole 30-s
period of sprint 2. The PCr content of the muscle -6.6 s
after sprint 1 was 16.9 t 1.4% of the resting value, and
PCr was resynthesized to 78.7 I~I 3.3% of the resting
value by 3.8 min into the recovery (Fig. 3). During the
first 10 s of sprint 2, PCr dropped rapidly to the
post-sprint I levels, with no significant decrease there-
after.
PCr levels at the end of the first sprint were similar
in all subjects, but subjects with the highest PPO and
MPO values in sprint 1 had the slowest resynthesis of
PCr. The percent resynthesis of PCr (%PCr) was nega-
tively correlated with PPO (r = -0.81) and MPO dur-
ingsprint 1 (MPOlo, r = -0.81 and MPOsO, r = -0.74).
Furthermore, %PCr resynthesis was closely correlated
with %4 mM (Fig. 4), linking endurance fitness to PCr
resynthesis. High correlations were found between the
%PCr resynthesis and the percent recovery of MPO and
mean pedaling speed during the first 10 s of sprint 2
(r = 0.84, P < 0.05 andr = 0.91, P < 0.01).
There was a -27% decrease in ATP immediately
after sprint 1, but no further changes were seen after
recovery or during the second sprint (Table 2). Calcu-
lated Pi concentration increased after sprint I but had
recovered considerably by 3.8 min after sprint 1. Dur-
ing the first 10 s of sprint 2, Pi increased to levels higher
than after sprint 1, but no further change was seen at
the end of 30 s. No correlation was found between Pi
and power output recovery.
880
ENERGY METABOLISM DURING REPEATED SPRINT EXERCISE
Table 2. Muscle metabolites in vastus lateralis at rest, immediately after sprint
1,
following 4 min of recovery,
and after second
lo-
and 30-s sprint
Rest Sprint 1 Recovery Sprint 2
(10 d Sprint 2
(30 d
Glycogen (total)
PCr
Cr
Pi
ATP
327.5 k 14.3
75.2 t 4.4
42.3 k 2.1
2.9
27.0 5 0.8
228.3 5 18.2”
12.6 + 1.2a
105.2 k 3.7”
16.2 t 1.3”
19.6 rt O.ga
240.5 t 25.5a
58.5 2 2.3”~~
58.6 t 3.0apb
6.4 t l.4a,b
22.2? l.oa
223.5 k 25.0”
15.3 2 1.4aJ
102.2 If: 3.5a,C
20.1 2 1.9a,ftc
19.7? 1.3a
183.5 5 17.1a,g
8.8 k 2.5a)C
108.8 5 3.0apc
20.4 t l.7a,fpc
20.5 + 1.2”
10.7 t l.O”J
1.3 f. 0.3b
22.5 t 1.4a,b,c
5.1+ 0.6a,b,c
Glucose
G-l-P
G-6-P
F-6-P
1.7 2 0.2
0.2 5 0.1
1.4 zt 0.1
0.3 5 0.1
7.0 IfI 0.4”
3.1 t 0.6”
27.4 k 1.3a
9.6 + 1.4”
7.8 2 0.5”
0.8 t O.lb
14.2 5 0.7”~~
2.7 t 0.3b
9.6.5 1.2a
1.1 t 0.3b
20.0 t 0.8a,bJ
3.8 5 0.5Q,”
1.15 0.2b
72.7 5 5.gayb 2.0 5 0.2a,b
106.6 t 4.gapc 2.4 t 0.3a7b,c
129.3 t 5.2a,b,c,d
Pyruvate
Lactate 0.5 k 0.1
5.820.9 . 4.1 t 0.4a
108.0 + 4.5”
Values are means t SE for 7 subjects, expressed in mmol/kg dry muscle. Muscle glycogen expressed in mmol glucosyl units/kg dry muscle.
Pi, calculated total inorganic phosphate (in mmol/liter muscle water). PCr, phosphocreatine; Cr, creatine; G-l-P, glucose l-phosphate;
G-6-P,
glucose 6-phosphate; F-6-P, fructose 6-phosphate. Significant differences: “P < 0.01 from Rest; bP < 0.01 from
sprint 1; cP
< 0.01 from
recovery, *
dP
< 0.01 from
sprint
2 (10 s);
“P
< 0.05 from rest;
fP
< 0.05 from
sprint 1; gP
< 0.05 from recovery.
