To investigate the hypothesis that changes in muscle submaximal exercise me
tabolism would occur as a result of fiber hypertrophy, induced by high-resi
stance training (HRT), active but untrained males (age 20 +/- 0.7 yr; mean
+/- SE) performed lower-limb weight training 3 days/wk for 12 wk using thre
e sets of 6-8 repetitions maximal (RM)/day. Muscle metabolism was examined
at different stages of training (4, 7, and 12 wk) using a two-stage continu
ous cycle test performed at the same absolute power output and duration (56
.4 +/- 2.9 min) and representing 57 and 72% of pretraining peak aerobic pow
er ((V) over dot o(2peak)) Compared with pretraining, at the end of exercis
e, HRT resulted in a higher (P < 0.05) phosphocreatine (PCr; 27.4 +/- 6.7 v
s. 38.0 +/- 1.9 mmol/kg dry wt), a lower lactate (38.9 +/- 8.5 vs. 24.4 +/-
6.1 mmol/kg dry wt), and a higher (P < 0.05) glycogen content (132 +/- II
vs. 181 +/- 7.5 mmol glucosyl units/kg dry wt). The percent change from res
t before and after training was 63 and 50% for PCr; 676 and 410% for lactat
e, and 60 and 43% for glycogen, respectively. These adaptations, which were
observed only at 72% (V) over dot o(2peak), occurred by 4 wk of training i
n the case of PCr and glycogen and before any changes in fiber cross-sectio
nal area, capillarization, or oxidative potential. Fiber hypertrophy, obser
ved at 7 and 12 wk of training, failed to potentiate the metabolic response
. No effect of HRT was found on (V) over dot o(2peak) with training (41.2 /- 2.9 vs. 41.0 +/- 2.1 ml kg(-1) min(-1)) or on the steady-state, submaxim
al exercise rate of oxygen consumption. It is concluded that the HRT result
s in muscle metabolic adaptations that occur independently of fiber hypertr
ophy.