Muscle metabolism during sprint exercise in man: influence

of sprint training

C B a r n e t t 1, M Carey 2, J Proietto 3, E Cerin 1, M A Febbraio 4 & D Jenkins 1

1SchoOl of Human Movement Studies, The University of Queensland, Queensland, Australia. 2Exercise
Metabolism Unit, Victoria University of Technology, Footscray, Victoria, Australia. 3Department of
Medicine, The University of Melbourne, Parkville, victoria, Australia. 4School of Medical Sciences,
RMIT University, Bundoora, Victoria, Australia.

In order to examine the influence of sprint training on metabolism and exercise performance
during sprint exercise, 16 recreationally-active, untrained, men (VO2peak= 3.8+0.1 1.rain -1)
were randomly assigned to either a training (n= 8) or control group (n= 8). Each subject
performed a 30-sec cycle sprint and a test to measure "~02peak before and after eight weeks
of sprint training. The training group completed a series of sprints three times per week
which progressed from three 30-sec cycle sprints in weeks 1 and 2, to six 30-sec sprints in
weeks 7 and 8. Three rains of passive recovery separated each sprint throughout the training
period. Muscle samples were obtained at rest and immediately following the pre- and post-
training sprints and analysed for high energy phosphagens, glycogen and lactate; the
activities of both phosphofructokinase (PFK} and citrate synthase (CS) were also measured
and muscle fibre types were quantified; Training resulted in a 7.1% increase in mean power
output (p<0.05), an 8 % increase in VO2peak (p< 0.001), a 42% increase (p< 0.01) in CS
activity and a 17% increase (p< 0.05} in resting intramuscular glycogen content. In contrast,
neither PFK activity nor fibre type distribution changed with training. An increase (p< 0.05)
in mean power output and attenuated (p< 0.01) ATP degradation were observed during sprint
exercise following training. Glycogen degradation during sprint exercise was unaffected by
sprint training. These data demonstrate that sprint training may have enhanced muscle
oxidative but not glycolytic capacity.
(J Sci Med Sport 2004;7:3:314-322)

Introduction
Unlike moderate intensity endurance exercise, which utilises primarily
oxidative pathways to meet the increased energy demand 1, intense sprint
e x e r c i s e r e s u l t s i n r a p i d i n c r e a s e s in e n e r g y t u r n o v e r f r o m b o t h a e r o b i c a n d
anaerobic metabolism TM. Accordingly, the relatively consistent metabolic
a d a p t a t i o n s w h i c h h a v e b e e n o b s e r v e d to o c c u r w i t h e n d u r a n c e t r a i n i n g
contrdtst w i t h t h o s e r e p o r t e d in t h e s p r i n t t r a i n i n g l i t e r a t u r e . S p r i n t t r a i n i n g
o f t e n 5,6,7 b u t n o t always3,s,9 i n c r e a s e s p e a k o x y g e n c o n s u m p t i o n °(VO2peak}. A
n u m b e r of s t u d i e s r e p o r t i n c r e a s e s i n t h e a c t i v i t i e s of k e y g l y c o l y t i c
e n z y m e s 6A°, w h i l e c h a n g e s in o x i d a t i v e e n z y m e a c t i v i t y h a v e b e e n l e s s
c o n s i s t e n t in r e s p o n s e to s p r i n t t r a i n i n g 11. Likewise, t y p e I fibre p e r c e n t a g e h a s
b e e n s h o w n to i n c r e a s e 12, d e c r e a s e 1°, 13,14 o r r e m a i n u n c h a n g e d 9 in r e s p o n s e
to s p r i n t t r a i n i n g .
G i v e n t h a t s p r i n t t r a i n i n g h a s involved r e p e a t e d b o u t s of efforts r a n g i n g i n
d u r a t i o n f r o m five to >30 s e c s c o u p l e d w i t h r e c o v e r y p e r i o d s r a n g i n g f r o m 30
s e c s to 2 0 m i n s , it is n o t s u r p r i s i n g t h a t c o n s i d e r a b l e d i f f e r e n c e s in t r a i n i n g
a d a p t a t i o n s e x i s t w i t h i n t h e l i t e r a t u r e . T h e r e a s o n for t h e d i v e r s e r e s p o n s e to
sprint training may be that there are relatively significant contributions from