A considerable proportion of Pi released during ATP
and PCr breakdown appeared in the form of hexose
monophosphates G-l-P, G-6-P, and F-6-P. The large
increase of hexose monophosphates, especially G-6-P,
after sprint 1 was attenuated during the second sprint
(Table 2).
Muscle La and pH. Muscle La increased to 108.0 t
4.5 mmol/kg dry muscle immediately after sprint I, and
67 t 3% of that remained in the muscle at 3.8 min into
the recovery period. Therefore, subjects started the
second 30-s sprint with a high muscle La content, and
the accumulation of La during that second 30-s sprint
was decreased by 45%. The rate of La accumulation
during the first 10 s of sprint 2 was about threefold
higher than that during the last 20 s of the same sprint.
Changes in muscle pH before, after, and during the
recovery between the two sprints are shown in Fig. 3.
A 100 1y
\ \ I
I I
\ I
I I
I I
.
cj 80 -
“, 60 -
E
‘E
g 40 -
# 20 -
O-
100 1
I r
= 0.94
tE I
a 6.9 -
w
4
c) 6.8 -
s I
E 6.7 -
6.6 -
.
6.5 -
0
1 2 3 4
TIME (min)
60 J I I I I I
50
60 70 80 90
Fig. 3. Time course of changes in muscle phosphocreatine (PCr;
A)
and muscle pH (I?) during 2 sprints separated by 4 min of passive
recovery.
Sprint 1
was 30 s and
sprint
2 was either 10 or 30 s (sprints
are represented by bars). Values for PCr are expressed as %resting
value
(n
= 7 subjects).
*P
< 0.01 from resting value;
tP
< 0.05 and
$P
< 0.01 from
pre-sprint
2 value; and
§P
< 0.01 from
post-sprint 1
value.
%VO,max
at 4 mmol+1
blood lactate
Fig. 4. Relationship between %maximal oxygen uptake (VOZ,,)
corresponding to a blood lactate concentration of 4 mmol/l and %PCr
resynthesis after 4 min of passive recovery following a maximal 30-s
sprint
(n
= 7 subjects,
P <
0.01).
ENERGY METABOLISM DURING REPEATED SPRINT EXERCISE
881
Muscle pH decreased to 6.69 t 0.02 immediately after contribution dropped to only 15.6 t 3.3% of anaerobic
sprint I and only increased slightly to 6.80 t 0.03 (NS) ATP turnover during the last 20 s of the second sprint.
during recovery During the second sprint, muscle pH The rate of glycogenolysis during the first 10 s of sprint
was lower in comparison with the recovery value at 3.8 2 was positively correlated with the ATP turnover rate
min at both 10 and 30 s (6.69 t 0.03 at 10 s and during the same time interval (r = 0.88, P < 0.01).
6.61 ~fi: 0.03 after 30 s). No relationship was found During the last 20 s of sprint 2, glycolytic rate was
between muscle pH before sprint 2 and %PCr resynthe- reduced to only about one-third of that calculated for
sis or power output recovery. the first 10 s of that sprint.
Blood La. Blood La increased to -9 mmol/l immedi-
ately after sprint 1 and continued to increase during
the recovery to reach -12 mmol./l before sprint 2. There
was no significant difference between blood La concen-
tration immediately after the second lo- and 30-s
sprint, but blood La was lower 3.5 min after the second
10-s sprint compared with 3.5 min after the second 30-s
sprint (14.3 - . + 0 7 vs 16.0 t 0.8 mmol./l, P < 0.05).
ATP turnover. The’ anaerobic ATP turnover, as calcu-
lated from changes in ATP, PCr, La, and Pyr, was 235 t
9 mmol/kg dry muscle during sprint 1 and was de-
creased to 139 t 7 mmol/kg dry muscle during the
second 30-s sprint. This -41% reduction in the calcu-
lated anaerobic ATP turnover from sprint 1 to sprint 2
was more than twice as high as the -18% decrease in
MPO during spritit 2. However, the contribution of
aerobic metabolism to energy supply was increased
during sprint 2, as indicated by the increase in
VO,
from
2.68 t 0.10 l/min (61 t 2% Vqamax) during sprint 1 to
3.17 t 0.13 l/min (72 t 3%
VoXmax)
during sprint 2
(P < 0.01). Ventilation was 110.0 2 10 and 136.0 t 7.7
l/min in sprint 1 and 2, respectively (sprint 1 vs.
sprint 2, . P < 0.01). High correlations were found
between
Vosmax
(in ml l kg-l l min-l) and the percent
aerobic contribution to both sprint 1 (r = 0.79, P < 0.05)
and sprint 2 (r = 0.87, P < 0.01).
