tion. This decline occurs principally via deami-
nation of AMP to inosine monophosphate (IMP)
but also by the dephosphorylation of AMP to
adenosine. The loss of AMP may initially appear
counterproductive because of the reduction in
the total adenylate pool. However, it should be
noted that the deamination of AMP to IMP only
occurs under low ATP/ADP ratio conditions
and, by preventing excessive accumulation of
ADP and AMP, enables the adenylate kinase
reactions to continue, resulting in an increase in
the ATP/ADP ratio and continuing muscle force
generation. Furthermore, it has been proposed
that the free energy of ATP hydrolysis will
decrease when ADP and Piaccumulate, which
could further impair muscle force generation.
For these reasons, adenine nucleotide loss has
been suggested to be of importance to muscle
function during conditions of metabolic crisis;
for example, during maximal exercise and in the
later stages of prolonged submaximal exercise
when glycogen stores become depleted (Sahlin &
Broberg 1990).
Glycolysis
Under normal conditions, muscle clearly does
not fatigue after only a few seconds of effort, so a
source of energy other than ATP and PCr must be
available. This is derived from glycolysis, which
is the name given to the pathway involving the
breakdown of glucose (or glycogen), the end
product of this series of chemical reactions being
pyruvate. This process does not require oxygen,
but does result in energy in the form of ATP being
available to the muscle from reactions involving
substrate-level phosphorylation. In order for the
reactions to proceed, however, the pyruvate
must be removed; in low-intensity exercise,
when adequate oxygen is available to the muscle,
pyruvate is converted to carbon dioxide and
water by oxidative metabolism in the mitochon-
dria. In some situations the majority of the pyru-
vate is removed by conversion to lactate, a
reaction that does not involve oxygen.
A specific transporter protein (GLUT-4) is
involved in the passage of glucose molecules
across the cell membrane. Once the glucose mol-
ecule is inside the cell, the first step of glycolysis
is an irreversible phosphorylation catalysed by
hexokinase to prevent loss of this valuable nutri-
ent from the cell: glucose is converted to G6P.
This step is effectively irreversible, at least as far
as muscle is concerned. Liver has a phosphatase
enzyme which catalyses the reverse reaction,
allowing free glucose to leave the cell and enter
the circulation, but this enzyme is absent from
muscle. The hexokinase reaction is an energy-
consuming reaction, requiring the investment of
one molecule of ATP per molecule of glucose.
This also ensures a concentration gradient for
glucose across the cell membrane down which
transport can occur. Hexokinase is inhibited by
an accumulation of the reaction product G6P, and
during high-intensity exercise, the increasing
concentration of G6P limits the contribution thatbiochemistry of exercise 23
Table 2.2bMaximal rates of adenosine triphosphate (ATP) resynthesis from anaerobic and aerobic metabolism and
approximate delay time before maximal rates are attained following onset of exercise.
Max rate of ATP resynthesis
(mmol ATP · kg-^1 dm · s-^1 ) Delay timeFat oxidation 1.0 >2h
Glucose (from blood) 1.0 Approx. 90 min
oxidation
Glycogen oxidation 2.8 Several minutes
Glycolysis 4.5 5–10 s
PCr breakdown 9.0 InstantaneousPCr, phosphocreatine.