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 Muscle metabollism during sprint exercise...

the high energy phosphagens, glycolysis and oxidative metabolism to ATP

turnover during a 30-sec sprint. While most researchers have used a 30-sec
"all-out" exercise bout to evaluate sprint performance and to describe
adaptations to sprint training, changes in the metabolic responses to sprint
exercise are yet to be compared to training-induced changes in oxidative
capacity, glycolytic capacity and muscle histochemistry.
The present study compared enzymatic and histochemical adaptations to
sprint training with sprint performance and exercise-induced changes in high
energy phosphagens, muscle glycogen and lactate. Relatively short recovery
periods separated the sprints during training and a control group was included
to account for seasonal changes in performance. Training was expected to elicit
significant improvements in sprint performance via increases in energy
provision through glycogenolysis and oxidative metabolism.
Methods
Subjects
Sixteen recreationally active, but untrained, male subjects (mean+SE: age
21.2+0.9 yr; mass 84.2_+2.4 kg; VO2peak 3.8_+0.1 1.rain -1) were recruited for the
present investigation. The experimental procedures were approved by The
University of Queensland's Medical Research Ethics Committee prior to the
commencement of the study; before giving their written informed consent, all
subjects were fully informed of the study's purpose and possible risks.
Experimental Procedures
In the week prior to testing, subjects performed as familiarisation six 10-sec
sprints separated by 60 secs of passive recovery, and an incremental cycle to
volitional exhaustion. Subsequently, all subjects completed an incremental
cycle to volitional exhaustion to m e a s u r e VO2peak and a 30-sec "all-out" sprint
both before and after the training period. The tests were separated by at least
24 hrs. The post-training measurement of VO2peak occurred between 72 and 96
hrs following the final training session; the post-training sprint was performed
within one week following the final training session.
On the days of testing, subjects arrived at the laboratory at least three hours
post-absorptive. They were asked to refrain from vigorous exercise and to
replicate their dietary intake in each 24-hr pre-exercise period.
The sprints were performed on a calibrated, multi-geared air-braked cycle
ergometer (South Australian Sports Institute - SASI, Adelaide, Australia). Each
subject sprinted in a gear ratio which elicited 8.87 flywheel revolutions per
pedal crank revolution as previous work had shown this gear ratio to optimise
both peak power output (PPO) and mean power output (MPO) during a 10-sec
all-out test 15. Software developed by SASI (Cycletest version 3. lb) was used to
calculate and record PPO, MPO and the fatigue index during the sprint;
sampling occurred at 10 Hz. To ensure that the subject remained seated
throughout the sprint, a harness was fitted to his waist and secured to the
ground.
Subjects completed the VO2peak test on an electrically-braked cycle ergometer
(Excalibur Sports, Lode, Groningen, The Netherlands). The subjects' initial
workload was 120W and this increased by 30W every three minutes until

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Muscle metabollismduring sprint exercise...

volitional fatigue. A plateau reflecting less t h a n a 100 ml.min -1 increase in "VO2

