To investigate the hypothesis that training-induced increases in muscle mit
ochondrial potential are not obligatory to metabolic adaptations observed d
uring submaximal exercise, regardless of peak aerobic power (V) over dot o(
2peak)) Of the subjects, a short-term training study was utilized. Two grou
ps of untrained male subjects (n = 7/group), one with a high (HI) and the o
ther with a low (LO) (V) over dot o(2peak) (means +/- SE; 51.4 +/- 0.90 vs.
41.0 +/- 1.3 ml . kg(-1) . min(-1); P < 0.05), cycled for 2 h/day at 66-69
% of (V) over dot o(2peak) for 6 days. Muscle tissue was extracted from vas
tus lateralis at 0, 3, and 30 min of standardized cycle exercise before tra
ining (0 days) and after 3 and 6 days of training and analyzed for metaboli
c and enzymatic changes. During exercise after 3 days of training in the co
mbined HI + LO group, higher (P < 0.05) concentrations (mmol/kg dry wt) of
phosphocreatine (40.5 +/- 3.4 vs. 52.2 +/- 4.2) and lower (P < 0.05) concen
trations of P-i (61.5 +/- 4.4 vs. 53.3 +/- 4.4), inosine monophosphate (0.5
20 +/- 0.19 vs. 0.151 +/- 0.05), and lactate (37.9 +/- 5.5 vs. 22.8 +/- 4.8
) were observed. These changes were also accompanied by reduced levels of c
alculated free ADP, AMP, and P-i. All adaptations were fully expressed by 3
min of exercise and by 3 days of training and were independent of initial
(V) over dot o(2peak) levels. Moreover, maximal activity of citrate synthas
e, a measure of mitochondrial capacity, was only increased with 6 days of t
raining (5.71 +/- 0.29 vs. 7.18 +/- 0.37 mol . kg protein(-1) . h(-1); P <
0.05). These results demonstrate that metabolic adaptations to prolonged ex
ercise occur within the first 3 days of training and during the non-steady-
state period. Moreover, neither time course nor magnitude of metabolic adap
tations appears to depend on increases in mitochondrial potential or on ini
tial aerobic power.