The calculated anaerobic ATP turnover during the
first 10 s and the last 20 s of sprint 2 was 9.8 ? 0.8 and
2.1 t 0.4 mmolkg dry *muscle++, respectively (a
78% decrease), whereas
Vo2
increased from 1.96 t 0.11
(45 t 2%Vo 2max) to 3.76 t 0.12 l/min (85 t- 3%), respec-
tively. The contribution of PCr during the first 10 s of
sprint 2 was high, amounting to =43% of the anaerobic
energy supply However, PCr concentration was very
low at the end of the first 10 s of sprint 2, and its
DISCUSSION
This study was designed to examine changes in
muscle metabolism during sprint 2 and to relate these
changes to the recovery of power output. There was a
41% reduction in the calculated anaerobic ATP turn-
over from sprint 1 to sprint 2, mainly as a result of a
45% decrease in glycolysis (Fig. 5). However, MPO
during sprint 2 was only 18% lower than in sprint 1.
One main finding of the present study was that this
mismatch between anaerobic energy release and power
output during sprint 2 was partly compensated for by
an increased contribution of aerobic metabolism as
reflected by the increase in
VO,
during the second
sprint. The other main finding of the study was that
PCr was almost completely broken down during the
first 10 s of sprint 2 and remained unchanged thereaf-
ter (Fig. 3). A relationship was found between the
recovery of power output in the first 10 s of sprint 2 and
the resynthesis of PCr and between the recovery of
power output and endurance fitness, as reflected by the
.
percentage of
VOzmax
corresponding to a blood La concen-
tration of 4 mmol/l(%4 mM) during submaximal exer-
cise.
In
was the present study, the number of muscle biopsies
kept to an absolute minimum, which was thought
to be consistent with a sound experimental design.
Thus biopsies taken in only one of the main trials
needed to be representative of muscle metabolism
during both main trials. Such assumptions were consid-
ered to be safe, as there was excellent reproducibility of
the performance variables during the two main trials,
and the pre-main-trial regimen controlling both exer-
cise and diet used in the present study has been shown
400 A
1
B
I
3009
,
2001
I
loo-
.
O-
ATP
El PCr
n
Glycolysis Fig. 5. Calculated ATP utilization during
2 30-s sprints (A: sprint 1; B: sprint 2)
separated by 4 min of passive recovery,
Boxes represent contribution of ATP-pro-
ducing processes to total ATP utilization
(n = 7 subjects).
I
0 30
TIME (set) TIME (set)
882
ENERGY METABOLISM DURING REPEATED SPRINT EXERCISE
to result in very similar resting muscle metabolites on
two separate occasions 1 wk apart (30). In addition, no
account was taken, in the calculati .ons of ATP turnover,
of the 1 2-s gap between th .e muscle biopsy before sprint
2
and the start of the sprint. However, from our
previous work (3) we know that the there is little
recovery of muscle metabolites between 3 and 6 min
after a single 30-s spri nt. For example, from our m .odel
of PCr resynthesis Iwe estimate that the change in PCr
during the 12-s period before sprint 2 in the present
study will be <l mmol/kg dry muscle
l
Thus any errors
due the assumption that the metabolic status of the
muscle at 12 s before sprint 2 is representative of the
metabolic status at the start of the sprint will be
minimal.
The range of muscle metabolites in the present study
and the additional information gained from the biopsy
at 1 Osi nto the second sprint have not been previously
reported for repeated sprint cycling of 30-s duration,
although the reduction in the glycolytic rate in the
second sprint was of the same magnitude as that
observed during isokinetic cycling (18, 27). All of the
decrease in ATP occurred during the first 30-s sprint, so
that, despite the loss of PCr during the first 10 s of
sprint 2 and the reduction in the glycolytic rate from
the first 10 s to the last 20 s of sprint 2, there was no
further loss of ATP This lack of change in ATP in the
second sprint is particularly surprising, as muscle pH
failed to recover and had decreased further by
10
and
30 s of sprint 2. Under these conditions, an increase in
AMP deaminase activity might have been expected.