and a RER >1.15 were accepted as evidence that VO2peak had been achieved.
Expired air was collected in Douglas bags during each work stage. Inspired
volume was calculated using a turbine ventilometer (Morgan Mark 2, England},
calibrated prior to each test, and attached to a two-way breathing valve (Hans
Rudolph, Kansas City, USA}. Expired 02 and CO 2 concentrations were
m e a s u r e d using electronic gas a n a l y s e r s (Ametek S-3A/1 and CD3A,
Pittsburgh, USA) which were calibrated prior to and following each test with
known gas concentrations. Although power on an electrically-braked cycle
ergometer is maintained independent of cadence, subjects were asked to cycle
at approximately 90 rev.min -1 during maximal testing in a n effort to minimise
variations in mechanical efficiency.
Sprint Training
Following the initial testing, the 16 subjects were m a t c h e d according to sprint
performance (PPO) and divided into two groups of eight (control and
experimental). The experimental group (EXP: ag e 20.4_+1.2 yr; mass 79.8+3.1
kg; VO2peak 3.8_+0.1 1.min -1) trained three times a week for eight weeks while
the control subjects (CON: age 22.0_+1.3 yr; mass 88.5+_3.1 kg; VO2peak 3.9_+0.2
1.min -1) continued their normal activities (eg, basketball, tennis, etc) for the
same period. Initially, the sprint sessions involved three 30-sec sprints; every
two weeks the n u m b e r of sprints was increased by one, so that by weeks 7 and
8 the subjects were performing six 30-sec sprints. Three mins of passive rest
separated each sprint t h r o u g h o u t the entire training period.
Muscle Sampling & Analysis
Muscle (~ 150 mg) was sampled from the vastus lateralis on four occasions (two
pre-training and two post-training) using a 6 m m biopsy needle with
suction16,17. Samples were taken at rest and immediately following the 30-sec
test before and after the training period. One portion of the resting sample was
frozen immediately (<20 secs for all subjects) in liquid nitrogen and stored until
subsequent biochemical analysis. A second portion was cleaned of obvious
connective tissue and m o u n t e d on cork in tissue embedding m e d i u m and
immersed in isopentane cooled by liquid nitrogen. Once frozen, the sample was
then immersed in liquid nitrogen, placed in a Cryotube, and stored in liquid
nitrogen for later histochemical analysis. The post-sprint muscle sample was
taken from a site (prepared at rest) approximately 3 cm proximal to the resting
sample and frozen in liquid nitrogen within 15 secs of the sprint being
completed. Serial c r o s s - s e c t i o n s (10 pm) were stained for myofibrilar
actomyosin ATPase following preincubations at pH 4.3, 4.54, and 4.6 and
incubation at pH 9.4. This staining procedure differentiates between the type I
fibres (stained dark), type IIa fibres (stained light), and the type lib fibres
(stained moderately dark or intermediate) is. Due to insufficient tissue,
histochemical analysis could not be carried out for one subject in CON.
Muscle samples were divided in two; one portion being freeze-dried and
divided into two further portions. One portion (approximately 2 mg) was
extracted, neutralised and analysed for lactate, ATP, phosphocreatine (PCr) and
creatine (Cr) using enzymatic analysis with fluorometric detection. The second
portion was hydrolysed in 250pl of 2M HC1, incubated for two hrs at 100°C,
subsequently neutralised with 750pl of 0.667M NaOH and analysed for muscle

316
 Muscle metabollism during sprint exercise...

g l y c o g e n (glucose)19. E x c e p t for g l y c o g e n a n d l a c t a t e (due to t h e i r extracellular

p r e s e n c e ) , m e t a b o l i t e c o n c e n t r a t i o n s w e r e c o r r e c t e d for t h e h i g h e r total Cr
c o n c e n t r a t i o n i n b o t h t h e p r e - a n d p o s t - t r a i n i n g s a m p l e s . T h e r e m a i n i n g wet
t i s s u e f r o m t h e r e s t i n g s a m p l e s w e r e h o m o g e n i s e d a n d a n a l y s e d for PFK a n d
C S 2°. D u e to i n s u f f i c i e n t t i s s u e , CS a c t i v i t y c o u l d n o t b e d e t e r m i n e d for one
s u b j e c t in EXP a n d t h r e e s u b j e c t s in CON.

Statistical Analysis
D a t a w e r e a n a l y s e d u s i n g t w o - w a y a n a l y s i s of v a r i a n c e (ANOVA) w i t h r e p e a t e d
m e a s u r e s o n t h e s e c o n d factor. T - t e s t s for d e p e n d e n t a n d i n d e p e n d e n t s a m p l e s
w e r e u s e d for follow-up a n a l y s i s of s i g n i f i c a n t i n t e r a c t i o n s . T h e level of sig-
n i f i c a n c e for all t e s t s w a s s e t a t 0.05.

ReSults
~QO2peak i n c r e a s e d in b o t h CON (3.91_+0.23 v s 4.07_+0.23 l . m i n -]) a n d EXP (3.78
+-0.11 v s 4.09-+0.12 1.min 4) (p< 0.001) following t h e e i g h t w e e k s of t r a i n i n g b u t
t h e i n c r e a s e w a s g r e a t e r (p< 0.05) i n EXP c o m p a r e d w i t h CON (315-+35 vs 162
•+55 m l . m i n -1) (Figure 1).

