high velocities, it is difficult to maintain such a
high limb speed, both in recovery of the driving
leg, and in the brief track contact time for force
generation (Radford 1990).
Air resistance at high velocities may also be a
significant factor in sprinting because it increases
with running speed. Davies (1980) calculated
that elite 100-m sprinters running 10 m · s–1
would run 0.25–0.5 s faster if they did not have to
overcome air resistance. Pugh (1970) estimated
that air resistance accounted for 16% of the total
energy expended to run 100 m in 10.0 s. Thus, it is
advantageous to perform sprints at high altitude.
For example, the altitude of Mexico City (2250 m)
provides an advantage of approximately 0.07 s
(Linthorne 1994).
The metabolic factors contributing to the onset
of fatigue are associated with the decrease of
PCr or ATP in the muscle (Murase et al. 1976;
Hirvonen et al. 1987, 1992). The consequent
decrease in the availability of high-energy phos-
phates within exercising muscles results in a
reduction in the power output. During the
middle part of the 100-m sprint, running speed
decreases as the contribution of the high-energy
phosphate stores is reduced (see Fig. 41.1), and at
the end of the 100-m race, anaerobic glycolysis is
the main energy source (Hirvonen et al. 1987). A
decline in running speed or power output
towards the end of a 400-m race and a 30-s tread-
mill sprint is also associated with very low PCr
values (Hirvonen et al. 1992; Greenhaff et al.
1994).
The importance of PCr is highlighted because
power output declines when PCr utilization
decreases, despite adequate stores of ATP and
glycogen. For example, during a maximal 30-s
treadmill sprint, muscle glycogen was reduced
by 27% and 20% in type II and type I fibres,
respectively (Greenhaff et al. 1994). ATP
decreased by a similar amount (20%) in both fibre
types. After 30 s of sprint cycling, there was still
sufficient glycogen and ATP left in both fibre
types in the muscle to sustain energy metabolism
(Boobiset al. 1987; Vollestad et al. 1992). Why,
then, do the sprinters fatigue when substrate is
still available for energy metabolism? A possible
answer is that initial force generation is depen-
dent on the availability of PCr, once intramuscu-
lar PCr stores are depleted. Sprinting speed
cannot be maintained because the available
glycogen cannot be used quickly enough to
sustain the high rates of ATP utilization required.
In addition, accumulation of inorganic phos-
phate (Pi) may inhibit the cross-bridge recycling
between actin and myosin filaments directly
(Hultmanet al.1987).
The decline in running speed observed
towards the end of a 400-m race is due to a reduc-
tion in the rate of glycogen hydrolysis, despitesprinting 539
1000755025Pre-exercisePhosphocreatine (mmol.kg–1
dm)Postexercise1000800600400Power output (W)*Peak powerEnd power*Fig. 41.4Muscle
phosphocreatine concentrations
in type I ( ) and type II ( )
fibres before and after a 30-s
sprint on a non-motorized
treadmill (Greenhaff et al. 1994).
*,P<0.01, type I vs. type II.