entering the electron transport chain. In the elec-
tron transport chain, NADH and FADH are
oxidized and the energy generated is used to
rephosphorylate ADP to ATP. The rate of flux
through the electron transport chain will be regu-
lated by the availability of NADH, oxygen and
ADP (Chance & Williams 1955). Finally, the
translocation of ATP and ADP across the mito-
chondrial membrane is thought to be effected by
creatine by way of the mitochondrial creatine
kinase reaction (Moreadith & Jacobus 1982),
thereby linking mitochondrial ATP production to
the ATPase activity in the contractile system.
Lactate production
Considerable controversy exists concerning the
mechanism responsible for lactate accumulation
during intense muscle contraction. The most
widely accepted theory attributes this to a high
rate of energy demand coupled with an inade-
quate oxygen supply. In short, when tissue
oxygen supply begins to limit oxidative ATP pro-
duction, resulting in the accumulation of mito-
chondrial and cytosolic NADH, flux through
glycolysis and a high cytosolic NAD+/NADH
ratio are maintained by the reduction of pyruvate
to lactate. However, it has been suggested that
the reduction in mitochondrial redox state
during contraction is insignificant, thereby indi-
cating that reduced oxygen availability is not the
only cause of lactate accumulation during con-
traction (Graham & Saltin 1989). In addition,
there are data to indicate that it is the activation
of the PDC and the rate of acetyl group produc-
tion, and not oxygen availability, which primar-
ily regulates lactate production during intense
muscle contraction (Timmons et al. 1996). Fur-
thermore, it has also been shown that for any
given workload, lactate accumulation can be
significantly altered by pre-exercise dietary
manipulation (Jansson 1980; Putman et al. 1993).
Taken together, these findings suggest that an
imbalance between pyruvate formation and
decarboxylation to acetyl-CoA will dictate the
extent of lactate formation during exercise as
88 nutrition and exercise
seen, for example, during the transition period
from rest to steady-state exercise.Glycogen utilization with respect to
exercise intensity
Maximal exercise
During submaximal (steady-state) exercise, ATP
resynthesis can be adequately achieved by oxida-
tive combustion of fat and carbohydrate stores.
However, during high-intensity (non-steady
state) exercise, the relatively slow activation and
rate of energy delivery of oxidative phosphoryla-
tion cannot meet the energy requirements of
contraction. In this situation, anaerobic energy
delivery is essential for contraction to continue.
Typically, oxidative energy delivery requires
several minutes to reach a steady state, due prin-
cipally to the number and complexity of the reac-
tions involved. Once achieved, the maximal rate
of ATP production is in the region of approxi-
mately 2.5 mmol · kg–1dry matter (dm) · s–1. On
the other hand, anaerobic energy delivery is
restricted to the cytosol, its activation is almost
instantaneous and it can deliver ATP at a rate in
excess of 11 mmol · kg–1dm·s–1. The downside,
however, is that this can be maintained for only a
few seconds before beginning to decline. Of
course, oxidative and anaerobic ATP resynthesis
should not be considered to function indepen-
dently of one another. It has been demonstrated
that as the duration of exercise increases, the
contribution from anaerobic energy delivery
decreases, whilst that from aerobic is seen to
increase.
Figure 6.1 shows that maximal rates of ATP
resynthesis from PCr and glycogen degradation
can only be maintained for short time periods
during maximal contraction in man (Hultman
et al. 1991). The rate of PCr degradation is at its
maximum immediately after the initiation of
contraction and begins to decline after only 1.3 s.
Conversely, the corresponding rate of glycolysis
does not peak until after approximately 5 s of
contraction and does not begin to decline until