[] pre-training 900 [] pre-training

4.5-
* [] post-training? [] post-training
850 q
T

4.0- 800 -4
......!..... i!iii!i!iiili
:+:,:,:,:.:.:+>:, ©
::::::::::::::::::::::: ~i~
::::::::::::::::::::::: 750 ......' " ~;~
c? i i i~i iii
:::::::::::::::::::::::::::::::::::::: ,.,...,..., ,,,.,....,...,

4 3.5- ii!i!iiiii!iiiii!i
i!iii!i
iiiiiiiiiiiiiiiii!ii!
..............
k:::::::::::::::.::::::
700 iiiii!jiiiiiiiiiiiiiiiiil
::::::::::::::::::::::::::::::::: : i:::::::::::::::::::::::

.:.:,:.:.:.:,:.:,:,:,:,
Iii!iiiiiiiiiiiiiiiiiiiiil 650
liiiiiiiiiiiii!iiiiiiiiili 600
3.0
CON EXP CON EXP

Group Group

* = significantly greater than pre-training * = significantly greater than pre-training

(p = 0.022) (p = 0.023)
? = significantly greater than pre-training t = significantly greater than pre-training
(p = 0.001) (p = 0.003)

Figure 1: Mean (+_SE)values of VO2peak (I.min9 for Figure 2: Mean (+SE) values of mean power
control (CON) and experimental (EXP) output (MPO) for the control (CON)
groups pre oand post-training. Although and experimental (EXP) groups pre.
both groups showed increases with and post-training. Although groups
sprint-training, the increase was increased MPO with training, the
greater for the EXP group (315 vs 162 increase was greater for the EXP group
ml; p = 0.035). (55.1 vs 21.6; p= 0.035).

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Muscle metabollism during sprint exercise...

Following. training the m e a n power o u t p u t (MPO) for the CON group

increased from 762.5_+41.1 to 784.1_+42.2 W, while MPO for the EXP group
increased from 779.8_+22.3 to 834.9+20.4 W (p< 0.001) (Figure 2). The increase
for the EXP group (55.1_+12.2 W) was greater t h a n t h a t for the CON group
(21.6v7.5 W) (p< 0.05) (Figure 2).
Peak power o u t p u t (PPO) increased for b o t h the CON (1183.4 vs 1288.6 W)
and EXP (1164.6 vs 1254.1 W) (p< 0.001) groups with training (Figure 3); these
increases were not different between g r o u p s (p> 0.05).
As shown in Table 1, the percentages of muscle fibre types I, IIa a n d lib
remained u n c h a n g e d for b o t h groups. Resting ATP concentrations r e m a i n e d
u n c h a n g e d with training (p> 0.05} (Table 2). There w a s however a reduced net
ATP degradation for the EXP group during the 30s sprint following training (9.9
vs 6.1 mmol.kg -1 dw, pre- a n d post-training respectively; p< 0.01).
Resting PCr contents were not different following the training for either
group. However, PCr degradation during sprint exercise increased (p<0.05)
following the intervention b u t this increase w a s not different between groups
(Table 2).
Whereas the p o s t - s p r i n t Cr content in the EXP group w a s higher following
sprint training (94.4_+6.3 vs 110.5+2.9 mmol.kg -1 dw, pre- and post-training
respectively; p< 0.01), post-exercise Cr content did not change for the CON
group.

* = significantly greater than pre-training

1500- [] pre-training (p = 0,003)
~ 1400- [] post-training = significantly greater than pre-training
t
(p = 0.032)
13oo-

o
t-L
12oo-
11oo-
Z ......

ii!ilil
1000- !ti
900- Figure 3: Mean (+_SE) values of peak power
output (PPO) for both the control
800-
(CON) and experimental (EXP)
700 groups pre- and post-training. There
CON EXP was no difference between the
improvements found for each
Group
group.