This continued decrease in pH, however, provides a
possible explanation for the reduction in the glycolytic
rate in the second 30-s sprint in comparison with the
first
30
-s sprint and in the last
20
s in comparison with
the first 10 s of the second sprint, through an inhibitory
effect on the key enzymes phosphorylase and phospho-
fructokinase.
PCr was almost entirely depleted during the first 10 s
of sprint 2, and the large contribution of PCr to energy
SUPPlY
during this period probably supported the ob-
served high power output. About 45% of the total work
during the second 30-s sprint was generated in the first
10 s, and power output decreased at a rapid rate
reaching 55% of peak power at 10 s (Fig. 2). During the
last 20 s of sprint 2, power output declined at a lower
rate, and the contribution of PCr was minimal. These
observations would imply that the availability (amount)
of PCr before a repeated sprint may be related to the
ability to generate high power during the initial sec-
onds of the sprint. This suggestion is supported by the
high correlations found in the present study between
the percentage of PCr resynthesis and the percentage
restoration of MPO and speed during the initial 10 s of
sprint 2 (r = 0.84 and r = 0.91), whereas no such
relationships were seen for power output during the
last 20 s of the sprint. Further support for the signifi-
cance of PCr during the initial seconds of repeated
sprints comes from the results of a previous study,
where the time course of PCr resynthesis after a 30-s
sprint was found to be parallel with the time course of
PPO restoration (3). Also two preliminary studies (15,
31) have shown that occlusion of the circulation to one
leg during the 4-min recovery between repeated 30-s
bouts of maximal isokinetic cycling prevents PCr resyn-
thesis and reduces total work in the subsequent sprints
bY
-15% in the occluded in comparison with the
nonoccluded leg. All of the observed decrease in work
occurred during the first
10-15 s
of the sprint, and no
differences in muscle me tabolites were found between
the occluded leg and the leg with the free circulation,
apart from the different PCr level before the second
sprint. Similar evidence demonstrating the importance
of PCr availability for muscle metabolism and power
generation during repeated bouts of maximal exercise
has been provided by studies in which muscle PCr
content was increased after oral Cr supplementation.
In one of these studies, ATP degradation was attenu-
ated and power output recovery was increased, whereas
there were no changes in muscle La accumulation
during the second of two 30-s bouts of maximal iso-
kinetic cycling separated by 4 min after, in comparison
with before, oral Cr ingestion (9).
It is recognized that the relationship between power
output recovery and PCr resynthesis may not be causal
and that the recovery of power output may be influ-
enced by many other factors (e.g., changes in pH,
electrolytes, etc.). However, in the present study, power
output recovery and changes in other metabolites (H+,
La, Pi, or H,PO,) were unrelated. The relationship
between PCr and power output recovery may indicate,
however, that when PCr is available, increases in
muscle metabolites such as ADP (in the cell microenvi-
ronment), which may cause fatigue, are prevented. If
this were the case, then PCr availability would be
crucial for removing the products of ATP hydrolysis
from all the cell adenosinetriphosphatases (myosin,
Ca2+, and Na+-K+) and thus it could have wide-ranging
effects on cell function.
In the present study, both the resynthesis of PCr and
the recovery of power output were related to endurance
fitness (%4 mM), but no relationship was found be-
tween the resynthesis of PCr or power output and
muscle pH. These results provide further support for
earlier suggestions that muscle pH has little influence
on PCr during the first few minutes of recovery and
that oxygen supply to the mitochondria may be more
important (24). Endurance-trained individuals (as re-
flected by %4 mM in the present study) are expected to
have an increased capillary network, a high muscle
oxidative capacity, and may, in addition, have a greater
proportion of type I fibers (6, 28, 29). Support for the
notion that endurance-trained individuals will have a
faster rate of resynthesis of PCr comes from studies
examining mainly isometric muscle actions, with the
use of the noninvasive method of phosphorus magnetic
resonance spectroscopy (31P-MRS). These 31P-MRS stud-
ies have provided evidence that PCr resynthesis is
faster in endurance-trained athletes (3 4) and that it
can be improved by endurance training (19). Further-
more, it has been reported that the PCr resynthesis
rate is positively correlated with the activity of citrate
ENERGY METABOLISM DURING REPEATED SPRINT EXERCISE
883
synthase (20), which in turn parallels capillary density
(29), and also that the PCr resynthesis rate is reduced
in patients with mitochondrial myopathies (22). A link
has therefore been established between oxidative capac-
ity and PCr resynthesis after exercising small muscle
groups (e.g., calf muscles) by using noninvasive meth-
ods. The present study provides evidence showing this
link following maximal sprint exercise, when PCr was
directly determined by using chemical methods.
