subjects was 534±85 W and was 50% of its peak
value at the end of the sprint. Biopsy samples
were taken from the vastus lateralis muscle
before and after the sprint. Muscle glycogen, PCr
and ATP declined from resting values by 25%,
64% and 37%, respectively. Three minutes after
exercise, muscle and blood lactate increased to
78 ±26 mmol · l–1and 13 mmol · l–1, respectively.
Similar intramuscular lactate concentrations of
73.9±16.1 mmol · kg–1dry matter were observed
for males by Jacobs et al. (1983) after 30 s of
maximal cycling using the Wingate anaerobic
test (WAnT) protocol. Blood pH decreased by
0.24 units to 7.16±0.07 3 min after the sprint, and
heart rate increased over the 30-s sprint, reaching
its maximum of approximately 182 beats · min–1
over the last few seconds of the sprint (Cheetham
et al. 1986). Anaerobic glycogenolysis supplied
64% of the ATP required during the 30-s sprint,
calculated from the changes in muscle glycogen,
lactate, pyruvate and PCr concentrations. Similar
metabolic responses to sprinting were observed
in a later study from the same laboratory (Nevill
et al. 1989).
Costillet al. (1983) examined muscle and blood
pH along with blood lactate concentration and
pH after sprint running. Four male subjects were
biopsied from the gastrocnemius muscle before
and after a treadmill sprint run at 125% V
.
o2max.
and a 400-m timed run on a track. After the 400-m
sprint, muscle pH in four of the subjects
averaged 6.63±0.03 and blood pH and lactate
concentration were 7.10±0.03 and 12.3 mmol · l–1,
respectively, highlighting the extensive meta-
bolic challenge of this event.
Thirty seconds of treadmill sprinting also pro-
vokes a marked increase in endocrine response.
Plasma noradrenaline and adrenaline increased
from resting values by six- and sevenfold, respec-
tively, and the plasma concentration of b-
endorphin doubled following 30 s of treadmill
sprinting. (Brooks et al. 1988). Plasma growth
hormone is elevated to more than eight times its
resting value following a 30-s treadmill sprint
(Nevillet al. 1996). The concentration peaked
after 30 min recovery and remained significantly
elevated above baseline for the 60 min. A greater
endocrine response is observed when maximal
538 sport-specific nutrition
sprints are repeated after a short recovery
(Brooks et al. 1990). In one study, nine men and
nine women performed 10 6-s sprints on a non-
motorized treadmill, with 30 s separating each
sprint. Peak plasma adrenaline was 9.2±7.3 for
the men and 3.7±2.4 nmol · l–1for the women,
and was recorded after only five sprints (Brooks
et al. 1990).
Most studies reporting the metabolic
responses to sprinting have analysed muscle
samples which contain a mixture of fibre types.
However, studies which have been carried out in
vitrohave suggested that maximal power output
and its decline are related to fibre type (Faulkner
et al. 1986). Energy metabolism in single muscle
fibres was measured in a study by Greenhaff and
colleagues (1994). Muscle biopsies were taken
from the vastus lateralis muscle before and after
30 s of maximal treadmill sprinting and the type I
and type II fibres analysed for concentrations of
ATP, PCr and glycogen (Fig. 41.4). Prior to the
sprint, PCr and glycogen concentrations were
highest in the type II fibres and a greater decline
was observed in these fibres after the 30-s sprint.
Peak power output declined by 65±3% during
exercise. Phosphocreatine was almost depleted
after the sprint, but those subjects with the higher
type II fibre PCr content showed a smaller
decline in power output during the sprint
(r=–0.93;P<0.01). The decline in ATP during the
sprint was similar in both fibre populations. This
illustrates the importance of the contribution
of PCr to energy production during maximal
exercise.Fatigue during sprinting
Elite male sprinters can maintain maximal speed
for 20–30 m, whereas females can maintain top
speed for only 15–20 m. The explanation, even in
elite sprinters, may be due to both mechanical
and metabolic factors.
The mechanical limitations to sprinting
include failure of neuromuscular coordination
(Muraseet al. 1976), the change in body position
relative to the foot striking the ground, and
deceleration caused by the grounding foot
(Mann & Sprague 1983; Mann 1985). At such