120
Biochemisny of Exercise
metabolism during intermittent, high intensity
cycling exercise. Four females and two males (25 f
2.1 yrs, 69 f 4.2 kg, VOzpeak= 47.5 f 2.8
ml.kg*'.min") participated in the study. Subjects
performed two trials on separateoccasions, one with
prior ingestion of 0.3g.kg-' bodyweight @.w.) calcium
carbonate (CON) and the other with 0.3g.kg-' b.w.
sodium bicarbonate (ALK). The exercise protocol
consisted of 4x1 min cycling exercise bouts at 115125% VOgeak, with 1 min rest between bouts,
followed by a fifth bout to fatigue. Arterialised
blood was drawn prior to ingestion, immediately
before exercise, at the end of each bout, and during
recovery from the final exercise bout. Blood was
analysed for pH, base excess (BE), bicarbonate
(HCO,), lactate, ammonia (NH,) and hypoxanthine.
Muscle biopsies were obtained at rest and
immediately after the fourth and fifth bouts of
exercise (n=4). These samples were analysed for
ATP, CP, Cr, IMP and lactate. Time to fatigue
during the fifth bout of exercise was 43% greater
(PcO.05, n=5) in the ALK trial compared with
CON.
Sodium bicarbonate ingestion resulted in
greater (Pc0.05, n=5) blood pH, HCO, and BE
prior to and during most bouts of exercise and
recovery compared with CON. Plasma lactate
concentrations were greater (Pc0.05, n=5) during
the early stages of recovery in the ALK compared
with CON. Plasma NH, and hypoxanthine were not
different (P>0.05) across the trials at any time.
Sodium bicarbonate ingestion did not influence any
of the muscle metabolites (Table 1).
Table 1: Muscle metabolite data (values means & SE, expressed
in mmol.kg* dw,n=4).
CON
ATP
CP
Cr
Lactate
IMP
Rest
Bout 4
Bout 5
26.620.7
89.021.3
51.724.4
4.520.3
0.0720.03
20.422.5
31.1 28.6
109.727.0
69.7217.7
2.921.4
19.321.4
21.4k4.8
119.327.1
79.1 k 10.6
3.320.6
ALK
ATP
CP
Cr
Lactate
IMP
Rest
Bout 4
Bout 5
27.421.9
91.422.6
49.224.8
4.720.4
0.1320.0
20.8?2.2
17.924.0
124.927.1
68.3 2 12.1
52.620.7
18.121.1
12.12 1.2
128.626.4
90.6210.4
3.820.4
These data indicate that adenine nucleotide
metabolism during high, intensity intermittent
exercise is unaffected by alkalosis.
CREATINE SUPPLEMENTATION AND
HIGH I NT E NSI T Y EXERCISE:
INFLUENCE ON PERFORMANCE AND
MUSCLE METABOLISM
K Siiderlund, PD Balsom and B Ekblom. Dept. of
Physiology and Pharmacology, Physiology 111,
Karolinska Institute, Stockholm, Sweden.
1%
Creatine supplementation in man has been
shown to improve the ability to maintain power
output during repeated bouts of high intensity
exercise. The aim of this study was to confirm these
findings and to further investigate if any changes in
performance following creatine supplementation
could be explained by changes in muscle
metabolism.
Methods. Eight male subjects, age (mean f
SD) 24 f 4 years and body mass 77.8 f 9.9 kg,
performed five 6 s, and one 10 s bout of high
intensity exercise, on an adapted friction-loaded
Wingate cycle ergometer, before and after 6 days of
creatine supplementation (20 g creatine
monohydrate per day). The rest period between the
exercise bouts was 30 s for the five 6 s bouts and 40
s before the 10 s bout. Subjects were instructed to
try to maintain a target speed of 140 revmin" during
each exercise bout (see Balsom et al. 1993). The
resistance applied to the ergometer (mean 6.7 kg)
was individually chosen to be as high as possible,
with the criteria that the target speed could be
maintained for the total duration of the first five
exercise periods but not for the 10 s bout. Thus,
during the first five exercise bouts the same amount
of work was performed on both test occasions.
Muscle biopsies were taken from m. vastus lateralis
at rest, and immediately after the 5th and 6th
exercise bout.
Preliminary Results (n=6). As a result of
the creatine supplementation, total muscle creatine
[creatine + phosphocreatine (PCr)] concentration at
rest increased by 24.6 mmolkg-' dm @c.05), this
was accompanied by a 1.5 (0.5) kg increase in body
mass (Pc.05). Immediatelyafter the five 6 s exercise
bouts PCr concentrations were higher, and muscle
lactate lower, after vs before supplementation
(pc.05). After creatine suplementation, all subjects
were better able to maintain the target speed
towards the end of the 10s exercise bout (pc.05).
Despite the fact that more work was performed
during this exercise period following creatine
supplementation, post-exercise muscle lactate was
lower compared to before creatine supplementation
(pc .05).
Conclusion. These preliminary results
suggest that enhanced fatigue resistance during high
121
Biochemistry of Exercise
i n t e n s i t y e x e r c i s e following c r e a t i n e
supplementation, may be partly explained by a
higher pre-exercise PCr concentration and also
possibly by a reduced accumulation of lactate in
muscle.
