To investigate the hypothesis that changes in muscle submaximal exercise metabolism would occur as a result of fiber hypertrophy, induced by high-resistance 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 three 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 continuous 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 power (V˙o 2 peak). Compared with pretraining, at the end of exercise, HRT resulted in a higher ( P < 0.05) phosphocreatine (PCr; 27.4 ± 6.7 vs. 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 ± 11 vs. 181 ± 7.5 mmol glucosyl units/kg dry wt). The percent change from rest before and after training was 63 and 50% for PCr, 676 and 410% for lactate, and 60 and 43% for glycogen, respectively. These adaptations, which were observed only at 72%V˙o 2 peak, occurred by 4 wk of training in the case of PCr and glycogen and before any changes in fiber cross-sectional area, capillarization, or oxidative potential. Fiber hypertrophy, observed at 7 and 12 wk of training, failed to potentiate the metabolic response. No effect of HRT was found onV˙o 2 peak with training (41.2 ± 2.9 vs. 41.0 ± 2.1 ml ⋅ kg−1 ⋅ min−1) or on the steady-state, submaximal exercise rate of oxygen consumption. It is concluded that the HRT results in muscle metabolic adaptations that occur independently of fiber hypertrophy.
High-resistance training and muscle metabolism during prolonged exercise