CON EXP
Fibre Type Pre-training (%) Post-training (%) Pre-training (%) Post-training (%)

I 57.4 (3.1) 56.6 (1,9) 48.7 (4,2) 48.8 (5.1)

Ila 30.3 (2,0) 30.7 (2,0) 38.8 (5.1) 39.5 (5.6)
lib 12.3 (3.0) 12.7 (1.6) 12.5 (1.7) 11.7 (1.6

Table 1: Mean ( +-SE)values of fibre type percentages for both the control (CON)and experimental
(EXP) groups pre- and post-training.

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 Muscle metabollism during sprint exercise...

CON EXP
Pre-train Post-train Pre-train Post-train
pre.sprint post.sprJ,t pre.sprint post.spri,t pre.sprint post.sprint pre.sprint post.sprint
ATP 25.4 (1.2) 16.1 (1.1) 25.7 (1.2) 16.4 (1.3) 24.0 (1.3) 14.0 (1.1) 22.4 (1.5)* 16.3 (1.5)
~ATP 9.3 (0.8) 9.2 (1.1) 9.9 (1.0)? 6.1(0.7)
PCr 79.7 (3.9) 20.8 (1.8) 79.4 (2.7) 16.7 (2.0) 80.8 (5.3) 22.8 (1.5) 86.6(3.0) 16.9 (2.5)
APCr 58.9 (3.2) 62.7 (2.7) 58.0 (4.6)?t 69.7 (1.7)
Cr 39.5 (3.5) 98.5 (5.8) 40.0 (3.5) 102.7(3.9) 36.4 (2.4) 94.4 (6.3) 40.8 (1.7) 110.5(2.9)
TCrY 119.3 (6.4) 119.4 (3.6) 117.2 (7.t) 127,4 (4.3)
La 9.1 (1.0) 101.0 (5.3) 7.9 (1.3) 96.5 (2.7) 8.7 (0.8) 107.8 (7.8) 7.9 (0.8) I01.5 (6.8)
ALa 92.0 (5.2) 88.5 (3.1) 99.0 (7.6 )93.7 (6.5)
Glycogen 388.5 (29.7) 296.1 (24.2) 366.6 (25.8) 277.1 (20.5) 400.2 (49.0) 308.7(41.0)** 468.3 (46.4) 320.6(30.3)
AGlycogen 92.3 (18.9) 89.6 (14.8) 91.4 (25.0) 147.6 (27.2)
* greater than pre-training post-sprint (p< 0.05) ~ less than pre-training (p = 0.01)
t t greater than pre-training (p< 0.05) ** greater than pre-training pre-sprint (p< 0.05)
Y Total creatine was corrected to the highest value (pre- or post-sprint) pre- and post-training.
Table 2: Muscledata [mean ( +_SE)]for the CONand EXP groups pre- and post-training, and pre- and
post.sprint. Units for ATP, Pcr, Cr and La are mmoLkg "1 (dw); units for glycogen are
mmol.kg "1 (ww).

Pre-training Post-training P
PFK ( v m o l . g l . m i n l ) CON 33.1 (3.0) 31.O (2,3) 0.558
EXP 30.8 (2.0) 34.9 (1.5) 0,101
CS ( p m o l . g l . m i n 1) CON 12.3 (1.6) 10.2 (1.4) O.186
EXP IO.5 (1.O) 14.9 (0,8) 0.005
Table3: Enzyme activity and ATPprovision for the control (CON)and experimental (EXP)groups pre-
and post-training [means ( + SE)I.

There was no significant difference in anaerobic ATP provision as a result of

training; for the EXP group, ATP provision was 226.4+17.4 a n d 222.4_+10.7
mmol.kg -1 dw pre- a n d post-training. For the CON group, ATP provision was
215.5+10.8 and 214.0+3.5 m m o l . k g -1 dw pre- and post-training. Anaerobic ATP
provision was estimated as:

ATP provision = APCr + 1.5 Alactate + 2 AATP

It should be noted t h a t as lactate efflux from the m u s c l e was not measured,

the values of ATP energy provision m a y have b e e n underestimated. Both the
resting and post-exercise glycogen values for the CON group were not different
post-training c o m p a r e d with pre-training (388.5 vs 366.6~ mmol.kg -1 dw,
p>0.05; a n d 296.1 vs 277.1 mmol.kg d dw, p> 0.05}. The resting glycogen
content for the EXP group w a s higher post-training c o m p a r e d with pre-training
(400.2 vs 468.3 mmol.kg -1 dw; p< 0.05). However, there was no difference (p
>0.05) in glycogen degradation pre-to post-training for the EXP group (Table 2).
Muscle lactate a c c u m u l a t i o n during the sprint was not different pre- to post-
training for either Group (Table 2).
PFK activity was not different pre- to post-training for either group (Table 3).