Balsom PD, Ekblom B, Siiderlund K, Sjodin B and
Hultman E (1993). Creatine
supplementation and dynamichigh-intensity
intermittent exercise. Scand J Med Sci
Sports 3~143-149
THE ACCUMULATION OF BLOOD
METABOLITES DURING A S-TED
2000 M ROWING RACE
MF Carey, J Baldwin, MA Febbraio, SE Selig and
RJ Snow. Exercise Metabolism Unit, Victoria
Universityof Technology, Footscray,301 1, Australia.
197
This study examined the time course of the
accumulation of various blood metabolites during a
2000 m rowing race. The investigation involved nine
oarswomen (20.920.4yrs; 64.321.1 kg; V0,max =
3.320.1 1.min-’) who rowed on an ergometer
(Concept 11), at simulated racing pace, for 2 min
(n=6), 6 min (n=6) and 2000 m (n=6), respectively.
Blood was sampled from an antecubital vein, at rest
and for 60 min in recovery from exercise, and
subsequently analysed for lactate, hypoxanthine and
ammonia. All blood and plasma metabolites were
elevated above resting values (P<0.05) following all
exercisebouts. Blood and plasma lactate levels were
greater (P<0.05), at most sampling times, in the 6
min and 2000 m trials compared with the 2 min trial.
Early in recovery plasma ammonia levels were
greater (P<0.05) in both the 6 min and the 2000 m
trials compared with the shorter trial. Similarly, at 5
min into recovery the levels of hypoxanthine were
greater (PcO.05) in the longer trials compared with
the 2 min trial. At this time point hypoxanthine
levels were also greater (P<0.05) in the 2000 m trial
compared with the 6 min trial. At no other time
were any blood or plasma metabolites different
between the two long trials (P>0.05). These data
demonstrate that lactate and purine nucleotide
metabolites accumulate in the blood beyond the
initial stages of the event. These findings suggest
that adenosine 5’- triphosphate (ATP) degradation
and glycolysis occur to a greater extent in the latter
phase of a rowing race compared with the earlier
stage of the race.
RECOVERY OF POWER OUTPUT AND
MUSCLE METABOLISM A F E R 10s
AND 20s OF MAXIMAL SPRINT
EXERCISE IN M A N
GC Bogdanis, ME Nevi& LH Boobis’ and HKA
Lakomy. Department of P.E. and Sports Science,
Lioughborough University, LE11 3TU; ‘Sunderland
District General Hospital, Sunderland, SR4 7TP.
198
During maximal sprint exercise muscle
phosphocreatine (PCr) and glycogen stores are
utilised at rapid rates resulting in very low [PCr] and
the accumulation of lactate and hydrogen ions
( N e d et al. 1989). The present study, which had
Ethical Committee approval, examined the recovery
of muscle metabolites and power output, when
sprint exercise was repeated after a short recovery
interval following either a 10s or a 20s sprint.
Eight male students performed two cycle
ergometer sprints separated by 2 min of passive
recovery on two occasions, one week apart. On one
occasion the duration of the first sprint was 10s and
on the other 20s (randomly assigned). The second
sprint lasted 30s on both occasions. Muscle biopsies
were obtained from the vastus lateralis at rest,
immediately after the first sprint and after the 2 min
of recovery on both occasions. Muscle samples were
snap frozen, and later freeze dried, homogenised,
and analysed enzymatically. Oxygen uptake during
the sprints was measured using the Douglas bag
technique.
Table 1. Muscle metabolites (mmol (kgdry weight)”) at rest, after
the 10s and the 20s sprints, and following 2 min of recovery after
the 10s (REC 10) and the 20s (REC 20) sprints. (mean f s.e.m.,
n = 8). Significant differences (ANOVA): a,e=P<O.Ol and
Pc0.05 from REST; b,f=P<O.Ol and P<0.05 from 10s SPRINT;
c,g=P<O.Ol and P-zO.05 from 20s SPRINT; d=P<O.Ol between
REC 10 AND REC 20.
REST
Glycogen 403.8220.1
PCr
ATP
G6P
Lactate
80.723.2
25.620.7
1.220.1
4.520.4
10s SPRINT
20s SPRINT
357.42 18.6(r)
36.123.qr)
20.221.3(r)
16.82 1.8(r)
51.024.qr)
322.7221.4(rf)
21.4+2.2(a.b)
19.821.4(~)
22.52 1.3(a,b)
81.7+4.7(a.b)
REC 10
Gtywgen
PCr
ATP
G6P
Lactate
364.1 +25.0(a.c)
69.5?3.3(e,b.c)
21.82 1.2(.)
9.62 l.O(a,b,c)
38.22 2.8(a,f.c)
REC 20
328.42 24.5(a.f,d)
61.422J(a.t+c)
19.821.3(~)
16.7214a,~,r,cd)
662244a.l&
Following the 2 min of recovery after the
10s sprint subjects were able to reproduce the peak
power output (PPO) achieved during sprint 1,