A depletion of phosphocreatine (PCr), fall in the total adenine nucleotide
pool (TAN = ATP + ADP + AMP), and increase in TAN degradation products inos
ine 5'-monophosphate (IMP) and hypoxanthine are observed at fatigue during
prolonged exercise at 70% maximal O-2 uptake in untrained subjects [J. Bald
win, R. J. Snow, M. F. Carey, and M. A. Febbraio. Am. J. Physiol. 277 (Regu
latory Integrative Comp. Physiol. 46): R295-R300, 1999]. The present study
aimed to examine whether these metabolic changes are also prevalent when ex
ercise is performed below the blood lactate threshold (LT). Six healthy, un
trained humans exercised on a cycle ergometer to voluntary exhaustion at an
intensity equivalent to 93 +/- 3% of LT (similar to 65% peak O-2 uptake).
Muscle biopsy samples were obtained at rest, at 10 min of exercise, similar
to 40 min before fatigue (F-40 =143 +/- 13 min), and at fatigue (F = 186 /- 31 min). Glycogen concentration progressively declined (P < 0.01) to ver
y low levels at fatigue (28 +/- 6 mmol glucosyl U/kg dry wt). Despite this,
PCr content was not different when F-40 was compared with F and was only r
educed by 40% when F was compared with rest (52.8 +/- 3.7 vs. 87.8 +/- 2.0
mmol/kg dry wt; P < 0.01). In addition, TAN concentration was not reduced,
IMP did not increase significantly throughout exercise, and hypoxanthine wa
s not detected in any muscle samples. A significant correlation (r = 0.95;
P < 0.05) was observed between exercise time and glycogen use, indicating t
hat glycogen availability is a limiting factor during prolonged exercise be
low LT. However, because TAN was not reduced, PCr was not depleted, and no
correlation was observed between glycogen content and IMP when glycogen sto
res were compromised, fatigue may be related to processes other than those
involved in muscle high-energy phosphagen metabolism.