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Muscle metabollism during sprint exercise...

Howevei-, CS activity was higher for the EXP group following training (10.5 vs
14.9 pmol.g-l.min-1; p< 0.01) (Table 3); CS activity for the CON group r e m a i n e d
u n c h a n g e d (p> 0.05).
DiSCUSSiOn
The d a t a suggest t h a t the increase in sprint p e r f o r m a n c e which resulted from
the p r e s e n t eight week sprint training p r o g r a m m a y have b e e n mediated b y the
increase in energy provision from oxidative m e t a b o l i s m of pyruvate r a t h e r t h a n
non-oxidative conversion to lactate. PPO, MPO a n d ~O2peak each improved for
b o t h the EXP a n d CON groups. However, the increases in MPO a n d ~'02peak
were significantly greater for the EXP group. These findings are s u p p o r t e d b y a
n u m b e r of sprint-training studies 5,6,7. The changes observed in the CON group
in the p r e s e n t investigation were probably due to seasonal c h a n g e s in their
recreational activity. Unfortunately, activity diaries were not u s e d a n d the
m a g n i t u d e of change in activity outside the s t u d y w a s not recorded.
The increase in CS activity is consistent with the findings of J a c o b s et aP °
and, more recently, MacDougall et al 6 who reported increases in CS activity of
12% a n d 23%, respectively, following sprint training. VO2peak w a s not reported
b y J a c o b s et aP °, b u t MacDougall et al 6 observed a n increase in VO~peak similar
to t h a t found in the p r e s e n t study. It is likely t h a t the increase in VO2peak with
sprint training was mediated, to a small degree, by a n increase in oxidative
enzyme activity. However, t h a t circulatory a d a p t a t i o n s m a y have also occurred
with training c a n n o t be ruled out. In fact, McKenna et al 5 found t h a t following
seven weeks of sprint training, p e a k p u l m o n a r y "~O2 a n d VCO 2 increased, as
did b o t h PPO a n d MPO during a 30-sec sprint, while arterial blood lactate
concentration r e m a i n e d u n c h a n g e d , which according to the a u t h o r s suggests
e n h a n c e d gas exchange across the lungs a n d active tissue.
The increases in VO2peak a n d CS activity indicate t h a t the p r e s e n t sprint-
training protocol evoked changes in the capacity to produce energy via
oxidative metabolism. The contribution of aerobic m e t a b o l i s m to the energy
yield during a single 30-sec sprint h a s b e e n estimated to be between 20% and
30% 4 . It is also k n o w n t h a t the aerobic contribution to sprint exercise
increases, depending on the recovery between bouts, as a function of
successive sprints 4. The relatively short recovery periods u s e d in the p r e s e n t
s t u d y (three mins) would have imposed a considerable d e m a n d on aerobic
m e t a b o l i s m in meeting ATP r e s y n t h e s i s in the latter sprint bouts. This m a y
e x p l ~ n the observed increases in b o t h CS activity a n d VO2peak.
Although oxygen u p t a k e w a s not m e a s u r e d during the sprints, the
u n c h a n g e d muscle anaerobic ATP yield suggests t h a t the p r e s e n t post-training
increase in MPO was due to a n increased aerobic contribution to ATP
resynthesis. It is also possible t h a t the subjects b e c a m e not only m o r e
chemically efficient, b u t m o r e mechanically efficient during the six weeks of
sprint training. Interestingly, comprehensive work by H a r m e r et al also found
a reduced anaerobic ATP synthesis during intense exercise following seven
weeks of sprint training, a n d also suggested a n e n h a n c e d aerobic m e t a b o l i s m 7.
The u n c h a n g e d PFK activity in the p r e s e n t investigation is consistent with the
u n c h a n g e d rates of glycogen degradation a n d m u s c l e lactate a c c u m u l a t i o n
during sprint exercise with training. Nonetheless, given t h a t two previous
sprint-training studies which involved 30-sec b o u t s h a d reported increases in

