The effects of marked muscle hypertrophy induced by chronic resistance training on oxidative function were evaluated in 11 young resistance-trained athletes (RTA) and 11 controls (C). Pulmonary O₂ uptake (V'O₂) and skeletal muscle (vastus lateralis) fractional O₂ extraction (by near-infrared spectroscopy) were determined during incremental cycle ergometer (CE) and one-leg knee-extension (KE) exercises. Mitochondrial respiration was evaluated by high-resolution respirometry in saponin-"skinned" vastus lateralis fibers obtained by biopsy.

MRI-determined quadriceps femoris (QF) cross sectional area was higher in RTA (129±5 cm²) vs. C (94±4). Peak V'O₂ was lower in RTA vs. C, both during CE (39.6±1.6 mL/min/kg vs. 45.9±0.9, respectively) and KE (49.4±2.3 mL/min/100g of QF mass vs. 61.7±3.6). Peak fractional O₂ extraction was lower in RTA vs. C, both in CE (53±3%vs. 72±3) and in KE (51±3%vs. 73±4). Maximal ADP-stimulated mitochondrial respiration was higher in RTA (56.7±7.1 pmolO₂/s/mg wet weight) vs. C (35.6±3.1); the coupling between oxidation and phosphorylation was higher in RTA.

Peak oxidative function in vivo was impaired in RTA, also after eliminating, by the adopted KE protocol, constraints related to cardiovascular O₂ delivery. However, maximal ADP-stimulated mitochondrial respiration in isolated fibers, in conditions of unlimited O₂ availability, was higher in RTA. The main limitation to oxidative function in RTA in vivo may reside in peripheral O₂ diffusion.

Supported by ASI-OSMA I/007/06/0 - WP 1B-32-1