Isometric electrical stimulation was delivered to rabbit dorsiflexor muscles at 10 Hz for 1 s on and 1 s off over 30 min, 5 days/wk for 3 wk to induce an increase in muscle oxidative capacity. Stimulation-trained muscles as well as untrained muscles were then subjected to a 30-min eccentric exercise bout to test whether increased oxidative capacity provided a protective effect against muscle injury. Electrical stimulation resulted in significant training of both the extensor digitorum longus (EDL) and tibialis anterior (TA) muscles, with EDL citrate synthase (CS) activity increasing an average of 67% (P < 0.0001) and TA CS activity increasing by 27% (P < 0.05). For all parameters measured, the magnitude of change was much greater for EDL than for TA muscle. Dorsiflexor fatigability decreased significantly during the 3-wk training period (P < 0.0001), whereas the EDL and TA individually showed strong decreasing trends in fatigability after training. TA and EDL capillary density measured histomorphometrically increased from 839 ± 56 to 1,026 ± 71 mm² (P = 0.07) and from 589 ± 37 to 792 ± 66 mm² (P < 0.05), respectively. TA and EDL capillary-to-fiber ratio increased from 1.32 ± 0.10 to 1.55 ± 0.16 (P > 0.2) and 1.08 ± 0.07 to 1.36 ± 0.14 (P > 0.1), respectively. Type 2A fiber type percentage increased after stimulation training by 68% (P < 0.0001) for the EDL and by 32% (P > 0.1) for the TA at the expense of type 2D fibers. Despite the large training effect for the EDL and the modest training effect for the TA, no differences were observed between stimulation-trained and untrained groups for maximum dorsiflexion torque (P > 0.3) or maximum tetanic tension (P > 0.3) after eccentric contraction-induced injury. Additionally, no significant correlation was observed between CS activity and maximum tetanic tension after eccentric contraction-induced injury for either muscle (P > 0.2). Thus we conclude that increasing muscle oxidative capacity by isometric electrical stimulation training did not protect muscle against eccentric contraction-induced injury.