320
 Muscle metabollisrn during sprint exercise.,.

PFK activity 6,1°, we expected similar changes following the present training
regimen. However, it is possible t h a t a training-induced increase in PFK activity
for the EXP group m a y have decreased during the one-week period between the
final training session and the post-training biopsy. In their study, J a c o b s et al 1°
imposed b o t h 15-sec and 30-sec sprints on their training group, so the present
data are b e s t c o m p a r e d with those reported by MacDougall et al 6. MacDougall
et al a observed a 49% increase in PFK in r e s p o n s e to seven weeks of training
which progressed from four 30-sec sprints during each training session in the
first week to 10 30-sec sprints in each session during the final week; recovery
between sprints decreased from four m i n s in week 1 to 2.5 m i n s in week 7 with
subjects training three times a week. The only notable differences in the
training d e m a n d s between the s t u d y by MacDougall et al 6 a n d the present
investigation are the n u m b e r of sprints performed and the recovery between
sprints.
In c o n t r a s t to the findings of Stathis et al 3 and Hellsten-Westing et al 8, ATP
r e t u r n e d to pre-training levels following sprint training. It is of note that, in the
p r e s e n t study, the post-training sprint and biopsy were conducted within one
week following the final training session. In the studies by Stathis et al 3 and
Hellsten-Westing et al s the final sprint was performed 48 to 72 hrs and 24 hrs
(respectively) following the final training session. It h a s b e e n d e m o n s t r a t e d that
high intensity exercise results in significant purine loss and therefore purine
nucleotide resynthesis m u s t occur via the de novo synthesis p a t h w a y a n d / o r
via purine salvage 3. While the former p a t h w a y is a n energy-consuming and
slow process, it is clear from our d a t a t h a t seven days is sufficient for adequate
purine nucleotide r e s y n t h e s i s following several weeks of sprint training.
Our finding t h a t fibre type distribution did not change with sprint training
c o n t r a s t s with the d a t a o f J a n s s o n et al la a n d E s b j o r n s s o n et a114 who observed
increases in the proportion of type IIa fibres at the expense of type I and type
lib fibres. Although these two groups determined fibre distribution using
similar staining p r o c e d u r e s to those u s e d in the p r e s e n t study, differences
between studies b e c o m e a p p a r e n t w h e n the training d e m a n d s (and in
particular sprint durations a n d recovery periods) are compared. Nonetheless it
r e m a i n s unclear as to w h e t h e r training protocols are responsible for the
different findings in fibre d i s t r i b u t i o n b e t w e e n studies. Unfortunately,
MacDougall et al 6 a n d H a r m e r et al 7 did not report fibre type distribution.
In s u m m a r y , the p r e s e n t investigation found t h a t i m p r o v e m e n t s in sprint
p e r f o r m a n c e .following eight weeks of sprint training were accompanied by
increases in VO2peak a n d CS activity coupled with a lower net ATP degradation
during sprint exercise. It is likely t h a t the i m p r o v e m e n t s in MPO resulting from
training m a y have b e e n due to a n increased contribution of aerobic metabolism
to the energy yield. However, the contribution to MPO of a n increased mech-
anical efficiency as a result of the sprint training c a n n o t be underestimated.
Although the p r e s e n t s t u d y suggests t h a t there was no change in either
glycolytic capacity or glycolytic flUx during sprint exercise, m e a s u r e s of oxygen
u p t a k e during sprint exercise and glycolytic intermediates were not available
and it could be argued t h a t glycolytic flux was underestimated.
Acknowledgments
The a u t h o r s would like to t h a n k Margaret Barber, Dr David Bishop, Alastair

321
Muscle metabollism during sprint exercise...

Hanna, Dr Scott McLean, Bradley Mifsud and Dr Simon Green for their
assistance.

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