sis is occurring at a near maximal rate during
intense exercise. Surprisingly, during intermit-
tent isometric contraction with circulation intact,
when the rest interval between contractions is of
the order of 1.6 s, the rate of glycogenolysis in
type I fibres is almost negligible. The correspond-
ing rate in type II fibres is almost maximal and
similar to that seen during contraction with cir-
culatory occlusion. This suggests that during
maximal exercise glycogenolysis in type II fibres
is invariably occurring at a maximal rate, irre-
spective of the experimental conditions, while
the rate in type I fibres is probably very much
related to cellular oxygen availability.
Submaximal exercise
In contrast to maximal exercise, the rate of
glycogenolysis during submaximal exercise is
greatest in type I fibres, especially during the
initial period of exercise (Ball-Burnett et al. 1990).
This phenomenon is likely to be the result of dif-
ferences in the recruitment pattern between
muscle fibre types. If exercise is continued, glyco-
gen utilization occurs in both fibre types but
depletion is observed first in the type I muscle
fibres. The consumption of carbohydrate during
exhaustive submaximal exercise has been shown
to offset the depletion of glycogen specifically in
type I fibres (Tsintzas et al. 1996).
Fatigue mechanisms related to
carbohydrate metabolism
What is clear from the literature is that glycogen
availabilityper se is not usually considered
to be responsible for fatigue development
during maximal exercise, providing the pre-
exercise glycogen store is not depleted to below
100 mmol · kg-^1 dm. It is even unlikely that gly-
cogen availability will limit performance dur-
ing repeated bouts of exercise, due to the decline
in glycogenolysis and lactate production that
occurs under these conditions. It is more prob-
able that fatigue development during maximal
exercise will be caused by a gradual decline
in anaerobic ATP production caused by the
depletion of PCr and a fall in the rate of
glycogenolysis.
Lactic acid accumulation during high-
intensity exercise is considered to produce
muscle fatigue as a result of H+and Piaccumula-
tion. An increase in hydrogen ion concentration
will negatively affect phosphorylase activity,
thereby delaying the rate of glycogenolysis, by
delaying transformation of the bform to the a
form (Danforth 1965; Chasiotis 1983) and by
decreasing the HPO 42 +, the dibasic form of Pi,
which is the substrate for phosphorylase. The
inhibition of PFK discussed previously seems to
be at least partly offset by an increase in the acti-
vators of PFK, especially ADP, AMP and Pi, when
the rate of ATP utilization is higher than the rate
of oxidative ATP resynthesis. The increase in
ADP and Pi, especially the H 2 PO 4 – form, in aci-
dotic muscle is known to have inhibitory effects
on contractile function (Cook & Pate 1985; Nosek
et al. 1987). However, there is no evidence of a
direct relationship between the decline in muscle
force during contraction and H+accumulation.
For example, studies involving human volun-
teers have demonstrated that muscle-force gen-
eration following fatiguing exercise can recover
rapidly, despite having a very low muscle pH
value (Sahlin & Ren 1989). The general consensus
at the moment appears to be that the initial gen-
eration of muscle force production is dependent
on the capacity to generate ATP but the mainte-
nance of force generation is also pH dependent.
Despite the wealth of information showing
that carbohydrate availability is essential to per-
formance during submaximal exercise, the bio-
chemical mechanism(s) by which fatigue is
brought about in the carbohydrate depleted state
are still unclear. Recent evidence suggests that
carbohydrate depletion will result in an inability
to rephosphorylate ADP to ATP at the required
rate, possibly because of a decrease in the rate of
flux through the TCA cycle as a result of a decline
in muscle TCA cycle intermediates (Sahlin et al.
1990). The consequent rise in ADP concentration
will bring about fatigue, perhaps as a direct
inhibitory effect of ADP and/or Pion contraction
coupling.