Some evidence suggests that resistance training may lower relative muscle mitochondrial content via "dilution" of the organelle in a larger muscle fibre. Such an adaptation would reduce fatigue resistance, as well as compromise oxidative ATP synthesis and the capacity for fatty-acid oxidation. We investigated the effect of resistance training on mitochondrial enzymes of the citric acid cycle (citrate synthase; CS) and beta-oxidation (beta-hydroxyacyl CoA dehydrogenase; beta-HAD), as well as markers of the potential for glucose phosphorylation (hexokinase; HK) and glycolysis (phosphofructokinase; PFK). Twelve untrained men (21.9 +/- 0.5 y; 1.79 +/- 0.03 m; 83.2 +/- 3.2 kg) participated in a 12 week progressive resistance-training program. Muscle biopsies were taken from the vastus lateralis before (PRE) and after (POST) training. Training increased mean muscle fibre cross-sectional area (p < 0.05) and the activities of CS (PRE = 4.53 +/- 0.44 mol.kg protein(-1).h(-1); POST = 5.63 +/- 0.40 mol.kg protein(-1).h(-1); p < 0.001) and beta-HAD (PRE = 2.55 +/- 0.28 mol.kg protein(-1).h(-1); POST = 3.11 +/- 0.21 mol.kg protein(-1).h(-1); p < 0.05). The activity of HK increased 42% (p < 0.05), whereas the activity of PFK remained unchanged. We conclude that resistance training provides a stimulus for improving muscle oxidative potential, as reflected by the increased activities of CS and beta-HAD following resistance training induced hypertrophy.