In addition to the relationship between endurance
fitness and PCr/power output recovery, aerobic metabo-
lism was found to contribute significantly to energy
supply, especially during sprint 2. The increase in
vo2
from sprint 1 to sprint 2 was -18%. This finding is
consistent with the previously reported increase in
Vo2
found between the first and fourth 1-min bouts of
constant-velocity cycling performed at an exercise inten-
sity of 120%
VOgmax
with a 4 min-rest interval between
bouts (8). The findings of the present study are also
consistent with the 13% (NS) increase in leg
vo2
in the
second bout of dynamic knee extensor exercise reported
by Bangsbo and colleagues (1). Thus it seems likely that
leg
voz
was increased in the second sprint in the
present study. If it is assumed that the active muscle
mass represented 20% of body mass [based on calcula-
tions (13) in subjects from the same population (33)],
that all of that mass was equally active, and that the
contribution from myoglobin and hemoglobin was the
same in both sprints, it may be estimated (21) that the
aerobic contribution to sprint I and 2 was 34 t 2 and
49 t 2%, respectively. The value for sprint 1 is similar
to estimates reported in other studies in which either
the oxygen-deficit method (28%; Ref. 32) or theoretical
calculations in combination with power output data
were used (28%; Ref. 26). Other authors have suggested
a higher percent aerobic contribution (-40%, assuming
25% body mass as muscle mass) for 30 s of constant-
velocity cycling (21). The difference in the percent
aerobic contribution between that study and the pres-
ent study may reflect a greater contribution by type I
fibers at the slower pedal velocites during constant-
velocity cycling in comparison with sprinting (90 rpm
compared with peak values of 170 rpm in the present
study). Although all of these estimates are subject to
the errors inherent in the assumptions (for example, in
the present study, if the active muscle mass was
assumed to be 25% of body mass, the aerobic contribu-
tion would be 29 t 2 and 44 t 2%, respectively, for
sprint I and 2), the findings of the present study do
highlight the importance of the aerobic contribution to
energy supply in sprint cycling, particularly in the
second bout of exercise where
Voz
reached 85%
Vozmax
during the last 20 s. The high correlations found
between
Vozmax
and percent contribution by aerobic
metabolism during sprint 2 show the significance of a
high aerobic power when performing repeated sprints.
The increase in
Vo2
during sprint 2 compensates, at
least in part, for the apparent mismatch between the
decrease in power output (18%) and the decrease in
anaerobic energy supply (41%) from sprint 1 to 2. Any
small remaining differences may be the result of an
improvement in muscle efficiency from sprint 1 to 2,
resulting from the reduction in pedal speed according to
the parabolic shape of the power-velocity relationship.
In summary, this study has shown that (1) an in-
crease in aerobic metabolism partially compensates for
the reduction in energy supply from anaerobic path-
ways during sprint 2 and that aerobic metabolism
makes an important contribution to energy supply
during repeated sprints; (2) that PCr is completely
utilized during the first 10 s of sprint 2 and that there is
a relationship between power output recovery and PCr
resynthesis but no relationship between power output
recovery and any other metabolite measured in this
study; and (3) that
VOW,,,
and endurance fitness ap-
pear to be important, respectively, in determining the
magnitude of the aerobic contribution to, and the
recovery of power output during, repeated sprints.
Address for reprint requests: M. E. Nevill, Dept. of Physical
Education, Sports Science, and Recreation Management, Loughbor-
ough Univ., Loughborough, LE 113TU, UK.
Received 29 March 1995; accepted in final form 22 September 1995.
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