ample availability of muscle glycogen. The paral-
lel increase in hydrogen and lactate ions during
sprinting may inhibit glycolysis, thus contribut-
ing to the development of fatigue (Sahlin 1996). A
further explanation for fatigue during the 400-m
sprint and repeated shorter sprints during train-
ing is that the increase in ammonia observed as a
consequence of decreases in PCr and ATP con-
centrations during sprinting (Schlict et al. 1990;
Tullson & Turjung 1990) may be implicated in the
fatigue process (Green 1995).
Influence of sprint training on
energy production
The main focus of many studies on the adapta-
tions to sprint training is the changes in energy
metabolism underpinning improvements in per-
formance. This approach has led to a greater
understanding of the metabolic causes of fatigue
during sprinting.
The main and consistent finding in the labora-
tory and in the field is that sprint train-
ing improves performance. This performance is
measured as an increase in maximum power
output during the initial period of exercise, an
increase in the amount of work done during a
brief exercise bout, or an increase in exercise
duration at high exercise intensities (Brooks et al.
1993).
Nevillet al. (1989), investigated the effect of 8
weeks of high-intensity training on metabolism
during a 30-s treadmill sprint. Sixteen matched
subjects were assigned to either a training or a
control group. After training, peak power
increased by 12% during the initial period of
exercise, and the total work done during the
test was increased by 6%. This improvement
in performance was equivalent to a 1.5-s reduc-
tion in 200-m running time. Maximum muscle
lactate concentration increased by 20% after
training, and an equivalent increase in the rate
of ATP resynthesis from anaerobic glycolysis
was also observed. The excess postexercise
oxygen consumption also increased by 18%
after training. However, despite the increase in
muscle lactate concentration, training did not
540 sport-specific nutrition
change muscle pH during maximal treadmill
sprinting.
The increased ATP required as a consequence
of the improvement in performance after sprint
training was provided from anaerobic glycolysis
(Nevillet al. 1989). No changes were observed in
the contribution from PCr or aerobic metabolism.
The increased resynthesis from anaerobic glycol-
ysis was facilitated by an increase in the activity
of phosphofructokinase (PFK), the rate-limiting
enzyme in anaerobic glycolysis, and by an
increased efflux of H+from the muscle cell after
training. This is in agreement with other studies,
which have reported that adaptations to sprint
training include an increase in the muscle’s
buffering capacity (Sharp et al. 1986), an increase
in the activity of muscle PFK (Fournier et al. 1982;
Robertset al. 1982; Sharp et al. 1986; Jacobs et al.
1987), and an increase in the proportion of type
IIa fibres (Jacobs et al. 1987).
However, factors other than increased anaero-
bic energy production may also contribute to
improvement in performance after sprint train-
ing. These include an improved regulation of
K+during exercise and changes in the Na+–K+-
ATPase concentrations (McKenna et al. 1993),
which are important in the excitation–contrac-
tion coupling in skeletal muscles. Other factors
include the determinants of muscle tension at
both the whole muscle and single fibre level.
These include action-potential frequency, fibre
length and fibre diameter. It is beyond the scope
of this review to consider these factors, which are
discussed in detail elsewhere (Brooks et al. 1993).Nutritional influences on sprinting
Dietary intake
In contrast to the plethora of information on
the dietary intake of endurance athletes, the
nutritional habits of sprinters are not well
documented. It is a well-established belief in the
power- and strength-training community that
strength is improved when a diet high in protein
is consumed. Quantitatively, the recommended
protein intake for these athletes is about 1.4–1.7 g